Related Experiment Video
Updated: Jul 6, 2025
Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
Published on: March 15, 2019
The effect of inhaled nitric oxide on maximal oxygen consumption during exercise in acute hypoxia: a randomized
Zahrah H Rampuri1,2, Sophie É Collins1,2, Benjamin S A Mickelsen1,3
1Division of Pulmonary Medicine, Department of Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Abstract:
In moderate hypoxia [partial pressure of inspired oxygen ([Formula: see text]) = 85-111 mmHg], the reduction in maximal oxygen consumption (V̇o2max) 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 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: 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 V̇o2max in either hypoxic condition. Despite reducing RVSP with iNO in hypoxia, peak [Formula: see text] and V̇o2max 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 V̇o2max. 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 V̇o2max were unaffected.
More Related Videos
08:44Author Spotlight: Integrating Alveolar-Capillary Reserve Measurements in Exercise Adaptation and Therapeutic Strategies
Published on: February 2, 2024
05:46A Novel Inhalation Mask System to Deliver High Concentrations of Nitric Oxide Gas in Spontaneously Breathing Subjects
Published on: May 4, 2021
Related Concept Videos
01:28Nitric Oxide Signaling Pathway
01:27Oxygen Transport in the Blood
01:21Acute Respiratory Failure-II
The underlying physiological abnormalities that contribute to hypoxemic respiratory failure include:
01:16Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure
Oxygen therapy is vital in increasing and maintaining blood oxygen levels in PAH patients. As a result, it aids in reducing fatigue,...
01:20Exercise and Cardiovascular Response
Light to moderate physical activity initiates a series of interconnected responses in the body. The heart rate modestly increases in anticipation of the workout, followed by widespread vasodilation as oxygen consumption by skeletal muscles increases. This results in decreased peripheral resistance, increased capillary blood flow, and accelerated...
01:20Respiration and Gaseous Exchange
Respiration involves the exchange of gases, especially oxygen (O2) and carbon dioxide (CO2), between the alveoli and body cells, a process facilitated by blood circulation. As a result, the cardiovascular system, which involves...