Corticospinal influences on two antagonistic muscles of the shoulder were studied in 6 normal volunteers. Recordings were made of the discharges of single motor units from the deltoid and pectoralis major muscles and poststimulus time histograms constructed following either anodal electrical or magnetic cortical stimulation via the scalp. Contralateral anodal stimulation caused narrow short-latency peaks of excitation in motor units from both muscles, probably indicative of the arrival of the D or direct corticospinal volley. The size of the peaks led to estimates of the underlying excitatory postsynaptic potentials (EPSP) amplitude of 5.5 mV for the deltoid and 2.2 mV for the pectoralis motor units. Magnetic stimulation over the vertex caused multiple early peaks of excitation in motor units from both muscles but these peaks began at a greater latency than those produced by anodal stimulation. Additionally, magnetic cortical stimulation (and, occasionally, contralateral anodal stimulation) caused a previously undescribed period of medium latency excitation in both muscles. These medium latency periods of excitation differed from the earlier events in that they occurred independently of the direction of current flow in the magnetic coil. This raises the possibility that they are the consequence of stimulation of bilaterally distributed cortical motor outflow pathways. The short-latency excitation strongly suggests that, in man, corticomotoneuronal projections exist to proximal as well as distal muscles of the contralateral arm. The strength of the projection to deltoid assessed by this method is similar to that to an intrinsic muscle of the hand and significantly larger than that to its antagonist, pectoralis. The possible bilateral organization of the additional medium-latency projection to these proximal arm muscles may contribute to two characteristic clinical features after a unilateral cerebral lesion, such as stroke: the relative sparing of proximal arm strength compared with distal and, secondly, ipsilateral weakness.