The Effect of Inhaled Nitric Oxide on Maximal O2 Consumption During Exercise in Acute Hypoxia: A Randomized Double-blind Crossover Trial, 2024,Rampuri

Abstract
In moderate hypoxia [partial pressure of inspired oxygen (PIO2) =85mmHg-111mmHg], the reduction in maximal oxygen consumption (V̇O2max) has been attributed to arterial desaturation, whereas in severe hypoxia (PIO2<85mmHg), elevated pulmonary artery pressure (PAP) is thought to impair peak cardiac output (Q̇) and therefore V̇O2max.

The purpose of this study was to examine whether reducing PAP with inhaled nitric oxide (iNO, a selective pulmonary vasodilator) would increase V̇O2max in moderate and severe acute hypoxia.

Twelve young, healthy participants (mean V̇O2max = 45.3 ± 12.2 mL/kg/min), with normal lung function completed the randomized double-blind crossover study over six sessions. Experimental cardiopulmonary exercise tests (CPET) were completed on separate days with participants under the following conditions: A) acute moderate hypoxia (PIO2=89 mmHg), B) acute severe hypoxia (PIO2=79 mmHg), C) acute moderate hypoxia with 40ppm iNO, and D) acute severe hypoxia with 40ppm iNO (order randomized).

On separate days, rest, and exercise (60 watt) echocardiography were conducted to determine right ventricular systolic pressure (RVSP/PAP) under conditions A-D. Resting RVSP was reduced by 2.5±0.8 mmHg with iNO in moderate hypoxia (p=0.01) and 1.8±0.2 mmHg in severe hypoxia (p=0.05); however, iNO had no effect on peak Q̇ or V̇O2max in either hypoxic condition.

Despite reducing RVSP with iNO in hypoxia, peak Q̇ and V̇O2max were unaffected, suggesting that iNO may not improve exercise tolerance in healthy participants during hypoxic exercise.

https://journals.physiology.org/doi/abs/10.1152/japplphysiol.00767.2022