ABSTRACT
At high exercise intensities elite athletes not infrequently demonstrate a fall in arterial levels of oxygen. The explanation for this hypoxemia, which potentially might diminish exercise performance, is uncertain. Among the candidate explanations: pulmonary edema secondary to disruption of capillary-alveolar membranes, limitations of capillary-alveolar membrane diffusion of oxygen due to decreased lung transit time, bronchospasm, and increased pulmonary secretions. It is well-recognized that Thoroughbred racehorses, as well as other animals bred for racing, often develop pulmonary edema/hemorrhage as well as arterial hypoxemia during races. It is not inconceivable that the pulmonary abnormalities observed in elite human athletes during high levels of exercise reflect the etiological mechanisms underlying the ventilatory derangements of these highly bred animals. This chapter examines the proposed mechanisms underlying exercise-induced arterial hypoxemia and pulmonary hemorrhage/edema in both humans and racehorses. In surveying these data, one is left with a puzzling question: why is the lung so poorly adapted to exercise?
