Va. Hughes et al., EXERCISE INCREASES MUSCLE GLUT-4 LEVELS AND INSULIN ACTION IN SUBJECTS WITH IMPAIRED GLUCOSE-TOLERANCE, The American journal of physiology, 264(6), 1993, pp. 855-862
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 an
d 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 hype
rinsulinemic-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 low
er plasma glucose concentrations after training (P < 0.05), whereas pl
asma 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 mumol . kg FFM-1 . min-1). Skeletal muscle glyc
ogen 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 dem
onstrate that chronic exercise training without changes in body compos
ition improves peripheral insulin action in subjects with impaired glu
cose tolerance. The lack of a statistically significant correlation be
tween the changes in GLUT-4 protein and insulin-stimulated glucose dis
posal rate suggests 1) that GLUT-4 levels may be related instead to ch
anges in exercise-induced glucose disposal resulting from exercise tra
ining and 2) that the mechanisms responsible for the improvement in gl
ucose homeostasis are multifactorial.