Faster adjustment of O2 delivery does not affect Vo2 on-kinetics in isolated in situ canine muscle

The mechanism(s) limiting muscle O-2 uptake ((V)over dot O-2) 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 (V)over dot O-2. Two conditions were mainly compared: 1) spontaneous adjustment of blood flow ((Q)over dot) [control, spontaneous (Q)over dot (C Spont)]; and 2) pump-perfused (Q)over dot, adjusted similar to 15 s before contractions at a constant level corresponding to the steady-state value during contractions in C Spent [faster adjustment of O-2 delivery (Fast O-2 Delivery)]. During Fast O-2 Delivery, 1-2 ml/min of 10(-2) M adenosine were infused intra-arterially to prevent inordinate pressure increases with the elevated (Q)over dot. The purpose of the study was to determine whether a faster adjustment of O-2 delivery would affect (V)over dot O-2 kinetics. (Q)over dot was measured continuously; arterial (Ca-O2) and popliteal venous (Cv(O2)) O-2 contents were determined at rest and at 5- to 7-s intervals during contractions; O-2 delivery was calculated as (Q)over dot.Ca-O2, and (V)over dot O-2 was calculated as (Q)over dot.arteriovenous O-2 content difference. Times to reach 63% of the difference between baseline and steady-state (V)over dot O-2 during contractions were 23.8 +/- 2.0 (SE s in C Spent and 21.8 +/- 0.9 s in Fast O-2 Delivery (not significant). In the present experimental model, elimination of any delay in O-2 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.