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Journal of Applied Physiology, Vol 58, Issue 5 1622-1629, Copyright © 1985 by American Physiological Society
ARTICLES |
A. Bonen, G. W. Ness, A. N. Belcastro and R. L. Kirby
Bicycle ergometric exercise was used to deplete glycogen by either 80 or 35% in the vastus lateralis of both legs. Thereafter, subjects from each group rested or maintained single-leg exercise [20% of maximal O2 consumption (Vo2max) for 4 h. All subjects ingested glucose (1.5 g/kg wt; 20% solution) at min 10-12 and min 130-132 of the 4-h period. With bed rest, significant glycogen increases occurred after exhaustive (+36%; P less than 0.05) and nonexhaustive exercise (+13%; P less than 0.05). With single-leg exercise, 1) a diminished glycogen repletion occurred in exercising (+11%; P less than 0.05) and nonexercising (+15%; P less than 0.05) muscle after exhaustive exercise, or 2) further glycogen loss occurred in exercising (-26%; P less than 0.05) and nonexercising muscle (-19%; P less than 0.05) after nonexhaustive exercise. Within both groups, glycogen concentrations did not differ between exercising and nonexercising muscles (P greater than 0.05). Single-leg exercise, not preceded by exercise, provoked differences in glycogen loss in exercising (-47%) and nonexercising (-24%) muscle (P less than 0.05). These experiments demonstrate that mild exercise 1) impedes glycogen resynthesis or 2) provokes glycogen loss in both exercising and nonexercising muscle. These findings cannot be ascribed to circulating glucose and insulin concentrations in these studies.
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