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1 Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA
* To whom correspondence should be addressed. E-mail: jhollosz{at}im.wustl.edu.
Exercise induces an increase in GLUT4 in skeletal muscle with a proportional increase in glucose transport capacity. This adaptation results in enhanced glycogen accumulation, i.e. "supercompensation", in response to carbohydrate feeding after glycogen depleting exercise. The increase in GLUT4 reverses within 40h after exercise in carbohydrate fed rats. The purpose of this study was to determine if prevention of skeletal muscle glycogen supercompensation after exercise results in maintenance of the increases in GLUT4 and the capacity for glycogen supercompensation. Rats were exercised by means of three daily bouts of swimming. GLUT4 mRNA was increased ~3-fold and GLUT4 protein was increased ~2-fold 18h in epitrochlearis muscle after exercise. These increases in GLUT4 mRNA and protein reversed completely within 42h after exercise in rats fed a high carbohydrate diet. In contrast, the increases in GLUT4 protein, insulin-stimulated glucose transport and increased capacity for glycogen supercompensation persisted unchanged for 66h, in rats fed a carbohydrate-free diet that prevented glycogen supercompensation after exercise. GLUT4 mRNA was still elevated at 42h, but had returned to baseline by 66h, after exercise in rats fed the carbohydrate-free diet. Glycogen-depleted rats fed carbohydrate 66h after exercise underwent muscle glycogen supercompensation with concomitant reversal of the increase in GLUT4. These findings provide evidence that prevention of glycogen supercompensation after exercise results in persistence of exercise-induced increases in GLUT4 protein and enhanced capacity for glycogen supercompensation.
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