Abstract

The time course of muscle V̇O2 recovery (i.e., muscle V̇O2 kinetics) from contractions, measured at the site of O2 exchange i.e., in the microcirculation, is unknown. It is known that, in the rat spinotrapezius muscle, blood flow (Qm) kinetics are slower in recovery (time constant, t ~41 s) than at the onset of contractions (t ~17 s, Ferreira et al. J. Physiol. 2006).PurposeWe tested the hypothesis that this Qm kinetics profile was associated with a slowed m V̇O2 recovery compared with that seen at the onset of contractions (t ~23 s, Behnke et al. Resp. Physiol. 2002).MethodsMeasurements of capillary red blood cell flux and microvascular PO2 (PO2) were combined to resolve the time course of muscle V̇O2across the moderate intensity contractions‐to‐rest transition.ResultsContrary to our hypothesis, in recovery muscle V̇O2 began to decrease immediately (i.e., time delay 0 s in all but one animal) and demonstrated rapid first order‐kinetics (t 22.4 ± 2.1 s).ConclusionsThe slowed Qm kinetics in recovery serves to elevate the Qm/ V̇O2 ratio and thus microvascular PO2. Whether this Qm response is obligatory to the rapid muscle V̇O2 kinetics and hence speeds the repletion of high‐energy phosphates by maximizing conductive and diffusive O2 flux is an important question that awaits resolution. Support NIH AG031327.

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