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  • Title: Anodal transcranial direct current stimulation enhances time to task failure of a submaximal contraction of elbow flexors without changing corticospinal excitability.
    Author: Abdelmoula A, Baudry S, Duchateau J.
    Journal: Neuroscience; 2016 May 13; 322():94-103. PubMed ID: 26892298.
    Abstract:
    BACKGROUND: The increase in corticospinal excitability in response to anodal transcranial direct current stimulation (a-tDCS) may contribute to decrease neuromuscular fatigability. OBJECTIVE: This study investigated the effects of a-tDCS on neuromuscular fatigability in relation with changes in corticospinal excitability. METHODS: Eleven adults participated in two experimental sessions consisting of two submaximal voluntary contractions (35% maximal torque) performed to failure, one hour apart with the right elbow flexor muscles. Sham stimulation (90 s) and a-tDCS (10 min) were applied in two separate sessions 10 min prior to the second fatiguing contraction. Corticospinal excitability was assessed by recording motor-evoked potential (MEP), elicited by transcranial magnetic stimulation (TMS) of the motor cortex, in biceps brachii, brachioradialis and triceps brachii during the first (C1) and second (C2) fatiguing contractions. The silent period (SP) in electromyogramme (EMG) that followed MEP was also recorded for biceps brachii and brachioradialis. RESULTS: Time to failure was briefer for C2 than C1 in both experimental sessions, but the decrease was less pronounced after a-tDCS (-14.4±12.7%) than sham stimulation (-23.3±11.9%; p=0.04). MEP amplitude (+9.7±4.0%) and SP duration (+22.5±12.8%) in biceps brachii and brachioradialis increased significantly (p<0.05) during C1 and C2, but to a similar extent in both sessions (p>0.05). A similar result was observed for MEP amplitude in triceps brachii. No association was found between changes in time to task failure of C2 and corticospinal excitability. CONCLUSION: The reduced neuromuscular fatigability induced by a-tDCS does not rely on changes in the excitability of the corticospinal pathway of both agonist and antagonist muscles.
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