Exercise increases muscle GLUT-4 levels and insulin action in subjects with impaired glucose tolerance
A decline in insulin sensitivity is associated with aging, inactivity, and obesity. The effects of exercise training on glucose homeostasis independent of weight loss in older glucose-intolerant individuals are not well established. We examined the effects of exercise training on oral glucose tolerance, insulin action, and concentration of the GLUT-4 glucose transporters in skeletal muscle. Exercise training at 50 and 75% of heart rate reserve was performed for 12 wk in 18 individuals (age = 64 ± 2, body fat = 37.0 ± 1.5%). Peripheral insulin action was determined 96 h after the last exercise bout using a two-step hyperinsulinemic-euglycemic glucose clamp (insulin = 192 and 708 pmol/l). Percent body fat and fat-free mass (FFM) were unchanged with training. Diet composition, assessed by diet record, did not change over the 12 wk. Improved oral glucose tolerance was observed, as exhibited by lower plasma glucose concentrations after training (P < 0.05), whereas plasma insulin response remained unchanged. The rate of glucose disposal was unchanged during the low insulin concentration but increased 11.0% at the high insulin concentration (P < 0.05) after training (54.4 ± 4.4 vs. 60.4 ± 5.5 μmol · kg FFM1 · min-1). Skeletal muscle glycogen and GLUT-4 concentration increased 24 and 60%, respectively, with training. There was no direct relationship between the change in GLUT-4 protein and the change in glucose disposal rate. These findings demonstrate that chronic exercise training without changes in body composition improves peripheral insulin action in subjects with impaired glucose tolerance. The lack of a statistically significant correlation between the changes in GLUT-4 protein and insulin-stimulated glucose disposal rate suggests 1) that GLUT-4 levels may be related instead to changes in exercise-induced glucose disposal resulting from exercise training and 2) that the mechanisms responsible for the improvement in glucose homeostasis are multifactorial.
Hughes, VA; Fiatarone, MA; Fielding, RA; Kahn, BB; Ferrara, CM; Shepherd, P; Fisher, EC; Wolfe, RR; Elahi, D; Evans, WJ
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