4.2 Article

Remote muscle priming anodal transcranial direct current stimulation attenuates short interval intracortical inhibition and increases time to task failure of a constant workload cycling exercise

Journal

EXPERIMENTAL BRAIN RESEARCH
Volume 239, Issue 6, Pages 1975-1985

Publisher

SPRINGER
DOI: 10.1007/s00221-021-06103-x

Keywords

Intracortical inhibition; Transcranial direct current stimulation; Transcranial magnetic stimulation; Exercise performance; Cycling exercise fatigue

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This study found that atDCS applied over the unexercised muscle M1 representation can enhance cycling exercise performance, possibly mediated by reducing the excitability of global GABA(A) inhibitory interneurons.
Anodal transcranial direct current stimulation (atDCS), a non-invasive neuromodulatory technique has been shown to increase the excitability of targeted brain area and influence endurance exercise performance. However, the effect of atDCS applied on an unexercised muscle motor cortex (M1) representation on GABA(A)-mediated intracortical inhibition and endurance exercise performance remains unknown. In two separate sessions, twelve subjects performed fatigue cycling exercise (80% peak power output) sustained to task failure in a double-blinded design, following either ten minutes of bicephalic anodal tDCS (atDCS) or sham applied on a non-exercised hand muscle M1 representation. Short interval intracortical inhibition (SICI) was measured at baseline, post neuromodulation and post-exercise using paired-pulse transcranial magnetic stimulation (TMS) in a resting hand muscle. There was a greater decrease in SICI (P < 0.05) post fatigue cycling with atDCS priming compared to sham. Time to task failure (TTF) was significantly increased following atDCS compared to sham (P < 0.05). These findings suggest that atDCS applied over the non-exercised muscle M1 representation can augment cycling exercise performance; and although this outcome may be mediated via a multitude of mechanisms, a decrease in the global excitability of GABA(A) inhibitory interneurons may be a possible contributing factor.

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