The effect of inhaled nitric oxide on maximal oxygen consumption during exercise in acute hypoxia: a randomized double-blind crossover trial.
J Appl Physiol (1985)
; 136(3): 514-524, 2024 Mar 01.
Article
de En
| MEDLINE
| ID: mdl-38174373
ABSTRACT
In moderate hypoxia [partial pressure of inspired oxygen ([Formula see text]) = 85-111 mmHg], the reduction in maximal oxygen consumption (VÌo2max) has been attributed to arterial desaturation, whereas in severe hypoxia ([Formula see text] < 85 mmHg), elevated pulmonary artery pressure (PAP) is thought to impair peak cardiac output ([Formula see text]) and therefore VÌo2max. The purpose of this study was to examine whether reducing PAP with inhaled nitric oxide (iNO, a selective pulmonary vasodilator) would increase VÌo2max in moderate and severe acute hypoxia. Twelve young, healthy participants (mean VÌo2max = 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 1) acute moderate hypoxia ([Formula see text] = 89 mmHg), 2) acute severe hypoxia ([Formula see text] = 79 mmHg), 3) acute moderate hypoxia with 40 ppm iNO, and 4) acute severe hypoxia with 40 ppm iNO (order randomized). On separate days, rest, and exercise (60 W), echocardiography was conducted to determine right ventricular systolic pressure (RVSP/PAP) under conditions 1-4. 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 [Formula see text] or VÌo2max in either hypoxic condition. Despite reducing RVSP with iNO in hypoxia, peak [Formula see text] and VÌo2max were unaffected, suggesting that iNO may not improve exercise tolerance in healthy participants during hypoxic exercise.NEW & NOTEWORTHY The elevation of pulmonary artery pressure (PAP) with hypoxia may impair peak cardiac output ([Formula see text]) and therefore VÌo2max. Our novel findings show that despite reducing resting RVSP in acute moderate ([Formula see text] = 89 mmHg) and severe hypoxia ([Formula see text] = 79 mmHg) with inspired nitric oxide, peak [Formula see text], and VÌo2max were unaffected.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Hypoxie
/
Monoxyde d'azote
Type d'étude:
Clinical_trials
Limites:
Humans
Langue:
En
Journal:
J Appl Physiol (1985)
Sujet du journal:
FISIOLOGIA
Année:
2024
Type de document:
Article
Pays d'affiliation:
Canada