Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation

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 (VO_2max) range = 65-77 ml·kg⁻¹·min⁻¹] performed a normoxic graded exercise test on a cycle ergometer toVO_2max at sea level. During incremental exercise atVO_2max 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 P_AO₂ andP_aO₂ atVO_2max 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 atVO_2max 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.