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Effect of Physical Activity on Oxidative Stress and Endothelial‐Dependent Cutaneous Microvascular Function in Non‐Hispanic Blacks: A Pilot Study
Author(s) -
Miller James,
Turner Casey,
Wong Brett
Publication year - 2020
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.2020.34.s1.09658
Subject(s) - oxidative stress , vasodilation , endothelial dysfunction , nitric oxide , microdialysis , medicine , sodium nitroprusside , laser doppler velocimetry , endothelium , blood flow , endocrinology , central nervous system
Cardiovascular disease is a dominant cause of morbidity and mortality in non‐Hispanic Blacks (NHB). This may be due, in part, to vascular endothelial dysfunction which causes reduced nitric oxide (NO) bioavailability and increased oxidative stress. Conversely, physical activity has been shown to attenuate and treat symptoms of cardiovascular disease, endothelial dysfunction, and oxidative stress. It remains unknown whether physical activity reduces oxidative stress and enhances endothelial‐dependent vascular function in NHB. The purpose of this study was to examine the extent to which physical fitness influences oxidative stress and nitric oxide‐dependent cutaneous vascular function in NHB. On the first visit, young, healthy NHB participants (n = 3 regularly active; n=2 inactive) completed a graded exercise test on a cycle ergometer to determine V̇O 2max to confirm self‐reported physical activity status. On the second visit, participants were instrumented with 4 microdialysis fibers for infusion of 1) lactated Ringer’s (control), 2) 0.1 mM 1400W (iNOS inhibitor), 3) 0.1 mM tempol to inhibit oxidative stress, 4) and combined tempol + 1400W, respectively. Following infusion of experimental drugs, local skin temperature was increased via rapid local heating to 39°C at a rate of 0.1°C/sec. Once skin blood flow plateaued, 20 mM L‐NAME was infused to quantify NO‐dependent vasodilation. Following L‐NAME infusion, the local heaters were increased to 43°C and 54mM of sodium nitroprusside was infused to elicit maximal endothelium‐independent cutaneous vasodilation. Skin blood flow was measured via laser‐doppler flowmetry (LDF) throughout the local heating protocol. Cutaneous vascular conductance (CVC) was calculated as LDF divided by mean arterial pressure and normalized to maximum (%CVCmax). iNOS inhibition increased %NO‐dependent vasodilation in both active (67 ± 10% vs. 54 ± 7%) and inactive (69 ± 4% vs. 56 ± 10%) groups compared to control. Combined inhibition of iNOS and oxidative stress increased %NO‐dependent vasodilation in both active (72 ± 9%) and inactive (71 ± 13%) NHB compared to control but these were not different compared to inhibition of iNOS or oxidative stress alone. Interestingly, inhibition of oxidative stress significantly increased %NO‐dependent vasodilation in only the active group compared to control (74 ± 8%). Taken together these data indicate that inhibition of iNOS with 1400W increases endothelial‐dependent cutaneous vasodilation in active and inactive NHB while inhibition of oxidative stress increases endothelial‐dependent cutaneous vasodilation in active NHB.