Recovery dynamics of skeletal muscle oxygen uptake during the exercise off-transient

The time course of muscle .V(O2) recovery from contractions (i.e., muscle .V(O2) off-kinetics), measured directly at the site of O(2) exchange, i.e., in the microcirculation, is unknown. Whereas biochemical models based upon creatine kinase flux rates predict slower .V(O2) off- than on-transients [Kushmerick, M.J., 1998. Comp. Biochem. Physiol. B: Biochem. Mol. Biol.], whole muscle .V(O2) data [Krustrup, et al. J. Physiol.] suggest on-off symmetry.

We tested the hypothesis that the slowed recovery blood flow (Qm) kinetics profile in the spinotrapezius muscle [Ferreira et al., 2006. J. Physiol.] was associated with a slowed muscle .V(O2) recovery compared with that seen at the onset of contractions (time constant, tau approximately 23s, Behnke et al., 2002. Resp. Physiol.), i.e., on-off asymmetry.

Measurements of capillary red blood cell flux and microvascular pressure of O(2) (P(O2) mv) were combined to resolve the temporal profile of muscle .V(O2) across the moderate intensity contractions-to-rest transition.

Muscle .V(O2) decreased from an end-contracting value of 7.7+/-0.2 ml/100 g/min to 1.7+/-0.1 ml/100g/min at the end of the 3 min recovery period, which was not different from pre-stimulation .V(O2). Contrary to our hypothesis, muscle .V(O2) in recovery began to decrease immediately (i.e., time delay <2s) and demonstrated rapid first-order kinetics (tau, 25.5+/-2.6s) not different (i.e., symmetrical to) to those during the on-transient. This resulted in a systematic increase in microvascular P(O2) during the recovery from contractions.

The slowed Qm kinetics in recovery serves to elevate the Qm/.V(O2) ratio and thus microvascular P(O2) . Whether this Qm response is obligatory to the rapid muscle .V(O2) kinetics and hence speeds the repletion of high-energy phosphates by maximizing conductive and diffusive O(2) flux is an important question that awaits resolution.