Abstract
The contribution of nitric oxide (NO) to exercise-induced hyperemia is debated. Previous conclusions that nitric oxide synthase (NOS) inhibition reduces endothelium-dependent vasodilation during exercise hyperemia may be confounded by inhibitor-mediated increases in resting vascular tone. In this study, nine healthy participants performed wrist flexion exercise before and during intra-arterial administration of the NOS-inhibitor NG-monomethyl-l-arginine (l-NMMA, 2 mg·min-1). Nine additional subjects performed this procedure while nitroprusside (0.2 mg·min-1) was co-infused with l-NMMA to maintain basal flow. Forearm blood flow was assessed with venous occlusion strain-gauge plethysmography at baseline, immediately after cessation of exercise, and continuously for 5 minutes thereafter. l-NMMA alone reduced resting flow by 26%, peak flow immediately after exercise by 20%, and integrated post-exercise hyper-emic volume by 50% (all p, 0.05). Stabilization of resting vasodilator tone by nitroprusside eliminated the effects of l-NMMA on peak flow after exercise, yet l-NMMA still attenuated total hyperemic volume. In a time-control study of 12 subjects, there was no change in peak blood flow or hyperemic volume. This study indicates that NO is not a major regulator of peak limb blood flow measured immediately after cessation of dynamic exercise. The contribution of NO to exercise hyperemia is limited to the recovery period after exercise.