The purpose of this study was to examine O 2 uptake (VO 2) on-kinetics when the spontaneous blood flow (and therefore O 2 delivery) onresponse was slowed by 25 and 50 s. The isolated gastrocnemius muscle complex (GS) in situ was studied in six anesthetized dogs during transitions from rest to a submaximal metabolic rate (̃50- 70% of peak VO 2). Four trials were performed: 1) a pretrial in which resting and steady-state blood flows were established, 2) a control trial in which the blood flow on-kinetics mean response time (MRT) was set at 20 s (CT20), 3) an experimental trial in which the blood flow on-kinetics MRT was set at 45 s (EX45), and 4) an experimental trial in which the blood flow on-kinetics MRT was set at 70 s (EX70). Slowing O 2 delivery via slowing blood flow on-kinetics resulted in a linear slowing of the VO 2 on-kinetics response (R = 0.96). Average MRT values for CT20, EX45, and EX70 VO 2 on-kinetics were (means ± SD) 17 ± 2, 23 ± 4, and 26 ± 3 s, respectively (P < 0.05 among all). During these transitions, slowing blood flow resulted in greater muscle deoxygenation (as indicated by near-infrared spectroscopy), suggesting that lower intracellular PO 2 values were reached. In this oxidative muscle, VO 2 and O 2 delivery were closely matched during the transition period from rest to steady-state contractions. In conjunction with our previous work showing that speeding O 2 delivery did not alter VO 2 on-kinetics under similar conditions, it appears that spontaneously perfused skeletal muscle operates at the nexus of sufficient and insufficient O 2 delivery in the transition from rest to contractions.
- Blood flow
- Muscle contractions