Muscle oxygenation does not affect the prior exercise effect

Abstract

The controlling factors responsible for the "turn-on‟ of oxidative phosphorylation at the onset of exercise (VO2 on-kinetics) are controversial. Current hypotheses center on delayed O2 delivery, the build-up of respiratory stimuli, and a combination of the two. Recently, speeded VO2 on-kinetics after priming exercise have further fueled the debate over controlling factors. However, investigations into the mechanistic controllers of the prior exercise effect in exercising humans are limited by experimental techniques. It was the purpose of this study to examine the prior exercise effect in the highly-oxidative canine gastrocnemius muscle complex (gastrocnemius plus superficial digital flexor; GS) contracting in situ. With arterial [O2] maintained constant, a step change in metabolic rate was elicited by stimulating canine GS muscles (n=5) via their sciatic nerves (6-8 V, 0.2 ms duration, 50 Hz, 200 ms train) at a rate of 2 contractions / 3 s for two, 2-min bouts separated by 2 min of recovery. VO2 on-kinetics were determined during both of these bouts for four experimental conditions: spontaneous adjustment of self perfused blood flow (spontaneous); maximized O2 availability (elevated flow) in which blood flow was maintained at the end-contractile level throughout recovery and the second bout of contractions; maximized metabolic respiratory stimuli (resting flow) in which blood flow was rapidly returned to the pre-contractile level during recovery and the on-kinetics were the same between contractile bouts; and maximization of both metabolic respiratory stimuli and O2 availability (additive) which was identical to the resting flow condition with the exception that blood flow was increased rapidly at the onset of the second bout. Near infrared spectroscopy (NIRS) was used to monitor muscle oxygenation ([O2Hb] and [HHb]). Despite significant alterations in [O2Hb] prior to the second contractile bout, tau remained unaltered (means: 11.8 vs. 10.6 s) for each condition. Time delay (mean: 6.2 s) and correspondingly mean response time (mean: 18.0 s) were significantly (p<0.05) speeded during bout 2 (mean: 1.9 and 12.5 s, respectively) and the amplitude of the VO2 slow component was significantly reduced in all conditions after priming contractions (means: 11.0 vs. 28.2 mlO2•kg-1•min-1). These data indicate that altered O2 delivery and muscle oxygenation as assessed by NIRS do not play a role in the prior exercise effect in highly-oxidative skeletal muscle. Thus, the prior exercise effect likely has its origin in elevations in metabolic respiratory stimuli prior to the second contractile bout (evidenced by an elevated bout 2 baseline VO2 for all conditions). These data also provide evidence that reductions in the slow component amplitude after priming contractions do not require altered motor unit recruitment as has been suggested for human exercise.