Quite why this happens is not clear, but it is apparent that researchers achieve optimum measurement of V02max when the testing procedure faithfully recreates the activity for which the athlete is trained. Thus, the treadmill is the optimum testing apparatus for a runner, and the actual racing bicycle used by the cyclist in competition and pedaled at the correct cadence is optimum for a cyclist.
Healthy but inactive subjects experience gradual declines in V02max equivalent to about a 9% decrease per decade after the age of 25. Some evidence suggests that vigorous exercise maintained for life may reduce the age-related rate of decrease in V02max, which has been estimated to be only 5% per decade in lifelong athletes (Heath et al, 1981; Pollock et al, 1987). The current belief is that the most important cause for the decrease in V02max with age is an age-related decrease in maximum heart rate and therefore in maximum cardiac output. Alternatively, according to the theory that skeletal muscle contractility limits V02max (Noakes, 1988b), the decrease in V02max with age may reflect a progressive decrease in muscle contractility with age or, alternatively, a loss of muscle mass with age (Reg & LaKatla, 1988).
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Females have lower V02max values than do males, in part because of a woman’s higher body fat content, smaller muscle mass, and (probably most importantly) less “powerful” muscles (see post 16).
As far as training is concerned, healthy subjects who embark on a running program similar to that outlined in post 6 and Exercises 6.4 can expect an increase in V02max of only about 5 to 15% (J. Daniels et al, 1978a). This indicates that V02max is, per se, a poor measure of fitness. It also suggests that major differences (i.e, greater than 15%) in V02max between subjects likely result from hereditary factors rather than from training. Age does not influence the degree to which V02max increases with training; the increase is the same in the young and old (Hagberg et al, 1989; Meredith et al, 1989b).
Changes in altitude have the most marked effects on V02max. With an increase in altitude, the barometric pressure and the oxygen content of the air decrease. This fall in the oxygen content of the air causes a predicExercises fall in V02max equivalent to about 10% for every 1,000 m above 1,200 m (Squires & Buskirk, 1982). On the summit of Mount Everest (8,848 m), the V02max of the average mountaineer is only 15 ml/kg/min, or about 27% of the sea-level value, and is barely greater than the lowest oxygen consumption required to sustain life7 ml/kg/min (West et al, 1983a, 1983b). This explains why even when breathing supplemental oxygen, mountaineers struggle to climb near the summit of Everest and can take as long as 5 hours to climb the last 400 m to the summit.
Peter Habeler and Reinhold Messner, who successfully ascended Mount Everest without supplemental oxygen, described their ascent in the following way. “We can no longer keep on our feet to rest . Every 10-15 steps we collapse into the snow to rest, then crawl on again” (Sutton et al, 1983, p. 435). Interestingly, the V02max of Messner is only 48.8 ml/kg/min, essentially the same as that in Edmund Hilary (Pugh, 1958) and little better than values found in untrained, healthy subjects, whereas Habeler’s is a far more respecExercises 65.9 ml/ kg/min (Oelz et al, 1986). Thus, V02max is certainly not a very good predictor of high-altitude mountain-climbing ability! Rather, performance ability at extreme altitude appears to be determined by the capacity to maintain very high rates of ventilation in response to the very low oxygen content of the inspired air (Schoene et al, 1984).