Four distinct but highly interactive motor subsystems make essential contributions to motor control: local circuits in the spinal cord and brainstem, descending upper motor neuron pathways that control these circuits, and the basal ganglia and cerebellum, which modulate the activity of upper motor neuronal circuits. Alpha motor neurons in the spinal cord and in the cranial nerve nuclei of the brainstem directly link the nervous system and muscles, with each motor neuron and its associated muscle fibers constituting a functional entity called a motor unit. Motor units vary in size, amount of tension produced, speed of contraction, and degree of fatigability. Graded increases in muscle tension are mediated by both the orderly recruitment of different types of motor units and an increase in lower motor neuron firing frequency.

Local circuitry involving sensory inputs, local circuit neurons, and α and γ motor neurons is especially important in the reflexive control of muscle activity. The stretch reflex is a monosynaptic circuit with connections between sensory fibers arising from muscle spindles and the α motor neurons that innervate the same, or synergistic, muscles. The γ motor neurons regulate the gain of the stretch reflex by adjusting the level of tension in the intrafusal muscle fibers of the muscle spindle. This mechanism sets the baseline level of activity in α motor neurons and helps regulate muscle length and tone. Other reflex circuits provide feedback control of muscle tension and mediate essential functions, such as the rapid withdrawal of limbs from painful stimuli.

Much of the spatial organization and timing of muscle activation required for complex rhythmic movements such as locomotion is provided by specialized local circuits called central pattern generators. Because of the essential role of lower motor neurons in all of these circuits, damage to them results in paralysis or paresis of the associated muscle and other changes, including loss of reflex activity, loss of muscle tone, and eventual muscle atrophy.