Abstract

Arterial oxygenation is well maintained in healthy untrained or moderately trained individuals during exercise. In contrast, approximately 40 to 50 of healthy elite endurance athletes (cyclists and runners) demonstrate a significant reduction in arterial oxygenation during exercise at work rates approaching VO2max. The mechanism(s) to explain this exercise-induced hypoxaemia (EIH) remain controversial. However, hypoventilation and venoarterial shunt do not appear to be involved. By elimination, this suggests that ventilation-perfusion inequality and/or pulmonary diffusion limitations must contribute to EIH in this population. Theoretical and direct experimental evidence exists to support the notion that both ventilation-perfusion inequality and diffusion disequilibrium contribute to EIH. However, the relative contribution of each factor remains to be determined. In athletes who exhibit a profound EIH, the exercise-induced decline in arterial oxygenation results in a limitation of VO2max. Further, athletes who exhibit EIH at sea level suffer more severe gas exchange impairements during short term exposure to altitude than athletes or nonathletes who do not exhibit EIH at sea level. This finding explains much of the observed variance in the decline in VO2max among individuals during short term altitude or hypoxia exposure. Verf.-Referat