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Background  Basal release of nitric oxide ( NO ) from the vascular endothelium regulates the tone of muscular arteries and resistance vasculature. Effects of  NO  on muscular arteries could be particularly important during exercise when shear stress may stimulate increased  NO  synthesis.    Methods and Results  We investigated acute effects of  NO  synthase inhibition on exercise hemodynamics using  N G  ‐monomethyl‐ l ‐arginine ( l ‐ NMMA ), a nonselective  NO  synthase ‐inhibitor. Healthy volunteers (n=10, 5 female, 19–33 years) participated in a 2‐phase randomized crossover study, receiving  l ‐ NMMA  (6 mg/kg, iv over 5 minutes) or placebo before bicycle exercise (25–150 W for 12 minutes). Blood pressure, cardiac output (measured by dilution of soluble and inert tracers) and femoral artery diameter were measured before, during, and after exercise. At rest,  l ‐ NMMA  reduced heart rate (by 16.2±4.3 bpm relative to placebo,  P <0.01), increased peripheral vascular resistance (by 7.0±1.4 mmHg per L/min,  P <0.001), mean arterial blood pressure (by 8.9±3.5 mmHg,  P <0.05), and blunted an increase in femoral artery diameter that occurred immediately before exercise (change in diameter: 0.14±0.04 versus 0.32±0.06 mm after  l ‐ NMMA  and placebo,  P <0.01). During/after exercise  l ‐ NMMA  had no significant effect on peripheral resistance, cardiac output, or on femoral artery diameter.    Conclusions  These results suggest that  NO  plays little role in modulating muscular artery function during exercise but that it may mediate changes in muscular artery tone immediately before exercise.

journal of the american heart association. cardiovascular and cerebrovascular disease

Effects of Inhibition of Nitric Oxide Synthase on Muscular Arteries During Exercise: Nitric Oxide Does Not Contribute to Vasodilation During Exercise or in Recovery