Pulmonary gas exchange during exercise in highly trained cyclists with arterial hypoxemia

The causes of exercise-induced hypoxemia (EIH) remain unclear. We studied the mechanisms of EIH in highly trained cyclists. Five subjects had no significant change from resting arterial Po-2 (Pa-O2; 92.1 +/- 2.6 Torr) during maximal exercise (C), and seven subjects (E) had a >10-Torr reduction in Pa-O2 (81.7 +/- 4.5 Torr). Later, they were studied at rest and during various exercise intensities by using the multiple inert gas elimination technique in normoxia and hypoxia (13.2% O-2). During normoxia at 90% peak O-2 consumption, Pa-O2 was lower in E compared with C (87 +/- 4 vs. 97 +/- 6 Torr, P < 0.001) and alveolar-to-arterial O-2 tension difference (A-aD(O2)) was greater (33 +/- 4 vs. 23 +/- 1 Torr, P < 0.001). Diffusion limitation accounted for 23 (E) and 13 Torr (C) of the A-aD(O2) (P < 0.01). There were no significant differences between groups in arterial PCO2 (Pa-CO2) or ventilation-perfusion (VA/Q) inequality as measured by the log SD of the perfusion distribution (logSD(Q)). Stepwise multiple linear regression revealed that lung O-2 diffusing capacity (DLO2), logSD(Q), and Pa-CO2 each accounted for similar to 30% of the variance in Pa-O2 (r = 0.95, P < 0.001). These data suggest that EIH has a multifactorial etiology related to DLO2, VA/Q inequality, and ventilation.