Exercise-induced improvement in vasodilatory function accompanies increased insulin sensitivity in obesity and type 2 diabetes mellitus.

Abstract

The present study was undertaken to determine whether improved vasodilatory function accompanies increased insulin sensitivity in overweight, insulin-resistant subjects (OW) and type 2 diabetic patients (T2DM) who participated in an 8-wk exercise training regimen. Before and after training, subjects had euglycemic clamps to determine insulin sensitivity. Brachial artery catheterization was done on another occasion for measurement of vasodilatory function. A lean, healthy, untrained group was studied as nonexercised controls. Training increased oxygen consumption (VO2) peak [OW, 29 +/- 1 to 37 +/- 4 ml/kg fat-free mass (FFM).min; T2DM, 33 +/- 2 to 43 +/- 3 ml/kg FFM.min; P < 0.05] and improved insulin-stimulated glucose disposal (OW, 6.5 +/- 0.5 to 7.2 +/- 0.4 mg/kg FFM.min; T2DM, 3.8 +/- 0.3 to 4.2 +/- 0.3 mg/kg FFM.min; P < 0.05) in insulin resistance. OW and T2DM, before training, had decreased acetylcholine chloride (ACh)- and sodium nitroprusside-mediated vasodilation and decreased reactive hyperemia compared with lean controls. Training increased the vasodilatory response to ACh [OW (30 microg ACh/min), 12.2 +/- 3.4 to 19 +/- 4.2 ml/100 g.min; T2DM (30 microg ACh/min), 10.1 +/- 1.5 to 14.2 +/- 2.1 ml/100 g.min; P < 0.05] in both groups without affecting nitroprusside response. Because vasodilatory dysfunction has been postulated to contribute to insulin resistance, the exercise-induced improvement in vasodilatory function may signify changes in the endothelium that could contribute to the improvement in insulin sensitivity observed after aerobic exercise training.