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. This phenomenon, in which anxiety decreases with benign exposure to threat, is called habituation.
Beatty, McCroskey, and Heisel (1998) apply the principle of BIS reactivity to communication apprehension. Highly apprehensive individuals possess a reactive BIS, whereas low apprehensive people possess an underactive BIS. For this reason, speakers with elevated communication apprehension often avoid public speaking situations (McCroskey & Beatty, 2000). When forced to communicate, apprehensive speakers exhibit inhibited public speaking behaviors, such as monotone vocal delivery, rigid gestures, and deadpan facial expressions (Freeman, Sawyer, & Behnke, 1997). Individuals with a highly reactive BIS experience greater anticipatory activation, autonomic reactivity, and physiological arousal during public speaking (Behnke & Sawyer, 2001b). Furthermore, Sawyer and Behnke (1999) have attributed habituation of psychological state anxiety to BIS activity during public speaking. Consequently, both psychological anxiety and physiological anxiety appear to be mediated by BIS activity.
A central component of the BIS or anxiety circuit is the response of the hypothalamus (Gray, 1982; Gray & McNaughton, 2000). Specifically, the hypothalamus controls two major neuroendocrine systems that are sensitive to stress: the hypothalamic-pituitary-adrenocortical (HPA) system and the sympathetic-adrenomedullary system (Boucsein & Backs, 2000). Both systems influence emotions and cognitive processes such as attention, vigilance, and effort, but only the HPA system is associated with fear or distress (Gunnar, 1994; Lundberg & Frankenhaeuser, 1980; Ursin, Baade, and Levine, 1978). Cortisol, the byproduct of HPA activity, is particularly responsive to the psychological stimuli that trigger state anxiety and provides a physiological index for state anxiety (Gray & McNaughton, 2000).
State Anxiety and Cortisol
Scholars have examined the psychological correlates of cortisol reactions for more than 40 years. These associations include regulation, temperament, and behavioral inhibition. For example, McBurnett, Lahey, Frick, and Risch (1991) found cortisol to be a useful biological marker of arousal associated with BIS activity in children with anxiety and conduct disorders. Relationships have been established between cortisol and both emotional and mental strain (Bouscein & Backs, 2000). Furthermore, psychologists have found correlations between behavioral inhibition, temperament, social competence, novel experiences, and cortisol reactivity (Davis, Donzella, Krueger, & Gunnar, 1999; Gunnar, Tout, Haan, Pierce, & Stansbury, 1996; Haan, Gunnar, Tout, Hart, & Stansbury, 1998). Apparently, the release of cortisol during stress is anatomically regulated by the BIS and represents a "global response to emotionally distressing and threatening circumstances" (Al Absi et al., 1997). Consequently, cortisol should serve as a valid measure in psychobiological studies of public speaking state anxiety.
Blanchard and Blanchard (1990) describe state anxiety as a function of anticipating a potential threat. Anxiety studies involving the anticipation of parachute jumping and final exam-taking have produced significant increases in cortisol concentrations (e.g., Cook, Read, Walker, Harris, & Riad-Fahmy, 1992). Gray and McNaughton (2000) further advance this distinction by suggesting that anxiety incorporates a cognitive, motivational approach goal (e.g. reward) in addition to the emotional avoidance goal (e.g. escape) produced by fear. Although public speaking tasks, such as the Trier Social Stress Test (Kirschbaum, Pirke, & Hellhammer, 1993), have been used increasingly in studies of cortisol response, participants in these studies typically had limited preparation time prior to public speaking performance (usually about 10 minutes). Consequently, the effects of preparing a speech, especially on anticipatory anxiety, require further investigation.
Based on the preceding discussion, the following hypotheses were advanced:
H1: The pattern of cortisol levels for public speakers will be a monotonicaly decreasing function.
H2: A positive relationship exists between cortisol levels and psychological measures of public speaking state anxiety.
Participants were 31 (10 male, 21 female) students between 18 and 22 (M = 20.1) years of age enrolled in a college-level basic speech communication course. There were four freshmen, 10 sophomores, 11 juniors, and six seniors. Participation was voluntary and students completed informed consent forms notifying them of the procedures to be carried out during the investigation.
Two weeks prior to the investigation, students were asked to prepare and present a 5-6 minute informative speech, to an audience of their peers, for evaluation by the instructor. Those who chose to participate were given extra-credit. They were instructed to refrain from smoking, physical exercise, meals, alcoholic beverages, and caffeinated beverages at least one hour prior to testing.
Speeches were given between 11 a.m. and 3 p.m. in a standard classroom setting before an audience of 20-25 fellow students and the instructor. Speaking order was established by random selection. Following the presentations, speakers went to an adjacent room where saliva samples were taken for the cortisol test. Immediately following their presentations, participants completed three narrow-band measures of state anxiety reflecting the confrontation (the first minute of the speech), adaptation (last minute of the speech) and release (one minute after the speech) milestones.
Psychological State Anxiety Measure
The five-item measure developed by O'Neil, Spielberger, and Hansen (1969) was used to measure psychological state anxiety for each public speaking milestone. The items were: I felt tense; I felt calm; I felt relaxed; I felt at ease; and, I felt jittery. In previous studies of public speaking state anxiety, this measure has performed according to theoretical expectations and consistently yielded acceptable levels of internal consistency (Beatty, 1987; Beatty, 1988a; Beatty, 1988b; Beatty, Balfantz, & Kuwabara, 1989; Beatty & Friedland, 1990; Beatty & Valencic, 2000).
Laboratory Procedures and Manipulation Checks
Previous empirical studies have established cortisol responses as a neurological concomitant of state anxiety (Kirschbaum & Hellhammer, 1989). Since then, threats to internal and external validity are generally controlled by observing strict data collection protocols, maintaining rigorous laboratory procedures, and by exerting statistical control over error, such as adjusting for baseline readings (Thayer & Friedman, 2000). (1) The following laboratory procedures and manipulation checks were used in the present study.
Manipulation check #1. Prior to sample collection (both basal and experimental), students completed a questionnaire containing control questions for outside biological influences shown to affect cortisol levels (i.e. smoking, alcohol, meals, beverages). Students who fit all criteria were allowed to give saliva samples; however, all students who volunteered to participate in the study received extra-credit to help ensure the integrity of questionnaire responses.
Sample collection. Saliva samples were obtained using commercial "salivettes" that provided accurate, quick, hygienic and stress-free sampling (Hellhammer, Kirschbaum, & Belkien, 1987). Commercially available enzyme-linked immunosorbant assay (ELISA) kits were used to determine cortisol levels in the saliva samples. In the ELISA procedure, microtitre plates were coated with antibodies to cortisol. During incubation, known concentrations of cortisol called standards and unknown concentrations of cortisol from the saliva samples compete for antibody binding sites. After incubation, unbound components are washed away and a substrate was added that reacts with the enzyme-linked cortisol. A standard plate reader was used to detect the presence of the bound substrate.
Citric acid salivettes were used to induce salivary flow. Baseline levels of salivary cortisol were taken one week prior to the study on a non-speaking day at the same time of day as the scheduled presentation. On the day of the presentation, each speaker gave five samples at 8-minute intervals after the beginning of the speech (confrontation = [t.sub.0]). Thus, samples [t.sub.1], [t.sub.2], [t.sub.3], [t.sub.4], and [t.sub.5] were obtained at minutes 8, 16, 24, 32, and 40, respectively. After centrifugation at 3000 rpm, the samples were frozen at -20 degrees Celsius for two months until laboratory analysis.
Manipulation check #2. Prior to laboratory analysis, the pH level of each sample was tested to ensure that the acidity was within optimal levels for the ELISA procedure. Two participants had samples with pH readings that were below optimal levels and these participants' data were discarded from the study.
Means and standard deviations of the salivary cortisol levels for each time period are reported in Table 1. Measures of salivary cortisol obtained from speaker saliva samples were correlated with the theoretical values predicted from the known standards (r = .99). Consequently, the ELISA procedure used in this study was a reliable method for measuring speaker cortisol levels. An analysis of variance for repeated measures was performed with individual baseline measures serving as covariates. Results show negative monotonically decreasing mean scores in the ordering of the five time periods (F(4,112) = 8.84, p < .0001, [[eta].sup.2] = .10). Scheffe tests detected significant differences between means for cortisol levels at eight minutes and 40 minutes and for cortisol levels at and 16 and 40 minutes. A power analyses (Buchher, Faul, & Erdfelder, 1997) for non-significant differences in mean cortisol levels appear in Table 2. Power for all non-significant results was below .80.
Means (with standard deviations in parentheses) for STAI (A-State) for the confrontation, adaptation, and release milestones were 14.27(4.67), 12.59(1.88), and 8.93(1.96), respectively. Alpha reliability for the confrontation, adaptation, and release stage STAI measures was .92, .91, and .93, respectively. The association between psychological state anxiety and salivary cortisol levels over time was analyzed repeated measures analysis of variance with time as the independent variable, psychological state anxiety as a covariate, and salivary cortisol as the repeated measure. Three such analyses were conducted, one for each narrow-band state anxiety measure. Associations were detected cortisol levels and confrontation ([F.sub.4,1,4,135] = 6.31, p < .05, [[eta].sup.2] = .05), adaptation ([F.sub.4,1,4,135] = 27.61, p < .05, [[eta].sup.2] = .21), and release ([F.sub.4,1,4,135] = 5.953, p < .05, [[eta].sup.2] = .04) state anxiety milestones. A correlational analysis comparing each narrow-band measure of psychological state anxiety with cortisol level at each eight-minute interval appears in Table 3. Psychological measures of state anxiety during public speaking were positively correlated with cortisol levels over time.
Participants in this study experienced a dramatic two-to-three-fold increase in salivary cortisol levels from baseline, a finding consistent with the view that cortisol levels representing individual differences in reactivity among public speakers. These results also show progressively decreasing levels of cortisol from the first time period (8 minutes) through the fifth time period (40 minutes). In previous studies, salivary cortisol has most often peaked approximately 30 minutes after confrontation with the stressor, yielding an inverted U pattern. This difference in response patterns can be attributed to the effect of anticipatory anxiety on psychological stress, and hence cortisol response. In the present study, participants had two weeks to prepare speeches that would ultimately be presented in front of a live audience including an instructor who would evaluate them. Previous research participants were only given 0-10 minutes of speech preparation time for a laboratory experiment with little lasting impact. Yet, the effects of anticipatory anxiety have been well documented in the communication literature (Behnke & Beatty, 1981a). Behnke and Sawyer (2001a) found the same progressively decreasing function for psychological state anxiety with the highest level of anxiety occurring during the anticipation period.
Gray's theory of anxiety sheds light on these findings by concentrating on the cognitive and physiological effects of anticipated potential threats. Gray (1987; 1990) contends that continued exposure to a fear-arousing stimulus yields decreasing levels of state anxiety. This phenomenon, called habituation, is set in motion when speakers experience fewer negative consequences during exposure than they had expected. Likewise, decreases in speaker stress levels are reflected in the corresponding physiological responses occurring over the remainder of the speech. Heart rate studies report similar habituation patterns during public speaking, although heart rate peaks during the confrontation period and dramatically drops throughout the adaptation and release periods (Beatty & Behnke, 1991; Behnke & Carlile, 1971; Booth-Butterfield, 1987).
The results of the present study indicate that salivary cortisol is correlated with psychological measures of public speaking state anxiety. Moreover, the attenuation of cortisol levels over time reflects the monotonic decreasing function observed in pattern studies of narrow-band psychological measures of state anxiety. Individual differences within the overall patterns of psychological anxiety have recently been explicated, identifying some individuals as habituators and others as sensitizers (Behnke & Sawyer, 2001a). Future research should examine the cortisol responses of these differing state anxiety pattern types.
In the current study, cortisol levels and measures of psychological state anxiety were taken at graduated intervals following the speech so as not to disrupt the speech itself. However, technological advancements may one day permit the sampling of speaker cortisol and other neurological concomitants of state anxiety in real-time before, during, and after public speaking. For example, telemetry heart rate and other physiological measurements have been conducted without distracting ambulatory subjects (Backs & Boucsein, 2000). Improvements of this type would help to overcome a limitation of the present study, specifically, the inability to directly observe habituation processes over time. Additionally, the self-selection of participants potentially allowed speakers with higher levels of speech trait anxiety to opt out of the study. In the future, researchers may be able to remedy these limitations through innovative technologies and improved experimental procedures.
Novel experiences have been shown to elicit mild reactions of the HPA system. Although there is no empirical evidence that the use of salivettes, such as those employed in this study, provoke HPA reactions, future researchers should weigh this consideration against the costs when planning to conduct salivary cortisol studies.
TABLE 1 Means and Standard Deviations for Cortisol Concentrations Across Time Periods Descriptive Statistics Mean ([micro]g/dL) Standard Deviation [t.sub.1,] Eight minutes .590 .394 [t.sub.2,] Sixteen minutes .579 .340 [t.sub.3,] Twenty-four minutes .456 .063 [t.sub.4,] Thirty-two minutes .427 .223 [t.sub.5,] Forty minutes .334 .178 TABLE 2 Power Analysis of Non-Significant Differences in Mean Cortisol Levels Power Statistics Mean Cortisol Levels Delta Effect Size (d) Power [T.sub.1] vs. [T.sub.2] .11 .03 .05 [T.sub.1] vs. [T.sub.3] 1.47 .38 .30 [T.sub.1] vs. [T.sub.4] 1.94 .51 .48 [T.sub.2] vs. [T.sub.3] 1.48 .39 .31 [T.sub.2] vs. [T.sub.4] 2.01 .53 .51 [T.sub.3] vs. [T.sub.4] .42 .11 .07 Critical value for all analyses was 2.003. TABLE 3 Correlation Matrix of Speech Anxiety Milestones and Salivary Cortisol Levels over Time Cortisol at Minutes from Initial Exposure STAI Milestones 8 Min 16 Min 24 Min 32 Min 40 Min Anticipation .38 * .07 .10 .07 .02 Confrontation .36 * .32 * .23 .31 * .26 Adaptation .25 .47 * .59 * .63 * .52 * Release .24 .35 * .41 * .47 * .41 * * p < .05, one-tailed test of significance
(1) Psychophysiology has been defined as "the study of psychological processes in the intact organism as a whole by means of unobtrusively measured physiological processes" (Furedy, 1983, p. 14). Because psychophysiological reactions are guided by the physical, biological, and chemical laws that direct the entire organism, the tendency to experience similar physiological reactions to like psychological stimuli is shared across the human species (Andreass, 2000). Differences in individual response, therefore, often reflect differing baseline conditions among subjects. It is a fairly common practice in psychophysiological research, therefore, to treat individual subjects as their own control group. For example, studies of public speaking state anxiety that involve measures of heart rate virtually never have control groups but nearly every one of them adjusts for baseline conditions, such as resting heart rate. Conducting psychophysiological research is expensive and time-consuming. Consequently, once a particular physiological response, such as cortisol, has been established as a reliable measurement strategy in controlled experiments, researchers frequently opt for quasiexperimental designs, such as the one used in the present study, and control threats to validity by adjusting individual scores for baseline conditions (Thayer & Friedman, 2000).
Al Absi, M., Bongard, S., Buchanan, T., Pincomb, G., Licinio, J., & Lovallo, W. R. (1997). Cardiovascular and neuroendocrine adjustment to public speaking and mental arithmetic stressors. Psychophysiology, 34, 266-275.
Andersen, P. A., Guerrero, L. K., Buller, D. B., & Jorgensen, P. F. (1998). An empirical comparison of three theories of nonverbal immediacy exchange. Human Communication Research, 24, 501-535.
Backs, R. W., & Boucsein, W. (2000). Engineering psychophysiology: Issues and applications. Mahwah, NJ: Lawrence Erlbaum.
Beatty, M. J. (1987). Communication apprehension as a determinant of avoidance, withdrawal, and performance anxiety. Communication Quarterly, 35, 202-217.
Beatty, M. J. (1988a). Impact of ambiguity reduction about performance expectations on audience anxiety. Communication Education, 37, 208-217.
Beatty, M. J. (1988b). Public speaking apprehension, decision-making errors in the selection of speech introduction strategies, and adherence to strategy. Communication Education, 37, 297-311.
Beatty, M. J., & Behnke, R. R. (1991). Effects of public speaking trait anxiety and intensity of speaking on heart rate during performance. Human Communication Research, 18, 147-176.
Beatty, M. J., & Friedland, M. H. (1990). Public speaking state anxiety as a function of selected situational and predispositional variables. Communication Education, 39, 142-147.
Beatty, M. J., & Valencic, K. M. (2000). Context-based apprehension versus planning demands: A communibiological analysis of anticipatory public speaking anxiety. Communication Education, 49, 58-71.
Beatty, M. J., Balfantz, G. L., & Kuwabara, A. Y. (1989). Trait-like qualities of selected variables assumed to be transient causes of performance state anxiety. Communication Education 38, 277-289.
Beatty, M. J., McCroskey, J. C., & Heisel, A. D. (1998). Communication apprehension as temperamental expression: A communibiological paradigm. Communication Monographs, 65, 197-219.
Behnke, R. R., & Beatty, M. J. (1981a). A comparision of anticipatory and performance anxiety in public speaking. Texas Speech Communication Journal, 1, 3-6.
Behnke, R. R., & Beatty, M. J. (1981b). A cognitive-physiological model of speech anxiety. Communication Monographs, 48, 158-163.
Behnke, R. R., & Carlile, L. W. (1971). Heart rate as an index of speech anxiety. Speech Monographs, 38, 65-69.
Behnke, R. R., & Sawyer, C. R. (2001a). Patterns of psychological state anxiety in public speaking as a function of anxiety sensitivity. Communication Quarterly, 49, 84-94.
Behnke, R. R., & Sawyer, C. R. (2001b). Public speaking arousal as a function of anticipatory activation and autonomic reactivity. Communication Reports, 14, 73-85.
Behnke, R. R., and Sawyer, C. R. (2000). Anticipatory anxiety patterns for male and female public speakers. Communication Education, 49, 187-195.
Behnke, R. R., Carlile, L. W., & Lamb, D. (1974). A psychophysiological study of state and trait anxiety in public speaking. Central States Speech Journal, 25, 249-253.
Benjamins, C., Asscheman, H., Schuurs, A. H. (1992). Increased salivary cortisol in severe dental anxiety. Psychophysiology, 29, 302-305.
Blanchard, R. J, & Blanchard, D. C. (1990). Anti-predator defense as models of animal fear and anxiety. In P. F. Brain, S. Parmigiani, R. J. Blanchard, & D. Mainardi (Eds.), Fear and defence (pp. 124-133). New York: Harwood Academic.
Bohnen, N., Houx, P., Nicolson, N. & Jolles, J. (1990). Cortisol reactivity and cognitive performance in a continuous mental task paradigm. Biological Psychology, 31, 107-116.
Booth-Butterfield, S. (1987). Action assembly theory and communication apprehension: A psychophysiological study. Human Communication Research, 13, 386-398.
Boucsein, W., & Backs, R. W. (2000). Engineering psychophysiology as a discipline. In R. W. Backs & W. Boucsein (Eds.), Engineering psychophysiology: Issues and applications (pp. 3-30). Mahwah, NJ: Lawrence Erlbaum Associates.
Buchner, A., Faul, F., & Erdfelder, E. (1997). G-Power: A priori, post-hoc, and compromise power analyses for the Macintosh (Version 2.1.2) [Computer program]. Trier, Germany: University of Trier.
Burgoon, J. K., & LePoire, B. A. (1992). Reply from the heart: Who are Sparks and Greene and why are they saying all these horrible things? Human Communication Research, 18, 472-482.
Cappella, J. N., & Greene, J. O. (1984). The effects of distance and individual difference in arousability on nonverbal involvement: A test of discrepancy-arousal theory. Journal of Nonverbal Behavior, 8, 259-285.
Cappella, J. N., (1997). The development of theory about automated patterns of face-to-face human interaction. In G. Phillipsen, & T. L. Albrecht (Eds.), Developing communication theories. SUNY Series in human communication processes (pp. 57-83). Albany, NY: State University of New York Press.
Cook, N. J., Read, G. F., Walker, R. F., Harris, B., Riad-Fahmy, D. (1992). Salivary cortisol and testosterone as markers of stress in normal subjects in abnormal situations. In C. Kirschbaum, G. F. Read, & D. H. Hellhammer (Eds.), Assessment of hormones and drugs in saliva in biobehavioral research (pp. 147-162). Seattle, WA: Sogrefe & Huber.
Davis, E. P., Donzella, B., Krueger, W. K., & Gunnar, M. R. (1999). The start of a new school year: Individual differences in salivary cortisol response in relation to child temperament. Developmental Psychobiology, 35, 188-196.
Freeman, T., Sawyer, C. R., Behnke, R. R. (1997). Behavioral inhibition and the attribution of public speaking state anxiety. Communication Education, 46, 175-187.
Furlan, P. M., DeMartinis, N., Schweizer, E., Rickels, K., & Lucki, I. (2001). Abnormal salivary cortisol levels in social phobic patients in response to acute psychological but not physical stress. Biological Psychiatry, 50, 254-259.
Gray, J. A. (1982). The neuropsychology of anxiety: An enquiry into the functions of the septo-hippocampal system. New York: Oxford University Press.
Gray, J. A. (1987). Perspectives on anxiety and impulsivity: A commentary. Journal of Research in Personality, 21, 493-509.
Gray, J. A. (1990). Brain systems that mediate both emotion and cognition. Cognition and Emotion, 4, 269-288.
Gray, J. A., & McNaughton, N. (2000). The neuropsychology of anxiety: An enquiry into the functions of the septo-hippocampal system (2nd ed.). New York: Oxford University Press.
Greene, J. O., & Sparks, G. G. (1992). Intellectual scrutiny as an alternative to replies from the heart. Toward clarifying the nature of arousal and its relation to nonverbal behavior. Human Communication Research, 18, 483-488.
Gunnar, M. R. (1994). Psychoendocrine studies of temperament and stress in early childhood: Expanding current models. In J. E. Bates & T. D. Wachs (Eds.), Temperament: Individual differences at the interface of biology and behavior (pp. 175-198). Washington, DC: American Psychological Association.
Gunnar, M. R., Tout, K., Haan, M. de, Pierce, S., & Stansbury, K. (1997). Temperament, social competence, and adrenocortical activity in preschoolers. Developmental Psychobiology, 31, 65-85.
Haan, M. de, Gunnar, M. R., Tout, K., Hart, J., & Stansbury, K. (1998). Developmental Psychobiology, 33, 93-101.
Hellhammer, D. H., Kirschbaum, C., Belkien, L. (1987). Measurement of salivary cortisol under psychological stimulation. In J. N. Hingtgen, D. H. Hellhammer, & G. Huppmann (Eds.), Advanced methods in psychobiology (pp. 281-289). Toronto: Hogrefe.
Hoehn, T., Braune, S. Scheibe, G., & Albus, M. (1997). Physiological, biochemical, and subjective parameters in anxiety patients with panic disorder during stress exposure as compared with healthy controls. European Archives of Psychiatry and Clinical Neuroscience, 247, 264-274.
Kahn, J. P., Michaud, C., de Talance, N., Laxenaire, M., Mejean, L., Burlet, C. (1992). Applications of salivary cortisol determinatiions to psychiatric and stress research: Stress responses in students during academic examinations. In C. Kirschbaum, G. F. Read, & D. H. Hellhammer (Eds.), Assessment of hormones and drugs in saliva in biobehavioral research (pp. 111-127). Seattle, WA: Sogrefe & Huber.
Kirschbaum, C., Pirke, K., & Hellhammer, D. H. (1993). The "Treir Social Stress Test": A tool for investigating psychobiological stress responses in a laboratory setting. Neuropsychobiology, 28, 76-81.
Le Poire, B. A., & Burgoon, J. K. (1996). Usefulness of differentiating arousal responses within communication theories: Orienting response or defensive arousal within nonverbal theories of expectancy violation. Communication Monographs, 63, 208-230.
Luecken, L. J. (1998). Childhood attachment and loss experiences affect adult cardiovascular and cortisol function. Psychosomatic Medicine, 60, 765-772.
Lundberg, U., & Frankenhaeuser, M. (1980). Pituitary-adrenal and sympathetic-adrenal correlations of distress and effort. Journal of Psychosomatic Research, 24, 125-130.
Lundberg, U., Hedman, M. Melin, B., & Frankenhaeuser, M. (1989). Type A behavior in healthy males and females as related to physiological reactivity and blood lipids. Psychosomatic Medicine, 51, 113-122.
Martel, F. L., Hayward, C., Lyons, D. M., Sanborn, K. Varady, S., & Schatzberg, A. F. (1999). Salivary cortisal levels in socially phobic adolescent girls. Depress Anxiety, 10, 25-27.
Mason, J. W. (1968). A review of psychoendocrine research on the pituitary-adrenal cortical system. Psychosomatic Medicine, 30, 576-607.
McBurnett, K., Frick, B. J., & Risch, C. (1991). Anxiety, inhibition, and conduct disorder in children: II. Relation to salivary cortisol. Journal of the American Academy of Child and Adolescent Psychiatry, 30, 192-196.
McCroskey, J. C., & Beatty, M. J. (2000). The communibiological perspective: Implications for communication instruction. Communication Education, 49, 1-6.
McNaughton, N., & Gray, J. A. (2000). Anxiolytic action on the behavioural inhibition system implies multiple types of arousal contribute to anxiety. Journal of Affective Disorders, 61, 161-176.
Nachmias, M., Gunnar, M. R., Mangelsdorf, S., Parritz, R. H., & Buss, K. (1996). Behavioral inhibition and stress reactivity: The moderating role of attachment security. Child Development, 67, 508-522.
O'Neil, F. H., Spielberger, C. D., & Hansen, D. N. (1969). The effects of state anxiety and task difficulty on computer-assisted learning. Journal of Educational Psychology, 60, 343-350.
Patterson, M. L., & Kitts, V. (1997). Social and communicative anxiety: A review and meta-analysis. In B. R. Burleson & A. W. Kunkel, (Eds.), Communication Yearbook, 20 (pp. 263-303. Thousand Oaks, CA: Sage.
Porhola, M. (1999) Arousal styles during public speaking. Paper presented at the annual meeting of the National Communication Association, Chicago, IL.
Rose, R. M., & Fogg, L. F. (1993). Definition of a responder: Analysis of behavioral, cardiovascular, and endocrine response to varied workload in air traffic controllers. Psychosomatic Medicine, 55, 325-338.
Roy, M. P., Kirschbaum, C., Steptoe, A. (2001). Psychological, cardiovascular, and metabolic correlates of individual differences in cortisol stress recovery in young men. Psychoneuroendocrinology, 26, 375-391.
Rubin, R. T., Miller, R. G., Arthur, R. J., & Clark, B. R. (1970). Differential adrenocortical stress responses in naval aviators during aircraft, carrier landing practice. Psychological Reports, 26, 71-74.
Sawyer, C. R., & Behnke, R. R. (1999). State anxiety patterns for public speaking and the behavioral inhibition system. Communication Reports, 12, 33-41.
Sawyer, C. R., & Behnke, R. R. (2002). Reduction in public speaking state anxiety during performance as a function of sensitization processes. Communication Quarterly, 50, 110-121.
Stansbury, K., & Gunnar, M. R. (1994). Adrenocortical activity and emotion regulation. Monographs of the Society for Research in Child Development, 59, 108-134.
Ursin, H., Baade, E., & Levine, S. (1978). Psychobiology of stress. San Diego, CA: Academic Press.
Wilson, E. O. (1998). Consilence: The unity of knowledge. New York: Vintage.
Young, E. A., Lopez, J. F., Murphy-Weinberg, V., Watson, S. J., & Akil, H. (2000). Hormonal evidence for altered responsiveness to social stress in major depression. Neuropsychopharmacology, 23, 411-418.
Zeier, H. (1994). Workload and psychophysiological stress reactions in air traffic controllers. Ergonomics, 37, 525-539.
Zeier, H, Brauchli, P., & Joller-Jemelka, H. I. (1996). Effects of work demands on immunoglobulin A and cortisol in air traffic controllers. Biological Psychology, 42, 413-423.
James B. Roberts (MS, Texas Christian University, 2002) is an instructor in the Department of Communication Studies at Texas Christian University, Fort Worth, Texas 76129. Chris R. Sawyer (Ph.D., University of North Texas, 1992) is Associate Professor and Ralph R. Behnke (Ph.D., University of Kansas, 1966) is Professor in the same department. James B. Roberts may be reached at (817) 257-7610 or email@example.com. Chris R. Sawyer may be reached at (817) 257-6666 or firstname.lastname@example.org. Ralph R. Behnke may be reached at (817) 257-6664 or email@example.com.…