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 difference (Aa Po₂) to increase. Until recently, the physiological basis for this was considered to be mostly ventilation/perfusion (V̇_A/Q̇) 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, F_IO2, 0.13), normoxia (F_IO2, 0.21) and hyperoxia (F_IO2, 1.0) undertaken in balanced order on the same day in seven fit cyclists (V̇O_2max, 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/ 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 P_O2 and hypoxaemia during heavy exercise.