ECSS Paris 2023: OP-BM23
INTRODUCTION: Local vibration is an afferent-targeted intervention that, when superimposed on submaximal contractions, can modulate force output. Previous studies suggest that the effects of superimposed local vibration (SLV) on force production are intensity-dependent (1). Beyond force modulation, brief local vibration has also been shown to transiently increase corticospinal excitability (2). However, whether SLV modulates corticospinal excitability across different contraction intensities, and at spinal or cortical levels, remains unclear. Therefore, this study aimed to investigate the effects of SLV on spinal and cortical excitability during submaximal contractions performed at different contraction intensities. METHODS: Fourteen participants performed submaximal knee extension contractions (6s, separated by 45s of rest) across three sessions at 30%, 50% and 70% of maximal voluntary isometric contraction. Contractions were performed either under control conditions (CON) or with SLV applied to the quadricipital tendon (100 Hz, 2-3 mm). Vastus lateralis background electromyographic activity (bEMG) was recorded during contractions. Single stimulations included maximal M-waves (MMAX), motor-evoked potential (MEP), and thoracic MEP (TMEP), with MEP and TMEP matched at 30% of MMAX during CON. Per condition, 2 MMAX, 6 TMEP, and 10 MEP were collected. Condition and contraction intensity order was randomized. To account for peripheral changes, spinal excitability was assessed by normalizing the peak-to-peak amplitude TMEP to MMAX, and cortical excitability by normalizing MEP to TMEP. Linear mixed model with Condition (CON vs. SLV) and Intensity (30%, 50%, 70%) as fixed effects were applied to knee extension force, bEMG, and normalized neurophysiological responses (MMAX, MEP, TMEP). RESULTS: Knee extension force and bEMG did not differ between conditions (all p > 0.299). MMAX was unaffected by SLV (p = 0.827), contraction intensity (p = 0.491), or their interaction (p = 0.962). Spinal excitability (TMEP) showed no main effect of Condition (p = 0.386), Intensity (p = 0.083), or interaction (p = 0.978). Similarly, cortical excitability (MEP) was not influenced by Condition (p = 0.548), Intensity (p = 0.235), or their interaction (p = 0.910). CONCLUSION: Superimposed local vibration did not modulate cortical or spinal excitability across contraction intensities, suggesting that brief SLV does not alter the overall balance between excitation and inhibition within the corticospinal pathway. Future studies should examine longer SLV exposure durations or fatiguing conditions to better characterize its neuromodulatory effects. (1) Spiliopoulou et al., “Tendon vibration during submaximal isometric strength and postural task”, Eur J Appli Physiol, 2012. (2) Rosenkranz et al., “Differential effect of muscle vibration on intracortical inhibitory circuits in humans”, J Physiol, 2003.
Read CV Tom TIMBERTECSS Paris 2023: OP-BM23
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.
Read CV Dylan TingleyECSS Paris 2023: OP-BM23
INTRODUCTION: Sensory feedback transmitted through afferent nerve fibers is essential for accurate motor control. Ischemic nerve blocks of Ia-afferents have been widely used as a model to investigate human motor control in a deafferented state. However, besides the Ia-afferent block, the neuromuscular effects induced by ischemia, and their subsequent effect on motor unit discharge rates (MUDR), are still unclear. Therefore, we investigated the effects of an ischemic Ia-afferent block on MUDR during submaximal isometric plantar flexions. METHODS: In this preliminary analysis, four participants (3 males) performed trapezoidal contractions at 20% of maximal voluntary isometric torque (MVT) before (PRE) and after (POST) an ischemic Ia-afferent block, both at the same absolute (ABS) and relative (REL) torque levels. Contractions were performed at 5% MVT/s with a 16-s plateau at the target torque. Ischemia was induced through an inflatable cuff strapped over the proximal thigh at pressures of 191mmHg (SD 34). Soleus MUDR were analyzed from high-density surface electromyography. Trapezoidal contractions under ischemia were performed with complete Ia-afferent block, which was verified by the disappearance of H-reflexes. Motor axon transmission was assessed through maximal M-waves. H-reflexes and M-waves were elicited before and every minute during ischemia via posterior tibial nerve stimulation. To define the REL torque level with ischemia, a maximal isometric contraction after ABS with Ia-afferent block was performed. RESULTS: Complete Ia-afferent block was achieved after 17.5min (SD 5.0) of ischemia. M-wave peak-to-peak amplitude did not change from PRE (2.9mV SD 1.7) to the end of ischemia (2.6mV SD 1.5). MVT was significantly reduced following Ia-afferent block (PRE: 69.3Nm SD 28.3; POST: 59.0Nm SD 30.1; p=0.03). A total of 52 motor units were tracked across the three measurements (PRE, POST ABS and POST REL). When pooling all motor units within each trial, MUDR was higher during POST ABS (9.3pps SD 1.4) compared to PRE (8.0pps SD 1.4, p=0.001) and POST REL (8.7pps SD 1.0, p=0.009), with no differences between PRE and POST REL. CONCLUSION: In this study, an ischemic block of Ia-afferents increased MUDR when contractions were performed at the same absolute torque, but not at the same relative torque-level compared to baseline. Given that previous pilot studies have shown a reduction in twitch torque to supramaximal stimulation at the time of Ia-afferent block, it is plausible that the increase in MUDR at ABS likely reflects a neural strategy compensating for peripheral changes to maintain the same absolute torque target. Further, motor unit discharge is regulated through an interplay of supraspinal drive, neuromodulatory input, and afferent feedback to motoneurons. The loss of afferent feedback during the ischemic Ia-afferent block induced in the present study, might therefore have increased the relative contribution of central and neuromodulatory mechanisms to sustain MUDR.
Read CV Amin Karim ChetouaniECSS Paris 2023: OP-BM23