Previously, our research included electromyographic, histologic, and physiologic studies of immobilized and denervated rat muscles. The effects of electrical stimulation and passive exercise on reinnervation of denervated muscles were determined. Also, we developed an animal model of myotonic dystrophy, in which we measured muscle tension and electrical activity in myotonic muscles and correlated the results with hormone levels. Our present research involves investigating the cause of the new neuromuscular symptoms which appear in polio survivors 20 to 30 yr after the initial infection, i.e., the post-polio syndrome. We followed the contractile properties, degree of sprouting, and fiber-type patterns over time in partially denervated rat plantaris muscles. Partial denervation was accomplished by sectioning the L4 spinal nerve. We recorded measurements at 3, 6, 9, 12, and 15 mo postsurgery. At 6 mo, we found twitch and tetanic forces were normal and type I and II fiber areas in the partially denervated muscles were significantly larger than those in controls. The number of branch points per endplate in experimental muscles resembled those seen at 3 mo. After 9 mo, twitch and tetanus were lower than those of control muscles. Also, both type I and II fiber areas were significantly lower than controls. The number of terminal branches per endplate were much greater than in controls. In addition, preterminal and intraterminal nerve sprouting increased. It appears that the longterm partial denervation imposes an excessive strain on the motor neuron cell body and over time the endplates degenerate and muscle flbers atrophy. Our results show that partially denervated rat plantaris muscle is a model of the human post-polio motor unit.