Friday, February 20, 2009

Testing for maximum oxygen consumption has produced a brainless model of human exercise performance.

Br J Sports Med. 2008 Jul;42(7):551-5. Epub 2008 Apr 18. Review
Noakes TD.

Perhaps the hallmark study in human exercise physiology was performed by Nobel Laureate Professor AV Hill on himself in Manchester, England in the early 1920’s. Hill circled an 88m grass running track at three different speeds each for four minutes whilst he measured his average oxygen consumption every 30 seconds. He concluded that his oxygen consumption reached a maximum at 16km/hr “beyond which no bodily effort can drive it”. This experiment established the single most popular test in the exercise sciences – the progressive exercise test for the measurement of the maximum oxygen consumption (VO2max). The experimental protocol in this test forces the subject progressively to increase the work rate until voluntary exhaustion.

According to the modern interpretation, the outcome of this test defines the limits of the human cardio-respiratory system since it apparently terminates when the cardiac output reaches a maximum value. It also established a model to explain the biology of human exercise performance. For if the cardiovascular system determines maximal exercise performance, then it must also determine performance during many other forms of exercise as argued by Bassett and Howley and others. Thus, champion athletes able to run very fast for long distances do so because of the metabolic consequences in their skeletal muscles of their superior cardiovascular function even though they exercise at intensities below that at which the VO2max is reached and at which, according to that model, cardiovascular function is not maximal and cannot therefore, by definition, be the “limiting” factor.

This explanation seems paradoxical since, if correct, it predicts that athletes should be able to exercise more vigorously and for longer simply by increasing their (submaximal) cardiac outputs until maximal values are reached. Only then should exhaustion occur. Or that any athlete chasing the race leader should be able to increase the cardiac output to a maximal value and so pass the leading athlete who is exercising at a lower and submaximal cardiac output. But this does not happen; as is well known, prolonged exercise always terminates at submaximal levels of cardiac output.

It is my opinion that the manner in which the VO2max test is conducted has encouraged a reductionist mindset which teaches that the “limits” of exercise performance can be explained by one or two cardiovascular variables, such as the cardiac output and muscle blood flow. But the VO2max test includes three components that are foreign to all forms of freely chosen exercise.

First, the tested subject does not know the expected duration of the exercise bout when it begins. Accurate knowledge of the exercise duration optimizes the exercise performance.

Second the intensity of the exercise increases progressively, sometimes rapidly from low to “maximal” work rates. Humans do not usually exercise this way.

Third, the tested subject cannot regulate the exercise intensity except by choosing when to stop. This adds a subjective component to the test since the athlete’s conscious brain makes the final decision when to terminate the exercise. Thus psychological and not purely physiological factors can presumably influence that decision.

More to the point, a characteristic of freely-chosen exercise is the choice of different pacing strategies that change continuously from moment-to-moment. Unique, constantly-changing pacing strategies are most likely produced by a central motor command that continually modulates the number of motor units recruited in the exercising limbs. But during the VO2max test this critical brain function cannot be evaluated since the change in work rate is preset and immutable, thereby controlling the tested subject’s level of central motor output in an unnatural way (Figure 1).



Finally the VO2max test has produced an unusual definition of the intensity at which exercise is performed. For the intensity is expressed relative to that at which the VO2max occurs. Workloads beyond those reached during the VO2max test are defined as “supramaximal”. But this does not make sense. For a (lower) exercise intensity cannot be maximal if a higher exercise intensity can be achieved, even if under different circumstances.

Experimental models such as the VO2max test have their uses for they can define the maximal capacity of each human for oxygen use but their generalizability must be carefully scrutinized. Thus one must ask: Is it appropriate to explain the physiological factors determining human exercise performance according to an experimental model of exercise (i) in which
humans do not usually engage and (ii) in which the brain of the tested subject
does not set the pacing strategy as is usual in freely-chosen exercise? If we
base our interpretations exclusively on a testing model which is so unnatural
that it excludes the usual function of the brain during exercise, we may miss
the obvious.

Thus this traditional reductionist explanation of the factors limiting the VO2max
excludes any possible contribution of the brain and central motor
command.[3-9, 11-14] For the point is, as Kayser[18] reminds us, that
exercise begins and ends in the brain. Thus before any movement can occur
the appropriate number of motor units in the exercising skeletal muscles must
first be activated by the central nervous system. As a result the power output
of the exercising limbs increases, raising the whole body oxygen consumption
consequent to metabolite-induced arteriolar vasodilation which directs the
increase in blood flow to the exercising muscles. Thus, as is usually taught in
standard textbooks of human physiology[22] increases in blood flow and
cardiac output during exercise are the consequence and not the cause of the
increase in power output by the exercising muscles. Attempts to point this out
are usually dismissed out of hand.[23]

But the logical point is that this critical role of central motor command cannot
be identified if its most important function – the setting of the pacing strategy –
is the controlled variable in the experimental model – the VO2max test – used

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