Effects of prior exercise on exercise-induced arterial hypoxemia in young women

Abstract

Twenty-eight healthy women (ages 27.2 ± 6.4 yr) with widely varying fitness levels [maximal O2consumption (V˙o 2 max), 31–70 ml ⋅ kg−1 ⋅ min−1] first completed a progressive incremental treadmill test toV˙o 2 max (total duration, 13.3 ± 1.4 min; 97 ± 37 s at maximal workload), rested for 20 min, and then completed a constant-load treadmill test at maximal workload (total duration, 143 ± 31 s). At the termination of the progressive test, 6 subjects had maintained arterial [Formula: see text] [Formula: see text]) near resting levels, whereas 22 subjects showed a >10 Torr decrease in[Formula: see text] [78.0 ± 7.2 Torr, arterial O2 saturation[Formula: see text]), 91.6 ± 2.4%], and alveolar-arterial O2 difference (A-[Formula: see text], 39.2 ± 7.4 Torr). During the subsequent constant-load test, all subjects, regardless of their degree of exercise-induced arterial hypoxemia (EIAH) during the progressive test, showed a nearly identical effect of a narrowed A-[Formula: see text](−4.8 ± 3.8 Torr) and an increase in[Formula: see text] (+5.9 ± 4.3 Torr) and[Formula: see text] (+1.6 ± 1.7%) compared with at the end point of the progressive test. Therefore, EIAH during maximal exercise was lessened, not enhanced, by prior exercise, consistent with the hypothesis that EIAH is not caused by a mechanism which persists after the initial exercise period and is aggravated by subsequent exercise, as might be expected of exercise-induced structural alterations at the alveolar-capillary interface. Rather, these findings in habitually active young women point to a functionally based mechanism for EIAH that is present only during the exercise period.