Training-related decrease in antagonist muscles activation is associated with increased motor cortex activation: evidence of central mechanisms for control of antagonist muscles

Abstract

During human contraction, net joint torque production involves the contribution of the antagonist muscles. Their activation protects the articulations and facilitates movement accuracy, but despite these fundamental roles, little is known about the brain mechanisms underlying their control. In view of previous studies that showed lesser antagonist muscles activation in participants engaged in regular strength training (ST) than in participants actively engaged in endurance disciplines (ED), we used this between-group comparison to investigate the possible role of motor cortex activity on the control of antagonist muscles. Electroencephalographic (EEG) and electromyographic (EMG) activity as well as the net joint torque were recorded, while ten ST and eleven ED participants performed isometric knee muscles exertions at different force levels. EEG data showed a linear increase in the suppression of cortical oscillations in the 21-31 Hz frequency band with increasing force level in ST but not in ED participants. This effect was associated with lesser EMG activation of the antagonist muscles in ST than in ED participants, the difference between groups also increasing with the force level. Both effects were found specifically during flexion exertions, indicating that ST participants developed sharp central adaptations to control the antagonist muscles involved as prime movers in their usual training task. This result suggests that the cortical adaptations induced by regular strength training could exert a specific encoding of the antagonist muscles, leading to the minimization of their activation and improved energetic efficiency of the muscle contraction.

Increased antagonist muscle activity in cervical SCI patients suggests altered reciprocal inhibition during elbow contractions

“…The net torque corresponds to the sum of the individual torques developed by the muscles and other structures crossing the joint (Zajac et al, 2002). Antagonist muscles, acting in the opposite http direction to the net torque, have an important functional role in movement coordination and accuracy (Gribble et al, 2003;Rao et al, 2009;Wiegner, 1992, 1996), joint stiffness and stability Kellis, 1998;Kellis and Baltzopoulos, 1997;Lestienne, 1979;Solomonow et al, 1988), and effective net torque production (Dal Maso et al, 2012;Häkkinen et al, 1998).…”

Impaired corticomuscular coherence during isometric elbow flexion contractions in humans with cervical spinal cord injury

“…Dal Maso et al . () suggested that the cortical oscillations ~ 20 Hz recorded over the M1 might have a critical role in the modulation of antagonist muscle activations. The decrease in the magnitude of the CMC ~ 10 and ~ 20 Hz with the force level could thus reflect a functional neurophysiological mechanism that would take part in the control of the exerted force by modulating agonist and antagonist muscle activations.…”

“…Prior the experimental session, participants performed 3 so‐called relative Maximum Voluntary Contractions (rMVC) around the right elbow joint in flexion. The rMVC was determined as the highest net moment reached while keeping at rest all the muscles not involved in the task, especially face and neck muscles, to avoid muscles artifact in EEG recordings (Dal Maso et al ., ; Cremoux et al ., ,b). The experimental protocol consisted of 21 elbow isometric flexion contractions at 25, 50 and 75% rMVC randomized in seven sets of contractions.…”

“…For CMC calculation, the following steps were used. The EEG and EMG data were first band-pass filtered at [3-100] Hz and notched at [45-55] Hz (Sabri & Campbell, 2002;Baker & Baker, 2012;Dal Maso et al, 2012;Cremoux et al, 2013b). Channels visually identified as 'bad' channels were removed, and EEG signals were average referenced (Delorme et al, 2007; note that the C3 EEG channel has never been identified as 'bad' channel during this step; see Fig.…”

Effect of the phase of force production on corticomuscular coherence with agonist and antagonist muscles

“…The modulation in net joint torque stability could result from an altered control of the activation of agonist and antagonist muscles, respectively, acting in the direction or in the opposite direction of the net joint torque (Basmajian, ). Recent studies showed the involvement of the primary motor cortex (M1) in the regulation of agonist and antagonist muscle activations with the force level (Cremoux, Tallet, Dal Maso, Berton, & Amarantini, ; Dal Maso, Longcamp, & Amarantini, ; Dal Maso, Longcamp, Cremoux, & Amarantini, ). However, M1 involvement in the regulation of agonist and antagonist muscle activations with the phases of contraction remains largely unknown.…”