Frequency-Following Response to Steady-State Vowel in Quiet and Background Noise Among Marching Band Participants With Normal Hearing

Abstract

Objective: Human studies enrolling individuals at high risk for cochlear synaptopathy (CS) have reported difficulties in speech perception in adverse listening conditions. The aim of this study is to determine if these individuals show a degradation in the neural encoding of speech in quiet and in the presence of background noise as reflected in neural phase-locking to both envelope periodicity and temporal fine structure (TFS). To our knowledge, there are no published reports that have specifically examined the neural encoding of both envelope periodicity and TFS of speech stimuli (in quiet and in adverse listening conditions) among a sample with loud-sound exposure history who are at risk for CS. Method: Using scalp-recorded frequency-following response (FFR), the authors evaluated the neural encoding of envelope periodicity (FFR ENV ) and TFS (FFR TFS ) for a steady-state vowel (English back vowel /u/) in quiet and in the presence of speech-shaped noise presented at +5- and 0 dB SNR. Participants were young individuals with normal hearing who participated in the marching band for at least 5 years (high-risk group) and non–marching band group with low-noise exposure history (low-risk group). Results: The results showed no group differences in the neural encoding of either the FFR ENV or the first formant (F1) in the FFR TFS in quiet and in noise. Paradoxically, the high-risk group demonstrated enhanced representation of F2 harmonics across all stimulus conditions. Conclusions: These results appear to be in line with a music experience–dependent enhancement of F2 harmonics. However, due to sound overexposure in the high-risk group, the role of homeostatic central compensation cannot be ruled out. A larger scale data set with different noise exposure background, longitudinal measurements with an array of behavioral and electrophysiological tests is needed to disentangle the nature of the complex interaction between the effects of central compensatory gain and experience-dependent enhancement.