Priming the Motor Cortex With tDCS

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Priming the Motor Cortex With Anodal Transcranial Direct Current Stimulation Affects the Acute Inhibitory Corticospinal Responses to Strength Training.

J Strength Cond Res. 2019 Feb;33(2):307-317

Authors: Frazer AK, Howatson G, Ahtiainen JP, Avela J, Rantalainen T, Kidgell DJ

Abstract
Priming the motor cortex with anodal transcranial direct current stimulation affects the acute inhibitory corticospinal responses to strength training. J Strength Cond Res 33(2): 307-317, 2019-Synaptic plasticity in the motor cortex (M1) is associated with strength training (ST) and can be modified by transcranial direct current stimulation (tDCS). The M1 responses to ST increase when anodal tDCS is applied during training due to gating. An additional approach to improve the M1 responses to ST, which has not been explored, is to use anodal tDCS to prime the M1 before a bout of ST. We examined the priming effects of anodal tDCS of M1 on the acute corticospinal responses to ST. In a randomized double-blinded cross-over design, changes in isometric strength, corticospinal excitability, and inhibition (assessed as area under the recruitment curve [AURC] using transcranial magnetic stimulation) were analyzed in 13 adults exposed to 20 minutes of anodal tDCS and sham tDCS followed by a ST session of the right elbow flexors. We observed a significant decrease in isometric elbow-flexor strength immediately after training (11-12%; p < 0.05), which was not different between anodal tDCS and sham tDCS. Transcranial magnetic stimulation revealed a 24% increase in AURC for corticospinal excitability after anodal tDCS and ST; this increase was not different between conditions. However, there was a 14% reduction in AURC for corticospinal inhibition when anodal tDCS was applied before ST when compared with sham tDCS and ST (all p < 0.05). Priming anodal tDCS had a limited effect in facilitating corticospinal excitability after an acute bout of ST. Interestingly, the interaction of anodal tDCS and ST seems to affect the excitability of intracortical inhibitory circuits of the M1 through nonhomeostatic mechanisms.

PMID: 30688872 [PubMed – in process]

 

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