Pulmonary gas exchange during exercise in pigs

Abstract

Increased ventilation-perfusion (V̇A/Q̇) inequality is observed in ~50% of humans during heavy exercise and contributes to the widening of the alveolar-arterial O2 difference (A-aD(O2)). Despite extensive investigation, the cause remains unknown. As a first step to more direct examination of this problem, we developed an animal model. Eight Yucatan miniswine were studied at rest and during treadmill exercise at ~30, 50, and 85% of maximal O2 consumption (V̇O2(max)). Multiple inert-gas, blood-gas, and metabolic data were obtained. The A-aD(O2) increased from 0 ± 3 (SE) Torr at rest to 14 ± 2 Torr during the heaviest exercise level, but arterial PO2 (Pa(O2)) remained at resting levels during exercise. There was normal V̇A/Q̇ inequality [log SD of the perfusion distribution (logSD(Q̇)) = 0.42 ± 0.04] at rest, and moderate increases (logSD(Q̇) = 0.68 ± 0.04, P < 0.0001) were observed with exercise. This result was reproducible on a separate day. The V̇A/Q̇ inequality changes are similar to those reported in highly trained humans. However, in swine, unlike in humans, there was no inert gas evidence for pulmonary end-capillary diffusion limitation during heavy exercise; there was no systematic difference in the measured Pa(O2) and the Pa(O2) as predicted from the inert gases. These data suggest that the pig animal model is well suited for studying the mechanism of exercise- induced V̇A/Q̇ inequality.