Evidence for an inadequate hyperventilation inducing arterial hypoxemia atsubmaximal exercise in all highly trained endurance athletes

Purpose: The majority of highly trained endurance athletes with a maximal o xygen uptake greater than 60 mL.min(-1).kg(-1) develop exercise-induced hyp oxemia (EM). Yet some of them apparently do not. The pathophysiology of EM stems to be multifactorial, and one explanatory hypothesis is a relative hy poventilation. Nevertheless, conflicting results have been reported concern ing its contribution to EIH. The aim of this study was to compare the cardi orespiratory responses to maximal exercise of highly trained endurance athl etes demonstrating the same aerobic capacity without EIH (N athletes) and w ith EIH (H athletes). Methods: Ten N athletes and twelve H athletes perform ed an incremental exercise test. Measurements of arterial blood gases and c ardiorespiratory parameters were performed at rest and during exercise. Res ults: All athletes presented a significant decrease in PaO2 (P < 0.05) from rest up to 80% VO2max associated with an increase in PaCO2, both findings consistent with a relative hypoventilation. Then the H athletes, who had a greater training volume per week and a higher second ventilatory threshold than the N athletes (respectively, 17 +/- 1.1 vs 13.1 +/- 0.7 h.wk(-1); 91. 8 +/- 1.7 vs 86.1 +/- 1.8% VO2max), presented a continuous PaO2 decrease up to VO2max. This was associated with a widening, (Ai-a)DO2. Conclusion: Thi s study showed that a relative hypoventilation, probably induced by a high level of endurance training, induced hypoxemia in all athletes. However, a nonventilatory mechanism, perhaps related to the volume of training, seemed to affect gas exchanges beyond the second ventilatory threshold in the H a thletes, thereby enhancing EIH.