Faster adjustment of O-2 delivery does not affect Vo(2) on-kinetics in isolated in situ canine muscle

The mechanism(s) limiting muscle O2 uptake (V̇O2) 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 V̇O2). Two conditions were mainly compared: 1) spontaneous adjustment of blood flow (Q̇) [control, spontaneous Q̇ (C Spont)]; and 2) pump-perfused Q̇, 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 Q̇. The purpose of the study was to determine whether a faster adjustment of O2 delivery would affect V̇O2 kinetics. Q̇ was measured continuously; arterial (Ca(O2)) and popliteal venous (CV(O2)) O2 contents were determined at rest and at 5- to 7-s intervals during contractions; O2 delivery was calculated as Q̇ · Ca(O2), and V̇O2 was calculated as Q̇ · arteriovenous O2 content difference. Times to reach 63% of the difference between baseline and steady-state V̇O2 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 V̇O2 kinetics, which suggests that this kinetics was mainly set by an intrinsic inertia of oxidative metabolism.