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J Appl Physiol 85: 1394-1403, 1998;
8750-7587/98 $5.00
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Vol. 85, Issue 4, 1394-1403, October 1998

Faster adjustment of O2 delivery does not affect VO2 on-kinetics in isolated in situ canine muscle

Bruno Grassi, L. Bruce Gladden, Michele Samaja, Creed M. Stary, 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); Department of Health and Human Performance, Auburn University, Auburn, Alabama 36849-5323; and Dipartimento di Scienze e Tecnologie Biomediche, Università di Milano, I-20090 Segrate (MI), Italy

The mechanism(s) limiting muscle O2 uptake (VO2) kinetics was investigated in isolated canine gastrocnemius muscles (n = 7) during transitions from rest to 3 min of electrically stimulated isometric tetanic contractions (200-ms trains, 50 Hz; 1 contraction/2 s; 60-70% of peak VO2). Two conditions were mainly compared: 1) spontaneous adjustment of blood flow (Q) [control, spontaneous Q (C Spont)]; and 2) pump-perfused Q, adjusted ~15 s before contractions at a constant level corresponding to the steady-state value during contractions in C Spont [faster adjustment of O2 delivery (Fast O2 Delivery)]. During Fast O2 Delivery, 1-2 ml/min of 10-2 M adenosine were infused intra-arterially to prevent inordinate pressure increases with the elevated Q. The purpose of the study was to determine whether a faster adjustment of O2 delivery would affect VO2 kinetics. Q was measured continuously; arterial (CaO2) and popliteal venous (CvO2) O2 contents were determined at rest and at 5- to 7-s intervals during contractions; O2 delivery was calculated as Q · CaO2, and VO2 was calculated as Q · arteriovenous O2 content difference. Times to reach 63% of the difference between baseline and steady-state VO2 during contractions were 23.8 ± 2.0 (SE) s in C Spont and 21.8 ± 0.9 s in Fast O2 Delivery (not significant). In the present experimental model, elimination of any delay in O2 delivery during the rest-to-contraction transition did not affect muscle VO2 kinetics, which suggests that this kinetics was mainly set by an intrinsic inertia of oxidative metabolism.

gas exchange kinetics; muscle oxidative metabolism; submaximal exercise


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