Abstract

Contractile activity is followed by an increase in the permeability of muscle to sugar. The increase in sugar transport rate persists unchanged for hours before gradually returning to base-line (Holloszy, J. O., and Narahara, H. T. (1965) J. Biol. Chem. 240, 3493-3500). This prolonged delay suggested that the recovery process might involve protein synthesis. We have investigated this possibility. A large increase in permeability to [3-3H]methylglucose occurred in frog sartorius muscles stimulated to contract 60 times/min for 30 min. Cycloheximide or puromycin at concentrations that inhibited protein synthesis completely blocked reversal of the increase in permeability to 3-methylglucose. The recovery process was not irreversibly impaired, as permeability returned to base-line in muscles that were washed and incubated without protein synthesis inhibitors for a second 24-h period. Reversal of the increase in permeability to 3-methylglucose induced by a high concentration of epinephrine was also prevented by cycloheximide. In contrast, cycloheximide did not prevent reversal of the increases in sugar transport rate induced by either insulin or trypsin. These results provide evidence that exercise and catecholamines activate sugar transport by a process that requires protein synthesis for its reversal, while the increases in permeability induced by insulin and trypsin involve a different mechanism.

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