A number of researchers have used the decrease in mitochondrial enzyme content that occurs when training stops as a measure of the rate at which fitness is lost when one stops training. In addition, they have studied the amount of exercise required to maintain these adaptations.
In rats and humans trained for 8 to 15 weeks, elevated mitochondrial enzyme contents are lost within about 8 weeks in rats and about 4 to 8 weeks in humans (Coyle et al, 1985b; Holloszy & Coyle, 1984; R.L. Moore et al, 1987) with no further loss thereafter (Coyle et al, 1985b). However, humans who have trained for much longer (6 to 20 years) show much more gradual declines in mitochondrial enzyme content; even after 12 weeks of inactivity these people have mitochondrial enzyme contents at least 40 to 50% above untrained levels (Chi et al, 1983; Coyle et al, 1984, 1985b). This is compatible with the empirical observation that once an athlete has trained for a few years, even 1 or 2 months of complete inactivity do not cause that athlete to go back to total unfitness. In these studies, V02max declined by 7% over the first 12 days of detraining and by 16% after 8 weeks, at which level it stabilized (Coyle et al, 1984). The work load or oxygen consumption at the lactate tumpoint declined by 20% after 8 weeks before stabilizing at that level (Coyle et al, 1985b).
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On the other hand, tapering by reducing training from 110 km/week to 40 km/ week for 10 days neither decreased nor increased V02max and exercise time to exhaustion in trained distance runners (Houmard et al, 1989).
Hickson and his colleagues (Hickson & Rosenkoetter, 1981; Hickson et al, 1982) exercised groups of subjects 40 minutes a day, 6 days a week, for 10 weeks, after which the subjects exercised either less frequently (2 or 4 days a week) or for shorter times (13 min/day or 26 min/day) but at the same intensities and frequencies. The authors found that the fitness levels of the subjects were
Maintained even though the times that some subjects spent exercising had been reduced by almost two thirds. However, similar one-third or two-third reductions in exercise intensities failed to maintain the elevated V02max values resulting from training (Hickson et al, 1985).
Interestingly, these researchers found that with detraining, performance time to exhaustion during short-duration (5 minutes) and prolonged (200 minutes) exercise did not decrease to the same extent as did the V02max, which again suggests that other factors, possibly muscle contractility, are important in determining performance during short-duration and prolonged exercise.
Researchers have also shown through studies of rats a dissociation of changes in running performance, in V02max, and in muscle mitochondrial adaptations, which also suggests that an unmeasured factor, probably muscle contractility (Noakes, 1988b), also changes with training and is an important, albeit unrecognized, component of those training adaptations that increase running performance (Lambert & Noakes, 1989).
Another interesting finding is that the decrease in V02max that results with detraining can be reversed simply by increasing the blood volume with a dextran/ saline infusion (Coyle et al, 1986b). We would not expect such an infusion to alter the muscle mitochondrial enzyme activities, thus this finding again shows a dissociation between changes in V02max, running performance, and mitochondrial enzyme activities.
Nevertheless, these studies have important implications for those who wish to become “fit” in a short period of time but who are then unwilling to continue exercise for the same amount of time after achieving this goal. Continuing to exercise at high intensity will maintain fitness most effectively.
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