Brachial Artery Flow-mediated Dilation Following Exercise with Augmented Oscillatory and Retrograde Shear Rate

Twelve men participated in four randomized exercise sessions (90？W for 20？minutes) on separate days. During three of the sessions, one arm was subjected to increased oscillatory and retrograde SR using three different forearm cuff pressures (20, 40, 60？mmHg) (contralateral arm served as the control) and subjects ingested placebo capsules prior to exercise. A fourth session with 60？mmHg cuff pressure was performed with 1？g of vitamin C ingested prior to the session.Post-exercise FMD following the placebo conditions were lower in the cuffed arm versus the control arm (arm main effect: P？<？0.05) and without differences between cuff pressures (20？mmHg: 5.7？±？2.2%; 40？mmHg: 4.7？±？1.3%; 60？mmHg: 5.4？±？2.4%) (P？>？0.05). Following vitamin C treatment, post-exercise FMD in the cuffed and control arm increased from baseline (P？<？0.05) but were not different (control: 7.1？±？3.5% vs. cuffed: 6.6？±？3.3%) (P？>？0.05).These results indicate that augmented oscillatory and retrograde SR in non-working limbs during lower body exercise attenuates post-exercise FMD without an evident dose–response in the range of cuff pressures evaluated. Vitamin C supplementation prevented the attenuation of FMD following exercise with augmented oscillatory and retrograde SR suggesting that oxidative stress contributes to the adverse effects of oscillatory and retrograde shear during exercise on FMD.Improvements in recognized traditional and novel risk factors account for approximately 59% of the benefits associated with exercise which leaves a large portion of the exercise-induced reduction of disease risk unexplained [1]. Exercise provides direct beneficial effects to the vasculature which may contribute to the unexplained cardiovascular disease risk reduction [2]. Data obtained from animals and humans demonstrate that exercise produces an increased superoxide dismutase expression/activity [3], improved endothelial nitric oxide synthase (eNOS) expression and phosphorylation [4], enhanced acetylcholin