Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation
- Cite this article as:
- Powers, S.K., Martin, D., Cicale, M. et al. Europ. J. Appl. Physiol. (1992) 65: 37. doi:10.1007/BF01466272
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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 (Pa02) 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 (PA-aO2) of above 5 kPa (range 5-5.7) and a decline from restingPaO2 (ΔPaO2) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise (PA-aO2) of 4.0-4.3 kPa with ΔPaO2 of 0.4-1.3 kPa while the remaining 3 subjects hadPA-aO2 of 4.3-5 kPa with ΔPaO2 between 1.7 and 2.0 kPa. The correlation between PAO2 andPaO2 atVO2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption VSPaO2 and arterial partial pressure of carbon dioxide VSPaO2 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.