Introduction: 1) During tES, increasing intracellular Ca2+ levels beyond those needed for inducing LTP may collapse aftereffects. 2) State-dependent plastic aftereffects are reduced when applied during muscle activation as compared to rest. 3) Cortical surround inhibition by antagonistic muscle activation inhibits the center-innervated agonist. Objectives: To determine the interaction of state dependency of tACS aftereffects at rest and under activation of agonist and antagonist muscles during stimulation with different intensities. Methods: In thirteen healthy participants, we measured MEP amplitudes before and after applying tACS at 140 Hz over the motor cortex in nine single-blinded sessions using sham, 1 mA and 2 mA stimulation intensities during rest and activation of agonist and antagonist muscles. Results: During rest, only 1 mA tACS produced a significant MEP increase, while the 2 mA stimulation produced no significant MEP size shift. During agonist activation 1 mA did not induce MEP changes, after 2 mA first a decrease and later an increase of MEPs were observed. Antagonist activation under sham tACS led to an inhibition, which was restored to baseline by 1 and 2 mA tACS. Conclusions: Increasing stimulation intensity beyond 1 mA does not increase excitability, compatible with too strong intracellular Ca2+increase. Antagonist innervation leads to MEP inhibition supporting the concept of surround inhibition, which can be overcome by tACS at both intensities. During agonist innervation a tACS dose dependent relationship exists. Significance: Our results integrate concepts of "leaky membranes" under activation, surround inhibition, intracellular Ca2+ increase and their role in the aftereffects of tACS.