Emily M Heiston1,2, Zhenqi Liu3, Anna Ballantyne2, Sibylle Kranz2, Steven K Malin2,4,5,6,7. 1. Department of Internal Medicine, Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia, USA. 2. Department of Kinesiology, University of Virginia, Charlottesville, Virginia, USA. 3. Division of Endocrinology & Metabolism, Department of Medicine, University of Virginia, Charlottesville, Virginia, USA. 4. Department of Kinesiology & Health, Rutgers University, New Brunswick, New Jersey, USA. 5. Division of Endocrinology, Metabolism & Nutrition, Department of Medicine, Rutgers University, New Brunswick, New Jersey, USA. 6. The New Jersey Institute for Food, Nutrition and Health, Rutgers University, New Brunswick, New Jersey, USA. 7. Institute of Translational Medicine and Science, Rutgers University, New Brunswick, New Jersey, USA.
Abstract
OBJECTIVE: This crossover study explored the impact of a single bout of exercise on insulin-stimulated responses in conduit arteries and capillaries. METHODS: Twelve sedentary adults (49.5 [7.8] years; maximal oxygen consumption [VO2 max]: 23.7 [5.4] mL/kg/min) with obesity (BMI 34.5 [4.3] kg/m2 ) completed a control and exercise bout (70% VO2 max to expend 400 kcal). Sixteen hours later, participants underwent a 2-hour euglycemic-hyperinsulinemic clamp (90 mg/dL; 40 mU/m2 /min) to determine vascular and metabolic insulin sensitivity. Endothelial and capillary functions were assessed by brachial artery flow-mediated dilation and contrast-enhanced ultrasound, respectively. Metabolized glucose infusion rate, substrate oxidation (indirect calorimetry), nonoxidative glucose disposal (NOGD), and inflammation were also determined. RESULTS: Exercise increased insulin-stimulated preocclusion diameter (p = 0.01) and microvascular blood flow (condition effect: p = 0.04) compared with control. Furthermore, exercise improved metabolic insulin sensitivity by 21%, which paralleled rises in NOGD (p = 0.05) and decreases in soluble receptors for advanced glycation end products (condition effect: p = 0.01). Interestingly, changes in NOGD were related to increased insulin-stimulated microvascular blood flow (r = 0.57, p = 0.05). CONCLUSIONS: A single bout of exercise increases vascular insulin sensitivity in adults with obesity. Additional work is needed to determine vascular responses following different doses of exercise in order to design lifestyle prescriptions for reducing chronic disease risk.
OBJECTIVE: This crossover study explored the impact of a single bout of exercise on insulin-stimulated responses in conduit arteries and capillaries. METHODS: Twelve sedentary adults (49.5 [7.8] years; maximal oxygen consumption [VO2 max]: 23.7 [5.4] mL/kg/min) with obesity (BMI 34.5 [4.3] kg/m2 ) completed a control and exercise bout (70% VO2 max to expend 400 kcal). Sixteen hours later, participants underwent a 2-hour euglycemic-hyperinsulinemic clamp (90 mg/dL; 40 mU/m2 /min) to determine vascular and metabolic insulin sensitivity. Endothelial and capillary functions were assessed by brachial artery flow-mediated dilation and contrast-enhanced ultrasound, respectively. Metabolized glucose infusion rate, substrate oxidation (indirect calorimetry), nonoxidative glucose disposal (NOGD), and inflammation were also determined. RESULTS: Exercise increased insulin-stimulated preocclusion diameter (p = 0.01) and microvascular blood flow (condition effect: p = 0.04) compared with control. Furthermore, exercise improved metabolic insulin sensitivity by 21%, which paralleled rises in NOGD (p = 0.05) and decreases in soluble receptors for advanced glycation end products (condition effect: p = 0.01). Interestingly, changes in NOGD were related to increased insulin-stimulated microvascular blood flow (r = 0.57, p = 0.05). CONCLUSIONS: A single bout of exercise increases vascular insulin sensitivity in adults with obesity. Additional work is needed to determine vascular responses following different doses of exercise in order to design lifestyle prescriptions for reducing chronic disease risk.
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