Journal of Applied Physiology AJP: Heart and Circulatory Physiology
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J Appl Physiol 85: 1404-1412, 1998;
8750-7587/98 $5.00
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Vol. 85, Issue 4, 1404-1412, October 1998

Peripheral O2 diffusion does not affect VO2 on-kinetics in isolated in situ canine muscle

Bruno Grassi, L. Bruce Gladden, Creed M. Stary, Peter D. Wagner, and Michael C. Hogan

Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623; Istituto di Tecnologie Biomediche Avanzate, Consiglio Nazionale delle Ricerche, I-20090 Segrate (MI), Italy; and Department of Health and Human Performance, Auburn University, Auburn, Alabama 36849-5323

To test the hypothesis that muscle O2 uptake (VO2) on-kinetics is limited, at least in part, by peripheral O2 diffusion, we determined the VO2 on-kinetics in 1) normoxia (Control); 2) hyperoxic gas breathing (Hyperoxia); and 3) hyperoxia and the administration of a drug (RSR-13, Allos Therapeutics), which right-shifts the Hb-O2 dissociation curve (Hyperoxia+RSR-13). The study was conducted in isolated canine gastrocnemius muscles (n = 5) during transitions from rest to 3 min of electrically stimulated isometric tetanic contractions (200-ms trains, 50 Hz; 1 contraction/2 s; 60-70% peak VO2). In all conditions, before and during contractions, muscle was pump perfused with constantly elevated blood flow (Q), at a level measured at steady state during contractions in preliminary trials with spontaneous Q. Adenosine was infused intra-arterially to prevent inordinate pressure increases with the elevated Q. Q was measured continuously, arterial and popliteal venous O2 concentrations were determined at rest and at 5- to 7-s intervals during contractions, and VO2 was calculated as Q · arteriovenous O2 content difference. PO2 at 50% HbO2 saturation (P50) was calculated. Mean capillary PO2 (<OVL>P</OVL>cO2) was estimated by numerical integration. P50 was higher in Hyperoxia+RSR-13 [40 ± 1 (SE) Torr] than in Control and in Hyperoxia (31 ± 1 Torr). After 15 s of contractions, <OVL>P</OVL>cO2 was higher in Hyperoxia (97 ± 9 Torr) vs. Control (53 ± 3 Torr) and in Hyperoxia+RSR-13 (197 ± 39 Torr) vs. Hyperoxia. The time to reach 63% of the difference between baseline and steady-state VO2 during contractions was 24.7 ± 2.7 s in Control, 26.3 ± 0.8 s in Hyperoxia, and 24.7 ± 1.1 s in Hyperoxia+RSR-13 (not significant). Enhancement of peripheral O2 diffusion (obtained by increased <OVL>P</OVL>cO2 at constant O2 delivery) during the rest-to-contraction (60-70% of peak VO2) transition did not affect muscle VO2 on-kinetics.

gas exchange kinetics; submaximal exercise; muscle oxidative metabolism


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