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

Abstract

We sought to determine the contribution of nitric oxide (NO) to the blood pressure (BP) responses to exercise and post‐exercise alterations in arterial stiffness. In 10 healthy subjects (31±5 years), BP, heart rate (HR) and oxygen consumption were measured before, during and after an incremental cycling exercise test. Trials were performed with placebo (saline) or following acute inhibition of NO synthase with NG‐monomethyl‐L‐arginine (L‐NMMA) on separate days, in a randomized, double blind, cross‐over design. Central (aortic) and peripheral (femoral) arterial stiffness was assessed with pulse wave velocity (PWV). BP was increased with L‐NMMA at rest and during sub‐maximal exercise, but not at maximal exercise (mean BP 118±8 vs. 117±5 mmHg, saline vs. L‐NMMA, P>0.05). L‐NMMA had no influence on exercising HR or maximal oxygen consumption (P=ns). Post‐exercise reductions in femoral PWV were attenuated with L‐NMMA (P<0.05), while aortic PWV was increased similarly with either saline or L‐NMMA (P=ns). Our findings suggest that reductions in NO bioavailability cause augmented BP responses to sub‐maximal exercise, but do not lead to exaggerated BP responses to maximal exercise or reduce maximal oxygen consumption. Furthermore, NO is an important contributor to reductions in femoral artery stiffness following maximal exercise in healthy individuals.This research was supported by the BHF.