P&P#80

P&P #80: Overtraining

Research based on the proliferation of the conveniently defined maladaptation states such as overtraining, overreaching, overuse and chronic fatigue may be confusing, more than solving, the problems of prescription of optimal training levels.

BACKGROUND

In the earlier days of training, we simply had fatigue and exhaustion. An athlete was either training too hard or not enough, and sometimes optimally trained. The temptation to define overtraining as the first-mentioned state msu have been obvious. Then the sports medical profession decided that overtraining is not quite that simple, because the overtraining may be due to too great an intensity or load at any one time (this became known as 'overload'), or to too sustained a work volume (this became known as 'overuse'). The former state apparently led to overload injuries (common among strength athletes) and the latter to overuse injuries (common among distance athletes).

The logical next step was to define acute and chronic states of overtraining and fatigue or exhaustion. Whether there is a difference between acute exhaustion and acute fatigue, and between chronic exhaustion and chronic fatigue, was never quite settled. Maybe it was simply a matter of semantics, but then again it might not be.

Next on the scene were the states of ACUTE OVERTRAINING and CHRONIC OVERTRAINING (or should they be called 'processes', because they might not be conditions extant at a given moment, but a flux of events in dynamic change?). Then someone decided that these definitions were not quite what the doctors ordered and acute overtraining became OVERREACHING (does this include acute overuse and acute overload?) and the latter simply became OVERTRAINING (presumably still comprising both overuse and overload).

ADAPTATION MODELS

While all of this was happening, someone recognised that Hans Selye's General Adaptation Syndrome (GAS) describing the physiological response to stress might serve as a convenient theoretical foundation for adaptation to training, because training may be regarded as a certain type of stress. Out of this melting pot arose the concept of overcompensation or supercompensation, even though this concept (Weigert's Law) was formulated about a decade (Folbrot, 1941) before Selye's first invaluable work ('Stress', 1950) was published. Selye's model was applied directly to sport only much more recently.

The relationship between physical adaptation and exhaustion-recovery processes under different types of loading was researched in the early 1950s by Yakovlev (1955), based upon earlier Russian concepts of adaptation of CAR (Current Adaptation Reserves) and stimulated by the adaptation or conditioning of reflexes at the turn of the 20th century by Pavlov. The CAR, the generalised pool of energy and physiological capabilities, which fuels the body's resistance or adaptation to stress, is analogous to what Selye called Adaptation Energy (comprising Superficial and Deep Adaptation Energy to cope with acute versus chronic stressors). Dipping into the Deep Adaptation energy stores, which are considered to be non-replenishable, was regarded as potentially harmful and possible life threatening.

SUPERCOMPENSATION AND SO FORTH

Today, the term SUPERCOMPENSATION or SUPERADAPTATION is still widely applied to the result of optimal training, while among Russian scientists the term ADAPTIVE RECONSTRUCTION seems to be more favoured, because of doubts about super-normal rises in level of adapted performance or homeostasis (we shall return to the idea of homeostasis later, since it is central to an understanding of all of the states or processes presented in this P&P). For instance, while acute supercompensation of glycogen stores (as in 'carbo loading') occurs, chronically increasing levels of glycogen storage have not been observed to occur in response to repeated use of 'progressive overload' with carbohydrates.

RELEVANCE OF BIOCHEMICAL MARKERS

We must be cautious of the consequences of rigidly following the Selye biochemical approach to stress and adaptation. Most work on overtraining, stress and allied processes seems to follow in his biochemical footprints, monitoring catecholamines and other stress markers and tending to pay less attention to structural adaptations at cellular and subcellular levels.

Enhanced or diminished performance is not simply the result of altered storage or release of biochemical substances, but also of structural changes in muscle and other tissues, as well as altered efficiency and rates of bioenergetic, central nervous and neuromuscular processing. Could it be that the release or altered response of various 'stress chemicals' do not serve as direct precursors of overtraining or cellular damage, but instead serve to initiate or modulate repair processes? Thus, no release of 'stress chemicals', no signal for adaptation to occur, no adaptation!

Is the relevance of these biochemicals often being misunderstood? If not, why then are top level performances still produced by some athletes who are clearly labelled as 'overtrained'? Why are lowered performances just as common among under-trained, over-trained and optimally trained athletes? Is this due to one's mental state? If this is so, are we then stating that psychological factors can override the negative effects of overtraining? Can we then ignore fears about moderate (and possibly even severe) overtraining or overreaching, because we may be able to train the athlete to implement psychological strategies to override these states to excel in vital events and overcome any lingering adverse effects by resting after such effort? The career of the great Zatopek and many other athletes is replete with instances of ignoring all the symptoms of serious overtraining and still excelling without long-term disaster.

Could we not surmise that the degree and rate of adaptation to specific physical stressors is proportional to the level of circulating 'stress chemicals'? Are we justified in associating impaired performance with the level of selected biochemicals released after exposure to certain regimes of training? Can we state categorically that states of overtraining, as suggested by the release of or rise in levels of specific biochemicals, invariably lead to diminished performance or injury? What can we learn from cases where injured, severely overtrained, mentally distraught or terminally ill athletes have still managed to excel against all the odds? Are we justified in stating that these are the exceptions rather than the rule? (after all, the bell-shaped distribution curve shall always rule!) Do they not suggest the presence of other processes and mechanisms that could benefit us more than sole focus on averages and means derived from selected populations in a laboratory setting?

MIND OR BODY OR BOTH?

Maybe we also need to be examining which psychological strategies will enable the so-called overtrained athlete to excel even in that state. After all, has anyone managed to separate the physiological from the psychological effects of training or competitive stress? We might then wonder how much of the loss of performance during overtraining is due to mental rather than physical factors? Then again, are we truly justified in trying to clinically separate the two? Of course, I can now sense the urge of some physiologists to invoke the findings emerging from the newer discipline of psycho- neuroimmunology and indeed, some relevant data may be applied from this source. However, we have to be careful not to confuse adaptation with pathology, for overtraining appears to be almost exclusively regarded as pathology rather than adaptation.

All of this brings us to a major issue in sports science. Why do we base so many of our theories on Gaussian or bell-shaped distributions which tell us about means, modes and medians - in other words about majorities and average subjects? Certainly, we have learned a great deal about the 'average' human being from these carefully controlled studies, but very often this statistically admirable approach tends to disguise the fact that average persons almost never break world records or produce unbelievable physical feats. Maybe we have become too devoted to the wrong percentile or to 95 percent confidence intervals and so forth. Maybe we need to pay far more attention to those at the extreme ends of the Gaussian distribution, to the singularities rather than the regularities, to the exceptions rather than the rules. Research does not seem to have significantly correlated degree of supercompensation or overtraining with enhanced or lowered levels of glycogen, ATP or any other biochemicals involved in the various bioenergetic processes in the body. For instance, ATP levels have never been shown to deplete dramatically, even after very strenuous exercise. Lowered immune response has been noted, but its direct effect on performance is still open to question. These are major reasons why our Russian colleagues often prefer to use the term adaptive reconstruction instead of supercompensation (Siff & Verkhoshansky 'Supertraining' 1996). Similarly, they hesitate to talk in terms of overtraining, but pay more attention to different phases and types of adaptation.

OTHER MODELS OF ADAPTATION OR OVERTRAINING

The Selye or Single Factor model offers an easily understood theoretical framework for the adaptational process, but it is not the only plausible model used. The Two Factor Model implicates the superimposed after-effects of two processes: fitness adaptation and fatigue, with the fitness after-effect decaying at a slower rate than the fatigue after-effect (Siff & Verkhoshansky: 'Supertraining', 1996; Zatsiorski: 'Science and Practice of Strength Training', 1995). The resulting adapted state known as the athlete's PREPAREDNESS (yet another definition!) which, unlike 'fitness', is influenced by acute changes in the organism. In other words, the Fitness-Fatigue Model would appear to offer a more logical foundation for what has been called 'overreaching'.

Then again, are we justified in this bipolar approach with acute overreaching as one discrete state and overtraining as another, instead of noting a continuum process between optimal adaptation towards one end of the scale and all the 'Big Ds' (deterioration, damage, disease and death) towards the opposite end?

If overtraining or overreaching are to be explained on the basis of the Two Factor Fitness-Fatigue Model, then one has to assume that the fatigue after- effect persists for a longer period or reaches a greater magnitude than the fitness after-effect at an acute or chronic level. Has any evidence of this yet been observed?

ADDITIVE EFFECTS OF STRESS?

Stress is commonly regarded as being additive, with successions of smaller stressors summing up to produce a seriously disruptive major stress. Presumably, overload would then be the result of one or very few large single stressful events, whereas overuse would be the summated result of many smaller stressors.

While stress may be additive, it must be remembered that the body is an adaptive organism and thus, biological responses to environmental change usually seem to grow or decay according to exponential or various sigmoidal functions (though some oscillatory changes may sometimes occur), so that it is only the remaining AFTER-EFFECTS of stress that may actually add at a given time. Thus, according to the Fitness-Fatigue Model, both fitness and fatigue may grow or decay and result in acute, delayed and chronic (positive or negative) after-effects.

How do we then deal with concepts of OVERTRAINING and CHRONIC FATIGUE (and, of course, their physical and mental aspects)? Do we regard them as synonymous? If we comment that chronic fatigue can occur in the absence of physical effort, then we have to retort that much of overtraining may then be strongly associated with mental, rather than purely physical, factors! Quo vadis?

HOMEOSTASIS AND EQUILIBRIUM

In a previous P&P we discussed the problems associated with postulating the existence of precisely defined and quantified points and states of equilibrium or homeostasis, in the light of recent work on the relevance of chaos processes in physiological and psychological systems. Once again, we have to stress the same point, namely that the existence of exact equilibrium states and conditions is often unwarranted and misleading. Instead, homeostasis has to be regarded as a dynamic process periodically swinging between various temporary set- points with a certain bandwidth of probabilities whose characteristics permit the existence of a dynamic adapting and self-correcting state to offer superior ability to cope with environmental change (known as 'stress').

The work on non-equilibrium systems by 1977 Nobel prize-winner, Ilya Prigogine, may be of particular value in this regard. He showed that non- equilibrium may be a source of impending order (Prigogine & Stengers, 1984). All systems comprise subsystems in a continual state of fluctuation in which one or more fluctuations can totally disrupt the existing organisation and pro duce an unpredictable leap to 'chaos' or to a more differentiated, higher level of organisation (known as a dissipative structure, because it requires more energy to sustain this state). One of the most controversial aspects of this concept is that Prigogine maintains that order can occur spontaneously or by chance through a process of self-organisation. Investigation into how specific patterns of training or mental states can promote the conditions for enhanced self- organisation may then be of profit in the quest to produce sporting excellence. Any attempts to understand and explain the concepts of overreaching, overtraining and chronic fatigue then may have to take this work into account.

OTHER RESEARCH

This P&P has already become far longer than intended, so we shall for the moment have to omit the considerable amount of Russian research carried out for more than 40 years into adaptation. This has been based on research into positive and negative acute, delayed (short and long-term), cumulative and transient after-effects of distributed, intermittent and concentrated training loads of different types, durations and densities. This work has examined the interactive concurrent (complex) and sequential imposition of cyclic, acyclic, resistance and 'plyometric' training with and without the intervention of restorative means and various ergogenic substances (including 'chrononutrition'). For those who may have access to our book 'Supertraining' (Siff & Verkhoshansky), this topic is covered at length in Ch 6.

Unfortunately, the large number of diagrams means that I cannot send them adequately via simple e-mail, though I will send some of the biochemical aspects of adaptation as an APPENDIX to this P&P. Nor has space permitted me to address research into fatigue in terms of central and peripheral processes, the phenomena of low-frequency and high-frequency fatigue, muscle-fibre types and changes in blood flow to the muscles (this work is summarised in Ch 1 of 'Supertraining').

APPENDIX

This extract from Siff MC & Verkhoshansky YV 'Supertraining' (1996) serves as an Appendix to P&P 80 for those who wish to comment in greater depth on any of the biochemical correlates of the adaptational process in training.

THE BIOCHEMISTRY OF ADAPTATION IN SPORT

Adaptation is primarily dependent on the interrelation between a cell's function and its genetic apparatus, which constitutes the constantly active mechanism of intracellular regulation.

Unlike immediate adaptation reactions, the process of prolonged adaptation to systematic muscular activity typically involves significant intensification of the biosynthetic processes, primarily those of protein synthesis, as well as the emergence of marked structural changes in the tissues.

The use of radioactively labelled amino acids has revealed that training intensifies the synthesis of proteins in the myofibrils, mitochondria, sarcoplasm, and microsomes of the skeletal muscles and the heart (Platonov, 1988). The synthesis of DNA and RNA precursors also intensifies, indicating activation of the genetic apparatus of the muscle cell, while RNA synthesis in the cardiac muscle also increases during training. In this respect there is increased activity of enzymes which are structural components in the synthesis of nucleic acids.

Training intensifies the formation of all cellular material including the mitochondria, myofibrillar proteins, endoplasmic reticulum and various enzymes. The motoneurons also thicken, and the number of terminal nerve shoots increases, as does the number of nuclei and myofibrils in the muscle fibres. In addition to the intensified synthesis of structural proteins, synthesis of enzymatic proteins (especially skeletal-muscle aspartate-amino-transferase) is increased during training.

The nucleotides (ADP, AMP - adenosine monophosphate), creatine, inorganic phosphate, and some amino acids, as well as the ADP/ATP and the creatine/CP ratios, play an important role in activating protein synthesis elicited by training. It appears that the accumulation of metabolites formed during muscle activity, as well as the decreased ATP and CP levels, might signal activation of the genetic apparatus of the muscle cells. The change in the metabolism of hormones such as glucocorticoids, somatotropin, androgens, insulin and the thyroid hormones is very important in intensifying protein synthesis during training. Thus, adaptive synthesis of proteins as a result of training is induced by both hormonal and non-hormonal components.

The overall process of intensifying enzymatic and structural adaptive biosynthesis that ultimately leads to their supercompensation is most important in biochemical adaptation during physical load training.

In the skeletal muscles, training increases the levels of energy substrates (glycogen, CP, and creatine), muscle proteins (e.g. myosin, actomyosin, sarcoplasmic and mitochondrial proteins), phospholipids, vitamins, minerals (e.g. iron, calcium, magnesium), dipeptides (carnosine, anserin) and nucleotides (Platonov, 1988).

However, the concentration of ATP does not increase under the influence of training, probably due to accelerated metabolism of ATP in the muscles that involves intensification of its synthesis and breakdown. The increased activity of a number of enzymes that catalyse the energy metabolism reaction is an integral component of biochemical adaptation during training, especially the activity of glycolytic enzymes (e.g. hexokinase, phosphorylase and pyruvate-kinase) and enzymes in the oxidative resynthesis of ATP.

Thus, as a result of training, supercompensation of some of the energy sources takes place, enzyme activity increases, and the activity ratios in the enzyme systems change. In turn, the state of energy SUPERCOMPENSATION serves as a starting point for intensifying adaptive protein synthesis, which requires a large quantity of ATP.

THE SPECIFICITY OF BIOCHEMICAL ADAPTATION

Biochemical adaptation is not simply a generalised and summated response of physical systems to training stress. Many components and processes of the muscular system display a definite specificity of adaptation to loading.

THE SEQUENCE OF BIOCHEMICAL CHANGES DURING TRAINING

The many biochemical changes that take place in the body during and after training (as well as overtraining) do not occur simultaneously. A definite sequence in the biochemical adaptation to training is discerned (Platonov, 1988). First, the potential for oxidative resynthesis of ATP and the level of glycogen increase. Next there is an increase in the level of structural protein in the muscles (myosin) and in the intensity of non- oxidative ATP resynthesis (glycolysis), following which the level of CP rises.

In OVERTRAINING the typical changes of biochemical adaptation acquired through training are gradually lost and work capacity decreases. The biochemical indices during overtraining change in an order that is the reverse of the order seen during training. Naturally, the dynamics of developing and losing the biochemical changes of adaptation depend on the characteristics of the previous training. In general, the longer the training period, the more thorough is the reorganisation by the adaptation mechanisms and the longer the accompanying biochemical changes last in the body after cessation of training, especially regarding glycogen and CP levels. Thus, the biochemical changes during IMMEDIATE and LONG-TERM ADAPTATION to systematic muscle activity are reversible, with the process of direct and reverse development of these changes being heterochronic.

During overtraining, the chemistry of the muscles and, above all, the oxidative processes, are disturbed. Here the glycogenolytic activity of the muscle tissue diminishes, and levels of ascorbic acid, glutathione, and glycogen in it decrease (Platonov, 1988). Dysproteinaemia of the blood plasma is noted, and there is an increase in the blood levels of glycoproteins, sialic acids, and urea. With prolonged chronic fatigue, athletes have reduced functional potential of the sympathico-adrenal system, which is closely linked to a disruption of the acid-base balance.

When training loads exceed the adaptation potential of the body and cause FATIGUE, another type of sympathetic nervous system reaction takes place: in fatiguing endurance events, a physical load that was previously of relatively little significance for the athletes causes a sharp increase in the excretion of catecholamines, their biological precursors, and the products of degradation, i.e. a particular hormonal reaction to the test load occurs. It is clear, then that the above-mentioned biochemical changes during 'overtraining' exert an unfavourable influence on work capacity and the level of sports results.

The biochemical rules governing bodily adaptation may be used to verify various principles of sports training such as the continuity of the training process, the undulatory nature of load dynamics, the cyclical nature of the training process, the unity of general and special preparation, the gradual increase in loading and the progression toward maximal loading.

A single physical load can cause an immediate biochemical effect, but this rapidly subsides. If a subsequent physical load is performed after the traces of the adaptation effect of the first load have completely disappeared, a summation of the biochemical changes does not take place. Therefore, the training process must be repetitive in order to develop long-term progressive changes in the energy reserves and the metabolism-regulating systems.

The rules governing fatigue and restoration, the specific nature of biochemical adaptation, and the sequence in which the biochemical components of adaptation are developed and lost underlie the principles of the undulatory nature of load dynamics, the cyclical nature of the training process, and gradual increase in the volume and magnitude of the training loads.

A scientifically substantiated use of diversified training regimes for alternating work and rest has become possible as a result of creatively combining these biochemical principles, the achievements of sports pedagogy and the experience of the coaches. The need to increase loads and progress towards maximal loading is based on the thesis that physical loads which are most capable of significantly disrupting homeostasis elicit the greatest training effect.

The biochemical changes caused by a physical load immediately after it is performed (the IMMEDIATE TRAINING EFFECT) are capable of activating the genetic apparatus of the cells. When physical loads are systematically repeated, there is an accumulation of immediate training effects which assures their transfer to long-term adaptation (the CUMULATIVE TRAINING EFFECT). Thus, the following important fundamentals of the trained body's biochemical adaptation may be identified:

Improvement of mechanisms of the nervous, endocrine, and adenylatcyclase systems to increase the efficiency of metabolic regulation.
Adaptive biosynthesis of enzymatic and structural proteins.
Supercompensation of energy substances and proteins.

All of the foregoing indicates that significant changes in metabolism occur in the body during training. As muscle work is performed, catabolism intensifies, but during the restoration period anabolic processes intensify.

All of these changes are closely related to nutrition. The increased energy expenditure during muscle activity demands adequate replenishment; increase in need for vitamins demands an increased intake of them; and increased mineral losses during sports activity necessitate compensating for them.

A number of other specific problems also arise: nutrition over a long period and during restoration stages; the athlete's feeding frequency; and the application of biologically-enriched sports nutrition products. Planning diets for athletes also requires a new approach to organising nutrition at different stages of the annual cycle of training and competitions, especially concerning the quantities of food components, the interaction between different nutrients and optimal timing of ingestion of specific substances (chrononutrition). One must achieve the maximal correspondence between all the goals of sports training and the effect of diet on the body. In this respect, the biochemical processes underlying sports training form the theoretical basis for scientific sports nutrition.

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