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J Appl Physiol 85: 1556-1563, 1998;
8750-7587/98 $5.00
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Vol. 85, Issue 4, 1556-1563, October 1998

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

Claudette M. St. Croix, Craig A. Harms, Steven R. McClaran, Glenn A. Nickele, David F. Pegelow, William B. Nelson, and Jerome A. Dempsey

John Rankin Laboratory of Pulmonary Medicine, Department of Preventive Medicine, University of Wisconsin, Madison, Wisconsin 53705

Twenty-eight healthy women (ages 27.2 ± 6.4 yr) with widely varying fitness levels [maximal O2 consumption (VO2 max), 31-70 ml · kg-1 · min-1] first completed a progressive incremental treadmill test to VO2 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 PO2 (PaO2) near resting levels, whereas 22 subjects showed a >10 Torr decrease in PaO2 [78.0 ± 7.2 Torr, arterial O2 saturation (SaO2), 91.6 ± 2.4%], and alveolar-arterial O2 difference (A-aDO2, 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-aDO2 (-4.8 ± 3.8 Torr) and an increase in PaO2 (+5.9 ± 4.3 Torr) and SaO2 (+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.

maximal exercise; diffusion; repeat exercise effects


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