Objective: 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. Design: 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. Results: Training increased oxygen consumption (VO 2) 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 μg ACh/min), 12.2 ± 3.4 to 19 ± 4.2 ml/100 g·min; T2DM (30 μg 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. Conclusion: 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.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical