brain | vital organs | exercise fatigue

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The theory that exercise fatigue sets in when the muscles' demand for oxygen exceeds what the heart can supply is popular and persuasive. Yet there are powerful arguments against it and other equally valid physiological 'models' to explain the fatigue process. In this abridged version of a major paper published in the Scandinavian Journal of Medicine and Science in Sports and presented at a seminar organised by Peak Performance in September, South African exercise physiologist Professor Tim Noakes considers the claims of the competing arguments and outlines his own unifying belief in a central 'governor', which forces the muscles to stop exercising whenever the vital organs are threatened with damage.

The nature of the physiological and biochemical adaptations that occur in response to physical training has been extensively studied in humans and other mammals. There is also an extensive literature on the cellular mechanisms believed to cause fatigue during exercise.

Fewer studies have evaluated the extent to which these adaptations explain the improvements in performance that occur with different types of physical training and which presumably result from changes that delay the onset or development of fatigue. There are at least three probable reasons for this:

* Many exercise physiologists may consider this to be the work of the coach, not the scientist. And some scientists may be reluctant to undertake field-based studies in which the variables influencing human performance are not easily controlled;

* Even in the laboratory there is a dearth of tools to measure human performance accurately, which means that training-induced changes cannot be quantified. As a result most studies use physiological 'surrogates' to predict these changes. The most widely used surrogate is maximum oxygen consumption (VO2 max) - which has helped to entrench an unquestioning belief in the cardiovascular theory of athletic performance;

* In consequence, most reported training studies have measured the physiological and biochemical responses to training and have paid less attention to the influence on performance of different training programmes and the specific physiological adaptations which explain these changes. The aim of this review is not to describe how the body adapts to physical training. Rather I will pose two questions:

* What physiological models have exercise scientists developed (and subconsciously accepted) for the study of the physiological and biochemical determinants of fatigue during exercise?

* Which specific physiological, metabolic or biomechanical attributes might explain superior athletic performance and enhanced resistance to fatigue?

I will consider the evidence for and against several different models that are commonly used to explain how training may improve performance, probably by keeping fatigue at bay. Each model has its own proponents, usually those with a special expertise in the specific areas embraced by the model.

Yet it is highly improbable that the factors explaining human exercise performance under all conditions are restricted to one physiological system or to one scientific discipline. And human performance is unlikely to be adequately defined by any of these unitary models that are often presented as if they are mutually exclusive.

The cardiovascular/anaerobic model

The argument
Endurance performance is determined by the capacity of the athlete's heart to pump unusually large volumes of blood and oxygen to the muscles. This allows the muscles to achieve higher work rates before they outstrip the available oxygen supply, developing skeletal muscle anaerobiosis (a reduced oxygen content of the cells). Training increases 'cardiovascular fitness', especially by increasing the body's maximum capacity to consume oxygen (VO2 max). This effect results from an increased maximum capacity of the heart to pump blood (the cardiac output) and an enhanced capacity of the muscles to consume oxygen. These adaptations delay the onset of skeletal muscle anaerobiosis during vigorous exercise, thereby reducing blood lactate concentrations in muscle and blood at all exercise intensities above the so-called 'anaerobic threshold' and so allowing the exercising muscles to continue contracting for longer, at higher intensities, before the onset of fatigue. In addition, these changes increase the capacity of the muscles to use fat as a fuel during exercise, thereby enhancing endurance performance.

The evidence
Most of the changes described above have been shown to occur in training and fully documented in the literature. But they have not been shown to be causally related to enhanced performance and delayed fatigue. And it is possible that they occur in parallel with other adaptations which are the real causes of changes in exercise performance.

The major limitation of this model is that if the capacity of the heart does indeed limit oxygen utilisation by exercising muscles, then the heart itself would be the first to suffer. A key point, identified 75 years ago and since ignored by subsequent generations of exercise physiologists, is that the heart itself is a muscle, dependant on an adequate blood supply, which is determined by its own pumping capacity. Any demand by the muscles which exceeds the heart's capacity to supply it would imperil the heart's own blood supply, so reducing its pumping capacity and thereby inducing a vicious cycle of progressive and irreversible myocardial ischaemia (inadequate blood flow to the heart, causing angina and compromised function).

It would seem logical that human design should include controls to protect the heart from ever entering this vicious cycle.

In fact we know that progressive myocardial ischaemia does not occur during maximal exercise in healthy athletes, even though there is good evidence that VO2 max is determined by cardiac output. Thus if it is true that cardiac output limits maximal exercise, as seems likely, exercise must stop before the heart reaches its maximum output and hence well before skeletal muscle anaerobiosis can develop.

An alternative view
It is logical to speculate that maximal exercise terminates as part of a regulated process before the absolute maximum cardiac output and coronary blood flow are achieved. The famous British physiologist and Nobel Laureate Archibald Vivian Hill, then of University College, London, suggested as early as 1925 that there was 'some mechanism which causes a slowing of the circulation as soon as a serious degree of unsaturation occurs, and vice versa. This mechanism would tend to act as a governor maintaining a high degree of saturation of the blood.'

Although no such 'governor' has been dis-covered, clear evidence for its existence has come from a number of studies of exercise at altitude. These have shown, among other things, that:

* Peak blood lactate concentrations fall during maximum exercise at altitude. In terms of the cardiovascular/anaerobic model, this response is paradoxical, as blood lactate levels should be the highest when exercise is undertaken under conditions of profound oxygen deficiency in the inhaled air. Hence the proponents of this model have termed this phenomenon the 'lactate paradox';

* Heart rate and cardiac output are substantially reduced during exercise at extreme altitude - equally paradoxical to those who believe that the delivery of an adequate oxygen supply to the exercising muscles is the cardinal priority during exercise.

So under the precise conditions likely to induce anaerobiosis in either the heart or skeletal muscles, neither show any evidence whatever of 'anaerobic' metabolism. This unexpected finding can be explained only by the presence of a 'governor', probably in the central nervous system, whose function is probably to protect the heart from ischaemia or (perhaps at extreme altitude) to protect the brain from the effects of an inadequate oxygen supply.

Final confirmation for the presence of this theoretical governor comes from another study showing that skeletal muscle recruitment, or activation, falls with increasing altitude but increases rapidly with the administration of oxygen which increases exercise capacity.

The hypothetical existence and actions of the governor can be summarised as follows: receptors exist in the heart to assess the adequacy of the circulation to the heart. Before this reaches some predetermined limit, the brain reduces skeletal muscle activation. As a consequence, skeletal muscle recruitment either fails to rise further or falls, limiting the work output of the body, signalling the onset of 'fatigue'. The fall in work output reduces the heart's oxygen requirement and so averts the threat of myocardial ischaemia. At altitude the same mechanism would spare the brain from damage caused by exercise that allows the blood oxygen content to fall too low.

The energy supply model

The argument
Whereas the cardiovascular model suggests that exercise performance is limited by oxygen provision to muscles, this one proposes that it is limited by the provision of energy in the form of adenosine triphosphate (ATP).

This model predicts that performance in events of different durations is determined by the capacity to produce energy (ATP) by the different metabolic pathways including the phosphagens, oxygen-independent glycolysis (breakdown of glucose), aerobic glycolysis and aerobic lipolysis (breakdown of fat). Superior performance would be explained by a greater capacity to generate ATP in the specific metabolic pathway(s) that predominate during that activity - eg aerobic lipolysis for ultramarathon runners and oxygen-independent glycolysis for sprinters.

The evidence
This hypothesis has yet to be systematically evaluated. To prove it would require evidence that:

* the metabolic capacities of these different pathways are causally related to performance in events of different durations;

* the specific metabolic pathways adapt predictably with specific training;

* these adaptations alone are responsible for training-induced changes.

The energy supply model predicts that exercise must stop when muscle ATP depletion occurs - ie when the muscle develops rigor. However, there is evidence that ATP concentrations, even in muscles forced to contract under ischaemic conditions, do not drop below about 60% of resting values, suggesting that these stores are 'defended' in order to prevent the development of skeletal muscle rigor.

An alternative view
Some researchers have posited the existence of a peripheral 'governor', which induces fatigue through acidosis whenever the rate of ATP production by oxidative sources threatens to become inadequate, although this has not been proven by research. Another possibility is that fatigue is induced by a central governor responding to factors as yet unidentified. In summary, a metabolic basis for exercise fatigue is widely assumed but incompletely documented - particularly by human studies. In addition, logic suggests that this model cannot serve as a sole explanation for performance limitation. There must still be some overriding mechanism which stops energy-depleted muscles from running out of ATP completely as this would give rise to rigor, the condition of irreversible contracture found in muscles after death.

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