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This study investigated the effects of short-term glucocorticoid administration on voluntary activation and intracortical inhibitory and facilitatory circuits.Seventeen healthy men participated in a pseudorandomized double-blind study to receive either dexamethasone (8 mg·d−1, n = 9 subjects) or placebo (n = 8 subjects) for 7 d. The ankle dorsiflexion torque, corresponding EMG of the tibialis anterior, and voluntary activation assessed by the interpolated twitch method using transcranial magnetic stimulation (TMS) were measured during a maximal voluntary contraction (MVC). Short-latency intracortical inhibition (SICI) and intracortical facilitation (ICF) were assessed at rest and during submaximal contraction (50% MVC torque) by paired-pulse TMS with the conditioning stimulus set at 0.8× of motor threshold and delivered 2 ms (SICI) and 13 ms (ICF) before the test stimulus (1.2× motor threshold).The MVC torque (+14%), tibialis anterior EMG (+31%), and voluntary activation (+3%) increased after glucocorticoid treatment (P < 0.05). The increase in voluntary activation was associated with the gain in MVC torque (r2 = 0.56; P = 0.032). The level of SICI and the duration of the EMG silent period that followed the test TMS decreased (−18.6% and −13.5%, respectively) during the 50% MVC after treatment (P < 0.05), whereas no significant change was observed for ICF. Neither SICI nor ICF changed after treatment when assessed at rest.Short-term dexamethasone treatment induced specific decrease in the excitability of intracortical inhibitory circuits that likely contributed to the increase in the voluntary activation and associated MVC torque.