Objectives: Mediated by the medial olivocochlear system (MOCS), distortion product otoacoustic emission (DPOAE) levels are reduced by presentation of contralateral acoustic stimuli. Such acoustic signals can also evoke a middle ear muscle reflex (MEMR) that also attenuates recorded DPOAE levels. Our aim is to clearly differentiate these two inhibitory mechanisms and to analyze each separately, perhaps allowing the development of novel tests of hearing function. Methods: DPOAE were recorded in real time from chinchillas with normal auditory brainstem response thresholds and middle ear function. Amplitude reduction and its onset latency caused by contralateral presentation of intermittent narrow-band noise (NBN) were measured. Stapedius and tensor tympani muscle tendons were divided without disturbing the ossicular chain, and DPOAE testing was repeated. Results: Peak reduction of (2f1 - f2) DPOAE levels occurred when the center frequency of contralateral NBN approximated the primary tone f2, indicating an f2-frequency-specific response. For a 4.5-kHz centered NBN, DPOAE (f2 = 4.4 kHz) inhibition was 0.1 dB (p < 0.001). This response remained present after tendon division, consistent with an MOCS origin. Low-frequency NBN (center frequency: 0.5 kHz) reduced otoacoustic emission levels (0.1 dB, p < 0.001) across a wide range of DPOAE frequencies. This low-frequency response was abolished by division of the middle ear muscle tendons, clearly indicating MEMR involvement. Conclusions: Following middle ear muscle tendon division, DPOAE inhibition by contralateral stimuli approximating the primary tone f2 persists, whereas responses evoked by lower contralateral frequencies are abolished. This distinguishes the different roles of the MOCS (f2 frequency specific) and MEMR (low frequency only) in contralateral modulation of DPOAE. This analysis helps clarify the pathways involved in an objective test that might have clinical benefit in the testing of neonates.