Effect of eccentric exercise-induced muscle damage on the dynamics of muscle oxygenation and pulmonary oxygen uptake

Abstract

Unaccustomed eccentric exercise has a profound impact on muscle structure and function. However, it is not known whether associated microvascular dysfunction disrupts the matching of O2 delivery (Qo2) to O2 utilization (Vo2). Near-infrared spectroscopy (NIRS) was used to test the hypothesis that eccentric exercise-induced muscle damage would elevate the muscle Qo2:Vo2 ratio during severe-intensity exercise while preserving the speed of the Vo2 kinetics at exercise onset. Nine physically active men completed "step" tests to severe-intensity exercise from an unloaded baseline on a cycle ergometer before (Pre) and 48 h after (Post) eccentric exercise (100 squats with a load corresponding to 70% of body mass). NIRS and breath-by-breath pulmonary Vo2 were measured continuously during the exercise tests and subsequently modeled using standard nonlinear regression techniques. There were no changes in phase II pulmonary Vo2 kinetics following the onset of exercise (time constant: Pre, 25 +/- 4 s; Post, 24 +/- 2 s; amplitude: Pre, 2.36 +/- 0.23 l/min; Post, 2.37 +/- 0.23 l/min; all P > 0.05). However, the primary (Pre, 14 +/- 3 s; Post, 19 +/- 3 s) and overall (Pre, 16 +/- 4 s; Post, 21 +/- 4 s) mean response time of the [HHb] response was significantly slower following eccentric exercise (P < 0.05). The slower [HHb] kinetics observed following eccentric exercise is consistent with an increased Qo2:Vo2 ratio during transitions to severe-intensity exercise. We propose that unchanged primary phase Vo2 kinetics are associated with an elevated Qo2:Vo2 ratio that preserves blood-myocyte O2 flux.

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

“…Nonetheless, heart rate (HR) and blood pressure responses at the onset of exercise were not exaggerated at D2 in previous studies (Fig. 2, 2-[1]) 11,16,17) . If the cardiodynamic hypothesis has any influence on the phenomenon ( Increase in intramuscular pressure (IMP), muscle mechanoreflex, and vascular distension hypothesis (Fig.…”

“…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.…”

“…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).…”

“…2, 1-[1]) 20,21) . As a result, effort sense during the same exercise increases after ECC compared with that before conducting ECC [11][12][13]15,35) . Since Williamson et al 36) suggested that effort sense is closely related to central command, central command might be augmented as a result of the loss of muscle strength after ECC (Fig.…”

“…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.…”