Effect of fatigue on intermuscular EMG-EMG coupling during bench press exercise at 60% 1RM workload in males

Objective: To explore the neuromuscular control mechanism and quantifying the fatigue response during bench press exercise is important references to prescribe an appropriate exercise program. However, current literature struggles to provide a concrete conclusion on the changes of intermuscular EMG-EMG coupling between synergistic and antagonist muscles during the exercise. Thus, the current study was designed to reveal fatigue-related changes of intermuscular EMG-EMG coupling during bench press exercise.

Methods: Thirty-one healthy male participants performed a bench press exercise on the Smith machine at 60% One Repetition Maximum (1RM) workload to exhaustion, while surface electromyographic signals (sEMG) were collected from triceps brachii (TB), biceps brachii (BB), anterior deltoid (AD), posterior deltoid (PD), and pectoralis major (PM). Surface EMG signals were divided into the first half and second half of the bench press exercise. Phase synchronization index (PSI) was calculated between sEMG of synergistic muscle pairs AD-TB, AD-PM and antagonist muscle pairs BB-TB, AD-PD.

Results: EMG power of TB, AD, PD, PM muscles in alpha (8-12 Hz) frequency band and EMG power of each muscle in beta (15-35 Hz), and gamma (35-60 Hz) frequency bands were all increased during the second half of contraction compared with the first half of contraction. PSI of gamma frequency band was significantly decreased in BB-TB muscle pair while EMG-EMG coupling of AD-TB in gamma frequency band was significantly increased during the second half of contraction compared to the first half of contraction.

Conclusions: The results indicated a decrease of interconnection between synchronized cortical neurons and the motoneuron pool of BB and TB, and an increase of interconnection between AD-TB muscles during fatiguing bench press exercise at 60% 1RM workload. The changes of intermuscular coupling may be related to the supraspinal modulations to compensate for the decrease of muscle force as well as a result of unbalanced changes of agonist and antagonist muscle contractility.