How physiological, biochemical and neural systems influence your training and competition performance
Different physiological systems determine performance under different conditions
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
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.
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
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.
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.
The energy depletion model
This model, which relates to exercise lasting more than 2-3 hours, holds that depletion of the body carbohydrate stores, especially the muscle glycogen stores, is the limiting factor.
Fatigue during prolonged exercise is definitely associated with depletion of glycogen stored in the liver (causing hypoglycaemia - low blood sugar) or in the muscles. It is also known that reversal of hypoglycaemia by intravenous or oral administration of glucose allows exercise to continue. Finally, pre-exercise carbohydrate loading and/or carbohydrate ingestion during exercise delays the onset of fatigue and improves exercise performance.
The fact that reversal of hypoglycaemia alone allows exercise to continue proves conclusively that liver glycogen depletion can limit exercise performance under certain specific conditions. Indeed the rapidity with which the restoration of blood glucose levels restores performance suggests that a central 'governor' is activated by changes in blood glucose concentrations and acts to prevent activity that would further reduce the blood glucose concentration, posing the risk of brain damage.
However, since no technique has yet been devised that will instantly reverse glycogen depletion in the muscles, it is impossible to prove that muscle glycogen depletion alone limits prolonged exercise performance.
Evidence against the energy depletion model comes from a study showing that athletes ingesting carbohydrate stopped exercising after four hours when their muscle glycogen concentrations and rates of carbohydrate oxidation were no lower than they had been one hour earlier, when they were not exhausted. Another study showed that athletes who adapted to a high-fat diet were able to exercise to significantly lower muscle glycogen concentrations at exhaustion than when they were carbohydrate-adapted. And a trial of previously untrained subjects, who trained on a high-fat diet for seven weeks before switching to a high-carbohydrate diet for one week, found that although they increased their pre-exercise muscle glycogen concentrations by 44%, there was only a small further improvement in performance.
To my knowledge, no human study has yet established that training improves endurance performance exclusively by increasing body carbohydrate stores and delaying the onset of carbohydrate depletion during prolonged exercise.
A strong empirical case against this model comes from the ability of athletes to complete ultra-endurance events. Take the final 42k running leg of the 226k Ironman triathlon, for example: after cycling at 40 k/hr for 4.5 hrs the lead cyclists would be expected to have near total muscle glycogen depletion according to data from lab studies. Yet the best performers are able to run at close to 16k/hr for a further 160 mins!
Finally, as with the energy supply model, the end result of energy depletion, from whatever cause, must be skeletal muscle rigor. Hence, even if muscle glycogen depletion does indeed cause fatigue, it must act via some sort of governor that terminates exercise when glycogen-depleted muscles are unable to generate ATP sufficiently rapidly to prevent the development of rigor.
An alternative view
It is possible that the capacity to oxidise fat at high rates when body carbohydrate stores are depleted may delay fatigue and determine performance during exercise of moderately high intensity that lasts more than four hours and is typified by ultradistance running and triathlon events.
The muscle recruitment: (central fatigue) model
This model proposes that it is not the rate at which either oxygen or fuel are supplied to muscle that limits its performance but rather the processes involved in skeletal muscle recruitment (activation), excitation and contraction. It suggests that the brain concentration of the neurotransmitter serotonin, and possibly others including dopamine and acetylcholine, alters the neural impulses from the brain to the exercising muscles to reduce skeletal muscle activation - the actual mass of muscle that is active during any exercise. Alternatively, fatigue may be induced by inhibitory reflexes arising from the exercising muscles and feeding back to the spinal chord.
A number of studies have shown that manipulating central nervous system neurotransmitter concen-trations, particularly by increasing dopamine and reducing serotonin, can enhance exercise performance, and vice versa. There is also direct evidence for reduced central nervous system drive to muscle after fatiguing muscle contractions.
I have already described the clear evidence that fatigue at high altitude is caused by reduced activation of exercising muscles by the central nervous system and that a central 'governor' must be involved in causing fatigue when liver glycogen stores are depleted. It is also likely that heat-induced fatigue is controlled by the central nervous system, as it cannot be explained by any other model. In all these cases, reduced central activation of muscle would function as a protective mechanism to prevent organ damage.
A contrasting finding that electrical activity within the skeletal muscles actually rises during exercise at a constant workload is usually inter-preted as evidence for increased activation by the central nervous system to compensate for a prog-ressive failure of muscle fibre contractile function.
But competitive athletes do not work at a constant rate. And our own studies of prolonged exercise, including bouts of self-chosen high-intensity work, show a progressive reduction in power output during successive bouts of high intensity exercise. This response is very strongly suggestive of central rather than peripheral fatigue. The fact that a relatively small percentage of the available muscle mass (perhaps as little as a maximum of 40%) is ever recruited, even during maximal exercise, remains a perplexing enigma. And proponents of any model of peripheral limitations for exercise performance need to explain why the body does not recruit all its available muscle mass to produce the necessary force under varying exercise conditions as so-called 'peripheral fatigue' develops.
An alternative view
I have argued that a reduced central activation of the exercising muscles may be necessary to protect humans under specific conditions. I believe these control mechanisms are necessary to prevent the following potentially dangerous developments:
* myocardial ischaemia during high-intensity exercise;
* muscle ATP depletion and rigor during high intensity exercise;
* myocardial ischaemia or cerebral hypoxia during exercise at altitude;
* falling blood pressure during exercise in patients with chronic heart failure;
* heatstroke during prolonged exercise in the heat;
* brain damage from hypoglycaemia during prolonged exercise, when liver glycogen stores are depleted.
The biomechanical model
There is growing interest in the role of muscles as elastic energy return systems which function both as springs and torque producers during exercise. This model predicts that the greater the muscle's capacity to act as a spring, the less torque it must produce and hence the more efficient it is. This more efficient, more elastic muscle will enhance exercise performance, especially in weight-bearing activities by:
1. slowing the rate of accumulation of metabolites that may cause fatigue and
2. slowing the rate of rise of body temperature, thereby delaying the achievement of the core temperature that prevents the continuation of exercise.
This argument shows up yet another logical weakness of the cardiovascular/anaerobic model, which predicts that superior performance will result from increased oxygen delivery to muscle and an increased rate of energy - and hence heat - production. A higher rate of heat production would induce fatigue prematurely due to excessive heat accumulation. A more logical biological adaptation would be to reduce the rate of oxygen consumption (and hence the rate of heat production) by increasing the athlete's efficiency or economy of movement.
Therefore according to this model the more economical the athlete, the faster he or she will be able to run before reaching a limiting body temperature. And the smaller and lighter the athlete, the more economical he is likely to be.
A number of studies indicate that the best endurance athletes are often the most economical. Indeed, most training studies suggest that improvements in running economy are the most likely response to training, allowing the athlete to run faster at the same oxygen consumption and thus complete a given distance more rapidly for the same average rate of heat accumulation but a reduced overall heat expenditure.
In a cross-sectional study of recreational ultramarathon runners, it was found that those who trained were more economical and hence could run faster at the same oxygen consumption (or % VO2 max). During competition the better trained athletes ran at the same or a slightly lower % VO2 max but completed the races in a shorter time. Hence being more economical appears to be a better route to endurance success than having a higher VO2 max.
A second component of the biomechanical model stems from the evidence that repeated high-velocity short-duration eccentric muscle contractions, as occur during running, induce a specific form of fatigue that develops during races and is measurable for at least seven days after a marathon.
Characteristics of this fatigue are a failure of the contractile capacity of the exercised muscles, with a reduced tolerance to muscle stretch and a delayed transfer from muscle stretch to muscle shortening. Since these abnormalities persist for many days after a race, they cannot be explained by acute changes in oxygen or energy delivery to the muscles, or by elevated body temperature.
Empirical observation of the running stride and the anatomical structure of Kenyan runners' legs suggests that an evaluation of their elastic elements and their resistance to stretch/ shortening cycle fatigue would be very rewarding. The superiority of Kenyan runners in endurance events may be explained by the fact that they have more elastic leg muscles, which are better able to resist eccentrically-induced damage in training. This would explain why they are able to train harder and for longer than other athletes. It would also enhance performance during competitive racing by delaying the onset of the stretch/shortening cycle fatigue that is an inevitable consequence of repeated eccentric muscle contraction.
The psychological/motivational model
The ability to sustain exercise performance comes from a conscious effort.
The separation between physiology and psychology has generally prevented adequate laboratory evaluation of this model, although any studies showing an ergogenic effect of any placebo (dummy) intervention on exercise performance would prove that it makes some contribution to athletic performance.
However it conflicts with the various 'governor' theories, which suggest that exercise performance is regulated at a subconscious level to protect the vital organs from damage.
The importance of the conceptual models described above is that they suggest that different physiological systems determine performance under different conditions. Hence exercise physiologists need to consider all these models when they design studies to determine which are the most important physiological, biochemical, neural and other factors determining the changes in exercise performance that come from training.
More importantly, this review shows that many research findings are incompatible with one or more of these models. Rather than simply continuing to accept these inconsistencies uncritically, modern exercise physiologists should challenge old dogmas and so approach more closely the unattainable truth.
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