A Neurological Representation of Speech State Anxiety: Mapping Salivary Cortisol Levels of Public Speakers
Roberts, James B., Sawyer, Chris R., Behnke, Ralph R., Western Journal of Communication
SOME SCHOLARS in the natural sciences now explore questions that were once the sole dominion of social science and the merging of these research traditions enables scholars to construct more powerful explanations of human behavior than was formally possible (Wilson, 1998). Consilence, the convergence of interests and knowledge from diverse fields, has taken place in the field of communication and is evident in recent studies of speech state anxiety.
When examining public speaking, various disciplines offer explanations of speech state anxiety based upon the functioning of certain biological mechanisms (Behnke & Sawyer, 2000; Behnke & Sawyer, 2001a; Behnke & Sawyer, 2001b; Porhola, 1999; Sawyer & Behnke, 1999). Imbedded within this framework is the assumption that specific neurological events account for human emotions, especially fear (Gray & McNaughton, 2000; McNaughton & Gray, 2000). Wishing to avoid invasive and cumbersome methods, such as magnetic resonance imaging and positron emission tomography, scholars have been somewhat restricted in their efforts to make direct observations of underlying biological anxiety mechanisms. Much of what is known about the biology of speech state anxiety has been derived from studies of physiological reactions, such as heart rate, commonly associated with arousal (Beatty & Behnke, 1991; Behnke & Beatty, 1981a; Behnke & Beatty, 1981b; Behnke, Carlile, & Lamb, 1974; Behnke & Sawyer, 2001b; Booth-Butterfield, 1987; Sawyer & Behnke, in press).
Despite its utility in constructing communication theory (e.g., Andersen, Guerrero, Buller, & Jorgensen, 1998), physiological arousal is seen as a secondary indicator of neural activity rather than a direct measure of an affective state. Although commonly associated with anxiety reactions, accelerated heart rate is also associated with increases in exhilaration and excitement. Consequently, scholars must differentiate between these forms of arousal within the context of the constructs under investigation (LePoire & Burgoon, 1996).
Several arousal circuits have been identified in humans, each one operating from a unique brain center and producing its own specific pattern of physiological reactions, including very specific neuroendocrine or hormonal responses (Boucsein & Backs, 2000; McNaughton & Gray, 2000). Cortisol, a byproduct of the hypothalamic-pituatary-adrenocortical (HPA) system, is associated with state anxiety. Although speech anxiety theories have utilized neurological components, hormonal responses have not been employed in communication state anxiety studies. The purpose of the present study is to examine one such neuroendocrine response, salivary cortisol, as a direct measure of a particular affect, public speaking state anxiety.
Public Speaking Anxiety as Behavior Inhibition
Scholars have identified several arousal systems within the human nervous system that are triggered by environmental stress (Boucsein & Backs, 2000). Gray (1982; Gray & McNaughton, 2000) maintains that one of these systems serves as the basis for state anxiety and has been linked to the survival of numerous species including man. According to this perspective, a feature of brain anatomy called the comparator, detects conflicts between an organism's goals and current environmental conditions. Once a conflict is detected, the comparator decides whether the situation is likely to produce punishment or reward. If a punishment is detected, the comparator switches control to the behavior inhibition system (BIS), a circuit in the brain that suppresses on-going motor responses while increasing an organism's vigilance and sense of alarm. Although BIS control will persist if the potential for punishment remains high, continued exposure to the threat often results in a lessening of BIS influence, provided that punishment does not ensue. …