An abnormally rapid rate of loudness growth for given increments in stimulus intensity is seen both in patients with cochlear pathology and in normal listeners under conditions of wide-spectrum noise masking. The phenomenological similarity between these psychophysical observations raises the question of whether a single mechanism, or set of mechanisms, underlies them. Recent neurophysiological studies in animals have addressed the effects of cochlear pathology and noise masking on the neural correlates of stimulus intensity in the central auditory nervous system. A comparison of the data presented in those studies reveals that there are sequelae of cochlear pathology seen in the discharges of auditory-nerve fibers that might reasonably be expected to contribute to a steepened loudness function. These sequelae are not seen at the same locus in normal animals studied with noise masking paradigms. Noise masking, however, may have effects on the tonal sensitivity of more central neurons that mimic some of the sequelae of cochlear pathology seen in the auditory nerve. These data suggest that the mechanisms underlying the two manifestations of recruitment may be quite different, one having a uniquely cochlear site, while the other reflects purely central processes.