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exercise and ventilation. This can increase the O2 cost of ventilation to over 15% of the whole-body VO2 in an elite athlete during maximum exercise; however, whole-body VO2 increases more than the O2 cost of breathing, so respiratory mechanics do not limit VO2max in elite athletes, either.

Although mechanical limitations do not cause hypoventilation, pulmonary gas exchange becomes less efficient during heavy exercise for other reasons. During light levels of exercise, gas exchange may actually improve as indicated by a decrease in the alveolar-arterial PO2 (Chapter 21). This is because ventilation-perfusion matching improves when blood flow increases to the tops of the lungs when cardiac output and pulmonary artery pressure increase during exercise (Chapter 18). At higher levels of exercise (VO2 > 3 L/min), however, all of the pulmonary capillaries are recruited and distended, so further increases in cardiac output and pulmonary artery pressure only lead to interstitial edema. This makes the distribution of blood flow more heterogeneous and worsens ventilation-perfusion matching.

Interstitial edema can also impair diffusion by thickening the blood-gas barrier. The lung diffusing capacity for carbon monoxide (DLCO ) decreases in runners after competing in a marathon. At VO2 levels > 3 L/min, diffusion limitation explains over half of the alveolar-arterial PO difference and becomes more important than ventilation-perfusion matching in determining the efficacy of gas exchange. Decreased transit times for red blood cells in the pulmonary capillaries and the decreased mixed-venous PO2 under these conditions could cause diffusion limitations at high levels of VO2 even if the blood-gas barrier was not thickened. Shunt does not change during exercise but an existing shunt can contribute to more arterial hypoxemia because mixed-venous PO2 decreases during exercise.

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