Effect of prolonged, heavy exercise on pulmonary gas exchange in athletes

Abstract

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 O 2 uptake (V˙o 2 max ) = 63 ml ⋅ kg −1 ⋅ min −1 ] by using 5 min of cycling exercise at 30, 65, and 90%V˙o 2 max . Multiple inert-gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained. Resting log SD of the perfusion distribution (log SD Q˙ ) was normal [0.50 ± 0.03 (SE)] and increased with exercise (log SD Q˙ = 0.65 ± 0.04, P < 0.005), alveolar-arterial O 2 difference increased (to 24 ± 3 Torr), and end-capillary pulmonary diffusion limitation occurred at 90%V˙o 2 max . The subjects recovered for 30 min, then, after resting measurements were taken, exercised for 60 min at ∼65%V˙o 2 max . O 2 uptake, ventilation, cardiac output, and alveolar-arterial O 2 difference were unchanged after the first 5 min of this test, but log SD Q˙ 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 Q˙ 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.