Inhaled nitric oxide does not improve maximal oxygen consumption in endurance trained and untrained healthy individuals

Abstract

Purpose

Previous work suggests that endurance-trained athletes have superior pulmonary vasculature function as compared to untrained individuals, which may contribute to their greater maximal oxygen uptake ($\dot{\text{V}}$O_2max). Inhaled nitric oxide (iNO) reduces pulmonary vascular resistance in healthy individuals, which could translate into greater cardiac output and improved $\dot{\text{V}}$O_2max, particularly in untrained individuals. The purpose of the study was to examine whether iNO improved $\dot{\text{V}}$O_2max in endurance trained and untrained individuals.

Methods

Sixteen endurance-trained and sixteen untrained individuals with normal lung function completed this randomized double-blind cross-over study over four sessions. Experimental cardiopulmonary exercise tests were completed while breathing either normoxia (placebo) or 40 ppm of iNO, on separate days (order randomized). On an additional day, echocardiography was used to determine pulmonary artery systolic pressure at rest and during sub-maximal exercise (60 Watts) while participants breathed normoxia or iNO.

Results

Right ventricular systolic pressure was significantly reduced by iNO during exercise (Placebo: 34 ± 7 vs. iNO: 32 ± 7; p = 0.04). $\dot{\text{V}}$O_2max was greater in the endurance trained group (Untrained: 3.1 ± 0.7 vs. Endurance: 4.3 ± 0.9 L min⁻¹; p < 0.01), however, there was no effect of condition (p = 0.79) and no group by condition interaction (p = 0.68). Peak cardiac output was also unchanged by iNO in either group.

Conclusion

Despite a reduction in right ventricular systolic pressure, the lack of change in $\dot{\text{V}}$O_2max with iNO suggests that the pulmonary vasculature does not limit $\dot{\text{V}}$O_2max in young healthy individuals, regardless of fitness level.