Audiometric measurements are typically limited to the determination of the TTS₂ value, the Temporary Threshold Shift within 2 min after the exposure at 4 kHz, a frequency which represents the highest sensitivity in most individuals. Measurements during the restitution phase are mostly carried out only in laboratory studies due to the long time that is required. Thus, economic considerations, results from previous studies, and the fact that the C₅ dip (characteristic hearing loss at 4 kHz) is considered an undeniable sign of beginning hearing loss due to noise exposure, are all arguments for limiting studies to a single measuring frequency. The objective of this study was, however, to examine whether such threshold shift measurements at a single frequency can reliably capture the main metabolic processes in the inner ear after noise exposure. With respect to practical relevance, this was to be shown for continuous and impulse noise exposures.

In a cross-over test design, 10 test subjects (Ss) with normal hearing (ages 28.7 ± 9 years) were exposed to 3 different kinds of sound exposures. In Test Series I (TS I), “White Noise” of 94 dB(A) for 1 h – which is energy equivalent to 85 dB(A) for 8 h – was used. In TS II, an energy equivalent impulse noise exposure with 9,000 impulses (5 ms, each, with a level of 113 dB(A)) in 1-s intervals was used. In TS III, the duration of each impulse was shortened to 2.5 ms, i.e., the applied noise dose was halved. In all 3 test series, the TTS₂ values and the hearing threshold shifts' restitution were determined until the individual resting hearing threshold was once again reached. This was done at the frequency at which the maximum threshold shift occurs as well as at the upper and lower adjacent frequencies. Additionally, using the areas underneath the restitution curves (the IRTTS values) at the 3 frequencies, the total physiological costs which the hearing must “pay” for the preceding exposure were quantified.

The results in all Ss and across all 3 experiments were consistent in the sense that the maximum hearing threshold shifts, i.e., the TTS₂ values, at the lower and upper adjacent frequencies were substantially lower than at the main frequency. Additionally, the restitution time was shorter. The IRTTS values, i.e., the areas under the restitution curves also displayed substantial differences. On average, the physiological costs of the 10 Ss after exposure to continuous noise at the adjacent frequencies were only approximately 25%, i.e., ¼, of the physiological costs which were measured at the main frequency. For the energy equivalent exposure to impulse noise, the calculated total threshold shifts were even less than 20%. Exposure to impulse noise which was reduced by half in terms of energy resulted in total hearing threshold shifts at the adjacent frequencies which were even less than 10%. In conclusion, the excitation of the hair cells in the inner ear seems to affect larger areas with continuous broadband noise than with impulse noise. However, measurements of hearing threshold shifts at the frequency of the hearing's highest sensitivity seem already to capture the main metabolic processes.