Cortical and Spinal Modulation of Antagonist Coactivation During a Submaximal Fatiguing Contraction in Humans

Abstract

This study investigates the control mechanisms at the cortical and spinal levels of antagonist coactivation during a submaximal fatiguing contraction of the elbow flexors at 50% of maximal voluntary contraction (MVC). We recorded motor-evoked potentials in the biceps brachii and triceps brachii muscles in response to magnetic stimulation of the motor cortex (MEP) and corticospinal tract (cervicomedullary motor-evoked potentials--CMEPs), as well as the Hoffmann reflex (H-reflex) and maximal M-wave (Mmax) elicited by electrical stimulation of the brachial plexus, before, during, and after the fatigue task. The results showed that although the coactivation ratio did not change at task failure, the MVC torque produced by the elbow flexors declined by 48% (P < 0.01) with no change in MVC torque for the elbow extensors. While the MEP and CMEP areas (normalized to Mmax) of the biceps brachii increased ( approximately 50%) over the first 40% of the time to task failure and then plateaued, both responses in the triceps brachii increased ( approximately 150-180%) gradually throughout the fatigue task. In contrast to the monotonic increase in the MEP and CMEP of the antagonist muscles, the H-reflex of the triceps brachii exhibited a biphasic modulation, increasing during the first part of the contraction before declining subsequently to 65% of its initial value. Collectively, these results suggest that the level of coactivation during a fatiguing contraction is mediated by supraspinal rather than spinal mechanisms and involves differential control of agonist and antagonist muscles.

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

“…This specific encoding leads to the minimization of antagonist muscles activation and improves the energetic efficiency of the muscle contraction (Baratta et al 1988;Carolan and Cafarelli 1992;Hakkinen et al 2000;Bru and Amarantini 2008). This result is in agreement with previous studies that evidenced that central mechanisms are involved in the regulation of agonist and antagonist muscles activations (De Luca and Mambrito 1987;Mullany et al 2002) and corroborates the hypothesis of a distinct central control of antagonist muscles (Levenez et al 2008). In addition, our results showed that the cortical control of antagonist muscles differed between groups specifically in the direction of contraction (flexion) in which the antagonist muscles corresponded to the prime-mover muscles (i.e., knee extensors) of the training task (squats) usually used by ST participants.…”

“…Antagonist muscles participate in joint stiffness and stability (Basmajian and De Luca 1985;Miller et al 2000;Stokes and Gardner-Morse 2003;Centomo et al 2008;Rao et al 2009), protect the articulation by lowering tension in the ligaments (for review, see Remaud et al 2007) and facilitate movement accuracy (Corser 1973;Tanaka 1974;Gribble et al 2003). Although prior studies have emphasized the important role of central mechanisms for the regulation of agonist and antagonist muscles activations (De Luca and Mambrito 1987;Mullany et al 2002;Levenez et al 2008), no study has directly investigated the brain correlates of the modulation of antagonist muscles activation during human voluntary contractions.…”

Assessment of Neuromuscular Function Using Percutaneous Electrical Nerve Stimulation

“…However, nerve stimulation presents potential methodological limitations for some muscles. For instance, obtaining a H-reflex from biceps brachii muscle can be difficult to obtain at rest 49 . Furthermore, stimulating the musculocutaneous nerve over the brachial plexus leads to contraction of both agonist and antagonist muscles 32 , inducing the erroneous evaluation of the voluntary activation level.…”

Effects of Different Antagonist Protocols on Repetition Performance and Muscle Activation – Orginal Research

“…The authors indicated that these adaptations could be associated with a specific encoding of antagonist muscles activation through cortical oscillations. In addition, Lévénes et al [27] observed that excitatory drive to the motor neuron pool of the antagonist muscle is increased during fatigue of the agonist muscle, and the different behavior of the Hoffman-reflex and cervicomedullary motor evoked potentials during the fatiguing action in the antagonist muscle, suggests that the level of coactivation is likely under the control of supraspinal rather than spinal mechanisms.…”