F. Durand et al., Evidence for an inadequate hyperventilation inducing arterial hypoxemia atsubmaximal exercise in all highly trained endurance athletes, MED SCI SPT, 32(5), 2000, pp. 926-932
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.