Badminton Players Show a Lower Coactivation and Higher Beta Band EMG-EMG Coupling between Antagonist Muscles

PURPOSE: Previous studies have suggested that skilled athletes may show a specific muscle activation pattern with a lower antagonist coactivation level. Based on the point, we hypothesize that the coupling of antagonistic muscles may be different between elite badminton players and non-skilled individuals during exercises. The current work was designed to verify the hypothesis. METHODS: Ten male college students and eight male badminton players performed three maximal voluntary isometric contractions (MVC) and a set of three maximal concentric ankle dorsiflexion and plantar flexion at angular velocity of 30°, 60°, 120° and 180°/s. Surface EMG were recorded from the tibialis anterior (TA) and lateral grastrocnemius (LG) muscles during the test. Normalized average amplitude of the integrated EMG and phase synchronization index (PSI) between the EMG of TA and LG were calculated. RESULTS: Antagonist muscle coactivation were significantly lower (22.1% ± 9.4%, 24.7% ± 12.8%, 22.4%±9.4%, 22.4% ± 9.7% for non-players and 10.7% ± 3.7%, 10.1% ± 4.9%, 11.2% ± 2.5%, 10.6% ± 2.5% for badminton players in four angular velocity speed, P\u3c0.05 for four group comparison) and PSI in beta frequency band were significantly higher (0.42 ± 0.06, 0.36 ± 0.13, 0.36 ± 0.10, 0.35 ± 0.12 for non-players and 0.47 ± 0.15, 0.47 ± 0.15, 0.48 ± 0.11, 0.49 ± 0.14 for badminton players in four angular velocity speed, P\u3c0.05 for four group comparison) in badminton players group compared to non-players group during isokinetic ankle dorsiflexion contraction, while no significant difference was found in antagonist muscle coactivation and PSI between two group subjects during ankle plantar flexion. CONCLUSIONS: The decrease of antagonist coactivation may indicate an optimal motor control style to increase the contraction efficiency, while the increase coupling of antagonistic muscles may be related to the compensation of joint stability as a result of the decrease of antagonist coactivation