Summary
These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (P a02) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO2max) range = 65-77 ml·kg−1·min−1] performed a normoxic graded exercise test on a cycle ergometer toVO2max at sea level. During incremental exercise atVO2max 5 of the 12 subjects had ideal alveolar to arterial P02 gradients (P A-aO2) of above 5 kPa (range 5-5.7) and a decline from restingP aO2 (ΔP aO2) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise (P A-aO2) of 4.0-4.3 kPa with ΔP aO2 of 0.4-1.3 kPa while the remaining 3 subjects hadP A-aO2 of 4.3-5 kPa with ΔP aO2 between 1.7 and 2.0 kPa. The correlation between PAO2 andP aO2 atVO2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption VSP aO2 and arterial partial pressure of carbon dioxide VSP aO2 atVO2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.
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Powers, S.K., Martin, D., Cicale, M. et al. Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation. Europ. J. Appl. Physiol. 65, 37–42 (1992). https://doi.org/10.1007/BF01466272
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DOI: https://doi.org/10.1007/BF01466272