Biophysical Foundations of Human Movement

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.

Age-Related Changes in the Skeletal and Articular Systems

For the musculoskeletal system, the major periods of growth are the fetal and pubertal stages. During the early fetal growth period there is rapid multiplication of cells (hyperplasia), whereas during the pubertal period growth is caused mainly by development and enlargement of existing cells (hypertrophy). Development can also occur via the replacement of one type of tissue by another.

Stages in the Development of Bone

Adult human bones appear in a variety of shapes and sizes. Their basic shape is genetically determined, but their final shape is influenced greatly by the environment in which they develop. Environmental influences include mechanical factors, such as muscle forces acting on the developing bone, and metabolic factors, which include the supply of nutrients.

Typical long bones, such as the humerus in the arm and the femur in the thigh, develop via a process of endochondral ossification in which a cartilaginous model precedes the bone formation. The cartilage is eventually replaced by bone. The cartilage model initially is small, and its replacement by bone begins at an early stage of development. The primary ossification centres appear near the middle of the shaft of the future long bone at about 8 wk after fertilisation, when the embryo is about 35 mm (1.4 in.) long (see figure 5.1).

The cartilage model of the future bone grows before it is replaced by bone. This replacement occurs in a series of stages. Initially, the cartilage model grows by two processes: an increase in the number of cartilage cells and then an increase in the size of each cell. Next, the gel-like matrix surrounding the cartilage cells is calcified. This hardening of the tissue surrounding the cells effectively cuts off their supply of nutrients and prevents the removal of metabolic waste products. These imprisoned cartilage cells eventually die so that the calcified cartilage has a honeycomb appearance. Invading blood vessels bring nutrients and bone-forming cells (osteoblasts) to the calcified cartilage to lay down new bone. This new bone has a disorganised appearance. If ossification were the final stage, a long bone would not develop its hollow structure. What happens instead is that some of the newly laid bone is removed from internal sites by special bone-eroding cells. These osteoclasts work with osteoblasts during remodelling of the bone, causing the cortex to drift away from the central axis of the shaft during growth. Changes in shaft diameter and compact bone thickness can occur at any age by a remodelling process. Bone can respond to changes in mechanical stimuli by changing its structure.

One type of remodelling that occurs is the replacement of the originally laid bone by compact bone that has an organised structure (figure 3.1). Most primary centres of ossification (in the developing shaft) appear before birth, whereas most secondary centres of ossification (in the developing ends of the bone) appear after birth. The times of appearance of these secondary centres of ossification vary widely. The centre in the femur near the knee is normally present at birth, but the centre in the clavicle (collarbone) closest to the sternum (breastbone) does not appear until about 18 yr of age.

Growth in Length and Width of Bone

When both the shaft and ends of a long bone are developing they are separated by a growth plate, or epiphyseal plate. In this region, all the stages of bone development can be seen under a microscope (see figure 5.2). Each zone in figure 5.2 represents a stage in the growth of bone and then replacement of cartilage by bone; that is, the zones illustrated do not migrate downward, but rather retain their position and change their nature. This effectively increases the distance between the growth plates at each end of the bone. The process illustrated continues for almost 20 yr. Growth in length of the long bones ceases when the process stops and epiphyseal plates fuse and disappear. Actually, the growth stops because the cartilage cells no longer respond to hormonal influence.

http://www.humankinetics.com/AcuCustom/Sitename/DAM/093/fig_5_Main.2.png

Although growth in height ceases at a certain age, changes in thickness of the compact bone of the shaft and the density of spongy bone can occur at any time of life (see chapter 6). Growth in the thickness and diameter of long bones occurs by appositional growth. In this process, bone is normally added on the outside of the shaft and removed from the inside of the shaft.

Skeletal Composition Changes Across the Life Span

The relative proportions of the inorganic salt crystals and the organic collagen change throughout the life span. In a child, the flexibility of the bone is related to the large proportion of collagen. It is thought that the rapid growth of children's bones and the consequent amount of remodelling results in less-than-optimal mineralisation. In a newborn baby, the skeleton accounts for about 13% of the total body weight, but about two-thirds of the skeleton is cartilaginous.

In bone of a young adult the inorganic material is close to the optimal two-thirds mineralisation, so the bone is strong and tough. Though the proportion of skeletal material in the mature adult is also about 13% of total body weight, just over 10% of the skeleton is cartilaginous. Of the bone, four-fifths is compact and one-fifth is spongy.

Eventually, aged bone becomes brittle. This change relates partly to the increased proportion of the inorganic salts, but of more significance is the reduced total mass of bone material in the aged musculoskeletal system. Bone mass decreases mainly because of a decrease in the number of trabeculae in spongy bone (see “In Focus: Why Trunk Height Decreases With Ageing”) combined with resorption and consequent thinning of the trabeculae. In compact bone, the size of the Haversian canals (see figure 3.1) increases and the cross-sectional area of the bone surrounding each Haversian canal decreases. This increased porosity of bone, in turn, causes decreased bone density (mass per unit volume of tissue). In an 80-yr-old male the density of bone in the spine is often 55% of the value found in a 20-yr-old; in females who are elderly, it is often only 40% of its peak value. With ageing, bone also becomes stiffer, partly because of the collagen cross-linking. A consequence of these mechanical changes is that aged bone can absorb less energy before it fractures, so it is more liable to fail when subjected to large forces.

Osteoporosis

For most tissues in the body, their mass at any time is determined by the balance between the simultaneous formation and destruction of the tissue. Osteopenia (“bone poverty”) is reduced bone density, particularly in women during the postmenopausal years, when the dramatic decrease in the female hormone estrogen allows the rate of synthesis to be lower than the rate of resorption. The initial effects are mainly to the spongy bone, but later the compact bone in the shafts of long bones also decreases in thickness.

According to the World Health Organization, osteoporosis (“bone porosity”) is present when the bone density is more than 2.5 standard deviations below the average bone mass of a young adult woman. In general, the porosity of bone in the human femur doubles from 40 to 80 yr of age and people with osteoporosis show an even greater change. Thus, osteoporotic bone is even less able to absorb energy before it fails than is normally aged bone. Moreover, even though a chemical analysis of osteoporotic bone material may indicate slightly increased levels of calcium per unit mass of bone, the overall mass of bone decreases so markedly that there is less calcium stored in the skeleton overall.

During maturation, the density and calcium content of bones is increased due to genetic predisposition aided by the interaction between dietary calcium and exercise. It is now thought that peak bone mass occurs at about 16 to 20 yr of age in women, so some health authorities claim osteoporosis is a pediatric disease and have promoted the idea of “bone banks” to help prevent osteoporosis. The idea is that if a person's lifestyle during maturation and early adulthood promoted maximum deposition of bone material, then later in life, when withdrawals of bone material are inevitable, the structural integrity of the bones will be maintained longer. Financial advisers tell everybody to start saving as young as possible, and this concept is even more important for prevention of osteoporosis.

Osteoporosis is commonly associated with women, but the prevalence among men is now the same as it was in women about 25 yr ago. This trend has been attributed to lifestyle changes, which include inadequate intake of calcium and less-than-optimal levels of physical activity. The personal lifestyle changes due to osteoporosis and the public health care costs of osteoporosis are so great that they are considered further in chapter 23.

Bone Failure in Relation to Bone Development, Age, or Activity

The modern automotive industry attempts to protect passengers by enclosing them in a cage that is lined by material that cushions the forces involved in a collision. In similar fashion, the soft tissues of the human body, including fat and muscle, perform the role of a crumple zone. However, despite this protection, sometimes the energy involved in a mishap is enough to cause a fracture anyway. Bone failure may be related to bone development, age, or activity.

Certain types of fractures are associated with particular stages of development. The flexible bones of a child tend to splinter in a manner similar to the broken branch of a growing tree; this type of fracture is called a greenstick fracture. Late in life the fracture is more likely to be of the brittle type because of the increased stiffness of old bones. The bones of adults who are elderly are also more likely to fail because of the decreased bone mass and density in osteoporosis.

Specific fractures are related to certain ages. For example, fractures of the neck of the femur (commonly called hip fractures) are common in women in the elderly population. Incidence of forearm fracture increases near the peak of the pubescent growth spurt. This is associated with increased porosity of compact bone as the remodelling space increases to provide calcium to the rapid-growth regions. A second increase in wrist fractures is seen in women who are elderly; this is related to the combination of osteoporosis and increased incidence of falls. In developing children, the cartilaginous growth plate may also fail; this most often occurs at the zone of maturation, or hypertrophy (see figure 5.2).

The development of bone has implications for potential injury to the musculoskeletal system. For example, injury to the cartilaginous growth plates can be produced by single excessive forces causing trauma or by repetitive compressive forces, or tensile forces produced by muscle-tendon pull on an area of developing bone.

In sports medicine, specific injuries have been attributed to certain activities. One of the best examples is Little League elbow, described in more detail in chapter 24. Other examples of the relationships between activity and types of growth-plate problems are wrist injuries in gymnasts and tibial tuberosity avulsions in sports involving sprinting and jumping. Pain over the tibial tuberosity (just below the knee cap) in a prepubescent child is indicative of Osgood-Schlatter's condition.

Effects of Various Factors on Range of Motion

Range of motion at joints is affected by joint structure and the mechanical properties of the tissues associated with the joints. A general perception is that joint range of motion decreases during life. Although this is the general trend, the rate of loss is not constant. Ranges of joint motion are very large in a newborn baby. As an example, the range of ankle dorsiflexion in a newborn is limited only by the contact of the top of the foot against the shin. Try this movement yourself to indicate how much flexibility you have lost since birth.

Between the ages of 6 and 15 yr, there is a general trend for joint range of motion to decrease in boys, whereas for girls the effects are variable and joint dependent. Girls are generally more flexible than boys during childhood and adolescence. Changes in joint ranges of motion between adolescence and young adulthood are variable and, as discussed in chapter 6, appear to be related to physical activity. Similarly, the general trend for joint flexibility to decrease during ageing may not be completely explained by biological ageing processes.

Ageing people may suffer arthritis (“inflammation of joints”), which markedly restricts range of motion. Rheumatoid arthritis involves inflammation of the synovial membrane, while osteoarthritis involves degeneration of the articular cartilage (see figure 3.6). In the total adult population, about three times as many women have osteoarthritis as do men. Thus there is some genetic determination of osteoarthritis, to which are added the effects of environmental factors. It would appear that the risk factors for rheumatoid arthritis are mainly related to a family history of the condition.

Age-Related Changes in the Muscular System

Mesoderm, which forms toward the end of the third week of development, eventually forms the muscle and connective tissues of the body. Some of the mesoderm is segmented such that it is in lumps on either side of the midline, and these lumps form the muscles of the trunk. Other mesoderm forms the muscles of the limbs; this tissue migrates into the limbs when they first appear. Limb muscles migrate toward their final position during further development.

Certain precursor cells differentiate into myoblasts (muscle-forming cells) that fuse longitudinally to form the long muscles and muscle fibres we can observe. The number of muscle fibres appears to be genetically determined so that large people often have more muscle fibres than persons who are smaller in stature. As muscles grow in length, the number of sarcomeres increases. Although direct evidence is sparse, many believe that the stimulus for growth of muscle is the bone growth that pulls on the attached ends of the muscle. Developmental growth occurs in both muscle length and cross-sectional area, and these factors may also be affected by activity. The effects of physical training on muscle is summarised in chapters 6, 10, and 13.

In an infant, muscle tissue accounts for about 25% of total body weight, but in a young adult the proportion of muscle is more than 40%. In terms of growth, muscle increases from about 850 g (1.9 lb) at birth to about 30 kg (66 lb) in a young adult male weighing 70 kg (154 lb).

Strength, which may be defined as the capacity to produce force against an external resistance, is related to the cross-sectional areas of the muscles producing the force. Muscle volume peaks at about 30 yr of age and then gradually decreases. The atrophy of skeletal muscle associated with disuse is much faster than any ageing-related atrophy. Muscle elasticity also decreases during ageing so that muscles are stiffer and less extensible. This is one contributing factor to the loss of joint range of motion described earlier.

Biomechanical Adaptations to Injury

Adaptations are common following injury and surgical treatment. One interesting example found in the orthopaedics literature is a phenomenon known as quadriceps avoidance gait. This particular adaptation occurs in ACL-deficient (ACLD) patients; that is, patients who have suffered a complete rupture of the ACL. ACLD patients usually have difficulty with movements involving either lateral thrusts (e.g., cutting from side to side) or twisting (i.e., rotation of the femur relative to the tibia in the transverse plane).

Gait analysis has been done on ACLD patients during various activities of daily living, including level walking, jogging, walking up and down stairs, and even running, cutting, and pivoting. Kinematic and force-plate data were used to estimate the net muscle moments exerted at the knee in all three planes of movement: flexion-extension, abduction-
adduction, and internal-external rotation. Interestingly, the greatest functional changes between ACLD patients and healthy subjects occurred while walking at preferred speeds on level ground. During the midstance portion of the gait cycle, the ACLD patients exhibited a net extensor moment that was significantly lower than normal (figure 10.9, solid line). One interpretation of these findings is that the ACLD patients walk by reducing the demand on their quadriceps during stance (i.e., the quadriceps muscles are activated less in the ACL-deficient patients, giving rise to a quadriceps-avoidance gait pattern).

It is important to realise that a lower net extensor moment at the knee does not necessarily mean that the moment exerted by quadriceps is lower. Because the net moment at the knee is a combination of quadriceps and hamstrings muscle action, a lower extensor moment could result from an increase in the flexor moment applied by hamstrings. However, muscle electromyography results tend to support the interpretation that quadriceps moment is lower because the activation level of the quadriceps is lower in the ACLD patients.

Gait analysis results have also shown that the ACLD patients reduce their net extensor moment by 25% during jogging compared with a 100% reduction in walking. However, the net extensor moment in stair climbing was the same in ACLD patients and normal subjects. When taken together, these results suggest that the observed quadriceps avoidance in ACLD patients is not a result of quadriceps weakness but rather is due to a change in neuromuscular control.

Dependence of Motor Performance on Changes in Muscle Properties

Strength and quickness are critical determinants of performance in explosive movements such as jumping, throwing, and sprinting. Together, these two factors determine the amount of power developed instantaneously during a task (i.e., muscle power is given by the product of muscle force and muscle contraction speed; see “In Focus: At What Speed Must a Muscle Shorten to Develop Maximum Power?”). As discussed earlier in this chapter, resistance strength training can alter both muscle force and fibre contraction speed. This section describes the effects that changes in the contractile properties of muscle have on motor performance, specifically, how biomechanical performance depends on muscle strength and muscle fibre contraction speed.

Vertical jumping is one of the most heavily studied motor tasks. Many scientists have studied jumping with the aim of learning more about the biomechanics and control of this task and, specifically, how performance may be influenced by training. In a recent jump-training program that incorporated stretching, plyometric exercises, and weight lifting, female high school volleyball players demonstrated a mean increase of 4 cm (1.5 in.) in jump height after training. This represented an almost 10% increase in jump height as a result of the 6 wk period of training. Even larger increases in vertical jumping performance have been documented in the literature. One extreme example is the 1984 United States Olympic gold medal volleyball team, which showed a 10 cm (4 in.) increase in jump height after 2 yr of jump training.

Using Computer Modelling to Study Vertical Jumping Performance

It is gratifying to learn that jumping performance can be increased significantly by strength and neuromuscular training. However, it is difficult, if not impossible, to explain why these increases occur. Noninvasive measurements of biomechanical performance cannot pinpoint the factor or factors responsible for the increase in jump height. The reason is that several properties of the neuromuscular and musculoskeletal systems change simultaneously during the training regimen. Alternatively, computer models may be used to study the relationships between training effects and performance; that is, a model of the neuromusculoskeletal system may be used to predict how changes to specific parameters affect the performance of a motor
task.

Models of the body similar to the one shown in figure 8.7 have been used to study how changes in muscle strength, muscle contraction speed, and motor unit recruitment affect jump height. The values of each of these parameters in the model were increased by amounts consistent with results obtained from strength-training programs. For example, the peak isometric strength and maximum shortening velocity of each muscle in the model were increased by 20% and the activation level of each muscle was increased by 10%. The three training effects were first applied to all muscles simultaneously and then to the ankle plantarflexors, knee extensors, and hip extensors separately. In this way, the modelling results were used to determine whether it is better to train all the leg muscles simultaneously or to isolate specific muscle groups such as the quadriceps (knee extensors) and gluteus maximus (hip
extensors).

Insights Into the Effects of Training Provided by Computer Models

Increasing the peak isometric force of all the leg muscles in the model by 20% produced the largest increase in jump height. In this case, jump height increased by 7 cm, or 5% of that obtained before the simulated training effect. Increasing the maximum shortening velocity of each muscle by 20% or the activation level of each muscle by 10% increased jump height by only 4 cm, or 3% of that obtained for the nominal (untrained) model. When all three training effects were introduced simultaneously, jumping performance increased by nearly 17 cm, or 12% of that calculated for the untrained model. Thus, training programs that increase strength, fibre contraction speed, and motor recruitment (i.e., activation level) of all the leg muscles simultaneously are most beneficial to overall jumping performance.

The modelling results also suggest that training the knee extensors is better than training either the ankle plantarflexors or the hip extensors. When peak isometric force and maximum shortening velocity of the quadriceps were increased by 20% and quadriceps activation was simultaneously increased by 10%, jump height increased by almost 10 cm, or 7% of the value calculated for the untrained model. The same changes made to either the ankle plantarflexors or the hip extensors produced increases in jump height of only 3 cm, or 2% of the value obtained for the untrained model.

The latter result is a little puzzling because the model calculations had previously shown that the quadriceps and gluteus maximus are the major energy producers—the prime movers—of the body in vertical jumping (see “In Focus: Which Muscles Are Most Important to Vertical Jumping Performance?” in chapter 8). It should be noted here that each time a change was introduced to the model, a new optimal pattern of muscle activations was found by re-solving the optimisation problem for a maximum-height jump. Thus, one interpretation of the result is that what matters most in terms of performance is the quadriceps:gluteus maximus muscle strength ratio and not the absolute strength of these muscles. In other words, jumping performance is most sensitive to a change in the knee-extensor:hip-extensor muscle strength ratio. Increasing quadriceps strength by 20% increases the knee-extensor:hip-extensor muscle strength ratio in the model, whereas increasing gluteus maximus muscle strength decreases this ratio. The same line of reasoning may be used to explain why increasing ankle plantarflexor muscle strength by 20% leads to an increase in jump height of just 3 cm in the model.

Training for strength is also better than training for quickness or speed. Figure 10.10 shows the effects of increasing muscle strength and muscle contraction speed on vertical jump height as predicted by the four-segment, eight-muscle, sagittal-plane model of the body described in chapter 8 (see figure 8.7). An increase in muscle strength was simulated in the model by simultaneously increasing body weight because muscle strength increases in proportion to muscle mass. Thus, changes in body strength:weight ratio are represented in figure 10.10 rather than changes in muscle strength alone. Also, jumping performance is normalised in these results by dividing by the value of jump height calculated for the untrained model. Similarly, body strength:weight ratio and muscle contraction speed are each normalised by dividing by the value of body strength:weight ratio and muscle contraction speed in the untrained model, respectively.

The simulation results show that the slope of the line predicted for changes in body strength:weight ratio is twice as large as that obtained when changes in muscle fibre contraction speed are made (compare solid and dashed lines in figure 10.10). Thus, muscle strength has a greater effect on vertical jump height than muscle fibre contraction speed, even when the accompanying increase in body mass is taken into account.

Another important lesson learned from the modelling studies is that musculoskeletal changes must be accompanied by appropriate changes in neuromuscular control; otherwise, the expected improvement in motor performance will not be seen. In vertical jumping, if the pattern of muscle activations remains unchanged subsequent to strength training, jump height actually decreases relative to the untrained state. Figure 10.11 shows a simulated jump in which the strength of the knee-extensor muscles has been increased by 20% but the control exerted over the joints is the same as that calculated for the untrained model before the training effect was introduced. When the pattern of muscle activations was not optimised to match the changes introduced to the neuromusculoskeletal model, the body left the ground prematurely (i.e., the centre of mass was at a lower height at liftoff than is optimal for a maximal jump).

One consequence of not optimising the pattern of muscle activations (i.e., the controls) is that a larger fraction of the total work produced by the muscles goes into rotating the body segments rather than accelerating the centre of mass upward. In a maximum-height jump, approximately 90% of the total work done by the leg muscles is used to propel the centre of mass upward. This number is closer to 80% when muscle coordination (i.e., the sequence and timing of muscle activations) is not optimal. So, even though jumping performance depends heavily on muscle strength, and to a lesser extent on muscle fibre contraction speed, optimal performance is also intimately related to neuromuscular control. For this reason, and as discussed at the beginning of this chapter, jump-training programs now focus on maneuvers that blend muscle strength with neural control.

Summary

Training can change both muscle strength and fibre contraction speed. Strength may be increased by increasing motor unit recruitment (net neural drive to the muscle) or by increasing muscle fibre size. Contraction speed may be altered by changing the shape of a muscle's force-velocity curve or by changing the value of its intrinsic maximum shortening velocity. Early in a training program (2-8 wk), increases in muscle strength are brought by neural adaptations rather than by increases in muscle size. Training can also change the way muscle action is coordinated during activity (i.e., neuromuscular control). Neuromuscular training programs are usually designed to improve stability (balance and coordination) and proprioception (joint position sense) in addition to muscle strength. Training is vital for improving biomechanical performance and for preventing injuries during sport.