We previously reported that repetitive combined stimulation (RCS) of pyramidal tract and peripheral nerve could induce long-term potentiation (LTP) in indirect cortico-motoneuronal (C-M) excitations in biceps brachii (BB) of human subjects, which are mediated by cervical propriospinal neurons (PNs). However, the LTP could be induced only when the target muscle was voluntarily contracted, which limits possible clinical use. In animal studies, PNs are known to project various forelimb motoneurons. Because RCS could induce plastic changes in synapses from pyramidal tract to PNs, we hypothesized that the LTP of C-M excitations could also be induced in non-target muscles in upper limb, which are relaxed during RCS. RCS intervention (0.2 Hz, 10 min) was the same as in the previous study. With EMG recording from right BB under weak contraction, transcranial magnetic stimulation (TMS) to the arm area of left motor cortex (M1) was delivered with right ulnar nerve stimulation. Inter-stimulus interval for the combined stimulation was set at 10 ms, where inputs by both stimuli to reach PNs simultaneously. Stimulus strengths were determined to observe the maximum spatial facilitation in BB by the simultaneous inputs. To observe LTP in non-target muscles, motor evoked potentials (MEPs) were obtained from flexor digitorum superficialis, extensor digitorum communis and first dorsal interosseous muscles, by TMS to the optimal point in M1, which was ~1 cm lateral to the arm area. As previously reported, MEPs in BB were potentiated after RCS, which lasted for ~65 min. Furthermore, the potentiation could be observed in hand muscles, which showed similar time course to that in BB. When the stimulation point in M1 was moved laterally by 2-3 cm, where MEPs could be evoked in hand muscles but less efficiently, the potentiation was not observed after RCS. These results show that LTP could be induced in muscles without contraction, if RCS induces LTP in another muscle under weak contraction. Differences between stimulation points indicate that the LTP was caused by plastic changes in synapses, which are activated by TMS during RCS.