Abstract

BackgroundAntagonist activation may contribute to fatigue-induced decreases in torque while assisting in the maintenance of joint stability. This study utilized a reciprocal, slow velocity (60°·s−1) forearm flexion and extension fatiguing task to examine the contributions of coactivation to torque production at slow and moderate (180°·s−1) velocities, as well as during a maximal voluntary isometric contraction (MVIC). MethodsTwelve recreationally active men (mean ± SD: age = 21.7 ± 1.6 years; body mass = 83.5 ± 8.8 kg; height = 179.4 ± 5.2 cm) completed isokinetic (60 and 180°·s−1) and isometric pre-testing of forearm flexion and extension, followed by 50 maximal, reciprocal, isokinetic muscle actions at 60°·s−1, followed by post-testing. The amplitude (AMP) of the electromyographic (EMG) signals from the biceps and triceps brachii were simultaneously recorded. Torque and EMG AMP were normalized to the corresponding values from the pre-testing peak torque movements. Repeated measures ANOVAs and pairwise comparisons were used to identify mean changes in torque, EMG AMP, and coactivation ratios. ResultsThe torque analyses indicated greater (p < 0.03) decreases for 180°·s−1 (24%) and MVIC (23%) than 60°·s−1 (14%) for forearm flexion. For forearm extension, there were no differences (p > 0.05) in fatigability between velocities. For EMG AMP there were no changes (p > 0.05) from pre- to post-testing for any velocity or movement. There were no changes (p > 0.05) in the coactivation ratio for forearm flexion, but significant increases (13.6 ± 6.6 to 16.9 ± 6.0; p = 0.003) for forearm extension, collapsed across Velocity. ConclusionsThere was velocity- and movement-specific fatigability for forearm flexion and extension. The parallel, fatigue-induced EMG AMP responses indicated that coactivation did not contribute to the decreases in torque and would not affect elbow joint stability.

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