Exercise‐induced arterial hypoxaemia in healthy human subjects at sea level.

Abstract

The incidence of exercise-induced arterial hypoxemia and its determinants in 16 highly trained, healthy runners who were capable of achieving and sustaining very high metabolic rates (maximal O2 uptake 72 .+-. 2 ml kg-1 min-1 or 4.81 .+-. 0.131 min-1) were determined. Arterial blood gases and acid-base status were determined at each load of a progressive short-term exercise test and repeatedly during constant-load treadmill running while breathing air and during inhalation of mildly hypoxic, hyperoxic, and He enriched gases. Three types of responses to heavy and maximum exercise were evident and highly reproducible within subjects. Four runners maintained arterial PO2 (Pa,O2) within 10 mm Hg of resting values, another 4 showed 10-15 mm Hg reductions in Pa,O2, and the remaining 8 showed reductions of 21-35 mm Hg, i.e., in all cases to a Pa,O2 of less than 75 mm Hg and to less than 60 mm Hg in 2 cases. During constant-load excercise, Pa,O2 was often maintained during the initial 30 s when hyperventilation was greatest; then hypoxemia occurred and in most cases was either maintained or worsened over the ensuing 3-4 min. Hypoxemia may be attributed to a diffusion limitation secondary to very short red cell transit times in at least a portion of the pulmonary circulation. These excessively short transit times may occur at high metabolic rates if pulmonary capillary blood volume has achieved its maximum expansion at a time when pulmonary blood flow continues to increase.