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AJP - Endocrinology and Metabolism, Vol 256, Issue 1 E167-E172, Copyright © 1989 by American Physiological Society
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J. T. Devlin, J. Barlow and E. S. Horton
Metabolism-Endocrinology Unit, University of Vermont College of Medicine, Burlington 05405.
We studied whole body and regional fuel metabolism 1-4 h after cycle exercise [70% maximum O2 consumption (VO2max)], using the insulin clamp technique (40 mU.M-2.min-1) with indirect calorimetry. Substrate fluxes were determined in nonexercised (forearm) muscle tissues. Total glucose utilization was not increased by exercise, either in the preinsulin or insulin-stimulated state. Glucose oxidation tended to decrease, and lipid oxidation was increased after exercise. Forearm glucose uptake (FGU) was increased 5 times by insulin in the resting state, due largely to increased fractional extraction (P less than 0.05). After exercise, FGU was not increased by insulin. Forearm alanine and lactate release was doubled 2 h after exercise. Branched-chain amino acid (BCAA) concentrations were increasing after exercise (P less than 0.01) at a time when forearm muscle was taking up these amino acids. Insulin infusion suppressed the elevated release of gluconeogenic precursors from the forearm and suppressed the elevated concentrations of BCAAs, free fatty acids, and glycerol present after exercise. In summary, basal and insulin-stimulated glucose utilization is not augmented by prior high-intensity exercise, partly because nonexercised muscle is insulin resistant. Insulin infusion attenuates the altered metabolic milieu seen during early recovery.
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