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

Mary Beth Gordon, Rajiv Jain, Joshua A. Beckman, Mark A. Creager

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


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 μg.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.

Original languageEnglish (US)
Pages (from-to)163-168
Number of pages6
JournalVascular Medicine
Issue number3
StatePublished - 2002
Externally publishedYes


  • Blood flow
  • Endothelium-derived relaxing factor
  • N-monomethyl-L-arginine
  • Nitric oxide

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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