In anesthetized, vagotomized, paralyzed, and artificially ventilated dogs, naloxone effects on respiratory responses induced by thin-fiber muscular afferents were studied by recording phrenic nerve discharges. Naloxone augmented respiratory outputs, before, during, and after the stimulation. Two different types were found in the returning phase of the respiratory response by thin-fiber muscular afferent stimulation: respiratory outputs were supressed below the pre-stimulus level within several minutes after the cessation of the stimulus in some cases, while in the other cases they remained above the pre-stimulus level. In the latter cases, naloxone did not change the pattern of returning phase of the response, on the other hand, in the former cases, the after-suppression was significantly reduced by naloxone. The present results suggest that endogenous opiates play a role in setting the level of respiratory outputs and that in addition to facilitatory effects on respiration, thin-fiber muscular afferents drive a negative feedback system via neurohumoral mechanisms.