The contribution of nitric oxide to exercise hyperemia in the human forearm.

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 x min(-1)). Nine additional subjects performed this procedure while nitroprusside (0.2 microg x 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 hyperemic 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.