The contribution of intrapulmonary shunts to the alveolar-to-arterial oxygen difference during exercise is very small

Exercise is well known to cause arterial PO2 to fall and the alveolar-arterial PO2 difference(Aa PO2 ) to increase. Until recently, the physiological basis for this was considered to be mostly ventilation/perfusion ((.)VA/(.)Q) inequality and alveolar-capillary diffusion limitation. Recently, arterio-venous shunting through dilated pulmonary blood vessels has been proposed to explain a significant part of the Aa PO2 during exercise. To test this hypothesis we determined venous admixture during 5 min of near-maximal, constant-load, exercise in hypoxia (in inspired O2 fraction, FIO2 , 0.13), normoxia (FIO2 , 0.21) and hyperoxia (FIO2 , 1.0) undertaken in balanced order on the same day in seven fit cyclists ((.)VO2max, 61.3 +/- 2.4 ml kg(-1) min(-1); mean +/- S.E.M.). Venous admixture reflects three causes of hypoxaemia combined: true shunt, diffusion limitation and ((.)VA/(.)Q) inequality. In hypoxia, venous admixture was 22.8 +/- 2.5% of the cardiac output; in normoxia it was 3.5 +/- 0.5%; in hyperoxia it was 0.5 +/- 0.2%. Since only true shunt accounts for venous admixture while breathing 100% O2, the present study suggests that shunt accounts for only a very small portion of the observed venous admixture, Aa PO2 and hypoxaemia during heavy exercise.