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J Appl Physiol 90: 926-932, 2001;
8750-7587/01 $5.00
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Vol. 90, Issue 3, 926-932, March 2001

Influence of inhaled nitric oxide on gas exchange during normoxic and hypoxic exercise in highly trained cyclists

A. William Sheel, Michael R. Edwards, Garth S. Hunte, and Donald C. McKenzie

Allan McGavin Sports Medicine Center and School of Human Kinetics, The University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3

This study tested the effects of inhaled nitric oxide [NO; 20 parts per million (ppm)] during normoxic and hypoxic (fraction of inspired O2 = 14%) exercise on gas exchange in athletes with exercise-induced hypoxemia. Trained male cyclists (n = 7) performed two cycle tests to exhaustion to determine maximal O2 consumption (VO2 max) and arterial oxyhemoglobin saturation (SaO2, Ohmeda Biox ear oximeter) under normoxic (VO2 max = 4.88 ± 0.43 l/min and SaO2 = 90.2 ± 0.9, means ± SD) and hypoxic (VO2 max = 4.24 ± 0.49 l/min and SaO2 = 75.5 ± 4.5) conditions. On a third occasion, subjects performed four 5-min cycle tests, each separated by 1 h at their respective VO2 max, under randomly assigned conditions: normoxia (N), normoxia + NO (N/NO), hypoxia (H), and hypoxia + NO (H/NO). Gas exchange, heart rate, and metabolic parameters were determined during each condition. Arterial blood was drawn at rest and at each minute of the 5-min test. Arterial PO2 (PaO2), arterial PCO2, and SaO2 were determined, and the alveolar-arterial difference for PO2 (A-aDO2) was calculated. Measurements of PaO2 and SaO2 were significantly lower and A-aDO2 was widened during exercise compared with rest for all conditions (P < 0.05). No significant differences were detected between N and N/NO or between H and H/NO for PaO2, SaO2 and A-aDO2 (P > 0.05). We conclude that inhalation of 20 ppm NO during normoxic and hypoxic exercise has no effect on gas exchange in highly trained cyclists.

exercise-induced hypoxemia; pulmonary edema; ventilation-perfusion inequality; diffusion disequilibrium


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