What is the clinical evidence from this study?

Study design: Other. Population: Healthy (canine model) (n=7). Intervention: Faster adjustment of O2 delivery (pump-perfused constant blood flow) vs. Spontaneous adjustment of blood flow. Primary outcome: Time to reach 63% of the difference between baseline and steady-state VO2 during contractions (t63% in seconds) (p=not significant).

October 1, 1998Journal of Applied Physiology252 citations

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

BGBruno GrassiUniversity of Udine LGL. Bruce GladdenAuburn University MSMichele SamajaUniversity of Milan

Key Result

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).

Structured PICO

Does faster adjustment of O2 delivery improve VO2 on-kinetics in isolated in situ canine muscle?

Population

7 adult mongrel dogs undergoing isolated in situ gastrocnemius muscle preparation to investigate the mechanism limiting muscle O2 uptake kinetics.

Intervention

Pump-perfused blood flow (Q) adjusted ~15 s before contractions at a constant level corresponding to the steady-state value during contractions, with intra-arterial adenosine (1-2 ml/min of 10^-2 M) to prevent pressure increases (Fast O2 Delivery).

Comparator

Spontaneous adjustment of blood flow (C Spont) and pump-perfused Q manually regulated to maintain constant perfusion pressure (C Pump).

Outcome

Time to reach 63% of the difference between baseline and steady-state VO2 during contractions.surrogate

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.

Main Result

Absolute Event Rate: 21.8% vs 23.8%

p-value: p=not significant

Limitations

The contraction pattern utilized was unphysiological.
Fiber type composition of dog gastrocnemius muscle is different compared with that of human muscle.
Resting blood flow to muscle in control conditions was 6- to 10-fold higher than those observed in humans.
The metabolic transition considered was from rest to submaximal contractions, so results might not apply to other transitions.
Cannot exclude that intramuscular blood flow patterns could be somewhat different from those obtained in animals in vivo due to acute denervation.
Peripheral diffusion of O2 from red blood cells to mitochondria could not be evaluated
Intramuscular O2 stores could not be evaluated

Abstract

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.

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