EFFECTS OF PRIOR EXERCISE ON EXERCISE-INDUCED ARTERIAL HYPOXEMIA IN YOUNG-WOMEN

Twenty-eight healthy women (ages 27.2 +/- 6.4 yr) with widely varying fitness levels [maximal O-2 consumption (Vo(2max)), 31-70 ml . kg(-1) . min(-1)] first completed a progressive incremental treadmill test to Vo(2max) (total duration, 13.3 +/- 1.4 min; 97 +/- 37 s at maximal wo rkload), rested for 20 min, and then completed a constant-load treadmi ll test at maximal workload (total duration, 143 +/- 31 s). At the ter mination of the progressive test, 6 subjects had maintained arterial P -O2 (Pa-O2) near resting levels, whereas 22 subjects showed a >10 Torr decrease in Pa-O2 [78.0 +/- 7.2 Torr, arterial O-2 saturation (Sa(O2) ), 91.6 +/- 2.4%], and alveolar-arterial O-2 difference (A-aD(O2), 39. 2 +/- 7.4 Torr). During the subsequent constant-load test, all subject s, regardless of their degree of exercise-induced arterial hypoxemia ( EIAH) during the progressive test, showed a nearly identical effect of a narrowed A-aD(O2) (-4.8 +/- 3.8 Torr) and an increase in Pa-O2 (+5. 9 +/- 4.3 Torr) and Sa(O2) (+1.6 +/- 1.7%) compared with at the end po int of the progressive test. Therefore, EIAH during maximal exercise w as lessened, not enhanced, by prior exercise, consistent with the hypo thesis 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 al veolar-capillary interface. Rather, these findings in habitually activ e young women point to a functionally based mechanism for EIAH that is present only during the exercise period.