Abstract

The purpose of this study was to test the hypothesis that the exercise-induced hypoxemia observed in endurance athletes is due to a reduction in the mean red blood cell pulmonary capillary transit time consequent to a plateau in pulmonary capillary blood volume (Vc) as exercise intensity progresses from moderate to heavy levels. Measurements of Vc, mean transit time, arterial O2 tension (PaO2), and end tidal-arterial O2 tension difference (AaDO2) were made in 16 subjects (mean maximal oxygen uptake (VO2max) = 4.90 l.min-1) at rest and during five cycle exercise bouts designed to elicit 55, 65, 75, 85, and 95% VO2max. Mean PaO2 fell from 101 mm Hg at rest to 85 mm Hg during heavy exercise. Mean AaDO2 increased linearly from one stage to the next and at the highest work rate equaled 22.3 mm Hg. Mean Vc failed to plateau with increasing exercise intensity and increased on average by 16 ml from one stage to the next. Mean transit time, on average, dropped from 1.05 s at rest to 0.46 s at the lowest work rate. Mean transit time did not decrease further with increasing exercise intensity (range, 0.42-0.46 s). We conclude that, under the conditions of this study, the AaDO2 increases and PaO2 decreases observed in endurance athletes during exercise of increasing intensity is not caused by a plateau in Vc and a consequent reduction in mean transit time.

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