Investigating the Modulation of Corticomotor and Neuromuscular Function by Contralateral and Ipsilateral Experimental...

Pain can impair exercise performance, but its influence on motor control, in particular the effect of robust experimental pain on the timecourse of corticomotor responses throughout prolonged, exhaustive cycling, remains unclear. We tested the hypothesis that an augmented experimental pain intervention applied to exercising and non-exercising limbs would modulate neuromuscular function, corticospinal excitability and inhibition, and exacerbate perceptual and cardiorespiratory responses to exercise. Ten healthy adults (two females) completed three single-leg cycling sessions at 60% peak power output to failure: without experimental pain (CTRL), with intermittent occlusions applied to the resting leg (CONTRA), and with occlusions upon the exercising leg (IPSI). Every 5 min, single- and paired-pulse transcranial magnetic stimulations were applied during cycling to assess corticospinal excitability ( $\mathrm{MEP}·M_{\max }^{-1}$ ) and short- and long-interval intracortical inhibition (SICI and LICI). Participants also performed 5-s isometric maximal voluntary contractions (MVC) coupled with superimposed and resting femoral stimulations. Perceptual responses and cardiorespiratory variables were recorded throughout exercise. Time to failure was blunted in CONTRA (37.2 ± 13.1 min, p = 0.015) and IPSI (27.1 ± 11.4 min, p = 0.003) compared to CTRL (61.1 ± 21.5 min). Though they declined across time, MVC force, voluntary activation, and resting twitch force did not differ across conditions. While $\mathrm{MEP}·M_{\max }^{-1}$ was similar, SICI was higher in CONTRA (p < 0.001) and LICI was higher in CONTRA but lower in IPSI (p = 0.02) than CTRL. Both conditions upregulated pain in the affected leg and exacerbated ratings of fatigue and effort (p < 0.001), while IPSI increased ventilation. Experimental pain augmented perceptual responses without impairing neuromuscular function, but the site of application can oppositely modulate cortical inhibition.