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Exercise training during human obesity protects against impaired microvascular function after acute exertion by enhancing hydrogen peroxide‐mediated flow‐induced dilation
Author(s) -
Bian Jing-Tan,
Yue Lili,
Franklin Nina C,
Mazzone Theodore,
Phillips Shane A
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.678.9
Subject(s) - enos , nitric oxide , medicine , endocrinology , exertion , vasodilation , endothelial dysfunction , vo2 max , chemistry , nitric oxide synthase , heart rate , blood pressure
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 (H 2 O 2 )‐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 H 2 O 2 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 H 2 O 2 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 H 2 O 2 scavenger, blocked FID (68% ± 11%) and AChD (61% ± 7%) after exercise training. Fluorescence studies showed reduced NO (0.70 ± 0.05 fold) and increased H 2 O 2 (4.55 ± 0.83 fold) production in RA post‐WL compared to pre‐WL. We conclude that H 2 O 2 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).