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

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

Purpose

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 recovery compared with that seen at the onset of contractions (time constant, τ  23 s, Behnke et al., 2002. Resp. Physiol.), i.e., on–off asymmetry.

Methods

Measurements of capillary red blood cell flux and microvascular pressure of O₂ (P_O2mv) were combined to resolve the temporal profile of muscle across the moderate intensity contractions-to-rest transition.

Results

Muscle decreased from an end-contracting value of 7.7 ± 0.2 ml/100 g/min to 1.7 ± 0.1 ml/100 g/min at the end of the 3 min recovery period, which was not different from pre-stimulation . Contrary to our hypothesis, muscle in recovery began to decrease immediately (i.e., time delay <2 s) and demonstrated rapid first-order kinetics (τ, 25.5 ± 2.6 s) 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.

Conclusions

The slowed Qm kinetics in recovery serves to elevate the ratio and thus microvascular P_O2. Whether this Qm response is obligatory to the rapid muscle kinetics and hence speeds the repletion of high-energy phosphates by maximizing conductive and diffusive O₂ flux is an important question that awaits resolution.