- Home
- Strength Training and Conditioning
- Physiology of Sport and Exercise
- Other Sports and Activities
- Kinesiology/Exercise and Sport Science
- Fitness and Health
- Athletic Training and Therapy
- Science and Application of High Intensity Interval Training
Science and Application of High Intensity Interval Training
Solutions to the Programming Puzzle
by Paul Laursen and Martin Buchheit
672 Pages
The popularity of high-intensity interval training (HIIT), which consists primarily of repeated bursts of high-intensity exercise, continues to soar because its effectiveness and efficiency have been proven in use by both elite athletes and general fitness enthusiasts. Surprisingly, few resources have attempted to explain both the science behind the HIIT movement and its sport-specific application to athlete training. That’s why Science and Application of High-Intensity Interval Training is a must-have resource for sport coaches, strength and conditioning professionals, personal trainers, and exercise physiologists, as well as for researchers and sport scientists who study high-intensity interval training.
Authors Paul Laursen and Martin Buchheit—both well-known, expert-level HIIT researchers as well as practitioners and endurance athletes—do a masterful job of blending science-based concepts of HIIT with practical application strategies. Laursen, Buchheit, and a team of highly qualified contributors—who bring hundreds of years of combined HIIT science and application experience from across all sports—have written Science and Application of High-Intensity Interval Training to provide practitioners and athletes an understanding of the foundational principles of HIIT programming. Chapters in the first section describe five types of training, how to manipulate HIIT variables to maximize improvements in physical performance, and how to incorporate HIIT into a general training program. Readers will also learn the influence HIIT can have on fatigue, stress, and an athlete’s overall health.
The final 20 chapters each focus on a different sport and are written by leading coaches or practitioners who have successfully applied HIIT principles at an elite level in their respective sport. These chapters describe specific ways to incorporate HIIT into a training regimen for everything from combat sports to endurance events to the most popular U.S. and international individual and team sports. Each chapter also contains sport-specific preparation and competition phases, an overall one-year training program, and a brief story of how the coach or practitioner who authored the chapter used HIIT to successfully prepare an athlete for a competition.
Knowing the proper ways to incorporate high-intensity interval training into a fitness or conditioning program is of vital importance: Not following proper protocols can lead to excessive and prolonged fatigue, illness, or injury. Science and Application of High-Intensity Interval Training is an essential guide for those who want to incorporate HIIT into their own training or their athletes’ programming.
Earn continuing education credits/units! A continuing education course and exam that uses this book is also available. It may be purchased separately or as part of a package that includes all the course materials and exam.
Chapter 1. Genesis and Evolution of High-Intensity Interval Training
Paul Laursen and Martin Buchheit with contributions from Jean Claude Vollmer
Chapter 2. Traditional Methods of HIIT Programming
Martin Buchheit and Paul Laursen
Chapter 3. Physiological Targets of HIIT
Martin Buchheit and Paul Laursen
Chapter 4. Manipulating HIIT Variables
Martin Buchheit and Paul Laursen
Chapter 5. Using HIIT Weapons
Martin Buchheit and Paul Laursen
Chapter 6. Incorporating HIIT Into a Concurrent Training Program
Jackson Fyfe, Martin Buchheit, and Paul Laursen
Chapter 7. HIIT and Its Influence on Stress, Fatigue, and Athlete Health
Philip Maffetone, Paul Laursen, and Martin Buchheit
Chapter 8. Quantifying Training Load
Martin Buchheit and Paul Laursen
Chapter 9. Response to Load
Martin Buchheit, Paul Laursen, Jamie Stanley, Daniel Plews, Hani Al Haddad, Mathieu Lacome, Ben Simpson, and Anna Saw
Chapter 10. Putting It All Together
Paul Laursen and Martin Buchheit
Part II. Sport-Specific Application of High-Intensity Interval Training
Chapter 11. Combat Sports
Duncan French
Chapter 12. Cross-Country Skiing
Øyvind Sandbakk
Chapter 13. Middle-Distance Running
Jean Claude Vollmer and Martin Buchheit
Chapter 14. Road Running
Jamie Stanley and Carlos Alberto Cavalheiro
Chapter 15. Road Cycling
Marc Quod
Chapter 16. Rowing
Daniel Plews
Chapter 17. Swimming
Tom J. Vandenbogaerde, Wim Derave, and Philippe Hellard
Chapter 18. Tennis
Jamie Fernandez-Fernandez
Chapter 19. Triathlon
Daniel Plews and Paul Laursen
Chapter 20. American Football
Johann Bilsborough and Moses Cabrera
Chapter 21. Australian Football
Aaron Coutts, Joel Hocking, and Johann Bilsborough
Chapter 22. Baseball
Robert Butler and Matt Leonard
Chapter 23. Basketball
Xavi Schelling and Lorena Torres-Ronda
Chapter 24. Cricket
Carl Petersen and Aaron Kellett
Chapter 25. Field Hockey
Dave Hamilton
Chapter 26. Ice Hockey
Matt Nichol
Chapter 27. Handball
Martin Buchheit
Chapter 28. Rugby Union
Nick Gill and Martyn Beaven
Chapter 29. Rugby Sevens
Nick Poulos
Chapter 30. Soccer
Martin Buchheit, Mathieu Lacome, and Ben Simpson
Paul B. Laursen, PhD, is an endurance coach, a sport scientist, and an adjunct professor for Auckland University of Technology in New Zealand. He earned his doctorate in exercise physiology from the University of Queensland, was formerly the physiology manager for High Performance Sport New Zealand, and now resides in British Columbia, Canada.
Laursen is well known throughout the international sport and strength and conditioning communities for his knowledge and research of high-intensity interval training. His other interests include health, longevity, heart rate variability, thermoregulation, and artificial intelligence application to training. He has published more than 125 peer-reviewed manuscripts in exercise and sport science journals; his publications with coauthor Martin Buchheit are among the most cited. He is an active endurance athlete, having completed 18 Ironman triathlons.
Martin Buchheit, PhD, is a sport scientist, a strength and conditioning coach, and the head of performance for the Paris Saint-Germain Football (Soccer) Club. He is also an adjunct associate professor of exercise science for Victoria University in Australia. He previously worked as an exercise physiologist for ASPIRE Academy in Qatar, and he has served as a lecturer, consultant, and strength and conditioning coach for various organizations.
Buchheit received his doctorate in physiology from the University of Strasbourg in France. He has published more than 160 peer-reviewed manuscripts, with much of his research focusing on high-intensity interval training. The training tools he has developed include the 30-15 intermittent fitness test, used to program high-intensity training, and the 5-5 running test, used to monitor training status using heart rate variability. Buchheit also has experience with match analysis and talent development and identification. He is an endurance athlete who has a personal best time of 2:54 in the marathon.
“The mix of science and practical experience in Science and Application of High-Intensity Interval Training makes it the definitive guide to getting the most out of your interval training.”
Alex Hutchinson—Author of Endure: Mind, Body, and the Curiously Elastic Limits of Human Performance
“Science and Application of High-Intensity Interval Training, written by world-class scientists and practitioners, is an authoritative guide to both the evidence and the delivery of conditioning programs. It will become one of the most dog-eared books on my shelf.”
David Joyce—Head of Athletic Performance for the GWS Giants Football Club and Editor of High-Performance Training for Sports
“With Science and Application of High-Intensity Interval Training, Paul Laursen and Martin Buchheit provide the definitive training guide for athletes and coaches of all levels.”
Steve Magness—Head Coach for the University of Houston Cross Country Team and Author of The Science of Running
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Nutrition's effects on HIIT
It’s no secret that we all have to eat to survive. You wouldn’t be reading this otherwise.
It's no secret that we all have to eat to survive. You wouldn't be reading this otherwise. Nutrition provides needed energy, the water that makes up the body, as well as everything we need to run our bodies (micronutrients, etc.). While this book is not about nutrition, nutrition clearly has an influence on the physiological effect of an HIIT bout, which is why we are covering it. While there are likely other subtle effects that can be caused by manipulating other dietary nutrients, including supplements, we will focus on what we believe are the key nutrient manipulations influencing physiological effects. These include the dietary carbohydrate availability, hydration status, and caffeine intake. Chapter 7 additionally explores some of the common pitfalls and detrimental effects a poor diet has on performance. Like environment, nutrition is an additional area that can help us make further benefits in training, if well manipulated.
Carbohydrate Availability
Carbohydrates are plant-derived sugars that come in a variety of forms. At the simplest level, and the level to which all carbohydrates are broken down eventually, is the compound glucose, a six-carbon molecule. Glucose is a primary metabolic fuel used by all cells to give us energy. Specifically it is the fuel of use for the process of anaerobic and aerobic glycolysis (chapter 3).
Notwithstanding the profound individual variance in the blood glucose response to the consumption of foodstuffs, there are some general principles we might appreciate around the topic of nutrition, acknowledging that refinement and optimization will exist at a monitored individual level. In the context of most athletes habituated to a mixed-Western diet high in carbohydrates, the act of lowering carbohydrate availability can create stress on (among others) muscle and nerve cells. The resultant lowered level of blood glucose, termed hypoglycemia, acutely creates a perceived feeling of fatigue and a reduced motivation to exercise. Ultimately this global effect of the lowered basal blood glucose level reduces systemic central nervous system activation. Under such conditions, acute high-intensity exercise capacity is typically reduced.
While high-intensity exercise capacity is typically lowered in the acute state, such a state can create an advantaged adaptive condition. Lower blood glucose concentrations reduce glycolytic capacity, which drives AMPk signaling for associated benefits (mitochondrial biogenesis and enhanced fat oxidation rates; chapter 3). The condition also makes training harder, without increasing mechanical (musculoskeletal and neuromuscular) load, which is something we often want during a training session. Alternatively, the condition can be nonoptimal in the context of the training condition, and could acutely impair aspects such as mood, confidence, coordination, agility, judgment, game intelligence, learning, and so forth.
A number of methods can be used to lower carbohydrate availability. The most obvious is to lower carbohydrate consumption in the diet. This can be challenging for many athletes as it requires nutrition knowledge, and as mentioned, the individual response to foodstuffs is extremely variable. The social aspect of food (i.e., habits, eating what others eat, eating what someone serves you, etc.) and access to appropriate foods (low-carbohydrate foods can be difficult to source in many places) additionally make this intervention difficult. Typically, when lowering carbohydrate content from the diet, additional calories need to come from somewhere, and generally speaking this largely will come from fat, a concept that can be difficult for many to appreciate based on tradition, ingrained mind models, or instilled beliefs surrounding the effect of dietary fat on health. Regardless, a number of methods can be used to manipulate systemic levels of carbohydrate content or blood glucose, including eating low-carb high-fat (LCHF), fasting, and sleeping low.
Low-Carbohydrate High-Fat (LCHF) Diet
The low-carbohydrate high-fat diet is just what it sounds like. With protein levels similar to that of a typical mixed Western-based or high-carbohydrate diet (about 20%), fat calories are increased toward 70%, with carbohydrate content falling to 10%, or below 100 g in a given day. The LCHF diet has received considerable attention in social media, but few studies have assessed its effects. In most studies that have examined the impact of an LCHF diet on high-intensity performance, the time course has been relatively short (3 d to 3 wk). For example, when Havemann et al. examined high- versus low-carbohydrate diets over 6 d in cyclists, overall 100 km performance time was not different; however, high-intensity 1 km sprint performance during the time trial was impaired on the high-fat relative to the high-carbohydrate diet. As well, the authors found significant increases in HR and effort perception with the LCHF diet after 6 d. However, as with training adaptation, which requires long periods of adaptation, dietary adaptation may follow a similar time course. To address this discrepancy in the literature, Cipryan et al. recently had recreationally trained participants change from their habitual mixed Western-based diet to a ketogenic (<50 g CHO) diet over a 4 wk period. After this 4 wk period, performance and cardiorespiratory responses during a graded exercise test and HIIT were not impaired in the LCHF diet group. The LCHF group did, however, substantially increase their rates of fat oxidation. While more research is needed, it appears that short-duration time course adaptation periods can compromise HIIT performance, with adaptation requiring at least 4 wk. Additionally, LCHF diets substantially enhance fat oxidation, which is of importance for fatigue resistance and prolonged exercise performance.
Fasted Training
Fasted training is simply that—training in the fasted state. This can occur any time we decide not to eat for a given time period. Under the fasted condition, blood glucose and insulin levels drop and fat oxidation rates increase to meet the energetic demands. When we train under such a condition, we drive further the fat adaptations previously mentioned with the LCHF diet and with high-intensity training even more so (increased AMPk signaling). Anecdotally speaking, this is a common approach to training for many athletes, especially endurance specialists.
Sleeping Low
When we feed in the evening (typical) and we go to sleep, we are in effect fasting. When we wake, still in the fasted state before breakfast, we can train without breakfast and we are in effect typically already 8 h fasted. Lowering carbohydrate content in the evening meal, which can subsequently lower muscle glycogen levels, termed sleeping low, can enhance the adaptations further. Indeed, Marquet et al. have shown significant improvements in submaximal cycling economy, supramaximal cycling capacity, and 10 km running time in trained endurance athletes using such an approach.
Two-a-Day Training
We all know that athletes train, and many more than once in a day. When training occurs without refueling carbohydrate levels after the first session, muscle and liver glycogen levels may be only partially restored, and as a result, the same adaptations are driven in the subsequent session. As such, the signals for increased mitochondrial biogenesis (i.e., AMPk; chapter 3) and fat oxidation rates are enhanced.
Hydration Status
When athletes train, specifically when they train in the heat, it's often emphasized that they need to maintain hydration status. While that might be true in some contexts, there are times in the healthy athlete context where exactly the opposite approach can enhance a physiological state. Indeed, a lowered hydration status, which acutely lowers plasma volume, creates stress in a number of different areas, including the heart and the kidneys. The endocrine system responds by retaining sodium at the level of the kidney (heightened aldosterone and arginine vasopressin levels), water follows, and plasma volume is increased. The enhanced plasma volume can be highly beneficial in a number of contexts, from creating partial heat acclimation to enhancing stroke volume through increased ejection fraction, thereby enabling cardiac stability. For example, Garrett et al. showed that dehydration increased the desired adaptations from a short-term (5 d) heat acclimation protocol (90 min cycling in 35°C, 60% RH) in well-trained males. Aldosterone was enhanced more with dehydration, which was positively related to the plasma volume expansion, which tended to be larger in the dehydration condition. Thus, plasma volume expansion may be more pronounced with permissive dehydration and is one further factor that can be considered around HIIT to skin the cat. Of course, caution must be warranted when applying such maneuvers as physiological strain is likely to additionally be high, which could jeopardize other aspects of performance, such as skill development and tactical learning within the team sport context.
Caffeine
While there are, in our opinion, only a very small number of silver bullet solutions to solving the performance puzzle relative to the number of commercial claims, caffeine supplementation does show relatively consistent positive effects on exercise performance across a number of different conditions. In particular, caffeine couples well with train-low strategies to enhance acute HIIT performance. As described, under conditions of low-carbohydrate availability in athletes adapted to traditional Western diets (typical) or in any condition in which muscle glycogen content is substantially lowered (i.e., two-a-day training), HIIT performance (but not necessarily the acute signal/response) is compromised. In any such condition when HIIT is planned, caffeine supplementation, typically taken in a variety of forms (including coffee and tea) approximately 1 h prior to the session, will enhance HIIT performance and potentially the acute metabolic signal in the larger motor units recruited. For example, Lane et al. showed that caffeine ingestion (3 mg∙kg∙BM-1) taken 1 h prior to an HIIT session (8 × 5 min maximal sustainable pace, 1 min recovery) conducted in a low-carbohydrate state enhanced power output by 3.5%. Thus, such a strategy may be particularly useful in athletes reluctant to train low for various reasons.
Key weapons, manipulations, and surveillance tools
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons.
Recall that weapons refer to the high-intensity interval training (HIIT) formats we can use to target the physiological responses of importance, while the surveillance tools are what we are using to monitor the individual responses to those weapons (figure 1.5). In this section, we present the different HIIT weapons, their manipulations, along with ways to monitor their effectiveness (surveillance).
HIIT Weapons
In our experience, we typically target throughout the season all HIIT target types (see figure 1.5), with the exception of type 5 (type 1: metabolic O2 system; type 2: metabolic O2 system + neuromuscular; type 3: metabolic O2 + anaerobic systems; type 4: metabolic O2 + anaerobic systems and neuromuscular). As shown in figure 30.2, the very large majority of the weapons used to reach these targets are game-based HIIT, with the majority of them being in the format of small-sided games (SSGs) (70%, both pre- and in-season), followed next by short intervals (20%, both pre- and in-season, essentially for individual top-ups and rehabilitation), repeated-sprint training (RST) (5%, both pre- and in-season, essentially for individual top-ups), and long intervals (5%, preseason exclusively).
Manipulations of Interval Training Variables
The running intensity and modality of each HIIT format is systematically modulated to reach the desired acute metabolic and locomotor responses (i.e., physiological targets, types 1, 2, 3, or 4), which, in turn, solves the programming puzzle on a weekly basis for us.
Factors to consider when choosing an HIIT session type for soccer include match-play demands, player profile, desired long-term adaptations, and training periodization. Together, these factors determine the desired physiological response target type, including type 1 aerobic metabolic, with large demands placed on the oxygen (O2) transport and utilization systems (cardiopulmonary system and oxidative muscle fibers); type 2 metabolic as per type 1 but with a greater degree of neuromuscular strain; type 3 metabolic as per type 1 with a large anaerobic glycolytic energy contribution but limited neuromuscular strain; type 4 metabolic as with type 3 but with a high neuromuscular strain. The type 5 target, a session with limited aerobic demands but with a large anaerobic glycolytic energy contribution and high neuromuscular strain, is rarely if ever used in our context. The type 6 response (not considered HIIT) refers to typical speed and strength training with a high neuromuscular strain only. Note that for all HIIT types that involve a high neuromuscular strain, possible variations of the strain include more high-speed running (HS, likely associated with a greater strain on hamstring muscles) oriented work or mechanical work (MW, accelerations, decelerations, and changes of direction, likely associated with a greater strain of quadriceps and gluteus muscles).
HIIT With Long Intervals (Outdoor)
Because of their important (but less soccer locomotor-specific) neuromuscular load and anaerobic contribution (type 4), we generally implement HIIT with long intervals exclusively during the preseason over a 300 m loop designed around the pitch. These typical HIIT exercise bouts are generally performed over 3 to 4 min at 90%-95% VIncTest or 80% VIFT (see chapter 2). This represents 800 to 1000 m efforts completed over 3 min, depending on player fitness, with athletes running 3 to 5 repetitions interspersed by 2 min of passive recovery. Players are generally spread across 4 groups (16 km/h, 17 km/h, 18 km/h, and >18 km/h for VincTest or 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and are requested to reach group-specific cones set across the running loop at appropriate times. These sessions are generally prescribed at the end of the day, so that athletes may benefit from a greater (O2 slow component, i.e., higher (O2 for a similar or lower running speed due to muscle fatigue and loss in metabolic efficiency), which may help in limiting overall musculoskeletal strain and fatigue. Importantly, this HIIT format also has an advantage in that it stresses the cardiopulmonary system at high rates without the need for reaching high running speeds (<18-19 km/h). This is of primary importance for the weekly high-speed running load management, since it leaves room for the other sessions to target this locomotor component with less risk of locomotor or musculoskeletal overload.
HIIT With Short Intervals
Our preferred HIIT short-interval weapons include 10 s on/10 s off, 15 s/15 s, 20 s/20 s, and more often 10 s/20 s (figures 30.3 and 30.4) since this latter format has been shown to be low with respect to acute neuromuscular fatigue (figure 5.41). We implement these HIIT formats for the main reason that both the volume and intensity of the locomotor load (i.e., high-speed running and mechanical work), and in turn, the associated neuromuscular load and fatigue and anaerobic contribution, can be tightly manipulated. For example, type 1, 2, 3, or 4 targets can all be hit with short intervals. While we may sometimes use these HIIT formats in the preseason during a few collective team training sessions, HIIT with short intervals is of greater use to us in-season for individual players requiring well-tailored locomotor loads, i.e., rehabilitating players or conditioning substitute players, for which collective game-based training may not be recommended or fulfill their needs completely. In fact, programming HIIT with low levels of neuromuscular load (type 1) may be required during the preseason to assist with preserving the quality of the conjoined soccer sequences (same session) as well as the type 6 strength and speed sessions planned the following day (see chapter 6). Similarly, during rehab, it may be prudent to start with type 1 HIIT before progressing, depending on the type of injury, toward hitting type 2 targets (tailored toward either more high-speed running versus mechanical work, figure 30.3), followed by type 3 targets, and finally, type 4 targets. For substitute players, HIIT with short intervals is generally the only weapon available as a top-up to compensate for the high-speed running load that players miss while not playing, since the large majority of SSGs in which they participate (figure 30.5) fail to overload this locomotor component respective to match demands.
In practice, we generally spread the players into 5 groups (17 km/h, 18 km/h, 19 km/h, 20 km/h, and >21 km/h for VIFT) and request they run over group-based distances using cones on the pitch. For example, for players with a VIFT of 19 km/h, and for a 15 s/15 s HIIT run at 95% VIFT (relief interval: passive), the target distance will be (19/3.6) × 0.95 × 15 = 75 m (19 is divided by 3.6 to convert the speed from km/h to m/s, for convenience). When we plan runs with changes of directions (CODs) to decrease the amount of high-speed running and modulate mechanical work, the time needed for COD must also be considered when setting the target run distance in order to ensure a similar cardiorespiratory load compared to straight-line runs. Therefore, in relation to the estimated energetic cost of COD during HIIT (see chapter 2, VIFT section), if the players have to run over a 40 m shuttle, for example, they would instead cover 71 m. If the shuttle length is divided in half (i.e., 20 m shuttle), the distance they must cover drops to 65 m. (A spreadsheet that completes this calculation for 180° CODs for 15 players at a time is available through the 30-15 IFT App: https://30-15ift.com/.) Finally, to further modulate the locomotor demands and, in turn, the neuromuscular load of these runs, we use turns at different angles that can either decrease or increase braking and acceleration demands. In fact, using research technology that included measures of ground impacts and muscle activity and oxygenation during (repeated) high-intensity runs (https://www.youtube.com/watch?v=KFL8STOyaB0), we showed that while straight-line runs promote stride work (and hamstring loading) via increased high-speed running (HS, type 2 or 4), sharp turns (90°-180°) rather increase thigh work (quads and glutes) via the increased neuromuscular requirements associated with deceleration and acceleration phases (i.e., increased mechanical work, type 2 or 4). Interestingly, we also showed that 45° turns were likely associated with the lowest neuromuscular load, since neither high-speed nor sharp decelerations and accelerations are involved within this condition (type 1).
To make HIIT with short intervals more appealing to players and a bit more specific in terms of movement patterns and locomotor loading, the ball is often integrated into the activity on different occasions. For example, players run following position-specific running patterns for the required duration while reproducing position-specific technical sequences including passes, receptions, and/or shots on mini-goals at the end of the run (figure 30.3).
Finally, while the optimal loading in terms of HIIT volume and, in turn, high-speed running distance and mechanical work is difficult to define, we often use match demands as targets. For example, we progressively build up locomotor loads during rehab to reach the match-play distance equivalent of 45, 60, and 90 min or sometimes more. We also use within-player load modeling such as the acute/chronic ratio (and associated predictions) for both rehab and healthy players to define volume targets at different times of the week. For example, considering that a competitive match requires players to cover 600 to 1300 m >19.8 km/h (2), compensation training the day following the match including a 6 min HIIT (in which series duration and volume are based on player's profile and position) may allow substitutes to maintain their weekly high-speed running volume at a stable level, which may limit injury risk before the next match.
The athlete's heart and sudden death
Physiologic adaptations that improve cardiac function are among the benefits of athletic training.
Physiologic adaptations that improve cardiac function are among the benefits of athletic training. They include increased stroke volume and cardiac output, longer diastolic filling time, and decreased oxygen demand, while maintaining normal systolic and diastolic function, with blood pressure and heart rate (HR) trending lower (see chapter 3). Training benefits, which include normal hypertrophic changes to the heart muscle walls, extend far beyond the cardiovascular system and are well known, with exercise far outweighing any health risks in most adults. Even extreme exercise training is well tolerated by healthy individuals, with increasing exercise volume and intensity further reducing cardiovascular risk. HIIT is recommended as a treatment strategy for patients with cardiovascular disease because it can provide benefits more rapidly than standard cardiac rehabilitation exercise.
Unfortunately, in the process of building fitness, athletes can also become unhealthy as discussed above, especially during high-intensity—high-stress—training. Combined with reduced health, high-intensity training and its associated increased HR and blood pressure and elevated stress hormones can contribute to sudden death in athletes with known or occult cardiovascular disease.
Among the signs evident in unhealthy athletes is sudden death due to various cardiac injuries such as an acute myocardial infarction (heart attack) or arrhythmia (irregular electrical heart beat). These individuals are often asymptomatic until during or within an hour of a cardiac event, and may be seven times more likely to die during activity than at rest.
The incidence of sudden cardiac death, the leading cause of death in athletes during exercise, has been estimated in young athletes <35 years of age at 1:917,000 athlete-years, however rates four to five times higher have recently been estimated, with men, African Americans, and male basketball players being at greatest risk.
A vital point about this important topic is that sport training in itself is not the cause of most sudden death in athletes, but acts as a trigger for cardiac arrest in the presence of underlying cardiovascular diseases predisposing to a cardiac event. In addition, sudden cardiac arrest does not always result in death, with many individuals surviving such an event, which may or may not occur during exercise.
In younger athletes (<35 years), the most common cause of sudden death is hypertrophic cardiomyopathy, accounting for approximately one-third or more of sudden deaths, with congenital coronary anomalies occurring in 15% to 20% of the cases and myocarditis (infection) much less common. In those >35 years of age, the most common cause of sudden death is atherosclerotic cardiovascular disease. As such, it is vital for clinicians to differentiate between normal hypertrophy developed from chronic training and its pathological state. Normal changes to an athlete's heart, which can imitate pathology, must be distinguished from serious cardiac disorders. Elite athletes are also not immune to cardiovascular disease, nor is it limited to athletes >35 years, and may account for 56% of the sudden deaths in young competitive athletes.
Cardiovascular causes for sudden cardiac death in athletes may be mostly preventative. For example, both genetic and lifestyle factors can contribute to pathologic hypertrophic cardiomyopathy, the latter being associated with cardiometabolic impairment including abnormal blood lipids and glucose, prediabetes and diabetes, and chronic inflammation. In athletes, hypertension is the most common risk factor for cardiovascular disease.
In athletes >35 years, the risk of sudden death due to ischemic heart disease increases progressively with age, where coronary artery disease accounts for more than half of the cases of sudden death, with atherosclerosis (a buildup of plaque in an artery) being a contributing factor. Coronary artery calcification is specifically associated with chronic high-intensity training, with vitamin D important in helping prevent calcification.
The prevalence of sudden death in athletes increased by 6% annually between study years 1980 to 1993 and 1994 to 2006, with 31% of the sudden death population occurring between 1980 and 1993 and 69% between 1994 and 2006. As the data were largely limited to sudden deaths that became part of the public domain and records, the increasing number of fatal events observed over the study period may reflect enhanced public recognition caused by increased media attention. Corrado et al. raised a reasonable concern about the reliability of the estimation of athletes' sudden cardiac death that could lead to an incorrectly low number of cardiac events and underestimation of mortality rates. Performance-enhancing drugs could also adversely affect heart health through cardiac toxicity, including anabolic-androgenic steroids, growth hormone, testosterone, erythropoietin (EPO), and others.
It is also possible that athletes experiencing fatal events previously had cardiac clinical screening that failed to detect a cardiac condition, with Maron et al. estimating 30% of athletes cannot be identified reliably by preparticipation screening, even with ECG. Despite this, early identification of cardiovascular disease risks or cardiac abnormalities through a screening program could prevent sudden cardiac death, as recommended by the European Society of Cardiology, the American Heart Association, the International Olympic Committee, the American Society for Sports Medicine, and the American College of Cardiology.
Related Books
