Objectives: Permanent threshold elevation after noise exposure, ototoxic drugs or aging is caused by loss of sensory cells; however, animal studies show that hair cell loss is often preceded by degeneration of synapses between sensory cells and auditory nerve fibers. The silencing of these neurons, especially those with high thresholds and low spontaneous rates, degrades auditory processing and may contribute to difficulties understanding speech in noise. Although cochlear synaptopathy can be diagnosed in animals by measuring suprathreshold auditory brainstem responses, its diagnosis in humans remains a challenge. In mice, cochlear synaptopathy is also correlated with measures of middle-ear muscle (MEM) reflex strength, possibly because the missing high-threshold neurons are important drivers of this reflex. We hypothesized that measures of the MEM reflex might be better than other assays of peripheral function in predicting difficulties hearing in difficult listening environments in human subjects. Design:We recruited 165 normal-hearing healthy subjects, between the ages of 18 and 63, with no history of ear or hearing problems, no history of neurologic disorders and unremarkable otoscopic examinations. Word recognition in quiet and in difficult listening situations was measured in four ways: using isolated words from the NU-6 corpus with either a) 0 dB signal-to noise, b) 45% time compression with reverberation, or c) 65% time compression with reverberation and d) with a modified version of the QuickSIN. Audiometric thresholds were assessed at standard and extended high frequencies (EHFs). Outer hair cell function was assessed by distortion product otoacoustic emissions (DPOAEs). Middle-ear function and reflexes were assessed using three methods: the acoustic reflex threshold as measured clinically, wideband tympanometry as measured clinically and a custom wideband method that uses a pair of click probes flanking an ipsilateral noise elicitor. Other aspects of peripheral auditory function were