Author(s): TINGLEY, D., PRICOP, M., ELEMINE, G., KOMEILI, A., SMIRL, J., MACINNIS, M., ABOODARDA, S.J., Institution: UNIVERSITY OF CALGARY, Country: CANADA, Abstract-ID: 2711

INTRODUCTION:
Joint pain is a pervasive and performance-limiting factor during athletic, recreational, and rehabilitative exercise that can lead to impaired force production, altered movement patterns, and a reduction in exercise tolerance. Despite this, the corticospinal responses to joint pain during dynamic movement remain poorly defined. Accordingly, the present study investigated cortical activity and corticospinal excitability (CSE) responses during constant-load cycling exercise with and without superimposed knee pain using electroencephalography (EEG), transcranial magnetic stimulation (TMS), and electromyography (EMG), respectively.
METHODS:
Twenty-two healthy participants (12 females, 10 males) completed a familiarization visit and two randomized, counterbalanced experimental sessions consisting of 42-minute cycling bouts performed at delta 50 (i.e., 50% of the intensity between gas exchange threshold and respiratory compensation point), once with and once without experimental knee pain. Pain was induced via continuous 10 Hz sinusoidal electrical stimulation of the right infrapatellar fat pad at an individually calibrated intensity corresponding to a perceived pain rating of 4/10. Throughout cycling, cortical activity was recorded using a 32-channel EEG system for quantification of spectral power in alpha (8-12 Hz) and beta (13-25 Hz) frequency bands. A series of six TMS and two femoral nerve stimuli were delivered every 7 minutes to assess CSE measures, including motor evoked potential (MEP) normalized to Mmax and EMG, along with corticospinal inhibition (CSI) (i.e., silent period). Linear mixed model statistics were used to examine condition differences in CSE and CSI, while permutation-based statistics evaluated pain-related changes in brain activity.
RESULTS:
Experimental knee pain elicited a significant increase in beta-band power over contralateral premotor and primary motor brain regions during cycling (P < 0.05). CSE (i.e., MEP/Mmax) did not differ between conditions (P > 0.05); however, MEP amplitude normalized to EMG (MEP/EMG) was significantly reduced during painful cycling (P < 0.01). Silent period duration was significantly longer in the pain condition (P < 0.001).
CONCLUSION:
This study demonstrated that experimentally induced knee pain alters cortical oscillatory dynamics while modulating excitatory and inhibitory corticospinal responses. These collective findings further our understanding of the relationship between neural oscillations and the excitability of the central nervous system, supporting the hypothesis that beta-oscillatory activity reflects antikinetic motor states. Overall, this investigation provides novel evidence linking pain-induced changes in cortical brain activity to functional corticospinal modulation during dynamic movement, advancing mechanistic understanding of pain and its impact on exercise performance.