Exercise training during human obesity protects against impaired microvascular function after acute exertion by enhancing hydrogen peroxide‐mediated flow‐induced dilation

Abstract

Our recent studies suggest that increased superoxide dismutase and endothelial nitric oxide synthase (eNOS) contribute to the protective effects of chronic exercise on nitric oxide (NO) and hydrogen peroxide (H2O2)‐mediated acetylcholine (AChD) dilation after acute exertion. The goal of this study was to determine the effect of exercise training on flow‐induced dilation (FID) and AChD in resistance arteries (RAs) of obese patients. We hypothesized that H2O2 mediates the protective effect of exercise training against impaired FID and AChD induced by acute exertion. A protocol of weight lifting (WL; 8 weeks) was applied to subjects (BMI: 30–35). RAs were dissected from gluteal fat biopsies and cannulated for measurements of intraluminal diameters. NO and H2O2 production was assessed by confocal microscopy. All subjects had similar BP responses to WL. The eNOS inhibitor L‐NAME blocked FID (75% ± 12%) and AChD (60% ± 8%) in sedentary subjects. In contrast, PEG‐catalase, a H2O2 scavenger, blocked FID (68% ± 11%) and AChD (61% ± 7%) after exercise training. Fluorescence studies showed reduced NO (0.70 ± 0.05 fold) and increased H2O2 (4.55 ± 0.83 fold) production in RA post‐WL compared to pre‐WL. We conclude that H2O2 contributes to the protective effect of exercise training against reduced NO‐mediated dilation after exposure to acute exertion‐associated with hypertension in obesity. NIH (K23HL085614, R01HL095701).