EXACERBATING PAIN IMPAIRS CYCLING PERFORMANCE WITHOUT ALTERING CORTICOSPINAL EXCITABILITY AND INTRACORTICAL INHIBITION

Author(s): ZHANG, J., MCCLEAN, Z.J., HONARVAR, N., MORGAN, S., MACINNIS, M.J., ABOODARDA, S.J., Institution: UNIVERSITY OF CALGARY, Country: CANADA, Abstract-ID: 752

INTRODUCTION:
During high-intensity exercise, pain arises from the accumulation of metabolites (e.g., H+, K+) and increased intramuscular pressure (1). While the contribution of pain on impaired exercise performance is poorly understood, studies using experimental pain models have suggested that the increased inhibitory afferent feedback and augmented feedforward central drive can accelerate the achievement of the sensory tolerance limit to compromise performance (2). While prior studies have investigated the effect of experimental pain on isometric exercise tasks, little is known about corticomotor modulations to painful stimuli during ecological dynamic tasks such as cycling. Accordingly, this study aimed to examine the effect of experimental pain on corticospinal excitability, intracortical inhibition, and neuromuscular function during cycling.
METHODS:
Nine healthy, adult participants (2 females) completed a counterweighted single-leg cycling ramp incremental test to obtain peak power output (PPO) followed by two experimental sessions wherein single-leg cycling at 60% of PPO was performed to task failure. Sessions were performed either without (CTRL) or with (PAIN) an experimental pain intervention consisted of a complete vascular occlusion of the contralateral resting leg combined with electrical stimulation of thigh muscles. To measure corticospinal excitability and intracortical inhibition, 2 femoral nerve stimuli, 5 unconditioned single-pulse transcranial magnetic stimuli (TMS), and 5 short- and 5 long-interval paired TMS pulses were elicited every five minutes during cycling to evoke Mmax, MEP, SICI, and LICI, respectively. Following each stimulation epoch, the bike pedals were locked and participants performed a brief maximal voluntary contraction (MVC) combined with femoral nerve stimuli to characterize neuromuscular function. Subjective ratings of leg pain, fatigue, and effort were also measured every 5 min.
RESULTS:
Despite a shortened time to task failure in the PAIN condition (37±12min vs. 61±21min; P=0.015), no differences in neuromuscular function (i.e., MVC force, voluntary activation, and quadriceps twitch force) were present between conditions. Additionally, there were no between-condition differences in Mmax, MEP, SICI, or LICI during cycling (all P>0.05). Contralateral leg pain ratings were higher in PAIN than CTRL (P<0.001), but exercising leg pain was higher in CTRL than PAIN (P=0.015). No differences between fatigue or effort appeared between conditions.
CONCLUSION:
Pain impaired exercise performance, but this impedance occurred independently from the intracortical, corticospinal, and neuromuscular pathways governing voluntary movement. Instead, regardless of the amount of inhibitory afferent feedback, exercise terminated once individuals achieved a maximal tolerable limit which was accelerated and primarily determined by perceived pain.
1. Cook et al., 1997, MSSE
2. Azevedo et al., 2022, APNM