Science of optimal performance Physiology of overtraining and fatigue

Dr. Christine BrooksUSA Track and Field Coaching Science Education Coordinator

1Endocrine system basics

What You Will Learn

When you have completed this module you will be able to:

1. Explain how hormones work

2. Describe the two clusters of hormones

3. Distinguish between the hypothalamus and pituitary gland and identify the endocrine glands relevant to training an athlete

4. Discuss the role of the following hormones: testosterone, growth hormone, insulin, cortisol and progesterone.

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Introduction

! The body is in a persistent effort to maintain homeostasis and the capacity to achieve homeostasis is determined by effec-tive communication among the cells. Two of the major homeo-static systems have evolved to provide this communication (Fig-ure 1). One is the nervous system that communicates very rap-idly, but the messages are destroyed very quickly. The other is the endocrine system that is typically slower, but the effect lasts quite a long time because the messages are available for a longer period of time before they are destroyed. Both are struc-tured to sense information, organize an appropriate response, and then deliver the message to the proper organ or tissue.

! Often the two systems work together to maintain homeo-stasis. The term 'neuroendocrine response' reflects the interde-pendence of the two systems. However, the two systems differ in their delivery mechanisms. The endocrine system uses hor-mone message carriers and the network of blood vessels to transport its messages to tissues. Nerves relay messages from one nerve to the next until it reaches the tissues. They use a messenger signal referred to as a neurotransmitter.

! Endocrinology is the science of intercellular and intracellu-lar communication via the secretion of a chemical substance called a hormone. The word 'hormone is from a Greek word

Section 1

Endocrine system basics

3

meaning to stimulate, or to spur into action Hormones play an essential role in an athlete's performance because they stimu-late the release of energy, and the building of muscle most ap-propriate for the athlete's performance requirements.

!

What You Will Learn

! The goal of this module is to provide you with sufficient knowledge about the endocrine system so you can understand

the role training plays in the activation or inhibition of hormone release from endocrine glands. We will take a look at how hor-mones work, the two clusters of hormones important for a coach to be familiar with, and some important anatomy of the endocrine system itself. Knowledge about the endocrine system adds greater depth to your understanding about overtraining syndrome and its symptoms.

Brief Anatomy Of The Endocrine System

! The endocrine system is a collection of ductless glands dis-tributed throughout the body. There are two types of endocrine organs: primary endocrine organs, whose primary function is the secretion of hormones, and secondary endocrine glands, for which secretion of hormones is secondary to some other function.

! Some primary endocrine organs are located within the brain, including the hypothalamus, pituitary glands and pineal gland. Other primary endocrine organs are located outside the nervous system. These include the thyroid gland, parathyroid glands, thymus, adrenal glands, pancreas and gonads (testes in male and ovaries in the female).

! Secondary endocrine glands include the heart, liver, stom-ach, small intestine, kidney and skin. You may come across

Figure 1. Relationship between the nervous system and endocrine system of communication

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readings that refer to hormones from any one of the endocrine organs. However, our focus will be to examine the primary endo-crine organs and hormones that have the highest implication to sports training—specifically the hypothalamus, pituitary gland, the adrenal gland, pancreas and the testes/ovaries.

! The hypothalamus and pituitary are particularly important endocrine glands (Figure 2). Together they control almost all the activity of organs throughout the body. The hypothalamus is a part of the brain and right underneath it is the pituitary gland connected. The main general function is homeostasis, or main-taining the body's status quo.

! To achieve this task, the hypotalamus receives information about the state of the body, and then initiates changes if any-thing drifts out of a certain range. Factors such as blood pres-sure, body temperature, and fluid and electrolyte balance, among other factors important to maintaining homeostasis are held to a precise range. To accomplish many of its regulation tasks the hypothalamus secretes hormones that affect the pitui-tary gland. The hypothalamus releases hormones that move to the pituitary gland to stimulate it to release hormones.

! The adrenal glands are also important glands for ath-letes. They sit on top of the kidneys (Figure 3) forming a little hat-like structure on top of each kidney.

! The pancreas is tucked underneath the liver – here's the liver up here and here's the pancreas. The pancreas secretes insulin and insulin is important for getting glucose into the cell.

Figure 2. The hypothalamus and pituitary glands are two important endocrine organs for athletes

Figure 3. The adrenal glands, pancreas and liver

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Hormone Actions

! The hypothalamus affects the pituitary gland and this is why any damage to the hypothalamus is so serious to an ath-lete. The hypothalamus receives input from nerves. It’s for this reason the hypothalamus-pituitary complex is often called the neuroendocrine system. “Neuro” means nerve and the neuroen-docrine system simply refers to the release of hormones involv-ing the interface between the endocrine glands and the nervous system.

! The hypothalamus produces releasing hormones none of which have any direct effect on tissues or cells (Figure 4). Their job is to instruct the pituitary to release hormones depending on feedback the hypothalamus receives about the state of the body’s internal environment.

! There are two subdivisions of the pituitary. One is referred to as the anterior pituitary and the other as the posterior pitui-tary. The posterior portion of the pituitary also releases hor-mones upon direction from the hypothalamus. One on those hormones controls the electrolyte balance in the body. The ante-rior pituitary releases numerous hormones including the follow-ing.

• Prolactin stimulates the mammary glands in females.

• Thyroid stimulating hormone stimulates the release of hor-mones from the thyroid gland that controls day-to-day me-tabolism of the body.

• Adrenocorticotrophic hormone (ACTH) is an important hor-mone because it stimulates the adrenal cortex to release cortisol. Cortisol is also known as the stress hormone be-cause it is elevated whenever the body is breaking down energy or protein structures.

• Growth hormone is another important hormone. GH di-rectly affects cells throughout the body. Another important action is to stimulates the liver to release insulin-like growth factor. Insulin-like growth factor is thought to be a

Figure 4. The hypothalamic and anterior pituitary hor-mones

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primary growth factor required for early development and for achieving maximal growth. It is thought to have impor-tant growth effects in adults. Almost every cell in the hu-man body is affected by insulin-like growth factor espe-cially cells in muscle, cartilage, bone, liver, kidney, nerves, skin, and lungs. Despite a lack of evidence that these metabolic effects translate to improved performance, GH abuse by athletes appears to be quite widespread.

• Testosterone is primarily secreted in the testes of males and the ovaries of females, although small amounts are also secreted by the adrenal glands.

Categories Of Hormones

! There are many different types of hormones and we have only addressed a small handful. The two classifications of hor-mones relevant to an athlete’s development are the catabolic and the anabolic hormones (Table 1). Anabolic hormones help build structures, especially protein structures. Catabolic hor-mones break down molecules and this is especially relevant when energy stores are needed for exercise. Anabolic hor-mones important to training are testosterone, growth hormone and insulin.

! Critical catabolic hormones include cortisol and progester-one. Anabolic hormones important to a coach include:

• Testosterone is the male sex hormone. It is also found in some degree in females. Its presence normally indicates an anabolic state of the organism. Elevated testosterone levels are nearly always associated with improved athletic performance.

• Growth hormone is a hormone connected with the regu-lation of growth. Its presence is important to foster recov-ery from exercise.

Anabolic Hormones Catabolic Hormones

Associated with putting molecules together

Associated with taking molecules apart

Testosterone: Associated with improved performance

CortisolTestosterone: Associated with improved performance

Causes the breakdown of stored protein

Testosterone: Associated with improved performance

Promotes fatty acid and glycogen release for energy

Growth Hormone: Vital to building muscle and other tissue

Promotes fatty acid and glycogen release for energy

Insulin: Controls the use of glucose by the body

Progesterone: Normally associated with a catabolic state

Table 1.Categories of hormones

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• Insulin is produced by the pancreas and controls the use of glucose by the body.

Catabolic hormones important to the coach include:

! Cortisol that is better known as the stress hormone. Corti-sol causes the breakdown of stored protein molecules, pro-motes fatty acid and glycogen release for energy use. Elevated cortisol levels are usually associated with heavy training or over-training.

! Progesterone is a female sex hormone and when proges-terone levels are elevated this is normally associated with a catabolic state.

How Hormones Work

! One of the considerations you will have when designing a training stimulus will be on what hormone you want to activate to generate a specific physiological effect relevant to an opti-mum performance. For this reason it is important to know how the endocrine system works.

! There are three parts to the endocrine system (Figure 5) – the endocrine gland responsible for producing the hormone, the

hormone itself, often referred to as the signal, and a target cell for the hormone (often referred to as the receptor). The endo-crine gland is responsible for producing the hormone. A hor-mone is a particular chemical with a specific shape.

! The hormone molecules circulate in the blood and are de-posited around the body where they are exposed to the cells (Figure 6). However, a specific hormone won’t affect all the tis-sues. It depends on whether the cell the hormone passes by has a special docking station with the exact shape of the hor-mone. Some cells will have no receptors on their cell mem-brane, or inside the cell, matching the hormone. Other cells will have docking stations or receptors that are the exact shape of the hormone. If the cell has a docking station matching the shape of the hormone it is called the target cell.

! When the hormone finds a matching docking station it binds to it. Depending on the message the hormone is carrying

Figure 5. Parts of the endocrine system

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this sets off activity inside the cell. The hormone itself is called the first messenger. When the hormone docks to a cell’s recep-tor it activates another messenger (referred to as the second messenger) inside the cell. The second messenger stimulates the physiological change. For example, the second messenger might be designed to change the functioning of the mitochon-dria, or to build a specific protein, or to break down fat for en-ergy, or any other action. It is the second messenger system that facilitates the physiological change the body wants to carry out. The hormone simply carries the message from the endo-crine gland in response to the initial stimulus from the hypothala-mus by way of the pituitary.

Testosterone

! Resistance training is a potent stimulant for increasing both muscle size and the functional qualities of the neuromuscu-lar system. Together these two effects lead to improved muscu-lar strength, power, hypertrophy and local muscular endurance. The steroid hormones, specifically, the biological effects of tes-tosterone and cortisol, help to control long-term changes in mus-cle growth and neuromuscular adaptation, and therefore, subse-quent performance.

! The most recognized effect of testosterone and cortisol lies in skeletal tissue remodeling – especially the type II fibers. Testosterone is considered a primary anabolic hormone, be-cause it increases protein synthesis and decreases protein deg-radation. Cortisol is the primary catabolic hormone, as it in-creases protein degradation and decreases protein synthesis.

! The net result is an increase, decrease or maintenance of muscle fiber and whole muscle size depending on the training program and other factors such as nutrition. The force-generating capacity of muscle is related to its cross-sectional area, so it is generally agreed that testosterone and cortisol con-tribute to human performance by regulating changes in skeletal muscle size over a time. However, skeletal muscle growth is not the only outcome influenced by these hormones. The motor

Figure 6. Hormone molecules circulate in the blood

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neuron is sensitive to testosterone and increases its size and function under its influence.

! There is often a small role played by testosterone in women, but growth hormone, and insulin-like growth factor 1 is more involved in the anabolic processes. We will discuss this shortly shortly. There has been considerable effort to determine how to use resistance training to enhance the body's natural re-lease of testosterone. It appears that the magnitude of the ef-fect relates to the size of the muscle mass involved in training.

! The general recommendation is to exercise large muscles first, followed by small muscles. Large muscle-mass exercises such as Olympic lifts, dead lifts and jump squats produce large elevations in testosterone compared with small muscle mass ex-ercises (Figure 7). Based on these data the recommended pro-grams are those designed to simulate high levels of testoster-one secretion. Performing small muscle mass exercises does not acutely elevate testosterone. It is thought that elevating tes-tosterone first benefits the small muscles, and this is the reason-ing behind performing large muscle mass, multiple joint exer-cises early in the workout, and smaller muscle mass exercises later in the workout when training to enhance strength.

! If you are just after a high testosterone response, it ap-pears that higher reps with short rest periods produce a greater testosterone response than high load, low volume training with long (3-minute) rest periods. The training for women is the

same. However, growth hormone appears to be the influential factor for promoting muscle hypertrophy in women with testos-terone having a smaller effect. The other important effect of re-sistance training is that it increases the concentration of recep-tors for testosterone and insulin-like growth factor 1 (IGF1) on the muscle cells.

How Human Growth Hormones Work

! Growth hormone (GH) is a small protein that is made by the pituitary gland and secreted into the bloodstream. GH pro-duction is controlled by a complex set of hormones produced in

Figure 7. Hormone molecules circulate in the blood

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the hypothalamus of the brain and in the intestinal tract and pan-creas. Secretion of hGH is slightly higher in women than in men, with the highest levels observed at puberty. Secretion de-creases with age by around 14% per decade.

! Growth hormone is secreted in 6-12 discrete pulses per day with the largest pulse coming around 1 hour after the onset of night-time sleep (Figure 8). Indeed sleep is one of the most powerful stimulants for hGH release. The other is exercise. GH is released from the anterior pituitary and has many varied roles including growth of muscle, bone and collagen, and is also in-volved in fat metabolism.

! The current accepted hypothesis about how hGH works is known as the Somatomedin Hypothesis. This hypothesis states

that hGH does not affect tissues directly, but rather it stimulates other hormones referred to as somatomedins, or insulin-like growth factor (IGF) into action. IGFs are produced in most tis-sues, although IGF-1 is mostly produced by the liver. IGF-1 is one of the more significant somatomedins. It is responsible for the growth of muscle and bone.

! It is GHRH from the hypothalamus that simulates the pitui-tary to release GH. When there is sufficient IGF-1 available it tells the hypothalamus to stop producing the GHRH. Also recall that there was another hormone released by the hypothalamus called somatostatin that blocks the release of GHRH. IGF-1 also stimulates the production of somatostatin. IGF-1 also has a direct inhibiting effect on GH release from the pituitary. It is thought that exercise blocks both these inhibitory feedback path-ways and this is why GH spikes during exercise.

! The body produces sufficient GH to maintain homeostasis based on activity. However, taken in large doses in excess of natural production, as would occur during supplementation, leads to irreversible effects on bone growth resulting in large hands and feet, enlarged internal organs, high blood pressure, diabetes and a range of cancers. One has to wonder if chronic high levels of natural GH production induced by sport training over long periods of time is causing the heart problems cur-rently showing up in older master athletes.

Figure 8. Growth hormone secretion

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Exercise Effects Of Growth Hormones

! Patients who are supplemented with GH have significant improvements in perception of energy level and mood. Memory and concentration are also improved. These changes in the CNS appear quite quickly – well before there are noticeable changes in lean body mass or strength. For an athlete, naturally produced GH potentially has psychological effect on perform-ance by allowing a higher quality training due to enhanced mood. For those in sports requiring a high level of concentration and attention the effect of GH appears particularly relevant.

! Results from a large number of studies have demon-strated that GH levels rise in response to acute exercise with a threshold level of approximately 70%VO2max. The extent of the rise depends on the type and intensity of exercise, with lev-els increasing by up to 100-fold in response to anaerobic exer-cise and hypoxia.

! This acute stimulation of GH also appears to affect noctur-nal secretion of GH. GH levels start to increase 10–20 min after the onset of exercise, peak either at the end or shortly after ex-ercise and remain elevated for up to 2 h following exercise. The magnitude of the GH response to exercise is influenced by age, gender, body composition, physical fitness and the intensity, and nature and duration of exercise.

Sleep

! As one ages, there is a decrease in sleep duration and GH secretion. Sleep deprivation in young individuals reduces GH secretion and may contribute to premature development of the metabolic syndrome. A summary of these effects of exercise on hGH is shown in Table 2.

! Research suggests that the greatest stimulus for hypertro-phy and improvement in muscle strength and power occurs via local production of IGF-1 – in our case this would be skeletal muscle. In other words, IGF-1 secretion can be stimulated by both muscle contraction or by hGH stimulating IGF-1 secretion from the liver. Indeed, it appears that the local production of

Mood Permits higher quality of training

Acute exercise>79% VO2max, very high with anaerobic

exercise

GH releaseIncrease 10-20 mins after onset of exercise.

Peak at end, or shortly after. Remain elevated for 2 hours

SleepRelease of GH during sleep is associated

with repair and remodeling

Age Decrease in sleep = decrease in GH

Table 2. Summary of exercise effects on hGH

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IGF-1 has a higher effect on protein synthesis than circulating hGH. Studies in rats have shown than GH is not essential for exercise-induced muscle hypertrophy or an improved cardiores-piratory response to training. This points to the important role played by the locally produced IGF-1.

! For endurance athletes the GH stimulates the release of fatty acids. The threshold for hGH secretion occurs above 40% VO2max. However, for a consistent EIGR an exercise intensity above 60% of VO2max is required. In this case the GH surge is consistent with lactate threshold.

References

Crewther, BT; Cook, C; Cardinale, M; Weatherby, RP; Lowe, T. Two Emerging Concepts for Elite Athletes: The Short-Term Ef-fects of Testosterone and Cortisol on the Neuromuscular Sys-tem and the Dose-Response Training Role of these Endoge-nous Hormones. Sports Medicine. February 2011, Volume 41, Issue 2, pp 103-123

Godfrey RJ, Madgwick Z, Whyte GP. The exercise-induced growth hormone response in athletes. Sports Med. 2003;33(8): 599-613.

Frystyk, Jan, Exercise and the growth hormone-insulin-like growth factor axis. Medicine and science in sports and exer-cise, 01/2010, Volume 42, Issue 1

Jenkins, Paul J. Growth hormone and exercise: Physiology, use and abuse. Growth Hormone & IGF Research, 2001, Volume 11, Issue 1

Saugy M, Robinson N, Saudan C, Baume N, Avois L, and Mangin P. Human growth hormone doping in sport. Br J Sports Med. 2006 Jul; 40(Suppl 1): i35–i39.

Strobl, J S; Thomas, M J. Human growth hormone. Pharma-cological reviews, 03/1994, Volume 46, Issue 1

Van CE, Plat L. Physiology of growth hormone secretion during sleep. J Pediatr. 1996 May;128(5 Pt 2):S32-7.

Widdowsona WM, Healyb ML, Sönksenc PH, Gibneya J, The physiology of growth hormone and sport. Volume 19, Issue 4, August 2009, Pages 308–319

2Autonomic nervous system

What You Will Learn

When you have completed this module you will be able to:

1. Explain the difference between the sympathetic and parasympathetic nervous system

2. Discuss the influence each system has on the heart and other organs

3. Discuss the meaning of the respiratory sinus arrhythmia

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Introduction

! The autonomic nervous system is particularly important to your understanding of overtraining symptoms. Much of the litera-ture on overtraining is confusing because the authors do not fully discuss the autonomic nervous system.

! An understanding of how the autonomic nervous system works. You will also be exposed to polyvagal theory will aid in your knowledge about overtraining. Polyvagal theory is a bit complicated and you might wonder at times why this knowledge has any relevance to you as a coach. However, overtraining symptoms make a lot more sense if they are placed in the con-text of polyvagal theory.

What You Will Learn

! In this module we overview the difference between the sympathetic and parasympathetic nervous system and discuss the influence each system has on the heart and other organs. We also discuss the meaning of the respiratory sinus arrhyth-mia and polyvagal theory

Section 1

Autonomic nervous system

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While much of this module might appear to contain more infor-mation than a coach needs to know, you will find that the knowl-eddge will be invaluable to you when you are reading the litera-ture about over training syndrome and how to use heart rate as an assessment of how deeply the athlete is in the over trained state. It will also help you understand why your athletes are per-forming poorly for no apparent reason even after several days of recovery.

Nervous System Components

! The nervous system consists of two broad divisions (Fig-ure 1). One division is the central nervous system (CNS) encom-passing the brain and spinal cord. The second component is the peripheral nervous system and includes all the nerves out-side the central nervous system. The peripheral nervous sys-tem is itself divided into a sensory division and a motor division. The sensory division collects all the information the brain needs to make sure the body is functioning properly according to exter-nal and internal conditions.

! Specially designed sensors incorporated in the structure of voluntary skeletal muscles and involuntary smooth muscles (found in blood vessels) inform the brain about their status.

The eyes, ears, nose, and touch, provide the brain with crucial information about the external environment. Numerous visceral sensors relay information about the status of the organs within the body. The brain has the massive task of synthesizing all this information and coordinating actions or adjustments necessary to ensure survival.

! The nerves traveling from the periphery to the brain are re-ferred to as afferent fibers. The flow of information through the afferent fibers is always from the peripheral toward the central nervous system.

Figure 1. The central and peripheral nervous systems

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! The motor division of the peripheral nervous system causes action in the body. The voluntary division involving the skeletal muscles is referred to as the somatic branch. The so-matic nervous system consists of nerves that exit the CNS and project out into the periphery. All nerves sending information from the CNS to the periphery are referred to as efferent nerves. Somatic nerves are responsible for sending instructions from the brain to muscles stimulating them to perform some type of movement.

! The involuntary or subconscious branch of the motor divi-sion is the autonomic nervous system. This branch also has ef-ferent nerves running from the CNS to most organs and tissues in the body including cardiac muscle, smooth muscle of the blood vessels and various visceral organs such as the stomach and lungs, etc. Our concern in this module is the sympathetic and parasympathetic components of the autonomic nervous system.

Dual Innervation

! The autonomic nervous system is also referred to as the involuntary nervous system. Both the sympathetic and parasym-pathetic branches of the autonomic nervous system innervate most organs. This is called dual innervation. The parasympa-

thetic nerves that innervate most organs in the body derive from the brainstem (Figure 2). The sympathetic nerves extend from the mid section of the spinal cord.

! The sympathetic and parasympathetic branches function in an opposing seesaw type action depending on whether the body is active or at rest. The sympathetic branch is most active when the body is moving around and the parasympathetic branch is most active when it is at rest. For example, at rest the

Figure 2. The sympathetic and parasympathetic nervous system

Vagus nerve

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parasympathetic slows the heart. The sympathetic nervous sys-tem has a sliding scale of influence. It is operating at a very low level during rest but is constantly adjusting its influence on the heart to ensure the body can meet its energy and oxygen needs.

! Fulfilling these needs usually requires a faster heart rate and deeper breathing and when this happens it is an obvious sign the sympathetic nervous system has increased its activity. The sympathetic nervous system basically ensures survival by activating the organs responsible for supplying energy and oxy-gen to the active tissues. As the sympathetic nervous system is gears up its activity the parasympathetic gears itself down.

! You can think of the sympathetic system as the accelera-tor and the parasympathetic system as the brake. Any change in heart rate usually involves a reciprocal action of these two components of the autonomic nervous system. When a higher activity is needed parasympathetic activity decreases and there is an increase in sympathetic activity. During rest, the opposite occurs. The parasympathetic branch has a higher influence and the sympathetic branch has less influence.

The Reciprocal Effect

! If we use a car as an analogy, the sympathetic nervous systems is the accelerator and the parasympathetic nervous system is the brake (Figure 3). However, in contrast to a car that you can turn off, the body is always set to idle mode. It never turns off. If you remove the effect of both the sympathetic and parasympathetic nervous system heart rate is around 100 beats per minute – this is the body's natural idle mode and this is very energy consuming.

! At rest, the parasympathetic nervous system turns the idle down to an average heart rate of approximately 70 beats per minute. Athletes usually have a much lower resting heart rate because of their highly tuned cardiovascular system. There also

Figure 3. Dual actions of the sympathetic and parasympa-thetic nervous systems

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appears to be higher parasympathetic effect at rest with a highly tuned body. The sympathetic nervous system is capable of turbo charging the body by stimulating the adrenal cortex to release catecholamines (epinephrine and norepinephrine). This hyper excites all the systems in the body and is referred to as the fight or flight response that prepares the body to cope with extremely high physical demands.

! Just as you would with a car when you want to accelerate it you take the foot off the brake. When the athletes body is un-der the stress of training the brake from the parasympathetic nervous system is removed and the sympathetic nervous sys-tem accelerates to meet the body's metabolic demands. In other words, it throttles up.

! The primary function of the autonomic nervous system is to regulate the organs of the body in order to maintain homeo-stasis. The accelerator and brake are pushed according to the metabolic demands of the body. Remember that the sympa-thetic and parasympathetic are always turned on. However, one will dominate the other according to the metabolic needs of the body. Under conditions of stress, parasympathetic influence is turned off and the sympathetic nervous system shifts into more accelerated state.

The Vagus Nerve

! If your athletes have an unexplained deterioration in per-formance, in conjunction with unexplained fatigue and lack of motivation, it is likely the autonomic nervous system is involved. Specifically, it is likely to involve the activity of the vagus nerve (cranial nerve X).

! Before discussing the actions of the vagus nerve we must overview polyvagal theory. The vagus nerve is a parasympa-thetic nerve and has wide connections throughout the body. It is

Figure 4. Cross-section of the brain stem showing the DMNX and nucleus ambiguus

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the longest and most complex of the cranial nerves extending from the brainstem and branching off to most organs of the body.

! Vagus is Latin for “wandering”. The brainstem is the lower extension of the brain where it connects to the spinal cord. Es-sential neurological functions necessary for survival (breathing, digestion, heart rate, blood pressure, etc.), and for arousal (be-ing awake and alert), are located in the brainstem. It is the old-est part of the brain and is important in basic survival functions of the body including heart activity, digestion and breathing.

! The portion of vagus nerve beginning in the Dorsal Motor Nucleus (DMNX) of the brainstem sends branches to a number of organs – including the heart. The branch beginning in the nu-cleus ambiguous is an important branch from a coaching per-spective. When this branch is functioning correctly the training program is well within the physiological recovery capacity of you athlete. This branch has a connection to the heart, to the facial muscles, and the muscles involved with swallowing, and breathing. It also has connections to the areas of the brain con-trolling emotions. The vagus fibers arising from the nucleus am-biguus are much faster and have a more dominant influence than the fibers coming from the DMNX. The significance of this will become apparent shortly.

Chromatin Tissue

! To fill in the picture about the autonomic nervous system and its regulation of the heart it helps to know how the regula-tion mechanism of the heart evolved.

If we start with primitive vertebrates and move through evolu-tion to the more complex mammals additional layers of heart regulation appear. Very early vertebrates called cyclostomes (Greek for “round mouth) only had chromatin tissue controlling the heat rhythm.

! Chromatic tissue is non-neural tissue designed to produce and release a heart stimulation chemical. This enabled cyclo-stomes to produce sufficient heart activity to mobilize a little bit. Lampreys are an example of this type of vertebrate. These long, jawless eel-shaped fish attach themselves to, and feed on other fish.

! Release of chemicals from the chromatin tissue into the blood of the heart enables lampreys to move around and attach themselves to their prey. Humans still have this chromatin tis-sue feature of the heart.

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Dorsal Motor Nerve

! As vertebrates evolved new heart regulation methods were added that permitted a wider range of heart regulation.! In Elasmobranches (an example is the shark) the dorsal motor nu-cleus of the vagus nerve (DMNX) appears. The DMNX acts as a break to slow the heart down. A shark’s heart is regulated by a chemical (noradrenalin or norepinephrine) released from the chromatin tissue.

! When food is available the influence of the chromatic tis-sue allows the shark to move quickly. The release of noradrena-lin is a conditioned response to food. However, if food is unavail-able the DMNX slows the shark’s metabolic output and heart rate. In other words, the dorsal motor nucleus of the vagus nerve provides the shark with a range of motion with excitation on the one end when food is available, and inhibition on the other end when food is not available. This provides sharks more survival strategies options than are available to the cyclo-stomes because sharks can move around in search of food.

! The DMNX branch of the vagus nerve persists in humans. It has a sedating effect and when we discuss overtraining syn-drome you will see how dangerous this sedating effect can be to athletes who have fatigued their sympathetic nervous sys-tem. Indeed, some sudden death occurrences of athletes have been attributed to the ancient survival strategy of DMNX branch of the vagus nerve of slowing heart rate way down to conserve energy.

SNS And The Adrenal Medulla

! The sympathetic nervous system appears in the Teleosts or bony fish. The sympathetic nervous system excites the heart way above what is possible under the influence of chromatin tis-

Chromatin tissue

Dorsal motor

nucleusSNS Adrenal

medullaNucleus

Ambiguus

Cyclostomes (jawless fish) +

Elasmobranchs (cartilaginous fish) + -Teleosts (bony fish) + - +

Reptiles + - + +Mammals + - + + -

Table 1. Evolution of heart regulation methods permitting a wider range of heart regulation

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sue. It provides an additional acceleration mechanism for the heart.

! In reptiles a further accelerating component is added to the sympathetic nervous system - the adrenal glands where adrenalin (epinephrine) is produced. Adrenalin acts like a turbo charger for the heart and accelerates delivery of fuel and oxy-gen to the tissues. Survival capacity increases again.

Nucleus Ambiguus

! The nucleus ambiguous first appears in mammals and pri-mates. Like the DMNX the NA produces an inhibitory effect. Its job is to counteract the SNS effect by slowing the heart down. The nucleus ambiguus also has connections to the emotional center of the brain and this provides the well known connection between emotion and heart rate.

! So now, instead of just a two pronged autonomic nervous system traditionally discussed, there are three prongs:

1. The old DMNX parasympathetic branch that acts as a brake on the heart;

2. The sympathetic branch with the added feature of the ad-renal medulla that acts as an additional accelerator;

3. The nucleus ambiguus vagus branch that acts as a brake. This branch also has connections to the skeletal muscles of the face and coordinates swallowing with breathing.

 ! In humans, the effects of these autonomic heart regulation features move from the newest to the oldest. When the nucleus ambiguus is not functioning properly it can result in increase in resting heart rate and lower mood. Both of these are common overtraining symptoms. When the NA and SNS are not function-ing properly the older DMNX has the highest influence.

DMNX Versus Nucleus Ambiguus

! The question is: How does the nucleus ambiguus differ from the DMNX in its effect on the heart? Why was the NA added as a regulation mechanism of the heart of a mammal? To understand this we need to focus on the size of the meta-bolic engine in mammals.

Let’s just look at reptiles and mammals. A really significant differ-ence between these two vertebrates is the size of their meta-bolic engine. Gram-for-gram mammals have a much larger en-gine than reptiles – seven to eight times larger in fact.

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! The liver, kidney, heart and brain are important parts of this biological engine. The liver of reptiles is only 62% the size of the mammal’s liver, the kidneys are 39%, the heart is 49% and the brain is 36%. If we use the metaphor of a vehicle, rep-tiles represent vehicles with one-liter engine. Volkswagen makes such a car. It sips on .99 liters of gasoline per 100 kilo-meters.

! Mammals represent vehicles with a four or five liter en-gine. The mustang is an example.

How The Engine Works

! Mammals move around using a large and supercharged engine demanding a high-energy consumption at rest. It de-mands an even a higher energy consumption when it is acceler-ated under the influence the sympathetic nervous system and adrenal medulla. Supercharged mammals need to have a decel-erator on their metabolic system to allow this high-powered en-gine to idle during rest and periods of low levels of activity.

! This is where the NA branch of the vagus nerve comes into play. Nucleus ambiguus acts as a persistent brake and liter-ally cuts the mammal metabolic engine back to a more energy efficient idle.

! The fibers in NA part of the vagus nerve are very fast. This means that the vagal brake can be released almost instantane-

ously to allow the engine to increase speed quickly whenever situations requiring a higher metabolic demand arise.

! Reptiles don’t need the NA vagal tone because their en-gines idle at a very low rate already. If they had the NA vagal bake their hearts would stop working. For this reason vagal con-trol over the reptile’s heart is virtually removed during periods of breathing and other daily motor activities. In addition, reptiles use the vagal influence of the DMNX to respond to stressful situations. This is the reverse of what you expect of a parasym-pathetic nerve.

! The under-powered reptiles use the DMNX to deal with en-vironmental challenges by slowing the heart down, orienting their head and freezing in response to predator or prey, and to conserve oxygen while submerged for lengthy periods. So, their vagal tone is highest during stress, and its job is to slow every-thing down to conserve energy. At other times there is no vagal tone.

Vagal Tones

! In contrast a mammal’s vagal tone is highest during rest-ing situations such as sleep. Vagal tone is reduced when there are metabolically demanding states such as exercise, stress, attention, and information processing.

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! Now here’s an important point. In mammals the ancient DMNX also increases its activity during stress, and does ex-actly the same thing it does in reptiles – it tries to slow every-thing down. In a healthy athlete who is responding normally to the stress, its effect is usually minimal.

! However, one of the effects of an active DMNX is to cause expulsion of all undigested food in the gut. This has a survival origin in that it served to reduce the energy requirements of di-gestion. This was important because oxygen delivery to tissues has been reduced due to the slow heart.

! An overactive DMNX may be one reason some athletes experience diarrhea when they are overly anxious about a com-petition. The DMNX has increased its activity in response to the stressful situation to the point where the athlete is experiencing its ancient effect. The existence of both the nucleus ambiguus and DMNX can also explain the two types of heart rate re-sponses when an athlete is overtrained. As you will soon learn, in some overtrained athletes their heart rate is accelerated above normal. In other overtrained athletes it is much slower than normal. In former case the NA is providing a lower braking effect on the heart and the sympathetic nervous system is hav-ing a higher influence. In the later case the SNS is exhausted and the DMNX is the next evolutionary line of defense. When the athlete has a consistent lower heart rate than normal they are seriously overtrained and may never recover.

! Indeed, the DMNX evolutionary survival slowing effect on the heart and other organs can be massive and lethal. This situation may occur during exercise where the athlete becomes hypoxic, leading to sudden and unexplained death.

Respiratory Sinus Rhythm

! When healthy athletes are at rest the heart does not beat at a perfectly regular rate. A slight beat-to-beat variation (ar-rhythmia) is normally present. The most common cause of ar-rhythmia is breathing. Respiratory sinus arrhythmia is normal and may be quite marked (up to 10 to 20 beats/min).

! RSA is a natural phenomenon. It is based on the cycling of sympathetic and vagal impulses to the heart. During inspiration the heart speeds up and during expiration the heart slows down. The nucleus ambiguus controls this arrhythmia by puls-ing its activity. The explanation for the RSA phenomenon is thought to relate to the right time to dump as much oxygen as possible into the blood as it passes through the lungs. Speed-ing the heart up while oxygen is in the lungs pushed more blood through the capillaries in the lungs and this allows more oxygen to be deposited from the lungs into the blood.

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! Heart rate slows down during expiration because there is a low oxygen level in the lungs and the blood flow needs to be a lot slower. The main issues regarding the respiratory sinus ar-rhythmia are as follows:

1. During rest you want to see RSA occurring on the ath-lete’s ECG (a measure of heart rate).

2. If RSA is not occurring during rest then this means there is a decrease in the NA vagal tone.

3. If a lower than normal heart rate is also occurring in the absence of RSA when the athlete is at rest then you probably have a seriously overtrained athlete on your hands because this indicates that DMNX is supplying the vagal tone not the nucleus ambiguus.

References

Porges, Stephen. Orienting in a defensive world: Mammalian modifications of our evolutionary heritage. A Polyvagal Theory. Psychophysiology, 32 (1995), 301-318.

Else, P. L., AND A. J. HULBERT. Comparison of the “mammal machine” and the “reptile machine”: energy production. Am. J. Physiol. 240 (Regulatory Integrative Comp. Physiol. 9): R3-R9, 1981

Berne, Robert. M and Matthew Levy. Cardiovascular physiology (8th ed). Mosby, Inc., St Louis, Missouri. 2001.

3Introduction to overtraining

What You Will Learn

When you have completed this module you will be able to:

1. Distinguish between acute overload, over-reaching and over-training

2. Appreciate the seriousness of overtraining to the health of the athlete

3. Discuss the symptoms of overtraining

4. Discuss how over-reaching is used appropriately

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Introduction

! So far we have overviewed the endocrine system and the autonomic nervous system. Now we are going to delve into the complexities of what overtraining is. Following this module we will discuss ways in which you can monitor overtraining states of your athletes. Then we will delve deeper into the physiology and biochemistry of overtraining so you have a solid insight into this very frustrating phenomenon.

! Overtraining, or 'unexplained underperformance syn-drome', is not fully understood. It appears to be due to a pro-longed maladaptation to training, possibly because of an imbal-ance between training and recovery, and manifests as chronic fatigue, in conjunction with mood and sleep disturbances, lack of motivation, and frequent minor infections.

! It is thought that the fatigue accumulation process is asso-ciated with a reduced efficiency of the immune system, possibly due to alterations in metabolic response to training stress. The criteria for diagnosing overtraining is unexplained under-performance despite the maintenance or increase of training load. Overtraining can lead to a cyclic phenomenon involving psychological, physiological and underperformance that posi-tively feed upon each other to deepen underperformance over time (Figure 1). The athlete is in a constant struggle to keep up

Section 1

Introduction to overtraining

27

with training, require a greater amount of time to recover, and their technical skills will suffer.

! Although overtraining research has focused on endurance sports and activities the phenomenon occurs in a wide variety of sports. Research indicates overtraining occurs in more than 60% of distance runners during their athletic careers, more than 50 percent of soccer players during a 5-month competitive sea-son, and in 33% of basketball players participating in a 6-week training camp. It is likely to become even more common as sport demands more of the athlete's time and energy reserves.

! There is little doubt the human body has remarkable adap-tive flexibility. However, there is also little question that limits ex-ist to the human body’s ability to adapt and endure intense exer-cise training for sport. Once this adaptation threshold is ex-ceeded, the body fails to adapt appropriately and physical and mental performance declines. The human body lacks the ability to adapt to any single, severe stress for an extended time. We

are designed to be movement generalists – not specialists in a small number of movements.

! Sport, by its very nature, demands specificity of training stress and it’s really important for you as a coach to understand the fragility of the human body, while you are training it to ac-complish remarkable feats. It’s important to match the athlete’s mental desires to the frailty of their body so their mind does re-peatedly demand more of their body than it can deliver.

What You Will Learn

! In this module we discuss the difference between acute overload, over-reaching and over-training. There are many symptoms of overtraining and we will examine how the health of the athlete is affected. We will also examine over-reaching can be used to an athlete’s advantage if used cautiously on older and more experienced athletes.

Training Load Continuum

! There is a continuum of training zones ranging from under-training on one end, to overtraining on the other (Figure 2). In between are two additional zones. One is referred to as

Figure 1. Overtraining leads to a cyclic phenomenon

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the 'acute overload zone' and the other as the 'over-reaching zone'. During their careers athletes can experience a full contin-uum of all the zones of training load. Periods of under-training occur between competitive seasons or during recovery.

! Acute overload is the deliberate overload of the physiologi-cal systems during a single workout session designed to cause specific types of adaptation. It takes several sessions of acute overload for the body to adjust to a specific training stimulus.

! Over-reaching refers to several training sessions linked by inadequate recovery between the sessions. This usually results in a temporary performance decrement lasting from several days to a couple of weeks. Overreaching is often a deliberate training adaptation strategy, but it can also be unplanned, unde-

sirable outcome of overly strenuous training. This can occur very easily when you are working with younger training aged athletes.

! If the athlete is working within the acute and over-reaching zones, enhanced performance can occur. If recovery does not occur within the allotted recovery time then the athlete enters into the maladaptation phase of 'overtraining' and will become quite sick both physically and psychologically.

! The only difference between overreaching and overtrain-ing is the time factor. According to the definition both are the out-come of extended training stress with inadequate recovery. Overreaching is a special form of adaptive overload suitable for more experienced athletes. Indiscriminate and prolonged over-reaching training strategies eventually progress into the over-training phase.

A Different Perspective

! The three types of training overload include acute over-load, over-reaching and over-training. All three result in perform-ance decrements – it's simply a matter of the degree to which performance decrements occur. It takes 24 hours to recover from acute overload, a few days to recover from over-reaching and several weeks to months to recover from over-training.

Figure 2. Range of training

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Over-training is never intentional and is definitely not a training strategy. Acute overload is the safest approach for younger and intermediate training aged athletes. So since acute overload is an acceptable method of training we will focus on the more problematic training overload – over-reaching and over-training.

! The European College of Sports Science task force offer an alternative to this simple two-component model of over-reaching and over-training (Figure 3). Intensified training can have three possible outcomes. Short-term overreaching is con-sidered as functional overreaching that has a useful training pur-pose for older and more experienced athletes. There is a per-formance decline, but with appropriate recovery a higher ‘‘super-

compensation’’ effect can occur that is not achievable with the simple acute overload/recovery strategy.

! Extreme overreaching is “non-functional” overreaching that occurs when functional over-reaching has continued for too long. There is consistent stagnation, or decrease in perform-ance that can take weeks for recovery to occur - . However, with sufficient rest, recovery can eventually occur. You don't ever want to take your athlete into non-functional over-reaching – it serves no purpose. Overtraining syndrome (OTS) occurs when a high training volume or intensity has been applied for too long. And you definitely do not want to take your athlete here because the athlete may never fully recover.

! In all cases there is a performance decline and athletes will often show similar clinical, hormonal, and other symptoms. The diagnosis of full blown overtraining is usually only made af-ter the athlete has experienced extended and unexplained un-derperformance problems. By this time the damage has already been done.

Symptoms

! In many athletes, the first obvious signs of overtraining can be any one or a combination of generalized fatigue, recur-rent headaches, diarrhea, weight loss, and loss of appetite for

Figure 3. Simple two component model

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food or work. Others find they are unable to sleep properly, and have worsening allergies, colds, flu, or respiratory infections. The symptoms vary from one athlete to the next, and they can be nonspecific and numerous.

! Case studies of elite athletes who have overdone their training indicate how devastating overtraining can be. Alberto Salazar is a classic case in point. Salazar raced in the late 1970s and early 1980s. He was the pick to win an Olympic Gold medal in Los Angeles.

! However, suddenly, his performance dropped dramatically and by 1983 he was no longer the worlds best marathoner. In-stead of winning the Los Angeles Olympic marathon he finished 15th. Over the following ten years he struggled to train and race effectively. He was diagnosed with adrenal exhaustion syn-drome.

! As you know, the adrenal glands are governed by the hy-pothalamus through the pituitary. For this reason another diag-nosis was exhaustion of the hypothalamus. Salazar had diar-rhea daily for 10 years. Here’s what he wrote about that period of his life:

! “I hated running. I hated it with a passion . . . In retrospect, I now know what was wrong and what caused my problems. I had three episodes of heat stroke. That, combined with all the years of hard training at such a high level without ever taking a

break, damaged part of my brain. . . My endocrine system was so screwed up that I had very low hormone levels . . For sev-eral years, I was on a wild-goose chase to get my hormone lev-els normal again. I wasn’t competing anymore but still felt awful. I was always so exhausted I’d fall asleep at my desk at work . . . I didn’t have the energy to do normal things and was always in a bad mood.”

! After dropping out of the 1992 US Olympic Marathon trials, Salazar began treatment with the antidepressant medication, Prozac. His health and mood changed and he began running 100 km per week. Before long he extended it to 200 km per week. In 1994 he won a marathon in South Africa. However, shortly after this race he could only manage around 30 minutes of running per day. He continued to take Prozac, but it no longer worked. On June 30th, 2007 the running world was stunned to hear Salazar had a major heart attack.

Self-monitoring Questions

! Another world-class marathoner, Grete Waitz, was known for her consistent marathon performances. She attributed this to her constant monitoring of signs for possible overtraining. Waitz claims the positive answers to three or more of the follow-

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ing questions gave here important clues she was taking her body beyond its adaptive capacity.

• Does my normally comfortable workout leave me breath-less?

• Do my legs feel heavy for far longer than usual after a hard workout or competition?

• Do I find it especially hard to climb steps?• Do I dread the thought of training?• Do I find it hard to get out of bed in the morning?• Do I have a persistent lack of appetite?• Am I more susceptible to colds, flu, headache or infec-

tions?• Is my resting heart rate 5 to 10 beats higher than usual?• Is my heart rate during exercise higher than usual?

! Waitz wrote that the feeling in her legs, and the way she breathed during training runs indicated when she could no longer push herself in training. Usually, heaviness in her legs would go away after a few minutes of running. When the feeling persisted, she knew she should rest rather than train. At the age of 51 Waitz was diagnosed with cancer. She died of cancer in 2011 at the age of 57.

! These are just two anecdotal stories about famous ath-letes known for their ability to push their bodies beyond what

was previously thought possible and developed serious health problems.

! There is some evidence that athletes from Eastern Euro-pean countries who allegedly overtrained for months, possibly years, finally succumbed to an illness known as Addison’s dis-ease. In this condition, there is depression, progressive weight loss, an inability to maintain blood pressure when standing, and severe physical incapacitation. The cause of Addison’s disease is a failure of the adrenal gland to secrete adequate amounts the hormone cortisol, which is essential for the adaptations the body makes when exposed to stress, including a training stress. The inability to exhibit a normal cortisol response has been observed in runners who are training heavily. The problem has been attributed to exhaustion of the hypothalamus.

Neurological Overtraining

! We don't often think about overtraining the nervous sys-tem. However, there is evidence from a phenomenon known as golfer 'yips' that overtraining the nervous system is indeed possi-ble. In golf, the 'yips' refer to a sudden or catastrophic break-down in skilled performance, and has been explained in terms of anxiety or stress. However, a 1992 study challenged this no-tion. It was found that golfer's yips was not associated with anxi-

32

ety disorder, or neurosis. Rather, the 'yips' appears due to re-peating the same movement over and over that the athlete ends up with peripheral or central nerve injury termed 'focal dystonia'.

! Focal dystonia refers to the fact that a muscle or group of muscles in a specific part of the body are causing involuntary muscular contractions and abnormal postures. Focal dystonia often strikes for no apparent reason to severely debilitate an ath-lete for months, or even for a whole career. The phenomena is most obvious in sports where precision and fine motor control are at a premium. Examples include cricket (bowling in particu-lar), tennis, table tennis, snooker and darts.

! Eric Bristow who was a well known darts player is a clas-sic example of how dystonia can affect careers. At the height of his career Bristow was unable to release the dart from his fin-gers. It took him 10 years to overcome this affliction.

! Focal dystonia has also more recently been described in runners and it's hard to describe running as a precise move-ment. Therefore, dystonia may be due more to countless hours of the same repetitive movement to the point where the nervous system runs out of the ability to adapt and make the necessary repairs before the next practice session. In essence, the athlete is likely to be training in the non-functional over-reaching mode for a long time and ultimately the nervous system becomes chronically overtrained.

! Medically, the condition is categorized as a task-specific movement disorder and characterized by the inability to perform a well-learned and well-practiced motor skill. The condition was first described in 1713. It occurred in high frequency among oc-cupations where writing was the prime skill (scribes and nota-ries). In 1911 the condition was called 'dystonia' and described very simply as abnormal increases in muscle tone and contrac-tions. In many cases dystonia interferes with the individual's ability to ever perform the specific motor skill effectively.

! The cause of dystonia is still open to debate, although it is appears related to a misfiring of neurons in the sensorimotor cortex. Under normal conditions, when the brain tells a muscle to contract, it simultaneously silences muscles that would op-pose the intended movement. In dystonia, it appears that the ability of the brain to inhibit the surrounding muscles is im-paired, leading to loss of muscle selectivity. Over a career, an athlete will perform similar repetitive movements hundreds of thousands of times, the result of which appears to cause some form of long-term neuromuscular overtraining injury.

Overtraining The Heart

! Can you overtrain the heart? Evidence is suggesting that we can. The first reporting of heart overtraining and its deadly

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consequences was 40 year old Athenian message runner, Phi-dippides. In 490 BC, the Persian King Darius the Great com-manded his army to attack the Greeks.

! Phidippides, was ordered to run 75 miles through moun-tainous terrain to Sparta to request military support. The Spar-tans could not assist the Greeks due to certain religious obliga-tions, so Phidippides ran back to Marathon, completing 150 miles in less than 2 days. When he arrived in Marathon, he learned that the Greeks had defeated the Persians under tre-mendous odds. Phidippides then ran to Athens, 26.2 miles from Marathon, to spread the news of this impressive victory with the other Greeks. When he arrived in Athens, Phidippides ex-claimed, “We are victorious!” He then collapsed and died. Since then there have been numerous accounts of endurance ath-letes suffering cardiac related complications.

! The research is coalescing around the idea that repetitive and sustained cardiac exertion causes heart chamber enlarge-ment, left ventricular hypertrophy, and increased rates of atrial and ventricular arrhythmias. Cardiac fibrosis is also seen. These structural and functional changes in athletes has been dubbed 'Phidippides cardiomyopathy'.

! Our palaeolithic ancestors walked a lot – not sustained run-ning for mile after mile after mile. Despite the myth presented in Born to run, there was no survival need for long sustained runs. Our ancestors did quick, short bursts of running interspersed

with lots of long distance walking. Micah True, the mythic ultra-runner in Born to Run, died at aged 58 from idiopathic cardiomy-opathy, which means a weak, stiffened, thick heart muscle. His heart was classic 'Phidippides cardiomyopathy'. The right ventri-cle and the two atria were particularly damaged.

! Many master runners in their early 60s and 70s are now facing a variety of cardiac problems after decades of intense forms of exercise. Younger hearts are able to tolerate extended workload – but around 35 – 40 years of age you begin to see the mounting damage. Atrial arrythmias is epidemic among en-durance athletes.

! Exercise is a drug and like any drug there is an optimal dose (Figure 4). Above that optimal dose and the drug becomes

Figure 4. Like any drug, exercise must be prescribed in the right dose to be effective

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toxic. The dose effect is a upside down U-curve – at either end the dose is unsafe. In the middle of the U-curve exercise can provide potent health benefits. High performance sports is on the very edge of being unsafe because the athlete is typically up here.

! The heart pumps about a gallon or 3.8 liters/minute. When the athlete is engaged in intense exercise it is 6 times the rest-ing value. Very elite athletes will generate a cardiac output of 35 – 40 L/ min. This is massive cardiac output and you can train to do this, but after a time of this type of volume starts causing tears in the heart muscle. Troponin levels are elevated in up to 50% of runners completing a marathon. Troponin indicates heart damage. At the end of a marathon, the heart does not con-

tract properly because the muscle fibers are stretched out. This has been replicated in rats who run over an hour per day. Scar tissue begins to form in their hearts – in effect inducing acceler-ated aging of the heart.

! With adequate recovery the damage to the heart is reversi-ble – however, as the athlete gets older it takes much longer to recover and may not recover if the athlete begins training again too soon. In other words we are back in the non-functional over-reaching mode that ultimately ends up as very devastating chronic overtraining of the heart.

Musculoskeletal Overtraining

! Muscles, bones, tendons and ligaments become stronger and more functional with exercise due to a process referred to as remodeling. During remodeling the damaged tissue is bro-ken down and then replaced and reinforced. The imposed stress will only cause a training effect if there is sufficient recov-ery time for remodeling to occur.

! Inadequate recovery leads to chronic tissue micro-trauma. The mounting micro-trauma usually due to a too rapid accelera-tion of training intensity, duration, or frequency. Both adult and pediatric athletes are susceptible. However, the child's musculo-

Figure 5. Troponin levels after a marathon indicating heart damage

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skeletal system is particularly vulnerable to excessive stress im-posed by most sports.

! You really need to avoid overtraining a child's musculo-skeletal system because their bones, ligaments and tendons can be permanently affected by the injury. Let's quickly over-view some of the more common pediatric overuse injuries you will likely see.

! Apophysitis is commonly seen at the heel, elbow, and knee during times of rapid growth. An apophysis is a secondary ossification center where the muscle tendon attaches. During rapid bone growth the muscle-tendon unit is unable to stretch sufficiently to maintain its previous level of flexibility, causing in-creased tension at the attachment site. Training and competi-tion across this tight muscle-tendon unit amplify traction forces. The result is chronic irritation, inflammation, and micro-tissue detachment at the bone-cartilage junction. Heel apophysitis is most commonly seen in running, and jumping such as soccer, basketball, track, gymnastics, and dance.

! Overuse injuries to the physis and epiphysis are com-mon in the sports requiring overhead throwing movements and gymnastics. The epiphysis is the bony section at the end of a long bone, while the physis is the growth plate itself. Examples include little league shoulder and gymnast's wrist.

! Repetitive stress can also lead to tendinitis. Patellar tend-initis and iliotibial band tendinitis are the most common, al-though foot and ankle tendinitis, and shoulder rotator cuff tend-initis can also occur in young athletes.

! Stress fractures are caused by chronic low level repeated stress that ulti-mately weaken the bone. Predominant sites of stress fractures in young athletes include the tibia, fibula, femur, metatarsals, and navicular bone in the foot.

! Patellar tendinopathy, more commonly known as “jumper's knee” is due to repetitive loading of the quadriceps muscle during jumping and running activities. Over time, the strain on the tendon causes structural changes within the tendon. The condi-tion is seen in jumping sports, such as basketball, volleyball, and track and field (high and long jump), although athletes in other sports such as soccer and football are also affected.

! Spondylolysis contributes to nearly 50% of the back pain experienced in young athletes. It is a defect in the pars interar-ticularis of the vertebal arch and reduces mobility. It occurs in

36

sports where there is repetitive flexion and hyperextension mo-tion, combined with trunk rotation. Gymnastics, football line-man, weight lifting, dance, and volleyball are sports that can lead to spondylolysis. The fifth lumbar vertebra in the lower back is usually affected. If the stress fracture weakens the bone so much that it is unable to maintain its proper position, the ver-tebra can start to shift out of place. This condition is called spon-dylolisthesis. If too much slippage occurs, the bones may begin to press on nerves and surgery can sometimes be necessary to correct the condition.

! Incidentally, back pain is very common in adult athletes as well, and the excessive core training these athletes undertake can exacerbate their back problems.

Concluding Comments

! Obviously, any condition as complex as overtraining, is in-fluenced by numerous physiological systems. We've looked at a few of them – endocrine, neurological, cardiac and musculo-skeletal. You have to consider all these forms of overtraining.

! When dealing with younger athletes it is better to under-trained than over-trained them. Adequate rest is an important component of any athlete's training, but this is especially true for youth.

! Consider all aspects of the athlete's life and modify train-ing loads when they are experiencing non-training stresses such as examination pressures or relationship difficulties, etc. These stresses add to the training stress and it is important to ensure that their ability to adapt is not compromised.

Figure 6. Damage to the lower back occurs with excessive bending

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References

Alberto Salazar’s story was reported by Wischnia B. Comeback at Comrades. Runners World, 29 (8): 76-77, 1994.

Czajkowski, W. (1982). A simple method to control fatigue in en-durance training. In P.V. Komi (Ed.) Exercise and Sport Biology, International Series on Sport Sciences. Human Kinetics, Cham-paign, IL, 207-212.

V. PICHOT, F. ROCHE, J. M. GASPOZ, F. ENJOLRAS, A. AN-TONIADIS, P. MININI, F. COSTES, T. BUSSO, J. R. LACOUR, and J. C. BARTHÉLÉMY. Relation between heart rate variability and training load in middle-distance runners. Medicine and Sci-ence in Sports and Exercise, Vol. 32, No. 10, pp. 1729–1736, 2000

Lehmann, M., Foster C; Dickhuth HH., Gastmann U. Autonomic imbalance hypothesis and overtraining syndrome. Medicine and Science in Sports and Exercise, Vol. 30, No. 7, pp. 1140-1145, 1998.

Cyril Petibois, Georges Cazorla, Jacques-Rémi Poortmans, Gé-rard Déléris. Biochemical Aspects of Overtraining in Endurance Sports. Sports medicine (Auckland), 2003, Vol 33., Issue 2. pp 83- 94.

Dhungana, Samish; Jankovic, Joseph Yips and other move-ment disorders in golfers. Movement disorders: 2013, Volume 28, Issue 5. pp 576 -581

Torres‐Russotto, Diego; Perlmutter, Joel S. Task‐specific Dysto-nias Annals of the New York Academy of Sciences, 10/2008, Volume 1142, Issue 1. p. 179 – 199.

Wu, Laura J.C. , Jankovic Joseph. Runner's dystonia. Journal of the Neurological Sciences. Volume 251, Issues 1–2, 21 De-cember 2006, Pages 73–76

Leveille, Lise A; Clement, Douglas B, Case report: action-induced focal dystonia in long distance runners. Clinical journal of sport medicine : official journal of the Canadian Academy of Sport Medicine, 09/2008, Volume 18, Issue 5. pp 467 – 468

Østerås H; Garnæs KK; Augestad LB. Prevalence of musculo-skeletal disorders among Norwegian female biathlon athletes. Open Access Journal of Sports Medicine, March, 2013. p 71 – 77

Trivax, Justin E; McCullough, Peter A. Phidippides Cardiomyo-pathy: A Review and Case Illustration. Clinical Cardiology, 02/2012, Volume 35, Issue 2. pp 69-73.

James H. O'Keefe, Harshal R. Patil, Carl J. Lavie, Anthony Ma-galski,Robert A. Vogel, Peter A. McCullough. Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise.

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Mayo Clinic Proceedings Volume 87, Issue 6, June 2012, Pages 587–595

Hoang, Quynh B; Mortazavi, Mohammed. Pediatric overuse inju-ries in sports. Advances in pediatrics, 2012, Volume 59, Issue 1. Pages 359-383.

4Monitoring overtraining states

What You Will Learn

When you have completed this module you will be able to:

1. Teach your athletes how to manually measure their heart rate

2. Teach your athletes how to assess a resting baseline heart rate

3. Design and implement an overtraining monitoring system and understand the physiological bases behind the system.

4. Discuss the potential value of a heart rate variability monitor

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Introduction

! A training effect only occurs if the training load is sufficient to induce disturbance in the homeostasis of cells, tissues and organs. It sounds quite simple, doesn't it. You disturb the ath-lete's homeostasis and it returns to homeostasis quite quickly. However, as you now know a training overload is a continuum of effects. There are times when an athlete might enter into the overreaching part of the overload continuum. In a general sense, overreaching is an intentional increase the total training load for a few days with inadequate recovery.

! The intent is to induce a longer and greater disturbance of homeostasis so that further training adaptation is attained. It is now common to categorize over-reaching into functional over-reaching (FOR), and non-functional over-reaching (NFOR). The former can be valuable to an athlete’s training while the other is not valuable. FOR is used by athletes during a typical training cycle to stimulate an improvement in performance capacity above what would be achievable after a normal training ses-sion.

! Recovery from FOR should only take a few days. If FOR is done for a too long period, fatigue accumulates, and this sends the athlete into NFOR phase of persistent fatigue, performance decrease, neuroendocrine and immunological changes, and al-

Section 1

Monitoring overtraining states

41

terations in mood states. This may take a couple of weeks – or longer – for homeostasis to return to normal. If NFOR continues for too long the athlete enters into the dangerous overtraining phase from which recovery can take from months to years. The athlete's endocrine system is way out of whack!

! The athlete can slip from FOR into NFOR without any no-ticeable clues until the athlete has a continual decline in per-formance. Therefore, it's aways a good idea to monitor physio-logical markers that will alert you that FOR is slipping into NFOR. Monitoring strategies are classified into two broad cate-gories of non-invasive and invasive. Invasive monitoring tech-niques require sophisticated laboratory testing. For the average coach the non-invasive methodologies are the most practical so we will only discuss these.

!

What You Will Learn

In this module you will learn how to teach your athletes how to manually measure their heart rate and their baseline heart rate. From this information you will be able to design and implement an overtraining monitoring system and understand the physiological bases behind the system.

Heart Rate Monitor

! A heart rate monitor is standard equipment for athletes these days. It is a portable electrocardiogram or ECG (also EKG). Both the electrocardiogram and the heart rate monitor measure the electrical activity that's produced by the heart. Every time the heart beats the beat is caused by the electrical activation of all the cells in the heart which beat essentially all at once.

! Electrodes on the skin can pick up this electrical activity and transmit it to a monitor. In the case of a heart rate monitor the computer that reads the signal is worn on the wrist.

! Heart rate monitors have a strap that goes across the chest with two leads that pick up the elec-trical activity of the heart and trans-mits the signal to the write monitor and lets you know your heart rate.

How To Measure Heart Rate

! Heart rate is the number of times the heart beats per min-ute. It can be measured by feeling the pulse created by the

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rhythmic expansion and contraction (or throbbing) of an artery as blood is forced through it when the heart contracts and re-laxes. A pulse can be felt where the artery is close to the skin and these locations include the wrist, neck, groin or top of the foot.

! The most common location to measure pulse is in the wrist.Taking a pulse is easy and only requires a watch with a second hand or digital second counter.

• Turn the palm side of the hand so it is facing upward.

• Place the index and middle fingers of the opposite hand on the wrist, approxi-mately 1 inch below the base of the hand.

• Lightly press the fingers down in the grove be-tween the middle ten-dons and the outside bone. Make slight posi-tion adjustments until a throbbing of the pulse become no-ticeable.

• Count the number of beats for 10 seconds, then multiply this number by 6 to obtain heat rate for a minute.

Assessing Resting Baseline Heart Rate

! It is important for all athletes to establish a baseline meas-urement of their resting heart rate. Use a recovery week to es-tablish these baseline values or begin monitoring resting heart rate during the off-season. Measure heart rate just after waking in the morning and before getting out of bed. Count the pulse for 10 seconds and multiply by 6 to obtain heart rate for 1 min-ute.

! Alternatively, the athlete can wear a heart rate monitor to bed for the week and check heart rate just after wakening. Pro-vide each athlete with a heart rate recording chart at the begin-ning of each month. It is easy to reproduce a heart rate monitor-ing chart by using Excel. Under normal conditions the athlete’s heart rate will not vary much – perhaps 1 to 2 beats every min-ute. When the athlete has a resting baseline heart rate estab-lished this is used for comparison purposes.

Tracking Resting Heart Rate

! The most basic test is to monitor resting heart rate before getting out of bed on an ongoing basis (Figure 1). This strategy has been used since the late 1950s. An increase in heart rate indicates a higher than normal sympathetic influence suggest-

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ing the athlete’s body has not reestablished homeostasis. It is a good method for picking up short-term fatigue quite quickly. The major drawback with this technique is the difficulty in placing any increase in heart rate in the context of normal day-to-day variation. A 1 to 2 beat increase for a couple of days is typically ignored. However, if the 1-to 2 -beat increase is consistently pre-sent after 2 or 3 days ask the athlete about how they feel and if they are obtaining adequate sleep. This will help you determine if some over-reaching has occurred. A drop in heart rate is typi-cal of an aerobically trained athlete.

! The physiology behind the increased heart rate appears to be due to a withdrawal of the parasympathetic influence on the

heart. When athletes, who are overtrained are compared with athletes who are not overtrained, the sympathetic influence on the heart is the same. Overtrained athletes, though, have a lower parasympathetic tone than those not who are not over-trained and as a result the sympathetic nervous system is hav-ing a higher influence on heart rate than normal. A withdrawal of the parasympathetic tone is an indication that the nucleus am-biguus branch of the vagus nerve has been compromised.

The Orthostatic Test

! There are many variations of the orthostatic test. One sim-ple test involves measuring the athlete’s resting heart rate be-fore getting out of bed as we discussed above. Then a second heart rate measurement is taken exactly 20 seconds after the athlete stands up. If overtraining occurs the waking pulse rate rises for the reason we discussed above. In addition, the differ-ence between their supine and standing heart rates increases (compare a and b in Figure 2).

! Assume an athlete shows a constant drop in both resting and standing heart rate while training aerobically between April and July (Figure 2). As the athlete becomes better trained aero-bically this drop in heart rate is expected and is thought to be due to an increase in parasympathetic tone. In August note the

Figure 1. Resting heart rate of an athlete immediately after waking can indicate periods of over-reaching

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steep and sustained increased in the resting heart rate ( b in Figure 2). This indicates the athlete has not recovered from the previous training sessions. The enlarged gap between the standing and supine heart rate provides some idea as to how bad things are. At this point an adjustment in training is neces-sary. As you watch the gap close you can assess the success of the recovery. It can take several months for an athlete to re-cover from the overtrained state.

! Physiology of the orthostatic test: Changing from a su-pine to a standing position produces changes in gravitational forces causing a redistribution of blood into the compliant veins of the legs. This creates a drop in blood pressure and reduction

in blood returning to the heart. There are many intrinsic sensory mechanisms in strategic locations to sense the drop in blood pressure so that the brain is not deprived of oxygen. The sympa-thetic nervous system increases its activity to restore blood pressure back to normal. One response is an increase in heart rate. When the athlete stands quickly, the SNS must quickly snap into action to compensate for the change in blood pres-sure and redistribution of blood volume. The increase in resting heart rate is due to a withdrawal of the parasympathetic influ-ence. The increase in heart rate upon standing of an over-trained athlete is due to an increased sensitivity of the sympa-thetic nervous system to stress. In this case the stress imposed is standing.

! If you see the gap between resting heart rate and standing heart rate increasing this represents lack of recovery from previ-ous training sessions. Standing heart rate will always be higher than supine heart rate and the difference between the two heart rates is athlete specific. When a baseline has been established it is simply a matter of watching for changes.

Heart Rate Variability

! Heart rate variability is also known as respiratory sinus ar-rhythmia (RSA) and refers to heart rate variability in synchrony

Figure 2. The orthostatic test for monitoring overtrain-ing

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with respiration. The R-R interval on an ECG is shortened dur-ing inspiration and prolonged during expiration (Figure 3). Al-though RSA is used as an index of cardiac vagal function, it is also a physiologic phenomenon reflecting the efficiency of pul-monary gas exchange. RSA potentially saves energy expendi-ture by suppressing unnecessary heartbeats during expiration. It reflects efficient functioning of the heart.

! Polar now has a heart rate monitor capable of measuring heart rate variability. The Polar monitor has good reliability and is thought to provide an objective indication of early overtrain-ing. The test includes a combination of resting heart rate, stand-ing heart rate, and heart rate variability.

! The athlete lies down on the floor for 3 minutes resting peacefully and fully relaxed. After the 3 minutes the athlete slowly stands up. The 5-minute test is recorded using heart rate

monitor. The heart rate monitor provides an orthostatic heart rate and heart rate variability.

! Polar provides an analysis of the results in terms of good recovery, a stagnant state, an overreached state, sympatheti-cally over-trained and parasympathetically over-trained. The in-structions also provide suggestions on what to do to recover from any of the over-trained states. A return of heart rate vari-ability during a recovery week after a few days of over-reaching has been used to indicate a supercompensation effect.

! Heart rate variability is thought to produce more reliable in-formation about an over-reached state than simple heart rate. Reduced heart rate variability shows up sooner than an in-crease in heart rate does allowing you to catch possible excess fatigued states early. For this reason tracking heart rate variabil-ity in conjunction with the training protocol reveals threshold-training volumes and/or intensities athletes should not cross if they wish to avoid an over-trained state.

Questions To Ask

! If you suspect that there is some over-reaching, or over-training, and the monitoring strategies you have set up sug-gests that this is indeed the case, ask the athlete some addi-tional questions.

Figure 3. Heart rate variability is a normal phenomenon

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Table 1 summarizes the athlete’s aspects of the athlete’s health that can indicate the state of the athlete’s sleep, and if possible overtraining is occurring.

• There will be a lack of sleep - i.e. the athlete will not be sleeping many hours each night. Athletes in training need around 10 hours of sleep each night.

• Sensation of being tired will be quite high.

• There will be a lack of willingness to train and lack motiva-tion.

• Appetite will not be good.

• Competitive willingness is lacking and there may be mus-cle soreness.

• Explore each of these with your athletes if you suspect overtraining.

More Insight Into Heart Rate Variability

! Training and recovery each comprise 50% of the perform-ance improvement equation. The body need recovery to repair and adapt itself before the next training session. Quality of sleep, nutrition and an absence of additional life stresses are also components of increased performance. Neither training nor recovery can be optimized without adequate sleep, nutrition, and minimal non-training stress. The difficult part is figuring out how much training stress the athlete's body can tolerate and how much recovery is needed before training becomes counter-productive.

! We've discussed how overtraining progresses from func-tional overreaching and is equated with the healthy application of the overload principle of training, through non-functional over-reaching (when the body is unable to repair itself fast enough)

Length of sleep (H)Length of sleep (H) 12+ 10 99 8 7 6 5 0

Quality of sleepVery deep

NormalNormalNormal RestlessRestlessBad with breaks

Bad with breaks

Not good at

all

Not good at

all

Tiredness sensation

Very rested

NormalNormalNormal TiredTired Very tiredVery tiredPainfully tiredPainfully tired

Training willingness

Excellent GoodGoodGood PoorPoor UnwillingUnwillingDid not

trainDid not

train

AppetiteVery good

GoodGoodGood PoorPoorEat

because should

Eat because should

Did not eat

Did not eat

Competitive willingnessCompetitive willingness HighHighHigh AverageAverage LowLowNot at

allNot at

all

Muscle sorenessMuscle soreness No PainNo PainNo PainLittle painLittle pain

Mod painMod painSevere

painSevere

pain

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to sympathetic overtraining. This is the state that can often be detected by elevated pulse during the morning pulse check.

! The sympathetic branch of the nervous system that we call the 'fight or flight' branch involves production of stimulant hormones such as adrenaline and cortisol. These are chemical messengers that signal the heart to pump faster and blood ves-sels to constrict or dilate. We are not designed to have these hormones flowing around us for long, extended periods, and if they do they can lead to problems including heart disease. Ath-lete's often push through sympathetic overtraining into a state known as parasympathetic overtraining, when the fight or flight hormones become exhausted and extreme fatigue follows. Clearly we need some means to detect if the athlete is overdo-ing things based on their physiological capabilities and heart rate variability is thought to be one method IF we can get the technology sufficiently sensitive to provide useful information.

! The most comprehensive report on HRV published in 2008 in the British Journal of Sports Medicine by Bosquet. In this study it was concluded that HRV alterations that do occur in ath-letes who are over-reached and are within the range of normal physiologic variability. The fact that this study didn’t produce any groundbreaking information is frustrating because anecdo-tal data from athletes tell a slightly more positive story about the value of HRV. It's worth discussing some of the data obtained and the insight provided.

Case Study

! Figure 5 illustrates the major players in the HRV test. The SNS increases heart rate and decreases HRV, and the PNS de-creases the hearts activity and increases HRV.

! Figure 6 illustrates an athlete's HRV while at rest and while standing. The HRV data was collected for 3 minutes lying down, and then for 3-minutes standing up. When the parasym-pathetic system dominates and the SNS withdraws the lines on the graph will be very jagged. This illustrates considerable HRV

Figure 4. Relationship between sympathetic and para-sympathetic activity and overtraining

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and occurs when the athlete is resting or lying down. Notice how the lines smooth out when the athlete stood. This indicates the dominance of the sympathetic nervous system. The job of the SNS is to increase blood pressure and redistribute blood vol-ume so the athlete does not faint due to blood pooling in the

legs. The HRV is reduced when sympathetic nervous system dominates.

! The same principle is used in HRV software such as that developed by Firstbeat Technologies that is based in Finland. When an athlete is not recovered, the SNS remains overactive and therefore HRV is reduced. You see that effect in Figure 7. When the athlete is well recovered the lines are very jagged. The HRV software analyzes the 'jaggedness' of the lines to de-termine the athlete's recovery state.

Figure 5. Major players in the HRV test.

Figure 6. Athlete's HRV while at rest and while standing.Figure 7. HRV can measure chronic stress, overtraining, health disorders and disease. It can also measure the

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! An analysis of the athlete's rest/stress states is measured during sleep. The software provides the athlete with a stress and recovery score on a scale from -100 to +100. The stress and recovery index is the balance between stress and recovery. The ‘dark’ red represents stress reactions whereas ‘light’ repre-sents recovery. A score of 20 and above is considered complete recovery.

! Figure 8 is an example of an analysis. The gray area repre-sents the athlete's recovering zone. The autonomic nervous sys-

tem is in the correct balance. The red line represents HRV data over one month taken several days apart. It is possible to meas-ure recovery scores every night, but this is not necessary for most athletes if you are doing the simple hard-easy day training model. This athlete here is adding several days of FOR.

! There are points where the athlete is well recovered and points where the athlete is not fully recovered. An easier train-ing session was prescribed to allow the recovery index to return to normal. At the end there was a good recovery and super-compensation effect for competition.

Use In The Field  

! The role of technology in sports is growing. The scientific input and output is used to try to improve the athlete's perform-ance. One goal to educate the player how to train effectively. It is also being used to assess sufficient recovery. The underlying purpose is to gain a competitive edge.

Final Comments

! The effect of a training session not only depends on the ex-trinsic load, which you might measure by duration, intensity,

Figure 8. State of an athlete’s stress-recovery based on HRV measures during sleep.

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sets, repetitions, and terrain. It also depends on the athlete’s in-trinsic state. If they are tired, they will not adapt.

! While heart rate variability is a relatively new concept in sport, it has long been recognized as as a predictor of sudden cardiac death in the medical field. The Autonomic Nervous Sys-tem is the master controller of all organ systems and cells in the body. It provides a fine-tuned mechanism for the regulation all all the body's physiological functions. Ideally, the two compo-nents of the ANS – the sympathetic and parasympathetic - work in perfect harmony. If this system is not functioning well then many health problems develop.

! Heart rate variability is useful insight into the ANS and it is particularly useful in sports because it indicates completion of the repair and recovery process the body undergoes after a training session. The sympathetic nervous system is the stress

component of the nervous system – kicking it into action to meet increased metabolic needs. The parasympathetic nervous system relaxes the body and heals it.

! Training interferes with the SNS and PNS balance by caus-ing the sympathetic system to increase its activity to cope with the stresses created by training. The SNS activity will remain high until all the repairs are done. When the body is over-reached the autonomic nervous system has difficulties in return-ing to and maintaining its balance. The foundation underlying an athlete's improved performance is recovery of the autonomic nervous system back into the correct balance. The HRV test evaluates this balance. In other words, it provides an insight into how well the body has recovered from the stress of train-ing.

! You can think of HRV as an audit of whether you have the correct training planned on that particular day. It’s certainly not perfect. But, it does call out coaches and athletes who treat fa-tigue as a test of character to be conquered each day. Instead, fatigue is the body's method for protecting itself from harm. HRV refines our understanding of stress and recovery and can help prevent careless training workload decisions that poten-tially harms the athlete over the long-term.

! Whatever overtraining monitoring method you use de-pends on your resources and what works best for your athletes. Select one method and refine it to suit your situation and then

Figure 9. Training session effect depends on several vari-ables.

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stick with it. Evaluate heart rate data in conjunction with other data you gather from your athlete. Monitoring the state of the autonomic nervous system, whether objectively or subjectively, can help you better individualize an athlete’s training and mini-mize their chance of slipping into an over-trained state. By do-ing this the athlete has a better opportunity to reach their opti-mal potential as they enter into the elite phase of their perform-ance later on in their sport’s career.

References

Yasuma F, Hayano J. Respiratory sinus arrhythmia: why does the heartbeat synchronize with respiratory rhythm? Chest. 2004 Feb;125(2):683-90.

Kreider, R., Fry, A. C., & O’Toole, M. (1998). Overtraining in sport: terms, definitions, and prevalence. In R. Kreider, A. C. Fry, & M. O’Toole (Eds.), Overtraining in sport (pp. vii -/ix). Champaign, IL: Human Kinetics.

Halson, S., & Jeukendrup, A. (2004). Does Overtraining exist? An analysis of overreaching and overtraining research. Sports Medicine , 34, 967- 981.

Urhausen, A., & Kindermann, W. (2002). Diagnosis of overtrain-ing/ what tools do we have? Sports Medicine, 32, 95-102.

Meeusen R, Duclos M, Gleeson M, Rietjens G, Steinacker J, & Urhausen A. Prevention, diagnosis and treatment of the Over-training Syndrome ECSS Position Statement ‘Task Force’ Euro-pean Journal of Sport Science, March 2006; 6(1): 1 – 14

Bosquet L, Merkari S, Arvisais D, Aubert A. Is heart rate a con-venient tool to monitor overreaching? A systematic review of the literature. Br J Sports Med 2008;42:709–714

Hynynen E., Uusitalo A., Konttinen N., Rusko H. Heart Rate Variability during Night Sleep and after Awakening in Over-trained Athletes. Med. Sci. Sports Exerc., Vol. 38, No. 2, pp. 313–317, 2006.

Vanderlei LCM, Silva RA, Pastre CM, Azevedo FM and Godoy MF. Comparison of the Polar S810i monitor and the ECG for the analysis of heart rate variability in the time and frequency domains. Braz J Med Biol Res 41(10) pp. 854-859 2008

Pichot V, Roche F, Gaspoz JM, Enjolras F, Antoniadis A, Minini P, Costes F, Busso T, Lacour JR, Barthélémy JC. Relation be-tween heart rate variability and training load in middle-distance runners. Med Sci Sports Exerc. 2000 Oct;32(10):1729-36.

Hynynen E, Uusitalo A, Konttinen N, Rusko H. Cardiac auto-nomic responses to standing up and cognitive task in over-trained athletes. Int J Sports Med. 2008 Jul;29(7):552-8. Epub 2007 Nov 30.

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Heart Beat Based Recovery Analysis for Athletic Training.White paper by Firstbeat Technologies Ltd. https://www.firstbeat.com/science-and-physiology/white-papers-and-publications/

5Endocrinology of over-training

What You Will Learn

When you have completed this module you will be able to:

1. Discuss the endocrinology involved in overtraining and overtraining syndrome.

2. Explain how functional over-reaching and non functional over-reaching to polyvagal theory

3. Explain the difference between sympathetic overtraining and parasympathetic overtraining.

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1. Introduction

! We will now establish the link between overtraining and its health consequences. The terms 'overtraining' and 'overtraining syndrome' are used interchangeably. The term 'over-training' re-fers to heavier than usual training, whereas 'overtraining syn-drome' refers to the outcome of overtraining where health symp-toms occur. Acute overload is the stress imposed in one training session that is recoverable within 24 hours if kept within the physiological capabilities of the athlete (Figure 1). Theoretically,

Section 1

Endocrinology of overtraining

Figure 1. Overtraining versus overtraining syndrome

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FOR and NFOR are both overtraining – that is, loads are heav-ier than the normal acute overload. Recovery is possible within a few days for FOR and is done strategically within a training cy-cle. Recovery takes longer for NFOR and has no training pur-pose.

! Non-functional over-reaching is more akin to ‘overtraining syndrome’ because this is where the serious health symptoms begin to appear. It can take months to recover once the symp-toms of extended overtraining become seriously obvious. Across the continnum the athlete's performance declines. It is simply a matter of degree to which it declines, and how quickly recovery occurs. The goal is adaptation. Earlier in the course we discussed Selye's general adaptation syndrome or GAS model. The athlete's original level of performance gradually de-clines during a training session due to acute overload. Then re-covery occurs followed by the adaptation effect and a new level of performance due to supercompensation.

! When an athlete is functional over-reach a more advanced athlete may follow an incomplete recovery regime for 2-3 days. The idea is to stimulate a higher adaptation effect so that the new performance level is higher than the original functional per-formance. when NFOR occurs FOR continues too many days and recovery will take too long for the supercompensation ef-fect to occur. Overtraining syndrome occurs when NFOR is al-lowed to continue for too long.

What You Will Learn

! In this module we discuss some of the more important en-docrinology involved in overtraining and overtraining syndrome. We will also connect FOR and NFOR to polyvagal theory and explain the difference between sympathetic overtraining and parasympathetic overtraining.

Figure 2. Selye’s general adaptation syndrome

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The Problem Of ANS Dualism

! In the overtraining literature, reference is made to sympa-thetic overtraining and parasympathetic overtraining. Sympa-thetic overtraining refers to the high heart rate during exercise and during recovery until homeostasis is restored.

! The simple dual sympathetic/parasympathetic antagonistic balance approach we have been discussing with respect to HRV certainly provides a valuable window into the state of the athlete's body after training. However, the notion of a see-saw effect between sympathetic-parasympathetic activity only works to explain OT symptoms so long as the athlete does not be-come severely overtrained. When the athlete is severely over-trained it is called 'parasympathetic overtraining' to reflect the fact that athletes in a severely over-trained state have a low heart rate. The explanation is that the sympathetic nervous sys-tem is exhausted and is no longer functioning and so the para-sympathetic has retaken control.

! This explanation makes no sense because the nucleus am-biguus branch of the vagus nerve acts as a brake on the sympa-thetic nervous system. The brake was added during evolution because under sympathetic nervous system control human en-gines run at a very high speed that cannot be retained at rest without eventually 'blowing up the engine'. The brake can be re-leased quickly to allow instantaneous high levels of mobiliza-

tion. The nucleus ambiguus brake will not be restored unless the body is back in homeostasis, which in a very overtrained athlete it is clearly not. So theoretically, the athlete should retain a high heart rate while in the overtrained state. Yet, they don't and the question is why?

! Polyvagal theory provides some insights in why an over-training athlete’s heart rate is low.

Stress And Stress Response

! Until 1936, the term 'stress' was employed primarily by en-gineers to mean the forces necessary to exert a strain on any given object. In 1936 Hans Selye introduced 'stress' as a medi-cal term to define a collection of symptoms produced by the body in response to various noxious stimuli, or stressors. The stress arouses the body and can lead to an adaptation that will improve performance or the stress can lead to a maladaptation that interferes with performance.

! In sport, we place stress on the body through specific forms of over-load training depending on the desired outcome in terms of a skilled motor performance. A training stress is in-tended to disturb the homeostasis of the athlete's body. The word 'stress' and stressor' during training refer to a 'manufac-tured' threat to the athlete's body with the intension of produc-

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ing a set of physiological responses. The 'training stress re-sponse' is the physiological outcome of the training stress and is characterized by activation of the sympathetic nervous sys-tem and the hypothalamic-pituitary-adrenal axis. The body's ad-aptation to a challenge on these systems depends greatly on the type of the training stress applied.

! In times of threat, the hypothalamic-pituitary-adrenal (HPA) axis is activated. The hypothalamus secretes corticotropin re-leasing hormone (CRH) in order to stimulate the pituitary gland to secrete adrenocorticotropic hormone (ACTH). ACTH travel through the blood vessels to the adrenal gland and in response the adrenal cortex secretes cortisol. It also stimulates the re-lease of epinephrine and norepinephrine – both of which allow the gas pedal to be more easily activate. Cortisol enters the blood and peaks between 10 – 30 after the end of the training session.

! The main role of cortisol is to allow the body to success-fully adapt to challenges that disrupt its internal environment. Cortisol is essential for survival and is critical in the return to and maintenance of homeostasis. It has a wide spectrum of es-sential tools for adaptation after a stress situation. However, when in excess, it can lead to a host of health problems includ-ing immune, cognitive and emotional disorders.

! At rest, cortisol is released in pulses about every 60 mins. This is thought to allow the body to continually regulate homeo-

stasis. The highest pulse occurs in the morning after waking, fol-lowed by decline throughout the day. The lowest cortisol pulse occurs around midnight. The cortisol waking response is thought to reflect the challenged of waking up and getting the body moving. It is believed to restore the body to a fully alert state, among other important actions that maintain survival. In-terference with this pulse activity has been associated with stress-related illnesses. Athletes in heavy training show higher evening and night-time cortisol levels compared with healthy

Figure 3. Hypothalamic-pituitary adrenal axis (HPA)

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non-training controls. It not clear what affect this has on the nor-mal rhythmic nature of cortisol release.

! The catabolic actions of cortisol creates an increased pool of free amino acids that are valuable building blocks for protein synthesis, Catabolic processes continue during the recovery pe-riod ensuring the destruction of physiologically exhausted ele-ments of protein structures in order to make their substitution by newly synthesize proteins possible.

These are some other important the effects of cortisol

• Accelerates mobilization and use of fats for energy

• Maintains adequate glucose levels during the night for the brain by stimulating the liver to release glucose

• Decreases the entry of glucose into muscles thus conserv-ing glucose for the brain. It does this by blocking insulin from activating the glucose channels at the muscle cells.

• Acts as an anti-inflammatory agent and reduces the im-mune reaction,

• Appears to be related to a number of cytokines secreted by adipose tissue. Cytokines are a broad category for a group of proteins important to cell signaling. Appear impor-tant regulators of adipose tissue metabolism.

Polyvagal Perspective

! After a training session sensors throughout the body are busy monitoring its internal state and sending this information back to the central nervous system. The CNS interprets this in-formation, simulates the necessary repairs, and organizes the refilling of the glycogen storage tanks. When everything is back to the baseline homeostasis the nucleus ambiguus will apply the brake. After a night's sleep, the athlete wakes up with the nervous system in balance and ready for another training ses-sion.

! However, during periods of over-reaching there are exten-sive levels of repair that must be done. Let's say that the ath-lete's natural resting heart rate is about 48 bpm. This would oc-cur with the Nucleus Ambiguus brake fully applied and is the resting idle rate of the athlete's heart. If there are a lot of repairs needed the nucleus ambiguus brake may be completely re-leased the athlete's heart rate will be 100. This is the inherent 'idle' rhythm of the heart without the influence of the nucleus am-biguus.

! This higher heart rate allows a higher metabolic rate, higher delivery of oxygen and substrates needed for repair to the cells quickly. The nucleus ambiguus brake is gradually ap-plied as the repairs are completed. If the athlete's is lower than 100, but above the athlete's normal resting rate, then the nu-

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cleus ambiguus brake is being applied slightly indicating there has been some recovery. When the athlete’s heart rate is 65 bpm has some nucleus ambiguus activity. We will come back and talk about the dorsal motor nerve X shortly.

! When functionally over-reaching the athlete is slightly be-yond the upper limit of adaptation capacity for their training age and genetics. You may see an improvement in competitive per-formance. However, this temporary improvement is due to a slightly higher activity of the sympathetic nervous system.

! Functional over-reaching stresses the hypothalamic-pituitary-adrenal axis and structures within the body beyond the athlete's current physiological recovery capacity. Nagging aches and pains may occur in the joints and ligaments. How-ever, the symptoms are so subtle the athlete will often ignore them. Legs take longer to recover from their “dead” feeling at the beginning of training. But, they do recover and the athlete can perform reasonably well during the training session. The slight increase in resting heart rate is often dismissed as insig-nificantly different from their normal resting heart rate.

! Signals that you might be pushing the functional over-reaching phase too long include:

• Nagging aches and pain in back, knee, ankle, and feet.

• Mild depression and anxiety

• Slightly higher than normal heart rate in the morning be-fore getting out of bed.

! Polyvagal theory suggests that the Nucleus Ambiguus is not able to apply the brake on the heart because the body is not in homeostasis. The sympathetic nervous system is hav-ing more influence over the body and cortisol levels will be high. When the athlete is not provided with a reduced train-ing load, and/or longer recoveries, the second phase of the overtraining syndrome will become noticeable – the sympa-thetic overtraining phase.

Sympathetic Overtraining

! When the athlete has extended functional overreaching too long, and is entering into non-functional over-reaching, there are clearly considerable repair and resource problems the body must address. This results in a chronically high sympa-thetic nervous system activity. The slightly elevated heart rate seen in Phase 1 is now persistently high each morning.

! Some refer to this phase as Basedow type overtraining be-cause it mimics the symptoms of Basedow illness. A more com-mon term is Graves’ disease, and is due to excessive secretion of hormones from the thyroid gland. Common symptoms of Bas-

60

edow illness include anxiety, irritability, difficulty sleeping, fa-tigue, rapid and irregular heart-rate, sensitivity to heat, change in menstrual cycle, and frequent bowel movements or diarrhea. These are all the symptoms associated with sympathetic over-training and possibly indicates that the thyroid gland is chroni-cally overactive so it can help the body meet the higher meta-bolic demands for recovery of homeostasis.

! Thyroid hormones control the rate of many activities in the body – including how fast calories are used. A higher core body temperature is found in individuals with overactive thyroids and they also often have a higher systolic and diastolic blood pres-sure. The anxiety and irritability associated with sympathetic overtraining affects the ability of the athlete to concentrate and motor skills will deteriorate. The chronically elevated cortisol lev-els lower testosterone and lower DHEA significantly, both of which are important for muscle recovery. Chronic over-stimulation of the sympathetic nervous system for a long period of time is thought to lead to adrenal insufficiency that is often called sympathetic 'fatigue' or parasympathetic overtraining.

How The SNS Fatigues

! The sympathetic nervous system is not designed to be chronically active. When there are very high levels of prolonged

intensive training and there is a recovery imbalance several things can happen to cause the sympathetic nervous system to deactivate. With a higher level of sympathetic activity there is an increase in circulating cortisol released from the adrenal glands, and an increase in thyroid hormones. Both these are re-sponsible for increasing the body's metabolism so the body can readjust itself back to homeostasis.

! When there are an oversupply of hormones – such as corti-sol and thyroid hormone—being chronically released feedback messages are sent back to the hypothalamus telling it things are a lot higher out here than they should be. The hypothala-mus stops telling the pituitary to produce its hormones. Without the instructions from the hypothalamus, the pituitary will not re-lease ACTH that tells the adrenal gland to release cortisol.

! Without cortisol there will be a decrease in SNS activity. This is one explanation for why chronically overtrained individu-als have a lower than normal cortisol level. Thyroid hormones increase metabolism that, in turn increases core body tempera-ture. A prolonged increase in core temperature affects the func-tioning of the delicate hypothalamus that does not like a chroni-cally higher core temperature. This chronic increase in metabo-lism can also lead to metabolic error signals to the brain. In this way, the increase in body core temperature and the metabolic error signals both decrease the activity of the sympathetic nerv-ous system.

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! In addition, if target organs are being overwhelmed by too many hormones it is thought that sensors in the organs letting the brain know about the organ status eventually send informa-tion back to the brain informing it that things are working too hard. This negative feedback from the organ sensors to the brain have the effect of decreasing sympathetic activity.

! All these things that are going on will make it appear that the sympathetic nervous system has fatigued. You could look at it that way, but another way to view it is that the organ systems have been working too hard for too long and they are all screaming for the brain to slow things down. When adequate cortisol is not being produced to meet the repair needs of the body it is referred to as adrenal insufficiency. The athlete is un-able to fight infections, regulate blood sugar, and react to stress. Weight loss, and electrolyte disturbances are also possi-ble. Recovery from adrenal insufficiency can take several years.

Parasympathetic Overtraining

! When the activity of the sympathetic nervous system is compromised, and the body remains under stress, the nucleus ambiguus vagal brake is unable to apply its effect and the body is left with one final defensive strategy – the dorsal motor nu-

cleus. The name, 'parasympathetic overtraining' is used to re-flect the abnormally low resting heart rate and a delayed heart-rate recovery from training.

! However this is not caused by the nucleus ambiguus – rather it suggests that the heart is now being controlled by the dorsal motor nucleus. When the nucleus ambiguus is applying its brake there is a high heart rate variability. When the dorsal motor nucleus is applying its effect on the heart there is hardly any heart rate variability. This phase is typically accompanied by the lack of desire to compete and train, depression, chronic injuries, exhaustion and a markedly diminished performance.

Figure 3. Hypothalamic-pituitary adrenal axis (HPA)

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! This low heart rate, or bradycardia is a very bad symptom because it suggests the heart is being controlled by the DMNX and not the nucleus ambiguus. The DMNX provides too much vagal tone. Athletes who are in the third phase of parasympa-thetic overtraining are seriously ill. Recovery and return to previ-ous optimal levels of performance is a very difficult task.

! Parasympathetic overtraining is often referred to as Addi-sonian overtraining because the symptoms are similar to those exhibited by people who have Addison’s disease. Addison's dis-ease occurs when the adrenal glands do not produce enough cortisol. As we discussed previously, in the case of the severely overtrained athlete the reduced cortisol is possibly due to adre-nal insufficiency. The DMNX explains many of the symptoms de-scribed by Alberto Salazar. Recovery and return to previous opti-mal levels of performance is a very difficult task and serious long-term health problems can occur.

Things You Can Do

! Avoiding non-functional overreaching and overtraining syn-drome is critical to consistent long-term athlete development. The European Task Force provide the following recommenda-tions for coaches:

• Maintain accurate training and competition records.

• Adjust daily training intensity/volume, or allow a day of complete rest, when performance declines, or the athlete complains of excessive fatigue.

• Avoid excessive monotony of training.

• Always individualize the intensity of training.

• Encourage and regularly reinforce optimal nutrition, hydra-tion status and sleep.

• Be alert to multiple stressors such as sleep loss (e.g. jet lag), exposure to environmental stressors. Occupational pressures, change of residence, and interpersonal or fam-ily difficulties may add to the stress of physical training.

• Treat overtraining symptoms with rest! Reduced training may be sufficient for recovery in some cases of overreach-ing

• Resume training based on the signs and symptom.s There is no definitive indicator of recovery.

• Communicate with the athletes about their physical, men-tal, and emotional concerns is important. Include regular psychological questionnaires to evaluate the emotional and psychological state of the athlete.

• Maintain confidentiality regarding each athlete’s condition (physical, clinical, and mental). Regular health checks are recommended.

• Allow the athlete time to recover after illness/injury.

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• Note the occurrence of upper respiratory tract infections and other infectious episodes. Suspend training or reduce the training intensity when the athlete suffers from an in-fection.

• Rule out an organic disease in cases of performance dec-rement.

• Unresolved viral infections are worth investigating in adults experiencing fatigue and underperformance in train-ing and competition.

References

Kreider, R., Fry, A. C., & O’Toole, M. (1998). Overtraining in sport: terms, definitions, and prevalence. In R. Kreider, A. C. Fry, & M. O’Toole (Eds.), Overtraining in sport (pp. vii _ ix). Champaign, IL: Human Kinetics.

Meeusen R, Duclos M, Gleeson M, Rietjens G, Steinacker J, & Urhausen A. Prevention, diagnosis and treatment of the Over-training Syndrome ECSS Position Statement ‘Task Force’ Euro-pean Journal of Sport Science, March 2006; 6(1): 1 – 14

Fry A, Steinacker J, Meeusen, R. Endocrinology of overtraining. The Endocrine System in Sports and Exercise, pp.578 – 599.

William J. Kraemer and Alan Rogol (eds). Wiley-Blackwell; Mal-den, MA 2005

Dedovic K, and Duchesne A. Cortisol: Physiology, Regulation and Health Implications. P 28 - 43. Esposito, Alonzo & VitoBian-chi (Ed).Nova Science Publishers, Incorporated, 2012

Viru A, & Viru M. Cortisol—Essential Adaptation Hormone in Ex-ercise. Int J Sports Med 2004; 25(6): 461-464.

Bell, Lee M; Ingle, Lee. Psycho-physiological markers of over-reaching and overtraining in endurance sports: a review of the evidence. Medicina Sportiva. 17.3 (Sept. 2013): p81.

Kreher, Jeffrey B; Schwartz, Jennifer B. Overtraining Syn-drome: A Practical Guide. Sports health, 03/2012, Volume 4, Is-sue 2. 128-138

Lehmann M, Foster C, Dickhuth HH, Gastmann U. Autonomic imbalance hypothesis and overtraining syndrome. Med Sci Sports Exerc. 1998; 30:1140–1145.

Li-Ng, Melissa; Kennedy, Laurence. Adrenal insufficiency. Jour-nal of surgical oncology, 10/2012, Volume 106, Issue 5

Fadel, B M; Ellahham, S; Ringel, M D; Lindsay, Jr, J; Wartofsky, L; Burman, K D. Hyperthyroid heart disease. Clinical cardiology, 06/2000, Volume 23, Issue 6

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Lehmann, M; Foster, C; Dickhuth, H H; Gastmann, U. Auto-nomic imbalance hypothesis and overtraining syndrome. Medi-cine and science in sports and exercise, 07/1998, Volume 30, Issue 7.

Porges SW. (2007). A phylogenetic journey through the vague and ambiguous Xth cranial nerve: A commentary on contempo-rary heart rate variability research. Biological Psychology 74:301-307.

Porges SW. (2007). The polyvagal perspective. Biological Psy-chology 74:116-143

Porges SW, Riniolo TC, McBride T, Campbell B. (2003). Heart rate and respiration in reptiles: Contrasts between a sit and wait predator and an intensive forager. Brain and Cognition 52:88-96.

6Fatigue theories

What You Will Learn

When you have completed this module you will be able to:

1. Discuss how fatigue is defined from the perspective of the researcher's discipline

2. Discuss eight well-established theoretical fatigue models

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Introduction

! We have been talking about overtraining syndrome in which chronic fatigue is a major symptom along with many other problems. Overtraining is the accumulation of fatigue that occurs after a series of training sessions where the body does not have sufficient recovery time to make the necessary re-pairs. Consequently, organs and organ systems will not adapt adapt and will therefore be unable to manage higher physiologi-cal demands.

! During an athletic performance, the central nervous sys-tem is provided with the homeostatic challenge of balancing car-diovascular and respiratory demands, force output and coordi-nation of many muscle groups. The amount of fatigue incurred depends on the type and intensity of training, the muscle groups involved, and the physical environment in which the per-formance occurs.

! Over 3000 research studies have explored the reasons for why athletes fatigue, how to delay it, and how to quickly recover from it. The fragmented nature of the research has contributed more confusion than useful explanation. How and under what conditions adaptations to training incur a delayed onset of fa-tigue and/or minimizes its effects, remains unknown. We only have possible theories available at the moment.

Section 1

Fatigue theories

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! Understanding possible reasons for why fatigue develops during exercise, and how the perception of fatigue changes in response to training, provides insights into how to design effec-tive exercise training programs that will prolong and sometimes counteract the effects of fatigue. One immediate indicator of fa-tigue is a decline in performance.

! We commonly think of fatigue as a bad thing. However, there is a purpose behind every physiological response. Fa-tigue is thought to confer some sort of evolutionary advantage by preventing catastrophic organ system failure from which re-covery is excessively delayed or impossible.

What You Will Learn

! In this module we discuss how fatigue is defined and re-view the eight well-established theoretical fatigue models.

Models Of Fatigue

! Within the general population, fatigue is one of the most common complaints the doctor hears. In medicine 'fatigue' is usually defined as an abnormal state of physical or mental ex-haustion. It is thought to be due to chronic inflammatory condi-

tions and other abnormal health issues. Just as in sports, if the stress causing the fatigue is not removed then fatigue becomes chronic.

! To distinguish the fatigue due to training from non-training fatigue we use the term “exercise-induced fatigue”. It is an acute condition occurring during training or competition. With adequate recovery the athlete returns to normal homeostasis and the body is stronger.

! If recovery is insufficient the athlete exhibits all the symp-toms of the non-athletic population “chronic fatigue” with similar negative health outcomes. What precisely causes fatigue of any kind remains controversial and no precise explanation exists.

! Scientists describe exercise-induced fatigue according to their discipline. For example, a biomechanist explains fatigue as an exercise-induced decrease in maximal muscle force pro-duction, or an inability to sustain further exercise at a required force. A psychologist explains fatigue simply as a “sensation: of tiredness. A physiologist defines fatigue in terms of failure of a specific physiological system. For all of them, fatigue is a cata-strophic event eventually leading to termination of exercise as a result of some involuntary physiological or biochemical event oc-curring in the active muscle.

! Processes leading to fatigue begin at every level of the central and peripheral nervous system. The commonly ac-

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cepted definitions of fatigue it a general sensation of tiredness associated with decrements in muscular performance and func-tion.

! There are currently eight broad models offering an explana-tion for fatigue. These are:

• Cardiovascular/anaerobic model• Energy supply/energy depletion• Neuromuscular fatigue• Muscle trauma• Biomechanical model• Thermoregulatory• Psychological/motivational model• Central governor model

! Each model proposes different explanations for the under-lying causes of fatigue.

The Cardiovascular - Anaerobic Model

! This model provides an explanation for an athlete's endur-ance capacity. It extends the observation that oxygen delivery to a muscle and it's ability to use that oxygen rises linearly up to a certain point – referred to as the athlete's VO2max. Here is

the oxygen uptake and this is the blood lactate level rising as workload rises.

Fatigue occurs when:

1. the heart has reached its maximum ability to supply oxy-gen

2. waste products have risen to a level where muscular con-traction is catastrophically compromised,

3. the mitochondria within the muscle fiber are at their maxi-mum ability to use oxygen for ATP production.

! These factors reduce the ability of skeletal muscle to work and the athlete has to stop exercising to permit recovery to oc-cur. In other words, this module predicts that the capacity of the athlete’s heart to pump large volumes of blood and oxygen to the muscles, the ability of the mitochondria in the athlete’s mus-cles to extract oxygen from the surrounding capillaries, and the ability of the cardiovascular system to remove waste products determines endurance performance.

! The prime goal of training then, is to improve the heart’s capacity to deliver oxygen to the working muscles and increase mitochondrial volume within the muscle cell itself. Relevant train-ing adaptations are those resulting in an increased VO2 max, capillary growth around the muscle, and an increase in mito-chondrial volume in the muscle cell that enables a higher aero-

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bic ATP production. Another training adaptation includes an in-crease in the capacity of the muscles to use fat as a fuel during exercise, and this delays the use of the acid producing glyco-gen for fuel. These adaptations collectively delay the build up of blood acidity permitting muscles to continue contracting at high intensities for a longer period of time before the onset of fa-tigue.

! The rationale for EPO therapy, red blood cell re-infusion, and the administration of oxygen is to increase oxygenation of the heart and skeletal muscle. The theory is that this will result in a greater cardiac output, higher oxygen consumption and a reduction in acid conditions that interfere with skeletal muscles contraction and relaxation.

! The major drawback with this model is that if the pumping capacity of the heart limits oxygen delivery to the exercising skeletal muscle, then the heart itself will also be affected by oxy-gen deficiency. When the heart pumps blood throughout the body it also pumps blood to itself. Here you see the coronary arteries and the blood supply to these arteries arise here at the aorta. Here's the left coronary artery and this is the right coro-nary artery. If the skeletal muscles are low in oxygen and high in waste then the same would be true for the heart. In a healthy athlete there is no evidence the heart ever reaches a danger-ously low supply of oxygen. Athletes do not suffer from ischemic pain that would indicate the heart is not getting suffi-

cient oxygen. As well, among elite endurance performers the best athlete often is not always the one who has the highest VO2max.

! Despite these limitations this model is frequently use to ex-plain why fatigue affects endurance performance and has be-come a significant rationale in the design of certain types of training stimuli for endurance runners.

The Energy Supply - Energy Depletion Model

! As you know, there is a small store of ATP in the cell. As this ATP store is used the three energy systems replenish it al-most instantaneously replenish it. You are already familiar with this chart showing the power and capacity of the three ATP pro-duction mechanisms. The underlying premise of the energy sup-ply/ energy depletion model is that insufficient ATP is available to sustain the appropriate level of muscular activity. The muscle stops working when it runs out of ATP

 This can occur in two ways:

• The ATP production mechanisms are not keeping up with ATP demands

• Insufficient fuel is being delivered to the ATP production mechanisms.

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• The training implications are

• Improve the capacity of the ATP production mechanisms.

• Improve the athlete's movement economy so less ATP is needed to maintain specific intensity levels of exercise.

! Improve the fuel stores for each of the energy systems. That is, a power and speed athlete will want to strengthen their phosphocreatine ATP production capabilities, the 400 m runner will want to strengthen their anaerobic glycolytic ATP production mechanism capabilities, and the endurance athlete will want to strengthen their aerobic ATP production capabilities.

Researchers draw support for this line of thinking in the follow-ing ways:

• Depletion of liver and/or muscle glycogen stores cause hy-poglycemia (low blood sugar) adversely affecting the ath-lete’s performance – proof there is a delivery problem for glycogen.

• Replenishing the glucose level in the blood allows exer-cise to continue – proof that when the fuel is available then fatigue is delayed.

• Carbohydrate loading improves exercise performance – proof that supercompensating glycogen stores delays the onset of fatigue.

• Supplementation of creatine phosphate improves the per-formance of power athletes.

! At present, no study has shown that training in humans im-proves glycogen or creatine phosphate storage even though elite athletes have higher stores of both substrates depending on whether their specialty is power, speed or endurance. These higher stores are possibly due to genetics and not to training.

! An alternate explanation is that training increases the ath-lete’s capacity to use fat at higher exercise intensities, and this would conserve glycogen stores and delay fatigue. The ‘‘cross-over’’ concept of fuel use is of particular interest here. At 60% of VO2max the mitochondria begins move from using predomi-nantly fat to predominantly glycogen.

! When athletes train at intensities below their ‘‘crossover’’ point, they improve their ability to use fat, whereas when they train at higher exercise intensities they improve their capacity to use glycogen. Exercise intensities over 70% VO2max for longer than 2 hours is limited by the athlete’s glycogen stores. Mara-thon runners typically run at around 80% of VO2max. You can see from this chart they are using an awful lot of glycogen. Use of glucose from the blood is also increasing – this glucose pre-dominantly comes from the liver although lactate is also being converted back into pyruvate – we'll talk more about this is sub-sequent modules.

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! The problem with both the energy supply and energy de-pletion perspective is that they claim ATP depletion limits exer-cise. Either the muscle cell runs low on ATP due to the produc-tion mechanisms failure to produce sufficient ATP. Or, there is a problem with delivery of fuel to the ATP production mecha-nisms.

! However, the cell protects its ATP supply by never permit-ting levels to go below about 60%. Therefore any model claim-ing the muscle cell runs out of ATP is fundamentally wrong and is too simplistic to explain the cause of fatigue. If the muscle cell ran out of ATP it would develop rigor. If this happened, then the heart muscle would also develop rigor and this never hap-pens in a healthy athlete. In essence, it appears that the ATP used by the contracting muscles never exceeds the maximum rate of the ATP production mechanisms. The energy supply/energy depletion model does provide some interesting insights, though, into the role fuel storage and delivery plays during an athlete’s performance.

The Neuromuscular Fatigue Model

! Advocates of the neuromuscular fatigue model argue that it is a signal transmission failure at the neuromuscular level that

causes fatigue. This results in a reduction in muscle force or power production.

! To carry out a goal-directed skilled movement, the motor cortex of the brain must first receive various kinds of informa-tion from other lobes of the brain: information about the body's position in space – this comes from the parietal lobe. Informa-tion about the goal to be attained and an appropriate strategy for attaining it – this information comes from the anterior portion of the frontal lobe. And memories of past strategies that are fed from the temporal lobe, and so on.

! In the human brain, planning for any given movement is done mainly in the forward portion of the frontal lobe. This part of the cortex receives information about the individual's current position from several other parts.

! Then, it issues its commands, to Area 6. Area 6 decides which set of muscles to contract to achieve the required move-ment, then issues the corresponding orders to the primary mo-tor cortex, also known as Area 4. This area in turn activates spe-cific muscles or groups of muscles via the motor neurons in the spinal cord.

! The axons of the neurons of the primary motor cortex de-scend all the way into the spinal cord, where they make the fi-nal relay of information to the motor neurons of the spinal cord. These neurons are connected directly to the muscles and

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cause them to contract. Finally, by contracting and by thus pull-ing on the bones of the arm and hand, the muscles execute the movement that enables the athlete to perform whatever skilled performance they are trying to achieve.

! In addition, to ensure that all of these movements are fast, precise, and co-ordinated, the nervous system must constantly receive sensory information from the outside world and use this information to adjust and correct the movements of the athlete's body. The nervous system achieves these adjustments mainly from the cerebellum, which receives information about the posi-tions in space of the joints and the body from the propriocep-tors. In other words, when a conscious decision is made to move, processes in the (1) central and (2) peripheral nervous system work together to send electrical activation signals to (3) muscles where a number of responses put the movement sig-nals into action. Signal failure can occur at any of these three levels.

! This could be due to failure of neurotransmitters, such as acetylcholine, to generate the necessary neural impulses. Ace-tylcholine is one of many neurotransmitters in the autonomic nervous system (ANS) and the only neurotransmitter used in the motor division of the somatic nervous system. The impulse potentially fails to cross the synapses of interlinking nerve cells and at the muscle's neuromuscular junction. Without acetylcho-

line an action potential is not possible and will prevent muscle contraction.

! Another explanation is that signals are sent from the exer-cising muscles to the central nervous system informing it of re-ductions in ATP to the 60% level, or there are low fuel stores. As a result the brain reduces motor unit recruitment. This would induce the sensation of fatigue because of the limited number of active motor units available. The reduced central nervous sys-tem activation of the exercising muscles is theorized to protect the heart from catastrophic low oxygen levels.

! At the muscle level fatigue is thought toinvolve the excitation-contraction coupling mechanisms. There are many parts to the excitation-coupling process. Excitation-contraction uncoupling possibly occurs disrupting the normal excitation-coupling process. Action potentials are still generated, but they do not produce a contractile response. This would be perceived as fatigue. One characteristic of uncoupling is a slowed rate of muscle contraction and relaxation time. This could be due to a slow re-uptake of calcium into the sarcoplasmic reticulum. If cal-cium remains in the muscle fiber there will be a slowing of the muscle's relaxation time.

! Clearly, the neuromuscular model of fatigue suggests many possible sites for fatigue. The goals of training are to:

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1. enhance the neuromuscular system so it increases its fre-quency of muscle stimulation,

2. enhance recruitment of the muscle fibers,

3. improve the ability of the muscle cross-bridges to produce force.

Muscle Trauma Model Of Fatigue

! All cells in the body, including muscle cells are confined to a fairly narrow range of function and structure based on its spe-cialization. Muscle is able to handle reasonable physiologic de-mands and maintain its homeostasis. Adaptations are reversi-ble. Functional and structural responses to more severe physi-ologic stresses during which an altered steady state is achieved, allowing the cell to survive and continue to function. The adaptive response may consist of an increase in the size of cells (hypertrophy) and functional activity, an increase in their number (hyperplasia), or a decrease in the size and metabolic activity of cells (atrophy).

! In all these situations, when the stress is eliminated the cell can recover to its original state without having suffered any harmful consequences. If the limits of adaptive responses are exceeded, or if cells are exposed to injurious agents or stress, or deprived of essential nutrients, a sequence of events follows

that is termed cell injury. Cell injury is reversible up to a certain point, but if the stimulus persists, or is severe enough from the beginning, the cell suffers irreversible injury and ultimately cell death.

! Four mechanisms within the cell are particularly vulnerable to injury: membranes, aerobic ATP production, protein synthe-sis and the genetic apparatus (where all the codes for cell struc-ture and activity are located). Exercise-induced muscle damage (EIMD) is a common muscle cell injury following unaccustomed physical activity, or activity of high intensity or prolonged dura-tion such as you see in endurance sports.

! Symptoms include stiffness and swelling, decreased force or muscular contraction, and delayed-onset muscular soreness. EIMD also results in higher levels of lactate production and in-creased heart rate at submaximal exercise, indicating a physio-logical stress response.

! Histological examination has shown damage to myofibrils and cyoskeleton (the scaffolding holding the cell together). Dam-age is visible in the mitochondria and the sarcoplasmic reticu-lum. This reduces ATP production in the cell thereby compromis-ing work output. EIMD remains poorly understood. There are two explanations for the initial damage during exercise. One is mechanical stress and the other is metabolic stress. The me-chanical stress is the most popular explanation and the reason

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is that EIMD is more common following eccentric rather than concentric contractions.

! It is thought that reductions in force production during and after exercise may be due to:

• Disruption in intracellular calcium homeostasis

• Cytosolic calcium levels are closely regulated with muscle cells. When these mechanisms are overwhelmed follow-ing muscle injury, several intrinsic degenerative actions are activated that degrade the myofibril proteins, poisons the mitochondria and inhibit cellular enzymes.

• High levels of reactive oxygen species (ROS) due to in-crease use of oxygen during prolonged exercise can dam-age the mitochondria, reducing its ability to use oxygen. Some evidence also suggests that ROS also reduces the activity of membrane proteins that maintains homeostatic ionic gradients at the sarcolemma. This damage reduces actin/myosin coupling.

• Cell membrane disruption permits the contents leak out into the bloodstream.

• Protein damage and DNA damage activates the enzymes of cell death.

! All these disruptions to the cell activates the pain recep-tors that reduce the muscle excitement, that in turn, reduces

actin/myosin coupling. The end result is the feeling and percep-tion of fatigue.! There has been many efforts to decrease the amount of muscle damage after a bout of exercise, but few inter-ventions have proven very effective. Massage, microtherapy, ic-ing, hyperbaric oxygen treatment, fish oil, and whole body vibra-tion are just a few methods that have been tried with anecdotal success. A thorough warm up before exercise can reduce EIMD. Interestingly a powerful protection against muscle dam-age is a preceding damaging exercise bout.

Biomechanics Model

! This model proposes that superior performance is predomi-nantly due to enhanced efficiency of motion that results in bet-ter economy.

When economy of movement is improved, less demand is placed on other physiological mechanisms that may be respon-sible for fatigue:

• less oxygen and energy consumption is required reducing demand on the cardiovascular system.

• fewer intramuscular metabolites are produced potentially resulting in less muscle trauma

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• there is a slower rise in core body temperature thereby re-ducing the impact of the temperature effect on tissues sen-sitive to increased temperature.

! Recall that the cardiovascular/anaerobic model predicts su-perior performance results from increased oxygen delivery to muscle and an increased rate of fuel delivery—and hence a higher heat production. A higher rate of heat production would prematurely induce fatigue. Advocates for the biomechanical model point to this clear weakness of the cardiovascular/anaerobic model of fatigue. A more logical biological adaptation, they claim would be to reduce the rate of oxygen consumption (and hence the rate of heat production) by increasing the ath-lete's efficiency or economy of movement.

A number of training studies suggest that improvements in movement economy is the most likely training response, allow-ing the athlete to perform at a reduced oxygen consumption and accumulate less heat.

! Economy of movement explains, in part, why an elite ath-lete with slightly lower VO2max capacity within a cluster of highly elite athletes can be the superior performer.

! Part of the economy is thought to come from a superior stretch-shortening cycle. Repetitive eccentric muscle contrac-tion, as occurs in the quadriceps and calf muscles during run-ning, produces altered muscle function with a loss of elastic en-

ergy production, requiring an increased work during the push-off phase of the running stride. This would lead to an even faster progression of fatigue. A superior stretch-shortening cycle would delay the onset of the stretch/shortening cycle fatigue that is an inevitable consequence of repeated eccentric muscle contraction.

Thermoregulatory Model Of Fatigue

! The mouth is a convenient place to measure temperature. But the temperature inside the body, the core body tempera-ture, is what counts. Core temperature is generally a degree or so higher than the temperature in the mouth and is regulated at around 37°C (± 0.5-1°C).

! A core body temperature of > 40 °C cannot be tolerated for prolonged periods. Well trained cyclists, for example, are un-able to continue when their core body temperature reaches 39.5 °C. Therefore, there appears to be a critical core body tem-perature beyond which exercise is terminated. Body tempera-ture is affected by the rate of heat being produced by muscle ac-tivity and by the rate of heat removal through the skin. An inade-quate heat removal system results in a progressive increase in core body temperature as the exercise continues.

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 ! It is not uncommon for exercise to elevate core body tem-perature to the upper limit of its safe zone beyond which the thousands of internal chemical reactions can not occur properly. Severely low or high body temperature can lead to permanent organ damage, even death.

! There are two views as to what mechanisms cause per-formance decline as core body temperature rises.

• As core body temperature rises there is a rapid increased demand on the glycogen stores. Performance is reduced to protect muscle glycogen stores.

• Blood flow to the active muscle is reduced in order to maintain blood pressure so that blood flow to critical ar-eas, such as the brain, can be maintained. A reduced blood flow to muscles impacts oxygen and substrate deliv-ery.

In both cases, information from thermosensors in the skin and muscle and from the core is fed to hypothalamus, which in turn speeds up heat removal activities. If core temperature contin-ues to rise, the central nervous system reduces arousal, and/or down-regulates activation of motor units. Interestingly, the CNS can recruit muscle units for short periods of time even if core temperature is high. This may suggest that only prolonged con-tractions disrupt CNS function and the inhibitory signals coming

from the periphery takes some time to build up to a level indicat-ing pending danger to homeostasis.

! Adaptations: Repeated exposure to heat stress results in thermal adaptations permitting more effective defense mecha-nisms against heat build up. Expansion of plasma volume is the first adaptation to occur and this can be maintained for about 3 weeks if the stimulus is appropriate. Expansion of blood volume is associated with improved blood pressure regulation, that in turn leads to increased cardiovascular efficiency, permitting al-terations in skin blood flow that aid heat loss.

! Increased steady-state sweat rate, glandular hypertrophy and alterations in sweat gland function such as a reduced possi-bility of hidromeiosis. Hidromeiosis is a condition of reduced sweating that occurs when a sweat gland is producing a lot of sweat for more than a couple of hours. The sweat glands begin to shut down. As well, with training there is a decreased loss of electrolytes in sweat.

Psychological tolerance to heat is increased. It appears the physiological adaptations to heat must be in place before psy-chological tolerance levels to heat is possible. The elevated tol-erance of internal temperature is not much – only about 0.28 deg C (.5 deg F).

! Pre-cooling : Pre-cooling can reduce body temperature thereby enhancing the athlete's capacity to store heat during

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the subsequent bout of exercise. This strategy is particularly useful in sports requiring extended periods of exercise under high environmental temperatures, and where there is limited op-portunity to consume fluids. Hand cooling appears to have promise in reducing whole-body temperature.

Psychobiological Model

! This model is based on Brehm's motivational Intensity the-ory, which encompasses two main constructs: potential motiva-tion and motivational intensity.

• Potential motivation refers to the maximum effort the ath-lete is willing to exert to satisfy a goal (e.g., to succeed in the exercise task),

• Motivation intensity is the amount of effort the athlete actu-ally expends.

• From this perspective an athlete will continue to exert ef-fort as long as: 

• the level of maximal effort the athlete is willing to exert (po-tential motivation) is not reached or

• the task is viewed as possible.

! If the maximum effort the athlete is willing to exert is reached, or the task is perceived as impossible, the athlete will disengage and not produce good effort. The point of exhaustion is a psychological point at which the athlete completely disen-gages from performing the task.

! The Psychobiological model predicts that an improved ex-ercise tolerance can occur when the athlete's is taught how to expend a higher level of effort or when perception of effort of a physical task is reduced because the athlete has faith in their training and has developed a higher level of belief in their skill and physiological capacity. Both of these scenarios can delay the onset of perceived fatigue and exhaustion will be post-poned.

! In essence, the psychobiological model suggests that per-formance is ultimately regulated by perception of effort, and how much effort the athlete is willing to expend before giving up, and not due to physiological failures

The Central Governor Model

! The final model is the central governor model. This model hypothesizes that fatigue is due to a complex interaction be-tween multiple physiological systems in the periphery and the central nervous system. It suggests that all changes in the pe-

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ripheral such as fuel depletion, or waste product accumulation, will signal the brain so it can make the necessary adjustments to maintain homeostasis. The brain's job is to defend the body’s internal environment.

! The model proposes that the brain can anticipate when ho-meostasis will be severely disrupted and modifies the athlete’s ability to perform by inhibiting the number of muscle fibers avail-able for recruitment. Signals are sent down the spinal cord to adjust the number of motor units that can be recruited.

! Another interesting aspect of the central governor model is the focus on the heart. The model states that the heart is at the greatest risk of developing an oxygen deficiency during stress-ful conditions. Therefore, the monitoring mechanisms in the brain also monitor the state of oxygenation of the heart and per-haps the state of oxygenation of other essential life sustaining organs such as the brain and diaphragm. The diaphragm is an important breathing muscle.

! When the oxygen levels in the blood approaches unsafe levels, the motor cortex in the brain responsible for recruiting the skeletal muscles, is informed, and it stops recruiting addi-tional muscle fibers. In essence, the brain can anticipate the in-tensity of the upcoming bout of exercise and will “pace” the use of resources.

! How does the brain anticipate? It's believed to be a train-ing memory effect. Power athlete's will attempt to overstimulate their muscles and in so doing they are teaching their brain to an-ticipate a higher effort so it will recruit the highest number of mo-tor units possible.

! There are individual differences among athletes as to how their brain reads the feedback it receives from the muscles re-garding fuel supply, temperature and acid conditions among other feedback mechanisms.

! During training you are trying to teach the athlete's brain to anticipate a higher level of activity than it would normally antici-pate so it will not shut down the muscle fiber recruitment before the athlete has reach the level of activity that you want them to be able to produce during the competition. This model illus-trates the importance of the overload training principle.

Summary

! The precise causes of neuromuscular fatigue are not fully understood. As well, how fatigue presents within the athlete var-ies among sport. Competitive cyclists can ride all day, covering well over 100 miles. Olympic-class weight lifters cannot lift at or near their maximum capacity for more than a few seconds.

! Although fatigue eventually sets in after any kind of muscu-lar activity, it generally occurs more quickly when a muscle is

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stimulated at higher frequencies and when larger forces are generated. In all instances fatigue affects physical performance and is defined as a failure to maintain the required or expected output for the desired performance.

! As we have seen, fatigue can occur at both the level of the central nervous system and at the periphery. Central fatigue mechanisms refer to poor motivation through altered central nervous system transmission, or to reduced neural drive. Pe-ripheral fatigue involves impaired signal transmission, reduced muscle electrical activity, and motor unit activation.

! All the models we discussed provide interesting insight into how fatigue occurs and all have something to offer a coach. The central governor model integrates all of them in some way. The central governor model remains under debate because its exact location of the central governor has not yet been found.

7Fatigue during sprinting

What You Will Learn

When you have completed this module you will be able to:

1. Explain how the PCr, glycolytic and aerobic energy systems interact to provide ATP during sprinting

2. Discuss the recovery time necessary to replenish the fuel sources for the PCr and glycolytic energy systems after sprint training and/or competition

3. Explain how you would decide when the athlete’s PCr energy system is no longer being trained and you are training the glycolytic and/or the aerobic energy system.

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Introduction

! The models of fatigue we have been discussing open up alternative ways to view fatigue providing possible training in-sights. In this module we will examine the metabolic causes of fatigue during bouts of sprinting up to 60 seconds. In essence, we are looking at fatigue from the point of view of the energy supply/energy depletion theoretical perspective and from the muscle trauma perspective.

! Most sports involve short bouts of sprinting, so insights into what causes fatigue during sprinting has wide application. The mean distance and duration for sprinting in team sports is between 10 – 20 meters and 2 – 3 seconds, respectively achiev-ing speeds in excess of 90% of maximal velocity. Rate of recov-ery is an important consideration so the athlete is ready for the next sprint bout within minutes. In track sprint events, a runner performs a single bout of sprinting with very little consideration about the rate of recovery from this effort.

! However, during training all athletes who must master sprinting undertake repeated bouts of sprinting of various dura-tion and distance. What is the impact of repeated sprinting on muscle fatigue and how does it occur? We know that maximum speed cannot be maintained for vary long. Power output de-clines with increasing distance and duration as you see here –

Section 1

Fatigue during sprinting

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power is lowest at 30 seconds and highest at 6 seconds (Figure 1).

! Our knowledge for why this happens has advance due to the needle biopsy technique for sampling muscle and tech-niques to freeze the samples very quickly (within 4-6 seconds). In this way the samples are able to closely reflect the state of the muscle during exercise.

What You Will Learn

In this module we examine how the PCr, glycolytic and aerobic energy systems interact to provide the athlete with ATP during sprinting and the recovery time necessary to replenish the fuel

sources for the PCr and glycolytic energy systems after sprint training and/or competition. We will also provide insights into how to decide when the athlete’s PCr energy system is no longer being trained and you are training the glycolytic and/or the aerobic energy system.

PCR And Glycogen Use

! The two main energy systems used in sprinting are the PCr and glycolytic energy systems. To see how these two en-ergy systems interact during sprinting we need to set up an ex-periment. Most research of this type is done using a bicycle er-gometer because it is easier to collect the data. However, the same trends are seen during running as well. 

! The subjects performed three maximal sprints on a cycle ergometer (Figure 2). Each bout lasted 30 seconds and there was a 4 min rest period between each 30 second bout. Muscle biopsies were taken at rest, then they were taken after 6, 15 and 30 s during the first and third bouts of cycling. The muscle biopsies were used to estimate these metabolites – PCr, glyco-gen, lactate and hydrogen ions indicating the level of acidosis in the muscle.

Figure 1. Overtraining versus overtraining syndrome

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! Lactate content and H+ are both byproducts of glycolysis and provide an estimation of how hard the glycolytic energy sys-tem is working.Let's examine power output first (Table 1).

! During the first 6 seconds the subjects averaged 800W, be-tween 6 seconds and 15 seconds they averaged 700W and be-tween 15 and 30 seconds they averaged 500W. This reduction in power output indicates fatigue is occurring.

The first muscle biopsy at rest provided the following results:

• The phosphocreatine content of the muscle = 88 mmol/kg dry muscle (dm);

• Glycogen content = 480 mmol/kg dm;

• Lactate content = 5 mmol/kg dm;

• H+ content = 62 nM (nanomoles = a quantity of measure of hydrogen ions).

! The subject begins peddling as fast as he can – his power output during the first 6 seconds averages 800 watts. At 6 s PCr content was at 46mmol/ kg dm and H+ ion content had in-creased to 110 nM. This increase in H+ ion content is a good in-dication that anaerobic glycolysis was supplementing the declin-ing phosphocreatine energy system.

! Between 6 seconds and 15 seconds power output dropped to an average of 700 W. This makes sense because the anaerobic energy system cannot produce the power that the PCr energy system can produce and glycolysis is more

Figure 2. Anaerobic testing protocol

Power output

PCr content (mmol/kg/dm)

Glycogen content (mmol/kg/dm)

Lactate content (mmol/kg/dm)

H+ content

nM

Rest 88 480 5 62

At 5 secs800 W

average46 110

At 15 secs700 W

average28 157

At 30 secs500 W

average8 400 60 183

Table 1. Data from anaerobic test

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dominant between 6 and 15 second. At the 15 s point the mus-cle biopsy showed that the PCr content has dropped to 28-mmol/kg dm and H+ has increased to 157 nM.

! Between the 15 s and 30 s period average power output dropped to around 500 W due to rapidly decreasing PCr store. At 30 s the muscle biopsy showed that the PCr was almost de-pleted and H+ has risen to 183 nM. This is quite acidic.

Derivation Of ATP

! Now we will take a closer look at where the ATP is coming from (Figure 3). We will just examine Bout 1 for now. During the first 6 seconds of Bout 1 much of the ATP is coming from PCr – almost 15 units. Anaerobic glycolysis is contributing quite a sig-nificant portion as well (around 7 units). It might surprise you that there is also 3 units of ATP coming from the aerobic energy system. This is not much, but it is important to note that there is some ATP derived from this system.

! During the period between 6-15 seconds the ATP contribu-tion from PCr drops substantially and anaerobic glycolysis is contributing a larger portion. The aerobic energy system has also increased its ATP contribution a bit more. As anaerobic gly-colysis and the aerobic energy systems contribute more ATP

overall power the athlete can produce decreases as you can see here.

! Here's the power produced during the first 6 seconds and here is the power production between 6 and 15 seconds – it has dropped. In the final 15 seconds PCr has dropped again and so has anaerobic glycolysis. The aerobic energy system has picked up the slack. When aerobic energy becomes a more significant ATP contributor power drops quite a bit. PCr pro-duces the highest ATP production and the highest power out-put.

! Now let's go back Table 1 and take a look at the data. After the 30 seconds bout glycogen levels in the muscle drop to 400mmol/kg dm and lactate content is 60mmol/kg dm. So you can see that some of the muscle's glycogen store has been

Figure 3. Source of ATP and power output during the An-aerobic test

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used, and the PCr store has been completely depleted. At this level of acidity the athlete is unable to continue with much effort at all. Clearly fatigue during this 30 second bout of exercise is due to a depletion of PCr stores, and the acidity. It's not due to the lack of glycogen – this has depleted, but there is still plenty available.

Now the athlete takes a 4 min rest.

What Happens During The 4 Min Rest Period

! I will draw from several studies to discuss recovery. As you have seen creatine phosphate stores are rapidly activated dur-ing sprint activity. In the first 6 seconds PCr accounts for around 50% of ATP energy. Studies using maximal running show PCr stores become almost completely depleted after the first 10 sec-onds.

! However, PCr is quickly resynthesized during recovery Fig-ure 4). The time course of PCr resynthesis, and muscle pH re-covery from the 30 second sprints separated by 1.5, 3 or 6 min-utes of recovery is shown on Figure 3. Here is the restoration of peak power output. After 60 s of rest muscle PCr levels are re-stored by approximately 50%, and by up to 80- 90% after about 3 mins. In essence, sufficient PCr is available to power a subse-quent sprint after about 3 mins of rest. In contrast, the muscle

pH indicating of the amount of free H+, shows little recovery even after 5 – 6 mins of rest! Whenever glycogen is being used at a high rate hydrogen ions and lactate will accumulate. You've also seen that lactate increases immediately after the first sprint. Lactate falls to ap-proximately 70% of its peak value after 6 mins of recovery. This indicates the amount of clearance of H+. In essence, the ath-lete still retains significant acidosis. It takes roughly 2-hours to remove all the lactate and hydrogen ions from the blood and muscle if the athlete does no light activity during recovery. Walk-ing, or light jogging will restore the muscle pH in around 1 hour. So while you will expect to see some removal of lactate and hy-

Figure 4. Recovery of PCr and blood acidity during rest

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drogen ions during the 4 min rest period, a significant level of lactate and H+ will remain.

! Now let’s examine the power output after the various rest duration periods. After 4 mins, you can expect around 90% of the athlete's sprint capacity to be restored despite the remain-ing acid conditions. I hope you are wondering why sprint per-formance continues to improve despite high levels of acidosis remaining in the muscle. It appears that the resynthesis of PCr is the dominant factor influencing the performance of repeated bouts of sprint exercise. Acidosis does not interfere with the PCr energy system.

Effects Of Recovery

! Now let's reexamine the data in Table 1 by adding data from exercise bout 2 (Table 2). Biopsies were not done for Bout 2. The data for Bout 3 are shown in brackets on this chart along-side the data for Bout 1. PCr recovered to around 70mmol/kg dm during the rest period between Bout 2 and Bout 3. This is only around 80% of its starting value of 88mmol/kg dm and ex-plains why the athlete produces only 580 W during the first 6 seconds of Bout 3 compared with 800 during the first 6 seconds of Bout 1.

! The athlete begins Bout 3 with a glycogen level of 370mmol/kg dm. Remember that glycogen cannot rebuild in a short time period. The athlete begins Bout 3 with a glycogen level of 370mmol/kg dm. Remember that glycogen cannot re-build in a short time period.

! The lactate level is quite high at the start of Bout 3. Rest-ing level of lactate before Bout 1 was 5 mmol/kg dm compared with 95 mmol/kg dm at the beginning of Bout 3. H+ level is also high (216 nM compared with 62 before Bout 1). It is clear that the metabolic by-products of anaerobic glycolysis from the previ-ous two bouts are still present.

Power output

PCr content (mmol/kg/dm)

Glycogen content (mmol/kg/dm)

Lactate content (mmol/kg/dm)

H+ content

nM

Rest 88 (70) 480 (370) 62 (216)

At 5 secs800 W

average46 (26) 110 (254)

At 15 secs700 W

average28 (14) 157 (254)

At 30 secs500 W

average8 (2) 400 (300)

60 (no data)

183 (254)

Table 2. Data from anaerobic test for Bout 1 and Bout 3 (in brackets)

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! We can see what is going on by examining the ATP charts (Figure 5). The ATP source for Bouts 1 and 2 are indicated. PCr contributes the largest amount of energy in the first 6 seconds of the third bout. However, the amount of ATP produced is less than it was in Bout 1. There was a much smaller contribution from anaerobic glycolysis compared with Bout 1. The amount of ATP produced aerobically is slightly more. The high level of aci-dosis is clearly interfering with the athlete's ability to produce

ATP using anaerobic glycolysis.

! During the 6 to 15 second time period of the third bout here is the ATP produced by PCr. It is about half of the ATP than was being produced in Bout 1. Here is what is produced by anaerobic glycolysis – about the same as was being pro-duced during the first 6 seconds. The ATP energy that is de-

rived aerobically is providing almost as much ATP as the PCr and anaerobic glycolysis.

! The power output during the final 15 s is fueled almost equally by the three energy systems – here is PCr, here is an-aerobic glycolysis, and here is the aerobic ATP. Creatine phos-phate was used up during the first 6 seconds of bout 3 and the high level of hydrogen ions was inhibiting the ATP production via anaerobic glycolysis. Clearly the PCr made the difference in power output during the first 6 seconds.

The key points here are as follows:

• Anaerobic glycolysis cannot recover from extended bouts of intense activity.

• Extreme acidosis in the muscle prevents the breakdown of glucose and the muscle has to use fats for fuel. The only place fats can be used is in the mitochondria.

• If the athlete can’t produce ATP by anaerobic glycolysis very little power can be produced.

• The PCr energy system is unaffected by acidosis.

• Because the aerobic system does not fully return to rest-ing rates during recovery it turns on quicker, and reaches higher levels during subsequent bouts of sprinting.

Figure 5. Source of ATP for Bout 1 and Bout 3

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Application To Sprint Training

! The word 'sprinting' is used to describe bursts of maximal effort of less than 60 seconds. The duration and purpose of the bursts of speed is different depending on the sport. In track and field the competition sprint is a single all-out effort, although training for that single effort consists of performing multiple bouts of all-out speed to induce the necessary adaptations for speed.

! In team sports, sprinting only occurs in multiple bouts over about an hour, with intermittent recovery periods ranging from standing still to slow walking or jogging. We will now apply the insights we have gained from our discussion about the way the energy systems are used to these sprinting situations.

Single Bout Of Sprinting

! The 100m and 400m races are both examples of single bout sprinting where there is no concern about recovery for a subsequent race within the next few minutes. During a 100 m sprint, most of the cell's PCr is used during the first 20 meters of the race (Figure 6). Here is the speed curve and here is the phosphocreatine curve. This is the phase of rapid acceleration where PCr is a critical source of ATP because of its ability to

produce very high power. Speed begins to decrease between 40 – 60 m when the PCr stores are approaching their lowest lev-els. We know from our previous discussion that glycolysis is pro-ducing a significant proportion of the ATP in the middle to final portion of the race.

! Over a 100 m sprint anaerobic glycolysis provides approxi-mately 65 – 70% of the ATP production. This is the reason aci-dosis increases throughout the race. Blood lactate levels are the highest in the fastest sprinters indicating the importance of the anaerobic glycolytic energy system to ATP production in the 100 m race.

Figure 6. PCr use during a 100 m race

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! The metabolic factors contributing to the onset of fatigue in the 100 m are associated with the decrease of PCr in the mus-cle. This explains the decrease in running speed during the mid-dle part of the 100 m sprint. At the end of the race anaerobic gly-colysis is the main source of energy. There is insufficient time for acidosis to interfere with anaerobic glycolysis.

! During a 400 m race PCr also plays in important role (Fig-ure 7). PCr concentration falls 89% during the race. Glycolysis is an important source of ATP during the entire race. The rise in lactate here indicates the activity of glycolysis. The rate of ATP yield from glycolysis reaches its maximum between 200 and

300m when PCr is relatively depleted. Over the last 100 m, when PCr is very low, and the rate of glycolysis also declining due to interference from acidosis, there is a dramatic decrease in running speed because the energy system now shifts to the aerobic energy system.

! At the end of a 400 m race there is still adequate glycogen to sustain energy metabolism. The high rate of acidosis is thought to inhibit the cross-bridge cycling. The decline in run-ning speed observed towards the end of a 400 m race is due to a reduction in the rate of anaerobic glycolysis, despite ample availability of muscle glycogen.

Multiple Bouts Of Sprinting

! Athletes train for speed by performing multiple bouts of high intensity sprinting separated by short periods of rest or low activity. Figure 8 is what the activity intensity might look like – this one has three maximum speed bouts included, but there can be more for a track sprinter. Team sports coaches will try to mimic the speed variations typical during a game. The energy system dynamics change with each subsequent burst of activ-ity.

! illustrates a comparison of the workload for a sprinter per-forming a race. It's just one single burst of maximum speed.

Figure 7. PCr use during a 400 m race and the lactate pro-duced

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Here's an endurance runner (very consistent speed below VO2max). Here is a basketball player and - - - - here is a hockey player. There is quite a bit of variability.

! There are constant fluctuations in muscle levels of PCr from very low to reasonably high to support this speed variabil-ity. During the short bouts of intense sprinting the PCr concen-trations can be as low as 40% of resting levels. After 15 sec-onds of rest the PCr can increase to about 70% of the resting level.

! Figure 9 illustrates the PCr concentrations over a 6 min in-termittent exercise. You can see that the amount of PCr in the

muscle fluctuates quite a bit. The availability of PCr when needed will determine the athlete's performance during the more intense periods of a game. The PCr energy system is sup-ported by glycolysis, and as a result lactate production during team sport training session and competition, can be very high indicating relatively high levels of acidosis.

! In multiple bouts of speed the aerobic energy system gradually increases its contribution to ATP production with each bout of speed. Part of the role played by the aerobic energy sys-tem is to provide the ATP needed to rebuild PCr.

Figure 8. Activity intensity profile during a sprint training ses-sion

Figure 9. PCr concentrations over a 6 min intermittent bout of exercise.

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! Figure 10 is an interesting graphic illustrating the sub-strates that are used with multiple bout sprinting. Over the course of 1 hour most of the ATP is coming from glycogen. A lit-tle bit of glycogen is used for anaerobic glycolysis until acidosis begins to interfere with the ability of anaerobic glycolysis to work effectively. Most of the glycogen is used to support aero-bic metabolism when the athlete is running at speed over about 60% of their VO2max.

! Producing ATP to support multiple bouts of speed requires a large consumption of substrates. Here is the approximate dis-tribution. The dominant substrates are carbohydrate either as

glycogen or blood glucose, and fat. The carbohydrate used dur-ing a typical team game competition is mainly the glycogen stored within the exercising muscle. Some resynthesis of glyco-gen occurs from lactate during periods of rest and low-intensity activity.

! The key point here is that some fat is used to support multi-ple bursts of speed by the aerobic energy system. However, gly-cogen is the most important substate supporting aerobic ATP production.

Factors Influencing Recovery

! The aerobic energy system provides the ATP needed to re-build PCr. It also helps remove the metabolic waste products fol-lowing a sprint. For this reason, the athlete's aerobic fitness is an important factor in their speed of recovery. Athletes with higher VO2max values have a larger aerobic metabolic machin-ery to provide more ATP for PCr resynthesis. In essence, sprint-ers with good aerobic fitness compensate for the decline in an-aerobic metabolism by using aerobic glycolysis.

! Glycogen will continue to deplete when aerobic glycolysis is operating, but there will be no associated rise in H+. If we go back to Table 2 you can see this effect. In bout 3 the number of

Figure 10. Substrates used with multiple bout sprinting

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hydrogen ions remained constant at 254 after the first 6 seconds.The higher the number of sprints being performed the less anaerobic glycolysis will contribute and hydrogen ions will remain constant. However, aerobically supported glycolysis can-not produce the same power output as anaerobic glycolysis and there will be a marked decline in power. This in conjunction with the declining PCr explains the reduction in power output as Bout 3 continued.

Here are three key points.

• Sprinting is not limited by muscle glycogen availability un-less glycogen concentrations fall below a critical thresh-old.

• Athletes training using multiple sprint or competing in mul-tiple sprint sports need to consume adequate carbohy-drate to replenish glycogen stores within 24 hours of in-tense training or competition.

• Inadequate intake of carbohydrate is detrimental to multi-ple sprint performances

Creatine Supplementation

! A number of studies indicate that dietary creatine supple-mentation enhances sprint and high-intensity exercise is some

individuals. The higher initial muscle creatine phosphate con-tent provides more energy for ATP resynthesis during exercise, and there will also be an increased rate of creatine phosphate resynthesis during the recovery periods. This means the PCr content of the muscle will be greater at the start of each subse-quent sprint.

! In running, body mass increases following supplementa-tion. Carrying and propelling this additional mass counteracts some of the potential improvements in performance that might come from the enhanced muscle power. Creatine supplementa-tion is not recommended for athletes who must sprint against gravity.

Active Versus Passive Recovery

! A significantly higher mean power output in the second sprint is obtained using active recovery compared with passive recovery. There is an increased blood flow to the previously ex-ercised muscles and this facilitates a greater rate of removal of waste products. In particular, active recovery increases rate of removal of blood lactate.

! It is important to keep the intensity of the active recovery low so lactate accumulation is not enhanced. Walking or gentle

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jogging between bouts of sprint running works quite well to en-hance recovery.

References:

Bangsbo, J. Team sports. P 535 – 549. Nutrition in Sport: Olym-pic Encyclopaedia of Sports Medicine. Wiley, Chichester, GBR. 2008 Maughan R (ed) Volume VII.

Bogdanis CG, Nevill ME, Lakomy HK, Boobis LH. Power output and muscle metabolism during and following recovery from 10 and 20s of maximal sprint exercise in humans. Acta Physiol Scand 1998, 163, 261-272

Gaitanos GC, Williams C, Boobis LH, Brooks S. Human muscle metabolism during intermittent maximal exercise. J. Appl. Physi-ology. 75(2): 712-719, 1993.

Lakomy, Henryk K.A. Physiology and biochemistry of sprinting. in Hawley JA (ed) Olympic Handbook of Sports Medicine-Running: Blackwell Science Ltd, 2000.

Nicholas, CW. Sprinting. P 535 – 549. In Nutrition in Sport: Olympic Encyclopaedia of Sports Medicine. Wiley, Chichester, GBR. 2008 Maughan R (ed) Volume VII

Robergs, R A; Ghiasvand, F; Parker, D. Biochemistry of exercise-induced metabolic acidosis. American journal of physi-ology. Regulatory, integrative and comparative physiology, 09/2004, Volume 287, Issue 3. R502 – R516.

Spencer, M, Lawrence, S, Rechichi, C, Bishop, D, Dawson, B, and Goodman, C. Time-motion analysis of elite field hockey, with special reference to repeated-sprint activity. J Sports Sci 22: 843–850, 2004.

Spriet L. Anaerobic metabolism during exercise. P 7 – 27 in Har-greaves M, Spriet L. Exercise Metabolism (2nd edition). Human Kinetics

8Introduction to lactate

What You Will Learn

When you have completed this module you will be able to:

1. Explain how lactate is an indirect measure of hydrogen ion production and therefore provides insight into the acidity of the blood and muscles

2. Discuss how the muscle fibers differ in their ability to produce and clear lactate.

3. Explain how lactate and hydrogen ions are moved out of one muscle fiber into a muscle fiber capable of using it for fuel

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Introduction

! Whenever glycolysis exceeds the capacity of the athlete's aerobic energy system to use pyruvate it begins to accumulate because it cannot enter into the mitochondria. To keep glycoly-sis working pyruvate is first converted into lactic acid and then almost instantly dissociated into lactate and hydrogen ions (Fig-ure 1). Both these molecules begin to accumulate in the muscle cells and blood.

! Early sport scientists thought the high quantities of lactate in the muscle cells and blood caused fatigue, muscle cramps, muscle stiffness and soreness, and breathlessness. Therefore,

Section 1

Lactate and hydrogen ions

Figure 1. Pyruvate is broken down into lactate and hydro-gen ions

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they believed lactate was a key factor limiting the athlete's per-formance. They didn't know about the hydrogen ions that were being produced in association with lactate production.

! Today we understand the relationship between hydrogen ions and lactate production and that the hydrogen ion is respon-sible for making the environment for cells very acidic. The lac-tate molecule itself is a harmless molecule and a valuable source of fuel for certain tissues. The reason we measure blood lactate levels is because it is easy to measure, and provides an indirect estimation of what we are really interested in, and that is the blood and muscle acidity.

What You Will Learn

! In this module you will discover why lactate is an indirect measure of hydrogen ion production and therefore provides in-sight into the acidity of the blood and muscles. We will also ex-amine how the muscle fibers differ in their ability to produce and clear lactate and how lactate and hydrogen ions are moved out of one muscle fiber into a muscle fiber capable of using it for fuel.

Key Points To Recall

! The three energy systems start producing ATP concur-rently, but differ in how quickly they gear up to full speed. They use different fuels and only the aerobic energy system requires oxygen to work. The other two are oxygen-independent or an-aerobic. Glycolysis is oxygen-independent and can work up to two times faster than the ability of the aerobic energy system to clear pyruvate. This is why lactate and hydrogen ions can quickly accumulate when the athlete is working above the up-per limit of their aerobic capacity. When glycolysis is working faster than pyruvate can be cleared by the aerobic energy sys-tem, lactic acid is produced. This quickly dissociates into lactate and a hydrogen ion.

! In other words, lactate is formed when glycolysis and the aerobic energy system are not in balance.

! The glycolytic energy system can accelerate its ATP pro-duction within a few seconds, allowing for a fast adjustment to the energy demands of the performance. Glycolysis (in conjunc-tion with the PCr energy system), is therefore an important source of ATP at the start of exercise, whenever there is an in-crease in pace, and when the intensity of exercise exceeds aerobic ATP production capabilities.

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Muscle Fiber Type And Lactate

! The three muscle fiber types - Type I (slow oxidative), Type II (fast oxidative glycolytic) and Type II (fast glycolytic) muscle fibers - differ in their concentration of mitochondria and glycolytic enzymes, and therefore in their ability to produce ATP aerobically or anaerobically. This, in turn determines if they are high producers or consumers of lactate.

! The FG muscle fibers have a high anaerobic capacity and very little aerobic capacity. They lack the mitochondria needed to clear the pyruvate as it is being produced by glycolysis and therefore produce a lot of lactate and hydrogen ions. The FG fi-ber is the chief culprit for creating the high acid conditions for cells because their main ATP production is via anaerobic glyco-lysis.

! The slow oxidative fibers have a high aerobic capacity. They therefore produce very little lactate and are able to con-sume considerable lactate. The FOG muscle fiber is a hybrid fi-ber capable of generating energy both anaerobically and aerobi-cally.

! They produce a lot of lactate and hydrogen ions but are also able to consume quite a bit of lactate for fuel in their mito-chondria. They are also thought to convert lactate to glycogen.

! While the three types of fibers are randomly mixed within the muscle, there is generally a higher portion of one fiber type depending on the athlete's genetics.

! Successful athletes in different sports exhibit a predictable pattern of Type I and Type II muscle fibers (Figure 2). The mus-cle of successful sprinters, jumpers and weightlifters contain a high percentage of both types of Type II fibers. Middle distance (400 to 1500 m) runners, cyclists and swimmers tend to have equal proportions of both Type I and Type II fibers. Long dis-

Figure 2. Dominant muscle fibers of different sports

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tance runners and cross-country skiers have a high percentage of Type I fibers.

How Blood Becomes Acidic

! The lactate molecule and its accompanying hydrogen ion produced by glycolysis leaves the muscle cell and enters into the spaces between the cells where it then moves into the bloodstream (Figure 3). The hydrogen ion moves with the lac-tate. It is these hydrogen ions that make the blood acidic.

! The amount of lactate in the blood depends on how quickly it is being produced by the lactate producing muscle fi-bers and how quickly it is removed by the lactate consuming tis-sues. Figure 3 depicts the FG fibers that are producing the lac-tate. Some of it is taken up by the neighboring SO fibers. What-ever lactate is left is moved into the bloodstream where it will go to the heart, liver and other remote muscle cells that can use lactate for fuel. Some lactate is thought to be converted into gly-cogen by the FG fibers. The liver also converts lactate into gly-cogen.

! Blood lactate concentration during rest is generally around 1 — 2 mM (millimoles). Blood lactate concentrations can reach 15 — 20 mM during intense activity. In top-level 800 m runners a post competition blood lactate concentration as high as 22

mM has been reported. These numbers will have more mean-ing to you when we discuss lactate curves. The blood lactate concentrations are always lower than the muscle lactate con-centrations.

Blood PH

! The pH of any fluid is the measure of the hydrogen ion con-centration. A pH of 7 is neutral (Figure 4). Normal pH of blood is 7.4 and is tightly regulated between 7.38 – 7.42. Blood pH

Figure 3. Lactate and H+ moves from the muscle cell into the bloodstream

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above 7.42 indicates alkaline conditions. A blood pH of 6.8 or lower can severely damage proteins interfering with cellular functioning and glycolysis grinds to a halt. Remember that en-zymes are all proteins.

! Strenuous physical activity can cause your blood pH to drop or become more acidic. In general muscle pH is reduced by 0.4 to 0.8 units during intense exercise. A buildup of lactate and H+ ions in the cell causes water to be drawn into the mus-cle cell. This is the reason weight lifters feel "pumped" after a workout. The body builder will work very hard to increase the acidity of the muscle fibers so water is drawn into the fiber and muscle size is increased.

! When water enters the muscle cell it removes fluid from the blood reducing blood volume. At the end of a race where acidity levels are high, the athlete will be working with a less effi-cient cardiovascular system because blood volume has been reduced.

! During rest, the pH of the muscle fiber is reduced, water leaves the muscle fiber and reenters the bloodstream. The car-diovascular system returns to its normal level of functioning. You can perhaps see why intense exercise is not safe for an in-dividual who has a diseased heart.

How Lactate Moves

! The three fiber types are illustrated in Figure 5. There is the FOG fiber, the slow oxidative fiber and the FG fiber. The FOG and SO fibers both have mitochondria and the enzymes for glycolysis. The FOG fiber has more glycolytic enzymes than the SO fiber does. The FG fiber has insignificant numbers of mi-tochondria and are unable deal with the lactate they produce. They are packed full of glycolytic enzymes.

! The lactate and hydrogen ions leave the FG fiber abd en-ter into the interstitial fluid. The SO fibers will absorb some lac-tate while the majority will go into the bloodstream. The FOG fi-

Figure 4. Ranges of blood pH

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ber can use its own lactate in the mitochondria or it can also get rid of it.

! All muscle cells are surrounded by a cell membrane com-posed of a lipid bilayer called the sarcolemma and is not perme-able to either lactate or hydrogen ions. There are lactate trans-port mechanisms made from protein inserted in the cell mem-brane. These transporters are called monocarboxylate transport-ers (MCT)

 ! There are two types of MCT transporters: MCT1 moves lactate and H+ INTO the cell. The MCT4 transporter moves lac-tate and H+ ions OUT OF the cell. Note that the fast glycolytic

fiber does not have any MCT1 transporters, it only has MCT4. So, it can only get rid of lactate it can't bring it back in.

! The SO fibers don't have MCT4 transporters because they don't need to export lactate and hydrogen ions. Whatever lac-tate they produce they can use in their mitochondria.

! The FOG fibers show the two different types of transport-ers – one for bringing lactate in and the other for moving it out. This means FOG fibers are a good consumer of lactate. FOG fibers can also convert lactate into glycogen. The process is called glyconeogenesis.

! MCT1 transporters are especially abundant in the heart and this is the reason the heart can consume a lot of lactate and use it for fuel. MCT1 can transport lactate inward at high rates even when lactate concentrations are rather modest. On the other hand, the MCT4 doesn't begin to truly work until lac-tate builds up to a high level inside the cell.

! Prolonged inactivity causes concentration of both MCT1 and MCT4 to decrease. Endurance training will increase the number of MCT1 transporters. However, intense exercise is nec-essary for an increase in MCT4 concentrations. Changes can be seen over the course of a couple of weeks of appropriate training.

Figure 5. Lactate transportation

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! The ability to remove lactate and H+ ions is highly variable among different athletes of the same skill level and among ath-letes of different skill levels (Figure 6). Elite athletes have a higher lactate transport capacity than the trained and untrained subjects suggesting that MCT transporters could be under ge-netic control. However, training does increase the lactate trans-port capacity — it's just that some athletes have a higher capac-ity to train lactate and H+ transporters than others. Athletes with a highly developed MCT1 transport mechanism recover quicker due to their improved capacity to remove lactate and H+ from the blood.

! Endurance training can increase the number of MCT1 transporters in SO and FOG fibers. Very intense training such that is designed to challenge the anaerobic glycolytic energy system will stimulate the FG and FOG fibers to build more MCT4 transporters.

References

Bonen, A. Skeletal muscle lactate transport and transporters in Exercise metabolism. Hargreaves, M and Spriet L. editors. Hu-man Kinetics, 2006.

Bonen, A. Lactate transporters in heart and skeletal muscles. Medicine and science in sports and exercise. Volume: 32 Issue: 4, 778-789, 2000

Thomas C, Bishop D, Lambert K, Mercier J, Brooks G. Effects of acute and chronic exercise on sarcolemmal MCT1 and MCT4 contents in human skeletal muscles: current status. Am J Physiol Regul Integr Comp Physiol 302: R1–R14, 2012.

Bishop D, Edge, J., Thomas, C., Mercier, J. Effects of high-intensity training on muscle lactate transporters and postexer-cise recovery of muscle lactate and hydrogen ions in women. Am J Physiol Regul Integr Comp Physiol 295: R1991–R1998, 2008.

Figure 6. Key points for lactate transporters

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Juel, C. Current aspects of lactate exchange: lactate/H+ trans-port in human skeletal muscle. European Journal of Applied Physiology. November 2001, Volume 86, Issue 1, pp 12-16