Delayed Onset Muscle Soreness Does Not Alter O₂ Uptake Kinetics during Heavy-Intensity Cycling in Humans

Abstract

The purpose of this study was to determine if exercise-induced delayed onset muscle soreness (DOMS) would alter O2 uptake kinetics during heavy cycling in 9 untrained females. O2 uptake kinetics were characterised during 8-min of constant-load cycling performed with and without DOMS. DOMS was caused by completing 30 min of bench-stepping at a rate of 15 steps.min(-1). Two days after bench stepping, all subjects reported significant leg muscle soreness. Both phase II kinetics (without DOMS tau1: 26.6 +/- 2.4 s; with DOMS tau1: 27.2 +/- 3.7 s) and the slow component amplitude (without DOMS: 277 +/- 15 mL.min(-1); with DOMS: 291 +/- 21 mL.min(-1)) were unaffected by DOMS. The change in blood lactate concentration from rest to end-exercise was significantly greater during exercise performed with DOMS. Eccentric exercise causing a moderate degree of DOMS does not appear to impact upon the mechanisms mediating phase II or the slow component of O2 uptake kinetics.

Mechanism and implications of hyperpnea exaggeration at the onset of exercise in mechanical hyperalgesia after eccentric exercise

“…Pulmonary V ・ O2 at phase I is assumed to reflect circulatory transit time from active muscles to lungs 69) . The results of most previous studies indicate that muscle condition with DOMS does not impact the duration of phase I 11,14,70,71) . Phase III corresponds to the V ・ O2 steady state when moderate exercise is performed at a given work rate that is below the anaerobic threshold (AT).…”

“…For detailed information on the slow component, see Jones et al 72) . Previous experimental results regarding the effects of the DOMS condition on amplitude of the slow component have not been consistent 11,14,73) . Further studies are warranted because there have been few studies making reference to this topic.…”

“…Gleeson et al 13) and Schneider et al 14) suggested that this phenomenon is due to ventilatory compensation for greater blood lactacidosis after ECC. Gleeson et al 13) and Schneider et al 14) also presumed that increased afferent discharges from pain receptors or metaboreceptors and sensation of muscle pain or soreness affected ventilatory response to exercise after ECC. Davis et al 12,15) proposed that the augmentation of ventilatory response and reduction in the gas exchange threshold, at least during incremental exercise after ECC, are most likely evoked by increased activation of thin muscle afferents (without using the terms "pain receptor" and "pain sensation") stimulated via mechanical disruption of muscle fibers and local microvasculature, and are not the result of altered blood lactate.…”

“…On the other hand, in comparable concentric contractions yielding a similar metabolic response, hyperventilation has been observed during ECC 10) , though the slope of the relationship between ventilation and arterial blood CO2 partial pressure in concentric exercise and that in ECC are almost the same 9) . Regarding the effect of a prior bout of ECC on ventilatory response to exercise, some investigators reported that the response at phases II and III during constant load or incremental exercise a few days after ECC was exaggerated [11][12][13][14][15] . Gleeson et al 13) and Schneider et al 14) suggested that this phenomenon is due to ventilatory compensation for greater blood lactacidosis after ECC.…”

“…Regarding the effect of a prior bout of ECC on ventilatory response to exercise, some investigators reported that the response at phases II and III during constant load or incremental exercise a few days after ECC was exaggerated [11][12][13][14][15] . Gleeson et al 13) and Schneider et al 14) suggested that this phenomenon is due to ventilatory compensation for greater blood lactacidosis after ECC. Gleeson et al 13) and Schneider et al 14) also presumed that increased afferent discharges from pain receptors or metaboreceptors and sensation of muscle pain or soreness affected ventilatory response to exercise after ECC.…”