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Center for Metabolic Biology (E.D.F., L.J.M.), Arizona State University, Tempe, Arizona 85287; Department of Medicine (K.C., G.O.), University of Texas Health Science Center, San Antonio, Texas 78229; Department of Obstetrics and Gynecology (R.B.), Case Western Reserve University, Cleveland, Ohio 44106; Texas Diabetes Institute (S.B.), San Antonio Texas 78207; and Department of Medicine and Aging Sciences (A.C.), University of Chieti, 66013 Chieti, Italy
Address all correspondence and requests for reprints to: Lawrence J. Mandarino, Ph.D., Center for Metabolic Biology, Arizona State University, 350 East Orange Street, P.O. Box 873704, Tempe, Arizona 85287-3704. E-mail: Lawrence.Mandarino{at}asu.edu.
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 (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 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.
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