Peripheral patterned electrical stimulation (PES) to the common peroneal nerve modulates the spinal reciprocal inhibition from the tibialis anterior muscle (TA) to the soleus muscle (SOL) through spinal plasticity mechanisms, which have essential roles in functional recovery of the lower limb after spinal cord injury or stroke. Furthermore, modulation of cortex excitability is thought to modify spinal plasticity.This study aimed to investigate the priming-effects of intermittent theta burst stimulation (iTBS) over the primary motor cortex on PES-induced spinal plasticity in healthy subjects.Ten healthy volunteers have participated in the single-masked, sham-controlled, crossover study. All participants received iTBS to the TA motor hot-spot in three separated sessions: (1) iTBS before PES; (2) iTBS after PES; and (3) sham iTBS before PES. iTBS consisted of 10 bursts, in each of which composed of three stimuli at 50Hz, at 5Hz repeated every 10s for a total of 600 stimuli (200s). For the sham stimulation, iTBS was delivered with a coil held flipped over on the TA hotspot at a reduced intensity following the same procedure of real iTBS. PES involved stimulating the right common peroneal nerve with a train of ten 100-Hz pulses every 2s for 20min. To counterbalance the intervention time of iTBS before and after PES, rest period (200s) was set for each task. Reciprocal inhibition from TA to SOL was assessed using a soleus H-reflex conditioning-test paradigm. The conditioning-test inter-stimulus intervals were 2 (RI2ms), 20 (RI20ms) and 100ms (RI100ms).Reciprocal inhibition was assessed at baseline, before PES, and at 0, 15, 30, and 45min after PES.iTBS before PES significantly enhanced RI2ms at 0 and 15min after PES as compared with the baseline values. In contrast, iTBS after PES and sham iTBS before PES only enhanced RI2ms at the time point immediately after PES. RI100ms was significantly increased only under the iTBS before PES protocol, immediately after PES.These findings confirm the hypothesis that spinal plasticity can be modified by altering the motor cortical excitability, and provide a greater understanding of the mechanisms underlying spinal plasticity to help for developing newer rehabilitation strategies.