co-contraction of agonist and antagonist muscles increased corticospinal excitability and muscular activity in arm muscles

Background: this research aimed to explore how the co-contraction (mco) of agonist and antagonist arm muscles influences the excitability of the corticospinal pathway. methods: a randomized, controlled, within-subject crossover design was employed. a total of seventeen healthy male volunteers, aged 20 - 27 years, were enrolled in the study following a comprehensive eligibility screening process. each participant completed four experimental sessions under controlled conditions. the protocol of this study included measuring the motor-evoked potential (mep)'s area under the recruitment curve (aurc) and the pre-stimulus electromyography (emg) in four states (rest, agonist activity, antagonist activity, and mco of agonist and antagonist muscles) and at 100%, 120%, 140%, 160%, and 180% of the resting motor threshold (rmt), with 10 pulses per intensity (50 pulses total). sessions were randomized and counterbalanced with ≥ 24-hour intervals to minimize carryover effects. results: the study revealed that muscle activation states, particularly agonist activation and mco, significantly increased pre-stimulus root mean square (rms) amplitudes (p < 0.001). the mco caused a significant increase in the total aurc compared to rest states [d = 4.15, p < 0.001 for biceps brachii (bb) and d = 2.47, p < 0.001 for triceps brachii (tb)]. furthermore, antagonist muscle activity also increased the aurc of mep relative to the resting state in the agonist muscle (d = 0.50, p < 0.001 for bb and d = 0.28, p < 0.001 for tb). conclusions: the present study's findings indicate that the simultaneous contraction of two muscles can lead to greater increases in mep's and the pre-stimulus emg in the arm muscles. furthermore, this research offers valuable methodological insights (standardized protocol development, enhanced experimental design, and upper-limb validation) for future transcranial magnetic stimulation (tms) studies and lays the groundwork for investigating mco-induced modulations in the corticospinal pathway.