Aging is characterized by loss of spinal motor neurons (MNs) due to apoptosis, elevated amounts of circulating cytokines and increased cell oxidative stress. The age-related loss of spinal MNs leads to a reduction in muscle fiber number and size (sarcopenia), resulting in impaired mechanical muscle performance that in turn leads to a reduced functional capacity during everyday tasks. At the same time, however, aging involves substantial reorganization in the neuromuscular system and the CNS, which includes partial reinnervation of deinnervated muscle fibers. Experimental findings comprise the presence of very large motor units with aging, fiber type grouping, compressed rate coding during graded muscle contraction, reduced resting H-reflex excitability, and reduced TMS-evoked motor potentials suggesting decreased excitability in corticospinal pathways. Maximum muscle strength and power are markedly decreased with aging, even in highly trained strength athletes. Strength training leads to increased muscle strength and power in the elderly, including very old individuals (80 yrs). Notably, maximum power increased more after strength training using heavy loads (80% 1RM) than less heavy loads (50% 1RM). While rapid muscle force production (rate of force development, RFD = ΔF/Δt) is reduced with aging, increases in RFD and contractile impulse (∫Fdt) can be observed following strength training concurrently with signs of elevated neuromuscular activity (increased surface EMG amplitude). Maximum RFD is influenced by maximal MN firing frequency and the presence of MN discharge doublets. Maximum firing frequency during isometric or dynamic MVC is reduced with aging, along with a reduced incidence of MN doublet firing. Importantly, maximum MN firing frequency is increased in the elderly with strength training. Frail elderly may show reduced central muscle activation (CA) assessed by electrical muscle stimulation superimposed during MVC. CA may increase with strength training in the elderly, where individual changes in CA and maximal muscle strength (MVC) were related in very old individuals (+80). Unilateral long-term limb disuse is accompanied by a selective reduction in CA for the affected limb. Short-term (2 wks) limb immobilization led to reduced CA in old but not young subjects, indicating that the neuromuscular system of old individuals may be affected more severely by short-term unloading. Subsequent re-training by means of resistance exercise (4 wks) appeared to fully restore CA in old individuals, while young subjects increased CA above pre training levels.Old individuals may show increased antagonist muscle coactivation during MVC, although not a universal finding. If elevated prior to training, antagonist coactivation typically decreases following strength training in the elderly, although increased antagonist coactivation may also occur. Nevertheless, elderly typically show elevated muscle coactivation during daily movement tasks such as stair climbing and step descent, which seems to be unaffected by strength training. Force steadiness is impaired with aging, as reflected by elevated SD during isometric and dynamic force tracking tasks. Notably, strength training leads to improved force steadiness. In conclusion, elderly individuals demonstrate substantial adaptive plasticity in the neuromuscular system in response to strength training (resistance exercise), which may effectively compensate for the age-related decline in muscle size and neuronal function.