Introduction Humans can acquire new motor behaviors via different forms of learning- positive reinforcement and the formation of internal model representations of the movement dynamics (adaptation). The neurophysiological mechanisms in the primary motor cortex (M1) and the cerebellum (CB) when learning motor tasks through reinforcement or adaptation are poorly understood. Objectives To investigate neurophysiological underpinnings of distinct learning mechanisms. Materials and methods We assessed M1 LTP-like plasticity and cerebellar excitability changes when healthy participants learned a reaching adaptation task, known to rely early on adaptation and later on reinforcement mechanisms. We determined the presence of LTP-like plasticity when we observed no significant increase in M1 excitability even after applying anodal tDCS (i.e. occlusion of M1 LTP-like plasticity), as determined by single pulse TMS-evoked potentials. We evaluated cerebellar inhibition (CBI) to indirectly investigate CB excitability changes during learning, using a paired-pulse TMS paradigm comprised of conditioning CB stimulation followed by a test M1 stimulation. We also assessed these physiological markers when participants learned the same reaching via binary feedback, which relies on reinforcement mechanisms. Results We found occlusion of M1 LTP-like plasticity only late, but not in the early phase of adaptation learning, whereas CBI changed early but not in the later phase of learning. We also found occlusion of M1 LTP-like plasticity when participants successfully learned the same reaching action via binary feedback. However, CBI did not change in this task. Conclusion We show a clear double dissociation whereby learning a task via reinforcement results in M1 LTP-like plasticity changes, while learning the motor actions via adaptation leads to cerebellar plasticity modifications. This indicates that learning motor actions can be accomplished by different neurophysiological mechanisms and neural substrates. Furthermore, deficits in one learning mechanism could be compensated by another intact mechanism, opening alternative interventions to enhance motor function after neurological disease.