Elimination of any delay in O2 delivery during the rest-to-contraction transition did not significantly affect muscle VO2 on-kinetics in isolated canine muscle (21.8 vs 23.8 seconds).
Does faster adjustment of O2 delivery improve VO2 on-kinetics in isolated in situ canine muscle?
Elimination of any delay in O2 delivery during the rest-to-contraction transition did not affect muscle VO2 kinetics, suggesting that these kinetics are mainly set by an intrinsic inertia of oxidative metabolism.
Absolute Event Rate: 21.8% vs 23.8%
p-value: p=not significant
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 V(O2)). Two conditions were mainly compared: 1) spontaneous adjustment of blood flow (Q) control, spontaneous Q (C Spont); and 2) pump-perfused Q, adjusted approximately 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 V(O2) kinetics. Q 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 Q x Ca(O2), and V(O2) was calculated as Q x 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 V(O2) kinetics, which suggests that this kinetics was mainly set by an intrinsic inertia of oxidative metabolism.
Grassi et al. (1998) studied Healthy (canine model) (n=7). Faster adjustment of O2 delivery (pump-perfused constant blood flow) vs. Spontaneous adjustment of blood flow was evaluated on Time to reach 63% of the difference between baseline and steady-state VO2 during contractions (t63% in seconds) (p=not significant). Elimination of any delay in O2 delivery during the rest-to-contraction transition did not significantly affect muscle VO2 on-kinetics in isolated canine muscle (21.8 vs 23.8 seconds).