Summary
This study investigated the effects of laboratory-induced stress and beta-adrenergic
blockade on acoustic and aerodynamic voice measures. In a double-blind, placebo-controlled
trial, 12 participants, six males and six females, underwent cold pressor-induced
sympathetic activation followed by placebo or treatment with 40 mg propranolol. Aerodynamic and acoustic parameters of voice were collected at baseline,
during cold pressor and after treatment with propranolol or placebo. Fundamental frequency,
jitter, shimmer, maximum airflow declination rate, voice onset time, speaking rate,
and subglottal pressure were measured at baseline, during cold pressor-induced stress,
and after treatment with propranolol or placebo. Cardiovascular measures served as
indicators of sympathetic nervous system (SNS) activation by cold pressor and antagonism
by propranolol, and were collected during all conditions. Cold pressor appeared to
adequately agonize the SNS as indicated by significant increases in resting systolic
and diastolic blood pressure and heart rate. Propranolol appeared to adequately antagonize
the SNS for the participants. Jitter ratio demonstrated a statistically significant
increase in the participants treated with propranolol. Speaking rate demonstrated
a small but significant increase in the placebo control group during cold pressor.
Gender differences were observed in a few measures. Cold pressor adequately agonized
and propranolol adequately antagonized the SNS. No statistically significant differences
across subjects were observed in the voice parameters during cold pressor-induced
stress before treatment. Jitter ratio increased significantly during propranolol treatment
and cold pressor. Speaking rate demonstrated a statistically significant increase
during cold pressor in the placebo control group. Gender differences were observed,
but were few.
Key Words
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Article info
Publication history
Published online: October 21, 2009
Accepted:
December 2,
2008
Identification
Copyright
© 2010 The Voice Foundation. Published by Elsevier Inc. All rights reserved.
