Faster adjustment of O₂delivery does not affect V˙o ₂ on-kinetics in isolated in situ canine muscle

The mechanism(s) limiting muscle O₂ uptake (V˙o₂) 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 peakV˙o₂). Two conditions were mainly compared: 1) spontaneous adjustment of blood flow (Q˙) [control, spontaneousQ˙ (C Spont)]; and2) pump-perfusedQ˙, 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 affectV˙o₂ kinetics.Q˙ was measured continuously; arterial (${\text{Ca}}_{O_2}$ ) and popliteal venous (${\text{Cv}}_{O_2}$ ) O₂ contents were determined at rest and at 5- to 7-s intervals during contractions; O₂ delivery was calculated asQ˙ ⋅ ${\text{Ca}}_{O_2}$ , and V˙o₂ was calculated asQ˙ ⋅ arteriovenous O₂ content difference. Times to reach 63% of the difference between baseline and steady-stateV˙o₂ 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 muscleV˙o₂ kinetics, which suggests that this kinetics was mainly set by an intrinsic inertia of oxidative metabolism.