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

Abstract

Grassi, Bruno, L. Bruce Gladden, Michele Samaja, Creed M. Stary, and Michael C. Hogan. Faster adjustment of O 2 delivery does not affect V O 2 on-kinetics in isolated in situ canine muscle. J. Appl. Physiol. 85(4): 1394-1403, 1998.-The mechanism(s) limiting muscle O 2 uptake (V O 2 ) kinetics was investigated in isolated canine gastrocnemius muscles (n ϭ 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 O 2 ). Two conditions were mainly compared: 1) spontaneous adjustment of blood flow (Q ) [control, spontaneous Q (C Spont)]; and 2) pump-perfused Q , adjusted ϳ15 s before contractions at a constant level corresponding to the steady-state value during contractions in C Spont [faster adjustment of O 2 delivery (Fast O 2 Delivery)]. During Fast O 2 Delivery, 1-2 ml/min of 10 Ϫ2 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 O 2 delivery would affect V O 2 kinetics. Q was measured continuously; arterial (Ca O 2 ) and popliteal venous (Cv O 2 ) O 2 contents were determined at rest and at 5-to 7-s intervals during contractions; O 2 delivery was calculated as Q ·Ca O 2 , and V O 2 was calculated as Q · arteriovenous O 2 content difference. Times to reach 63% of the difference between baseline and steady-state V O 2 during contractions were 23.8 Ϯ 2.0 (SE) s in C Spont and 21.8 Ϯ 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-tocontraction transition did not affect muscle V O 2 kinetics, which suggests that this kinetics was mainly set by an intrinsic inertia of oxidative metabolism. gas exchange kinetics; muscle oxidative metabolism; submaximal exercise IT HAS BEEN KNOWN FOR DECADES that on a step transition from rest to exercise, or from a lower to a higher workload, O 2 uptake (V O 2 ) lags behind the power output increase (12), following a time course usually termed V O 2 on-kinetics. The mechanism(s) determining this kinetics has been a matter of considerable debate, mainly between those who consider it mainly related to the rate of adjustment of O 2 delivery to the exercising muscles (13-15) and those who support the concept that V O 2 on-kinetics is mainly set by an inertia of intramuscular oxidative metabolism (3, 32).An experimental approach to discriminate between the two conflicting hypotheses would be to increase the rate of adjustment of O 2 delivery to muscles and then determine whether the V O 2 on-kinetics becomes faster or not. Unfortunately, previous studies conducted following this approach yielded conflicting results. Hughson and co-workers (14), for example, described a significantly faster V O 2 on-kinetics when their subjects cycled in a supine position during the application of lower body negative pressure, which presumably enhanced the rate of O 2 delivery to the exercis...

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