THE RESPONSE TO SUDDEN CHANGE IN VOCAL-TRACT RESISTANCE DURING STOP CONSONANT PRODUCTION

Citation
Jr. Kim et al., THE RESPONSE TO SUDDEN CHANGE IN VOCAL-TRACT RESISTANCE DURING STOP CONSONANT PRODUCTION, Journal of speech language and hearing research, 40(4), 1997, pp. 848-857
Citations number
46
Categorie Soggetti
Language & Linguistics",Rehabilitation
Volume
40
Issue
4
Year of publication
1997
Pages
848 - 857
Database
ISI
SICI code
Abstract
The speech respiratory system is configured in ways that tend to maxim ize its ability to respond to changes in the airway environment. Intra oral pressures remain at levels sufficient to generate reliably recogn ized consonant sounds even in the presence of structural deficits such as velopharyngeal inadequacy. Similar respiratory compensations occur when bite blocks and bleed valves are used to vent airway pressures, The purpose of the present study was to determine the sensitivity of t he monitoring system psychophysically and to assess its physiological response to sudden, unanticipated perturbations. Twenty adults were as ked to produce the utterance /pa/, and a calibrated perturbator valve permitted air to escape from the oral cavity on randomly selected prod uctions. Respiratory responses were recorded using PERCI-SARS instrume ntation. The results indicated that sudden openings of 0.14 cm(2) (SD = 0.04) were detected by speakers. Compensatory respiratory responses to suprathreshold pressure-venting occurred rapidly (i.e., 27 ms [SD = 8]) after valve opening. Although peak pressure and area under the pr essure pulse fell with valve opening, the magnitude of pressure was ne vertheless sufficient for sound generation. Measurements of the slope of the rise in intraoral pressure after subthreshold pressure-venting in 10 participants were compared to measurements obtained From an elas tic model of the upper airway. The data demonstrated a significant dif ference between vented and unvented conditions for the model, but not the participants. This suggests that elastic recoil is actively and un consciously controlled in humans to compensate For losses in airway pr essure during speech.