In:
Journal of Applied Physiology, American Physiological Society, Vol. 86, No. 1 ( 1999-01-01), p. 93-100
Abstract:
Increased ventilation-perfusion (V˙a/Q˙) inequality is observed in ∼50% of humans during heavy exercise and contributes to the widening of the alveolar-arterial O 2 difference (A-[Formula: see text]). 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 O 2 consumption (V˙o 2 max ). Multiple inert-gas, blood-gas, and metabolic data were obtained. The A-[Formula: see text]increased from 0 ± 3 (SE) Torr at rest to 14 ± 2 Torr during the heaviest exercise level, but arterial[Formula: see text] ([Formula: see text]) remained at resting levels during exercise. There was normalV˙a/Q˙inequality [log SD of the perfusion distribution (log[Formula: see text] ) = 0.42 ± 0.04] at rest, and moderate increases (log[Formula: see text] = 0.68 ± 0.04, P 〈 0.0001) were observed with exercise. This result was reproducible on a separate day. TheV˙a/Q˙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[Formula: see text] and the[Formula: see text] as predicted from the inert gases. These data suggest that the pig animal model is well suited for studying the mechanism of exercise-inducedV˙a/Q˙inequality.
Type of Medium:
Online Resource
ISSN:
8750-7587
,
1522-1601
DOI:
10.1152/jappl.1999.86.1.93
Language:
English
Publisher:
American Physiological Society
Publication Date:
1999
detail.hit.zdb_id:
1404365-8
SSG:
12
SSG:
31
