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The Science of Performance |
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How does a foundational myth become sacred scientific dogma? The case of A.V. Hill and the anaerobiosis controversy Part 4 by Tim Noakes1 The second pillar arose from a series of experiments in which Hill and his colleagues measured oxygen consumption (VO2) every 30 seconds in subjects who ran for 3 minutes at different speeds on a circular grass track 85 m in circumference. Their relevant findings are reproduced in the main graph of Figure 4.3.
Figure 4.3 The authors’ interpretation of their data was the following (Hill and Lupton 1923): When muscular exercise is taken in man at a constant speed, the lactic content of his active muscles increases gradually from its resting minimum at the start. This rise in lactic acid content increases the rate of oxidation, so that finally, if the oxygen supply be adequate, a ‘steady state’ is reached in which the rate of lactic acid production is balanced by the rate of its oxidative removal, and its concentration remains constant in the muscle as long as exercise at that speed is maintained . . .. The lower three curves represent a genuine steady state, the uppermost curve only an apparent steady state in which the oxygen intake is at its maximum and the oxygen debt is rapidly increasing (148–9). Hill and Lupton (1923) concluded that the constant VO2 they measured at the fastest running speed (16 km.h_1 in Figure 4.3) represented an apparent, not a true steady state. The basis for this conclusion was a circular argument based on Hill’s subconsciously held model explaining fatigue during exercise (Figure 4.4). For Hill began with the subliminal premise that fatigue during exercise is caused by an oxygen deficiency; for reasons described in the introduction, he naturally interpreted his findings within that conceptual framework. From the subjective feelings of the fatigue that he experienced when he ran at 16 km.h-1, Hill drew the equally subjective conclusion that this must have been caused by an oxygen deficiency, hence anaerobiosis, in his active muscles. As a result he concluded that his real VO2 must have been higher than that which was objectively measured at 16 km.h-1 (top line in the main graph of Figure 4.3). On this basis, Hill and Lupton (1923) produced their classic speculation that defines their cardiovascular/anaerobic model: ‘Considering the case of
Figure 4.4 running . . . there is clearly some critical speed for each individual . . . above which, the maximum oxygen intake is inadequate, lactic acid accumulating, a continuously increasing oxygen debt being incurred, fatigue and exhaustion setting in’ (Hill and Lupton 1923: 151) and that ‘However much the speed be increased beyond this limit, no further increase in oxygen intake can occur: the heart, lungs, circulation, and the diffusion of oxygen to the active muscle-fibres have attained their maximum capacity’ (Hill and Lupton 1923: 156). Hill (1925: 93) further concluded that: ‘The oxygen intake may attain its maximum and remain constant merely because it cannot go any higher owing to the limitations of the circulatory and respiratory systems’. Not only did Hill and his colleagues fail to measure concurrently either the oxygen debt or muscle or blood lactate levels or cardio-respiratory function during these or subsequent studies, they also failed to subject their hypothesis to the accepted process of refutation. For the next logical study would have been to measure Hill’s rate of oxygen consumption (VO2) when he ran at a speed faster than 16 km.h-1. Their hypothesis would have been supported if the VO2 at that higher speed was either the same or lower than that measured at 16 km.h-1. Given that that experiment was not performed, Hill and his colleagues could not conclude that Hill’s VO2 had ‘plateaued’ and was indeed maximal at 16 km.h-1. Thus, their major conclusion that VO2 reaches a plateau during exercise of progressively increasing intensity was not proven because this test of refutation was not conducted. I have since submitted their conclusions to such refutation, though some sixty-odd years later (Noakes 1988, 1997). The data shown in the inset panel of Figure 4.3 confirm that Hill did not reach ‘some critical speed . . . above which, the maximum oxygen intake is inadequate.’ For the data clearly show a linear relationship between Hill’s mean VO2 at three different speeds. This proves that his oxygen consumption rose appropriately without any evidence for a ‘plateau’ as Hill increased his speed from 10 to 16 km.h_1. Hence those data do not provide any evidence for a ‘plateau phenomenon’ which Hill believed was the necessary proof that his exercise terminated as a direct consequence of skeletal muscle anaerobiosis. Nevertheless this is the interpretation that has survived in the popular model depicted in Figures 4.1 and 4.2. The next significant event in this controversy was the publication in 1955 of a paper by Taylor et al. in which they attempted to define the criteria for the establishment of this oxygen ‘plateau phenomenon’. They began the article thus: The classic work of Hill [Hill and Lupton 1923] has demonstrated that there is an upper limit to the capacity of the combined respiratory and cardiovascular systems to transport oxygen to the muscles. There is a linear relationship between oxygen intake and workload until the maximum oxygen intake is reached. Further increases in workload beyond this point merely result in an increase in oxygen debt and a shortening of the time in which the work can be performed (78). Yet it is clear from the inset panel in Figure 4.3 that Hill had failed to show any such ‘increase in oxygen debt’. Further support for this interpretation came in 1971 when a paper describing the meaning of the maximum oxygen consumption was published in the New England Journal of Medicine (Mitchell and Blomqvist 1971), arguably the most influential medical journal in the world. Next, was the development of one of the most popular teaching diagrams in the exercise sciences, shown in Figure 4.5 (Rowell 1993). Under the heading ‘What limits the ability to increase the oxygen uptake’, this diagram suggests that such a limitation may occur in the respiration, the central or peripheral circulation, or in the muscle metabolism. Notably missing in the picture is the presence of the central (brain) and peripheral nervous systems. Thus a central tenet of this model is the belief that the brain plays no role in exercise performance. Of course at the time he undertook his studies, Hill would not have had access to equipment to measure the brain’s contribution to exercise performance; thus he would be expected to ignore that which he could not measure. Yet it is a measure of the strength of a ‘foundation myth’ (Waller 2002) that even though scientists now have the capacity to measure the brain’s potential contribution to exercise performance, yet so few do (Gandevia 2001; Kayser 2004; Nybo and Secher 2004).
Figure 4.5 Once I realized that Hill had failed to prove his hypothesis, I began to wonder how a system could fail even when there was no evidence that that failure was caused by ‘anaerobiosis’ (Graham and Saltin 1989; Mole et al. 1999; Richardson et al. 1998, 1999). Since my doctoral training was in cardiac physiology and metabolism (Resink et al. 1981a, 1981b; Van Der Werff et al. 1985) I was aware of the core teaching that the heart and skeletal muscles use quite different techniques to increase their total power output. Although both heart and skeletal muscles are a collection of many individual muscle fibres (cells), the heart acts as if it comprises just one. Thus a single nerve impulse is all that is required to produce a simultaneous contraction of all the heart muscle fibres. Thus complete recruitment of all heart muscle fibres occurs each time the heart contracts; none remain quiescent and are unrecruited. Thus for the heart to increase its power output, the strength of each of the molecular interactions (actin–myosin cross-bridges) that produce muscle contraction must increase. An increase in the power output of the individual actin–myosin crossbridges is known as an increase in contractility. In contrast, the total number of fibres in a particular skeletal muscle are innervated by many different nerve fibres, each of which therefore innervates only a portion of all the fibres making up a particular skeletal muscle. Thus the maximum power output of a particular skeletal muscle can only be achieved if there is a simultaneous contraction of all its multitude of muscle fibres. This requires that all the nerves innervating that muscle must be actively recruited by the (motor cortex in the) brain at the same time. This method for increasing skeletal muscle power output is known as an increase in skeletal muscle recruitment. Thus, unlike the case in the heart, the brain is the principal site regulating any increase in power output by the skeletal muscles; skeletal muscle power output rises as more fibres are recruited by the brain and falls when fewer fibres are recruited. This alternative model of exercise performance is depicted in Figure 4.6. Here the arrow of causality is reversed; the brain, not the heart, is the driver of performance. Thus to increase the power output of the skeletal muscles, the brain recruits more muscle fibres which then require an increased blood supply to cover their increased oxygen and energy requirements. In this way, the exercise performance causes the oxygen consumption, and not the reverse.
Figure 4.6 Alternative (neuromuscular recruitment) model of factors determining maximal exercise performance. Hill’s understanding of these concepts were of course limited by the knowledge of the day; thus he assumed that all available muscle fibres are recruited at exhaustion. Indeed he must have realized, even if only subconsciously, that the ‘poisonous’ lactic acid, that he considered to be the peripheral regulator of performance (Figure 4.1), could not regulate the function of those quiescent muscle fibres that have yet to be recruited. He supposed quite reasonably that, to avoid exhaustion, the brain would simply recruit more of those quiescent muscle fibres, thereby allowing the exercise to continue until all the available muscle fibres had been recruited. Rather more culpably, all the exercise scientists who have subsequently embraced his cardiovascular/anaerobic model must also have made this assumption. This explains why the central and peripheral nervous system are not included in Figure 4.5. The assumption has to be that there is complete skeletal muscle recruitment at exhaustion in all forms of exercise. Hence any contribution of the central nervous system to exercise performance can be ignored. Yet this clearly conflicts with the most basic physiological truth, which is that the power output of skeletal muscle is determined by the number of muscle fibres that are recruited by the brain (Gordon et al. 2001; Katz 1992). The contrasting assumption of the alternative (muscle recruitment) model (Figure 4.6) is that, if the force output of skeletal muscle is less than maximal, then there must be a less-than-maximal skeletal muscle fibre recruitment. If this is the case then the exercise performance is clearly regulated by the brain through its control of the number of muscle fibres that are recruited in the exercising muscles. Since, in the late 1980s, I too seem to have assumed at that time that skeletal muscle fibres is always maximal at exhaustion in all forms of exercise, it was also natural that my first attempt to explain how a muscle could fatigue during maximal exercise included this subconscious assumption that all the available muscle fibres are simultaneously active at exhaustion. That is, my assumption was that, at exhaustion, the skeletal muscle acts as if it is a heart in which all available muscle fibres are simultaneously active. In which case, skeletal muscle failure, expressed as fatigue or exhaustion, can only occur if there is widespread failure of the contractility of the individual muscle fibres. Thus I originally proposed that fatigue develops during maximum exercise because of a centrally (brain) initiated down-regulation of the contractility of all the muscle fibres in the maximally recruited muscles: [A] critical review of Hill and Lupton’s results shows that they inferred but certainly did not prove that an oxygen limitation develops during maximal exercise . . .. This review proposes that the factors limiting maximal exercise performance might be better explained in terms of a failure of muscle contractility (‘muscle power’), which may be independent of tissue oxygen deficiency. The implications for exercise testing and the prediction of athletic performance are discussed (Noakes 1988: 419). What, in retrospect, is quite surprising is that I did not consider that the far more likely factor determining large changes in skeletal muscle power production is an alteration in the number of skeletal muscle fibres that are recruited by the central nervous system, as is the classical teaching (Gordon et al. 2001, Katz 1992). For even a simple calculation could have shown how much more probable is this alternative explanation. For example, the maximum power that an athletic human can produce for a few seconds with his legs is about 2000 W (Calbet et al. 2003c). But during a maximum exercise test lasting more than a few minutes, there are few humans who can achieve a power output of more than about 500 W. Similarly during an hour’s exercise, few can exceed an average power output of about 400 W. This means that if all the available muscle fibres are recruited at all times, then the force output (contractility) of the multitude of individual molecular interactions that produce the total muscle power output would need to vary by a factor of 2000/400, that is five-fold. I am unaware of any known biological mechanism that could produce a five-fold increase in the contractility of individual skeletal muscle cross-bridges. Whilst mechanisms that can increase the contractility of heart (myocardial) cross-bridges are well understood (Gordon et al. 2001; Katz 1992; Resink et al. 1981a, 1981b), (i) these are unlikely to produce a five-fold increase in contractility and, more importantly (ii) such mechanisms are not known to exist in skeletal muscle (Gordon et al. 2001; Katz 1992). It is much more likely that the extent of muscle recruitment by the brain differs five-fold so that, for example, five times more muscle fibres are active during a few seconds of absolutely maximal exercise than are active during a maximal effort that lasts an hour or more. But this apparently obvious conclusion evaded my thinking at that time as, apparently, it has evaded the grasp of many of the world’s leading exercise physiologists to this day (Bassett and Howley 1997, 2000; Bergh et al. 2000; Ekblom 2000; Wagner 2000). Seven years later, I concluded the J.B. Wolffe Memorial Lecture at the 1996 Annual Conference of the American College of Sports Medicine with the proposal that whatever mechanisms limit exercise performance, there appeared to be a reason for such regulation: [A]n alternate physiological model is proposed in which skeletal muscle contractile activity is regulated by a series of central, predominantly neural, and peripheral, predominantly chemical, regulators that act to prevent the development of organ damage or even death during exercise in both health and disease and under demanding environmental conditions. . . . Regulation of skeletal muscle contractile function by central mechanisms would prevent the development of hypotension and myocardial ischemia during exercise in persons with heart failure, of hyperthermia during exercise in the heat, and of cerebral hypoxia during exercise at extreme altitude (Noakes 1997: 571). Clearly I had still not grasped the eminently more logical proposal that the easiest way for the brain to regulate skeletal muscle power production is through the regulation of the number of muscle fibres that it recruits during exercise (Gordon et al. 2001, Katz 1992). This imprecise thinking was again conditioned by my continuing subconscious assumption that muscle recruitment must be maximal at exhaustion in all forms of exercise (Figure 4.5). Predictably since the publication of the J.B. Wolffe lecture represented a radical departure from the accepted ‘foundation myth’ which had not been seriously challenged for more than 70 years, it was accompanied by a detailed rebuttal (Bassett and Howley 1997). That rebuttal made the somewhat crude point that A.V. Hill was a Nobel Prize winner whose opinion was far more likely to be correct than was that of an iconoclastic Third World scientist. In preparing my response (Noakes 1998) I was forced to reread all of A.V. Hill’s original papers. It was there that I uncovered his remarkable insight that had been overlooked, perhaps since he first described it in the 1920s. For what Hill realized, and which has been ignored ever since, was that if the pumping capacity of the heart does indeed limit oxygen utilization by the exercising skeletal muscle as predicted in Figure 4.1, then the heart itself will be the first organ affected by any postulated oxygen deficiency (Hill et al. 1924b). This is because the blood supply to the heart is dependent on the pumping capacity of the heart; once the maximum output of the heart is reached, the heart will be unable further to increase its own oxygen supply and must therefore begin to work ‘anaerobically’ (Figure 4.1). The interpretation of Hill and his colleagues was unequivocal: Certain it is that the capacity of the body for muscular exercise depends largely, if not mainly, on the capacity and output of the heart. It would obviously be very dangerous for the organ to be able, as the skeletal muscle is able, to exhaust itself very completely and rapidly, to take exercise far in excess of its capacity for recovery . . .. When the oxygen supply becomes inadequate, it is probable that the heart rapidly begins to diminish its output, so avoiding exhaustion . . . (1924b: 161–2). The point identified by Hill and his colleagues (and since ignored) is that the heart is also a muscle, dependent for its function on an adequate blood and oxygen supply. But, unlike skeletal muscle, the heart is dependent for its blood supply on its own pumping capacity. Hence any intervention that reduces the pumping capacity of the heart, or demands the heart to exceed its own maximum pumping capacity, imperils the heart’s own blood supply. Any reduction in coronary blood flow will consequently reduce the heart’s pumping capacity, thereby inducing a vicious cycle of progressive and irreversible myocardial ischaemia (inadequate blood supply to the heart). It would seem reasonable that human ‘design’ should include controls to protect the heart from ever entering this vicious circle. Hence if (skeletal) muscle function fails when its oxygen demand exceeds supply (Figure 4.1) then, for logical consistency, the inability of the pumping capacity of the heart to ‘raise the cardiac output’ at the VO2 max (Rowell 1993), must also result from an inadequate (myocardial) oxygen supply caused by a plateau in blood flow to the heart. This limiting coronary blood flow would cause myocardial ‘fatigue’, a plateau in cardiac output and hence in the VO2 max leading, finally, to skeletal muscle anaerobiosis. Thus, according to this argument, the coronary blood flow must be the first physiological function to show a ‘plateau phenomenon’ during progressive exercise to exhaustion. All subsequent physiological ‘plateaus’ must result from this limiting of coronary blood flow. Whereas the most influential modern exercise physiologists for the past 75 years have enthusiastically embraced what increasingly appears to be a mythical basis for a ‘plateau phenomenon’ (Day et al. 2003), none seems to have grasped this logical prediction of the ‘plateau phenomenon’, which requires that the heart fatigue first before skeletal muscle failure develops. But this was clearly a concept with which the pioneering exercise physiologists were entirely comfortable. In addition to the conclusion of Hill and his colleagues, already quoted, the pioneering United States exercise physiologists Arlie Bock and David Dill (Bainbridge 1931) also believed that myocardial ischaemia causes a fall in the cardiac output at the point of fatigue during high-intensity exercise: The blood supply to the heart, in many men, may be the weak link in the chain of circulatory adjustments during muscular exercise, and as the intensity of muscular exertion increases, a point is probably reached in most individuals at which the supply of oxygen to the heart falls short of its demands, and the continued performance of work becomes difficult or impossible (Bainbridge 1931: 15). Hence they proposed that: ‘Another factor, which may contribute to the production of this type of fatigue, is fatigue of the heart itself’ (Bainbridge 1931: 229). Although the occurrence of fatigue of the heart in health is not very clearly established, a temporary lowering of the functional capacity of the heart, induced by fatigue of its muscular fibres, might gradually bring about during exercise an insufficient blood supply to the skeletal muscles and brain. The lassitude and disinclination for exertion, often experienced on the day after a strenuous bout of exercise, has been ascribed to fatigue of the heart as its primary cause (Bainbridge 1931: 229). Hence they concluded: ‘The heart, as a rule, reaches the limit of its powers earlier than the skeletal muscles, and determines a man’s capability for exertion’. In summary, the early physiologists who believed that skeletal muscle anaerobiosis limits maximal exercise, clearly understood that any plateau in cardiac output, necessary for there to be a limiting skeletal muscle blood flow, must result from a plateau in coronary blood flow, which would expose the heart to a progressive myocardial ischaemia that would worsen if exercise continued at that intensity. Perhaps the reluctance of modern physiologists to acknowledge these concepts stems from the current appreciation that progressive myocardial ischaemia does not occur during maximal exercise in healthy athletes (Raskoff et al. 1976). Thus one postulate might be that the termination of exercise must occur before the heart actually reaches its maximum capacity and hence well before skeletal muscle anaerobiosis can develop according to Figure 4.1. Hence for over 75 years, exercise physiologists may have focused on the incorrect organ as the site of any potential anaerobiosis that may develop during maximal exercise (Noakes 1998, 2000; Noakes et al. 2001). Interestingly, Hill and his colleagues seem to have been the first to suggest a solution to this dilemma as early as 1924: From the point of view of a well co-ordinated mechanism, . . .. it would clearly be useless for the heart to make an excessive effort if by doing so it merely produced a far lower degree of saturation of the arterial blood; and we suggest that, in the body (either in the heart muscle itself or in the nervous system), there is 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 (161–2). On reading this text it immediately became clear to me why Hill was not quite correct and how such a governor would likely act to protect the heart. For Hill’s model requires that the heart must first fail before the governor is activated, in keeping with his idea that a catastrophic limitation must first develop before exercise terminates. But since we now know that myocardial function is not impaired in healthy persons at maximal exercise (Raskoff et al. 1976), any governor must act before the heart becomes ischaemic. At some time during this process, the scales finally fell from my eyes and I realized that the more logical conjecture would be for such a governor to regulate the function, not of the heart, but of the skeletal muscles, specifically by regulating the number of muscle fibres that can be activated during maximal exercise. Accordingly in my rebuttal I made the first tentative proposal of what has since become known as a ‘central governor’, that responds to sensory information about the metabolic status of the heart. This information then leads to a reduction in skeletal muscle recruitment by the motor cortex leading to a reduction in exercise performance before there is any catastrophic failure of blood flow to either the heart or skeletal muscles. Discussion with my colleagues, especially Professor Vicki Lambert, led to the suggestion that exercise in a profoundly hypoxic (oxygendepleted) environment, for example at high altitude, would show whether or not such a control exists and, in particular whether it is sensory feedback information from the heart or the exercising skeletal muscles that regulates maximal exercise performance, especially in an hypoxic environment. For if an oxygen deficiency really does develop in either heart or skeletal muscle, its appearance will likely be more easily identifiable during maximum exercise at altitude where the oxygen content of the inspired air is much reduced. Furthermore, such experiments should identify in which organ – heart or skeletal muscle – anaerobiosis first becomes apparent; the heart, according to the ideas of the pioneering British and North American exercise physiologists (Hill et al. 1924b; Bainbridge 1931) or the skeletal muscles, according to the influential group of modern exercise physiologists (Bassett and Howley 1997, 2000; Bergh et al. 2000; Ekblom 2000; Wagner 2000). But regardless of their level of commitment to the cardiovascular/anaerobic model of exercise physiology, more than 65 years of work have now established two ideas that are accepted by all exercise physiologists. First, that peak blood lactate concentrations during maximum exercise fall with increasing altitude (Edwards 1936; Green et al. 1989; Kayser 1996) a phenomenon since labelled the ‘lactate paradox’ (Hochachka 2002). Second, that maximum heart rate and cardiac output likewise fall during exercise at increasing altitude (Sutton et al. 1988; Calbet et al. 2003a, 2003b). Interestingly Edwards (1936) interpreted the ‘lactate paradox’ at altitude accordingly: The inability to accumulate large amounts of lactate at high altitudes suggests a protective mechanism preventing an already low arterial saturation from becoming markedly lower . . .. It may be that the protective mechanism lies in an inadequate oxygen supply to essential muscles, e.g. the diaphragm or the muscles (374–5). Hence, in as much as high muscle lactate concentrations would have to be present if the exercising muscles were contracting ‘anaerobically’, these studies prove that exercise at extreme altitude terminates when the exercising muscles are contracting in the presence of an adequate oxygen supply. Hence we can conclude that skeletal muscles do not become anaerobic during maximal exercise in an oxygen-deficient environment at altitude. The finding that the maximal cardiac output and heart rate are reduced at extreme altitude is equally paradoxical according to the model which holds that the delivery of an adequate oxygen supply to the exercising muscles is the cardinal priority during exercise (Figures 4.1 and 4.2). For according to the logic of this model, if the principal responsibility of the cardiovascular system is the achievement of an (ultimately inadequate) oxygen supply to skeletal muscle, then the cardiac output must always reach the same maximal value at exhaustion regardless of the conditions in which the exercise is undertaken. Yet here too the evidence is definitive. The heart makes the exactly opposite adjustment – maximum cardiac output falls with increasing altitude (Sutton et al. 1988; Calbet et al. 2003a, 2003b). Nor is there any evidence that the function of the heart is impaired at altitude (Reeves et al. 1987; Suarez et al. 1987) as would occur if the heart were hypoxic. Hence the conclusion must be that some currently unrecognized mechanism must exist to ensure that the heart does not become ‘anaerobic’ during maximal exercise at any altitude – from sea level to the summit of Mount Everest – in healthy humans. The point is that this mechanism must exert its control before the heart fails, in contrast to Hill’s model (Figure 4.1). Interestingly, Christensen, but not Dill, interpreted this phenomenon correctly in my view: Christensen and I differed in our interpretation of his measurements of respiratory and circulatory function in exercise (at altitude). In his opinion, the chief limiting factor is the ventilation of the lungs. In the hardest grade of work at any station, the pulmonary ventilation reached about as high a value as at sea level, while the maximal cardiac output became less as the altitude increased. He thinks this means that the heart has an untapped reserve; it is circulating blood fast enough to carry to the tissues all the oxygen supplied by the lungs (Dill 1938: 170–1). These studies invite two precise conclusions. First, that the oxygen demands of the skeletal muscles are not the cardinal priority and hence are not ‘protected’ during maximum exercise, at least at extreme altitude. Second, neither the skeletal muscles nor the heart becomes ‘anaerobic’ or ischaemic during maximal exercise under conditions of hypoxia. The sole conclusion must be that some form of ‘governor’, as originally proposed by A.V. Hill, must terminate maximum exercise at altitude even before skeletal muscle anaerobiosis or myocardial ischaemia develops. Furthermore, it would be difficult to explain why the same control mechanism should not also act during maximum exercise at sea level. For it would indeed be surprising if the human body evolved one specific control mechanism that acts only at extreme altitude. How could evolutionary forces have acted in anticipation of the possibility that one day humans would choose to climb to the roof of the world? More likely this form of control has a much wider application and is also active during exercise at sea level. In summary, a number of famous studies have shown that under the precise conditions of maximal exercise at altitude most likely to induce anaerobiosis or ischaemia in either the heart or skeletal muscles, neither the heart nor the skeletal muscle show any evidence whatsoever for ‘anaerobic’ metabolism. This unexpected finding can be explained only if there is a ‘governor’, probably in the central nervous system, whose function it is to prevent the development of an inadequate blood supply to one or more vital organs such as the brain, heart, muscles or diaphragm. The same governor could also serve the identical function at sea level, thereby preventing the development of myocardial ischaemia during maximum exercise at sea level. Dill’s conclusion is therefore incorrect: ‘The capacity of the heart, as has already been suggested, is restricted at high altitude because of the deficiency in supply of oxygen to it’ (Dill 1938: 15). For the important point is that the heart never actually develops an oxygen deficiency at altitude or at sea level; the ‘governor’ acts to terminate exercise well before any such deficiency can develop. Confirmation of the presence of this theoretical governor comes from the studies of Kayser and his colleagues (Kayser 2004; Kayser et al. 1994). They showed that the extent of skeletal muscle recruitment, measured as skeletal muscle electromyographic (EMG) activity at peak exercise, falls with increasing altitude, but increases acutely with oxygen administration. They conclude: ‘During chronic hypobaric hypoxia, the central nervous system may play a primary role in limiting exhaustive exercise and maximum accumulation of lactate in blood’ (Kayser et al. 1994: 634). Calbet et al. (2003a, 2003b) have also shown that inhalation of an oxygen-rich gas mixture at the point of exhaustion during maximal exercise in simulated altitude instantly reverses the fatigue and normalizes the exercise performance. Since the partial pressure of oxygen in the arterial blood (PaO2) is immediately normalized with the inhalation of oxygen enriched air, this finding suggests that the PaO2 provides the sensory feedback to the central governor during exercise in hypoxia. Interestingly, had the human body been designed to function according to the modern physiologists’ cardiovascular/anaerobic model which requires that anaerobiosis should first develop in skeletal muscle before maximal exercise is terminated, no climber would ever have reached the summit of Mount Everest or other high mountains, even with the use of supplemental oxygen. Rather all would have succumbed to a combination of myocardial ischaemia and cerebral hypoxia whilst their skeletal muscles were exercising vigorously, relentlessly and unrestrainedly, in pursuit of anaerobiosis and fatigue, according to the model depicted in Figure 4.1.
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