Introduction: Exercise reduces systolic augmentation in the peripheral pulse wave, an effect similar to that produced by the nitric oxide (NO) donor nitroglycerin (NTG). The changes produced by exercise persist into the recovery period for >30 min. The aim of this study was to investigate if the exercise induced changes are dependent on endothelium-derived NO. We used the NO synthase inhibitor N^G-monomethyl-L-arginine (L-NMMA) to test this.

Methods: Healthy volunteers (n = 10, 5 female, aged 19 to 33 years) participated in a 2-phase randomised controlled cross-over study. L-NMMA (6 mg/kg i.v. over 5 min) and saline placebo were given immediately before exercise on two occasions separated by at least 5 days. Mean arterial blood pressure (MAP by Finopress), radial augmentation index (RAIx by SphgymoCor) and cardiac output (Innocor) measurements were made at baseline, during infusion of L-NMMA/saline immediately before exercise, during exercise (except for radial artery measurements) and during recovery. Peripheral vascular resistance (PVR) was calculated from MAP and cardiac output. During exercise, workload increased from 25W to 150W by increments of 25W at 2min intervals.

Results: Before exercise, L-NMMA increased mean arterial blood pressure (85.1±3.8 vs. 101.2±4.3 mmHg, P < 0.01), peripheral vascular resistance (16.4±0.7 vs. 24.7±1.7 mmHg/ml/min, P < 0.01) and RAIx (50.2±4.5 vs. 70.2±6.5%, P < 0.01) and decreased heart rate (65.6±5.7 vs. 49.1±2.8 bpm, P < 0.01). During and after exercise, heart rate, MAP and PVR were similar after L-NMMA and saline. However, L-NMMA attenuated the exercise induced fall in RAIx so that RAIx was higher after L-NMMA compared to saline at 15 min in recovery (49.5±5.3 vs. 36.0±4.4%, P < 0.02).

Conclusion: These data suggest that, although endothelium derived NO has little effect in regulating PVR during/after exercise, it may have a role in mediating exercise induced changes in the pulse waveform.