Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial Po 2 (PaO2 ) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O2 uptake (V˙o 2 max) = 51 ml · kg−1 · min−1]. They were studied in random order (C or R), with a fastV˙o 2 max protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% ofV˙o 2 max (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in V˙o 2 maxbetween R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of V˙o 2 max. At 90% ofV˙o 2 max, PaO2 was lower during R (mean ± SE = 94 ± 2 Torr) than during C (105 ± 2 Torr, P < 0.0001), as was ventilation (85.2 ± 3.8 vs. 98.2 ± 4.4 l/min btps, P < 0.0001) and cardiac output (19.1 ± 0.6 vs. 21.1 ± 1.0 l/min, P < 0.001). Arterial Pco 2 (32.0 ± 0.5 vs. 30.0 ± 0.6 Torr, P < 0.001) and alveolar-arterial O2 difference (A-aDo 2; 22 ± 2 vs. 16 ± 2 Torr, P < 0.0001) were greater during R. PaO2 and A-aDo 2 were similar between slow and fast. Nadir PaO2 was ≤80 Torr in four women (24%) but only during fast-R. In all subjects, PaO2 atV˙o 2 max was greater than the lower 95% prediction limit calculated from available data in men ( n = 72 C and 38 R) for both R and C. These data suggest intrinsic differences in gas exchange between R and C, due to differences in ventilation and also efficiency of gas exchange. The PaO2 responses to R and C exercise in our 17 subjects do not differ significantly from those previously observed in men.
