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Contribution of nitric oxide to the blood pressure and arterial responses to exercise in humans


Campbell, R and Fisher, JP and Sharman, JE and McDonnell, BJ and Frenneaux, MP, Contribution of nitric oxide to the blood pressure and arterial responses to exercise in humans , Journal of Human Hypertension, 25 pp. 262-270. ISSN 0950-9240 (2011) [Refereed Article]

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Copyright © 2010 Nature Publishing Group

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DOI: doi:10.1038/jhh.2010.53


An exaggerated blood pressure (BP) response to exercise predicts future cardiovascular risk. The mechanisms underlying exercise-induced hypertension remain unclear, although endothelial dysfunction and elevated arterial stiffness may contribute. Given the association between reductions in nitric oxide (NO) and vascular dysfunction, we sought to determine whether acute inhibition of NO synthase with NG-monomethyl-Larginine (L-NMMA) would lead to exaggerated BP responses to maximal exercise and attenuate exerciseinduced reductions in arterial stiffness. In 10 healthy subjects (31±5 years), BP and heart rate (HR) were measured before, during and after an incremental cycling exercise test to determine maximal oxygen consumption (VO2max). Trials were performed with placebo (saline) or intravenous infusion of L-NMMA on separate days in a randomized, double-blind, crossover design. Central (aortic) and peripheral (femoral) arterial stiffness were assessed using pulse wave velocity (PWV). BP was increased with L-NMMA at rest and during sub-maximal exercise, but not at maximal exercise (mean BP 117±5 vs 118±8mmHg, saline vs L-NMMA, P40.05). Furthermore, L-NMMA had no influence on exercising HR or VO2max (P>0.05). Notably, aortic PWV was similarly increased after exercise with either saline or L-NMMA (P<0.05), whereas postexercise decreases in femoral PWV were attenuated with L-NMMA (P<0.05). Our findings suggest that NO is an important contributor to reductions in femoral artery stiffness after maximal exercise in healthy individuals. Furthermore, acute pharmacological inhibition of NO synthase causes augmented BP responses to sub-maximal exercise, but does not lead to exaggerated BP responses to maximal exercise or reduce maximal oxygen consumption.

Item Details

Item Type:Refereed Article
Keywords:blood pressure; exercise; nitric oxide; arteries; vasculature
Research Division:Biomedical and Clinical Sciences
Research Group:Cardiovascular medicine and haematology
Research Field:Cardiology (incl. cardiovascular diseases)
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Sharman, JE (Professor James Sharman)
ID Code:66350
Year Published:2011
Web of Science® Times Cited:31
Deposited By:Menzies Institute for Medical Research
Deposited On:2011-01-13
Last Modified:2013-11-15

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