Exercise increases muscle GLUT-4 levels and insulin action in subjects with impaired glucose tolerance

Abstract

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 mumol.kg FFM-1.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.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise training reduces fatty acid availability and improves the insulin sensitivity of glucose metabolism

“…We also demonstrated that after exercise training glucose uptake and clearance increased with the high-dose insulin infusion in agreement with a previous study showing an improvement in peripheral insulin sensitivity following exercise training in insulin-resistant men, who were studied 96 h after the last exercise session [34].…”

Early-onset type 2 diabetes in obese white subjects is characterised by a marked defect in beta cell insulin secretion, severe insulin resistance and a lack of response to aerobic exercise training

“…The duration (3 months) of exercise at the frequency and intensity chosen for the current study may simply have been insufficient for the improvements that were expected. However, previous studies including our own in equally obese but older subjects with obesity and type 2 diabetes, have shown improvements in insulin sensitivity and glycaemic control with similar or even less rigorous exercise regimes [13,14]. Another question is whether it would have been preferable to combine the exercise regime with a weight-losing low-energy diet.…”

“…Similar to our study, they demonstrated marked insulin resistance and beta cell failure although these subjects had very good chronic glycaemic control. Aerobic exercise has been shown to be effective in improving insulin sensitivity in patients with obesity, prediabetes and type 2 diabetes [13,14,16]. The landmark diabetes prevention studies have proven the efficacy of exercise intervention in preventing progression from IGT to diabetes [9,11,12].…”

“…Smaller studies have shown that exercise improves insulin sensitivity and glucose metabolism [13,14]. We have recently shown that short-term exercise training increased insulin sensitivity by more than 50% in obese middle-aged patients (mean age 45 years) with type 2 diabetes [15].…”

Is weight loss the optimal target for obesity-related cardiovascular disease risk reduction?

“…The improvement in insulin resistance through chronic physical activity independent of weight change likely involves changes in body composition -in particular, reductions in visceral fat (14), as well as augmented expression of GLUT-4 protein in skeletal muscle (56,57), and enhanced metabolic efficiency of muscle (58,59). The lipid improvements independent of significant weight reduction may also be mediated by improvements in body composition, such as reductions in visceral fat (60), but apparently are not due to improvements in CRF (51).…”