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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 (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 O₂ difference increased (to 24 ± 3 Torr), and end-capillary pulmonary diffusion limitation occurred …