Pulmonary gas exchange during exercise in pigs

Increased ventilation-perfusion ((V) over dotA/(Q) over dot) inequality is observed in similar to 50% of humans during heavy exercise and contributes to the widening of the alveolar-arterial O-2 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 similar to 30, 50, and 85% of maximal O-2 consumption ((V) over dot O-2max). 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 (V) over dotA/(Q) over dot inequality [log SD of the perfusion distribution (logSD((Q) over dot)) = 0.42 +/- 0.04] at rest, and moderate increases (logSD((Q) over dot) = 0.68 +/- 0.04, P < 0.0001) were observed with exercise. This result was reproducible on a separate day. The (V) over dotA/(Q) over dot 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 ts well suited for studying the mechanism of exercise-induced (V) over dotA/(Q) over dot inequality.