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1 Division of Physiology, Department of Medicine, University of California, San Diego, La Jolla, California 92093; 2 Department of Thoracic Medicine, University of Crete, Heraklion 711 10 Crete, Greece; and 3 Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, California 92354
During maximal
exercise, ventilation-perfusion inequality increases, especially in
athletes. The mechanism remains speculative. We
hypothesized that, if interstitial pulmonary edema is involved, prolonged exercise would result in increasing ventilation-perfusion inequality over time by exposing the pulmonary vascular bed to high
pressures for a long duration. The response to short-term exercise was
first characterized in six male athletes [maximal O2 uptake
(
O2 max) = 63 ml · kg
1 · min1] by using 5 min
of cycling exercise at 30, 65, and 90%
O2 max. Multiple inert-gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained. Resting log SD of the perfusion distribution (log
SD
) was normal [0.50 ± 0.03 (SE)] and increased with exercise (log
SD = 0.65 ± 0.04, P < 0.005), alveolar-arterial
O2 difference increased (to 24 ± 3 Torr), and end-capillary pulmonary diffusion limitation occurred at 90%
O2 max. The subjects
recovered for 30 min, then, after resting measurements were taken,
exercised for 60 min at ~65%
O2 max.
O2 uptake, ventilation, cardiac
output, and alveolar-arterial O2
difference were unchanged after the first 5 min of this test, but log
SD increased from
0.59 ± 0.03 at 5 min to 0.66 ± 0.05 at 60 min
(P < 0.05), without pulmonary diffusion limitation. Log
SD was negatively
related to total lung capacity normalized for body surface area
(r = 
0.97,
P < 0.005 at 60 min). These data are compatible with interstitial edema as a mechanism and suggest that lung
size is an important determinant of the efficiency of gas exchange
during exercise.
multiple inert-gas elimination technique; interstitial pulmonary edema
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