Public Speaking Task Research Articles

Serum NPY and BNDF response to a behavioral stressor in alcohol-dependent and healthy control participants.

Neuropeptide Y (NPY) and brain-derived neurotrophic factor (BDNF) have been implicated in both the stress response and alcohol addiction. However, few studies have assessed the NPY and BDNF response to stress in alcohol-dependent participants and the concurrent measure of NPY and BDNF has not been reported in human participants. The purpose of this study was to concurrently assess serum NPY and BDNF, as well as adrenocorticotropin (ACTH) and cortisol, in control and race- and aged-matched abstinent alcohol-dependent participants in response to a stress-inducing public-speaking task. Basal and post-stress serum values of NPY and BDNF, as well as ACTH and cortisol, were assessed in 14 abstinent alcohol-dependent and ten healthy control male participants. Basal measures were stable over short periods of time and stress induced a significant increase in both NPY (p = 0.002) and BDNF (p = 0.006) as well as ACTH (p < 0.001) and cortisol (p < 0.007). Alcohol-dependent and control groups did not significantly differ on any basal or stress-induced measure. Basal and delta responses of NPY and BDNF were not significantly correlated, and delta peak responses of NPY and BDNF did not correlate with one another or with their respective ACTH and cortisol responses. These findings reveal that both serum NPY and BDNF are responsive to behavioral stressors, although their regulatory mechanisms appear to differ from one another and those of the hypothalamic-pituitary-adrenal axis. Differences in basal and stress-induced responses of NPY and BDNF were not supported between control and abstinent alcohol-dependent subjects.

Depressive symptoms and attenuated physiological reactivity to laboratory stressors

There is evidence that depressive symptoms are associated with attenuated physiological reactivity to active stressors. However, it is not known whether blunted reactivity in depressed individuals is stressor-specific. We examined cardiovascular and electrodermal reactivity in non-clinical participants with varying levels of depressive symptoms to different active and passive stressors. Depressive symptoms were inversely related to both blood pressure and skin conductance reactivity during a public speaking task and the viewing of the speech video. However, no effects were found during a cold pressor task. Together these findings suggest that depressive symptoms are related to attenuated sympathetic nervous system reactivity in response to self-relevant stressors.

Neurofunctional correlates of expressed vocal affect in social phobia

We investigated the neural correlates of expressed vocal affect in patients with social phobia. A group of 36 patients performed an anxiogenic public-speaking task while regional cerebral blood flow (rCBF) was assessed using oxygen-15 positron emission tomography. The patients' speech was recorded and content masked using low-pass filtering (which obscures linguistic content but preserves nonverbal affective cues). The content-masked speech samples were then evaluated with regard to their level of vocally expressed nervousness. We hypothesized that activity in prefrontal and subcortical brain areas previously implicated in emotion regulation would be associated with the degree of expressed vocal affect. Regression analyses accordingly revealed significant negative correlations between expressed vocal affect and rCBF in inferior frontal gyrus, putamen, and hippocampus. Further, functional connectivity was revealed between inferior frontal gyrus and (a) anterior cingulate cortex and (b) amygdala and basal ganglia. We suggest that brain areas important for emotion regulation may also form part of a network associated with the modulation of affective prosody in social phobia.

Negative affective responses to a speech task predict changes in interleukin (IL)-6

Laboratory studies show that individuals differ appreciably in the magnitude of their inflammatory responses to acute psychological stress. These individual differences are poorly understood, yet may contribute to variation in stress-associated disease vulnerability. The present study examined the possibility that affective responses to acute stress contribute to these differences. For this purpose, 102 relatively-healthy community volunteers (mean age 50 years; 60% female; 91.2% white) performed an acute stress protocol and measures of affective state and serum levels of the proinflammatory cytokine, interleukin (IL)-6 were collected at the end of a 30-min resting baseline, a 5-min evaluative public speaking task, and a 30-min recovery period. Results of regression analyses, controlling for age, race, gender, menopausal status, and body mass index, revealed a positive association of task-related increases in anger and anxiety with increases in IL-6 ( R 2 change = .08, p = .004; R 2 change = .08, p = .005, respectively). Further examination showed that these affective responses to the task were independent predictors of change in IL-6. Cardiovascular reactivity to the task did not explain the association. These results suggest that individuals who exhibit angry or anxious responses to acute challenge are more vulnerable to stress-related increases in markers of systemic inflammation, possibly rendering them more susceptible to inflammatory disease.

An Examination of the Factor, Convergent, and Discriminant Validity of the Behavioral Inhibition System and Behavioral Activation System Scales

The Behavioral Inhibition System and Behavioral Activation System Scales (BIS/BAS scales) are the most widely used measures designed to assess Gray’s Reinforcement Sensitivity Theory. However, questions remain regarding its factor, convergent, and discriminant validity. We assessed these properties in two samples of undergraduates (N = 723, N = 103). In Study 1, confirmatory factor analysis supported previous findings that suggested removal of several items, resulting in acceptable fit for a four-factor model. Convergent and discriminant validity were assessed for the original and revised scales. In Study 2, a public speaking task was used to assess validity of the scales in reference to positive/negative affect. Convergent and discriminant validity for the revised scales were not substantially different from the original scales. We suggest that future researchers should consider the use of the revised measure we describe. We also suggest that the creation of a revised BIS/BAS scale using new items may be warranted.

Age and puberty differences in stress responses during a public speaking task: Do adolescents grow more sensitive to social evaluation?

During adolescence pubertal development is said to lead to an increase in general stress sensitivity which might create a vulnerability for the emergence of psychopathology during this period. However, the empirical evidence for increasing stress sensitivity is scarce and mixed. Biological responses (salivary cortisol and alpha-amylase) were investigated during a social-evaluative stressor, the Leiden Public Speaking Task, in 295 nine to 17-year olds. Specific attention was paid to different elements of the task, that is anticipation to and delivery of the speech. Biological reactivity to the speech task increased with age and puberty, particularly during anticipation. Current findings support the idea that biological stress sensitivity increases during adolescence, at least in response to a social-evaluative situation. The increasing stress sensitivity appears related to both age and pubertal maturation, but unique contribution could not be distinguished. The importance of measuring anticipation is discussed.

Associations between common arginine vasopressin 1b receptor and glucocorticoid receptor gene variants and HPA axis responses to psychosocial stress in a child psychiatric population

On the one hand, a suitable response to daily stressors is crucial for adequate functioning in any natural environment. On the other hand, depending on the individual's genetic makeup, prolonged stress that is accompanied by an inappropriate level of responsiveness may lead to physiological and psychiatric disorders. Several psychiatric conditions have been linked with stress and alterations in hypothalamic–pituitary–adrenal (HPA) activity. While stress is a general phenomenon, illness is only seen in a proportion of individuals, suggesting that genetic factors may play a role in the ability to cope with stress. In children, relatively little research has been conducted to determine the impact of genetic factors on the variability in HPA axis functioning. In the present exploratory investigation, 106 prepubertal children were studied to estimate the impact of four glucocorticoid receptor gene ( NR3C1) polymorphisms ( NR3C1-1 [rs10482605], ER22/23EK [rs6190], N363S [rs6195], N766N [rs6196]) and five arginine vasopressin (AVP) receptor 1b gene ( AVPR1b) polymorphisms ( AVPR1b_s1 [rs28536160], AVPR1b_s2 [rs28373064], AVPR1b_s3 [rs33976516], AVPR1b_s4 [rs33985287], AVPR1b_s5 [rs33933482]) on cortisol responses after a psychosocial stress test (public speaking task). ER22/23EK carriers had significantly lower cortisol responses to psychosocial stress compared with noncarriers. These findings provide evidence for the relevance of the ER22/23EK polymorphism in childhood HPA axis regulation. However, the small number of ER22/23EK subjects does not allow us to draw definitive conclusions about the genotypic effect.

Effects of manipulating the amount of social-evaluative threat on the cortisol stress response in young healthy women

Psychological stress is known to activate the hypothalamic–pituitary–adrenal axis, resulting in the release of cortisol from the adrenal cortex into the bloodstream. Cortisol is the major human stress hormone and its health correlates continue to be investigated by laboratories around the world. One line of research suggests that specific situational variables play a role in the creation of a stressful situation. The current study examined the effects of systematically varying several situational characteristics on the cortisol stress response in 80 healthy young women exposed to a public speaking task. Three main factors and its interactions were investigated by locating the expert panel either inside or outside of the room, having the subjects speak either about themselves or somebody else, and by asking half of the subjects to perform a distractor task in addition to performing the public speaking. We interpreted these manipulations as variations of social evaluative threat, ego-involvement, and divided attention. We hypothesized that the variations and their interactions would cause differences in endocrine stress responses.The results showed that only the manipulation of social-evaluative threat had a significant main effect on the cortisol stress response in women. There was a further trend (p = 0.07) for a four-way interaction effect. No other main or interaction effects could be observed. We conclude that in women, social-evaluative threat affects the endocrine stress response. This is in contrast to a previous study showing no effects of this variation in men. Thus, future studies should more closely investigate sex or gender effects that might be interacting with the situational aspects of a stressful task.

Elevated Macrophage Migration Inhibitory Factor (MIF) is associated with depressive symptoms, blunted cortisol reactivity to acute stress, and lowered morning cortisol

Macrophage Migration Inhibitory Factor (MIF) is a proinflammatory cytokine produced by leukocytes and the secretory cells of the HPA axis. Remarkably, glucocorticoids (GC) induce leukocyte MIF secretion, while MIF renders leukocytes insensitive to the anti-inflammatory effects of glucocorticoids. In light of reported associations between dysphoric states, increased inflammatory activity, and reduced GC sensitivity, the current study investigated the association between MIF, loneliness and depressive symptoms. The study further investigated the relation between plasma MIF and markers of HPA function, i.e., diurnal cortisol and the cortisol response to acute stress. Healthy university undergraduates ( N = 126; 64 women) were invited to participate if their scores on the Beck Depression Inventory or UCLA loneliness scale were in the upper or lower quintile of their peer group. Plasma MIF and salivary cortisol were measured in response to a public speaking task. Ambulatory diurnal cortisol was assessed for 5 consecutive days. MIF levels were 40% higher in the high-depressive symptoms group compared to the low depressive symptoms group. Elevated MIF was also associated with a smaller cortisol response to acute stress and lower diurnal morning cortisol values. The observed association between HPA function and MIF remained robust after adjustment for depressive symptoms, and demographic, anthropomorphic, and behavioural factors. High levels of depressive symptoms were likewise associated with lower morning cortisol, but this association became non-significant after adjustment for MIF. MIF may be an important neuro-immune mediator linking depressive symptoms with inflammation and HPA dysregulation.

Frontal brain oscillations and social anxiety: A cross-frequency spectral analysis during baseline and speech anticipation

Increasing evidence suggests that cross-frequency spectral coupling between slow (SW) and fast (FW) wave activity in the EEG supports information exchange between separate and functionally distinct neural systems. Further, evidence suggests that states of uncertainty, anticipation and anxious apprehension involve a high degree of SW–FW coupling. We examined whether adults pre-selected for high and low social anxiety showed distinct patterns of frontal brain oscillatory coupling during resting baseline and the anticipation of a self-presentation task. As predicted, the high socially anxious group showed significantly greater SW–FW coupling than the low socially anxious group, in the right, but not left, frontal electrode sites while anticipating a public speaking task. Additionally, the low socially anxious group showed a decrease in delta power from baseline to speech anticipation, suggesting that they found the same task potentially rewarding. Exploratory analyses indicated no effects of delta-gamma coupling. However, EEG gamma band power increased during the speech anticipation condition, in the parietal electrode sites. Our results are discussed in the context of previous studies on cross-frequency EEG coupling in relation to individual differences in motivation and emotion and future directions for studying the neural correlates of anxiety.

Emotion, Stress, and Cardiovascular Response: An Experimental Test of Models of Positive and Negative Affect

The nature of the relationship between positive affect (PA) and negative affect (NA) has been a topic of debate for some time. In particular, there are gaps in our knowledge of the independent effects of PA and NA on health under stress. The study examined the effects of a laboratory-induced stressor on the experience of PA and NA, and the effects of affect on cardiovascular (CV) reactivity and recovery. A sample of 56 female college students was randomly assigned to a public speaking (stress) task or a silent reading (control) task. Pre- and posttask PA and NA were measured using the Positive and Negative Affect Schedule (PANAS Watson J Pers Soc Psychol 54:1,063-1,070, 1988). Baseline, task, and posttask cardiovascular measures were also recorded. The results indicated that PA and NA responded differently to the stressor and contributed independently to the prediction of both CV reactivity and recovery. Of particular interest was the finding that higher levels of both PA and NA predicted greater CV recovery. Results are discussed in light of the debate concerning the (in)dependence of positive and negative emotions and the importance of understanding the dynamics of emotions, stress, and health.

The Effect of Acute Psychological Stress on QT Dispersion in Patients with Coronary Artery Disease

An acute psychological stress can precipitate ventricular arrhythmias and sudden cardiac death in patients with coronary artery disease (CAD). However, the physiologic mechanisms by which these effects occur are not entirely clear. Mental stress-induced myocardial ischemia occurs in a significant percentage of the CAD population. It is unknown if the proarrhythmic effects of psychological stress are mediated through the development of myocardial ischemia. To examine the effects of psychological stress on QT dispersion (QTd) among CAD patients and whether these effects are mediated via the development of myocardial ischemia. Psychological stress was induced using a public speaking task. Twelve-lead electrocardiograms (ECG) were recorded at rest, during mental stress, and during recovery. QTd was calculated as the difference between the longest and the shortest QT interval in the 12-lead ECG. Rest-stress myocardial perfusion imaging was also performed to detect mental stress-induced myocardial ischemia. Mental stress induced a significant increase in QTd compared to the resting condition (P < 0.001). This effect persisted beyond the first 10 minutes of recovery (P < 0.001). QTd was significantly associated with the development of mental stress ischemia with ischemic patients having significantly higher QTd during mental stress than nonischemic patients (P = 0.006). This finding remained significant after controlling for possible confounding factors (P = 0.01). An acute psychological stress induces a significant increase in QTd, which persists for more than 10 minutes after the cessation of the stressor. This effect seems to be, at least partially, mediated by the development of mental stress-induced myocardial ischemia.

Usefulness of Peripheral Arterial Tonometry in the Detection of Mental Stress‐Induced Myocardial Ischemia

Mental stress-induced myocardial ischemia (MSIMI) identifies a subset of coronary arterial disease (CAD) patients at increased risk for adverse cardiovascular events. Peripheral arterial vasoconstriction has been consistently reported as an underlying mechanism for ischemia development in this setting and as such affords a unique opportunity for the noninvasive detection of this phenomenon. We studied the usefulness of a peripheral arterial tonometry (PAT) technique in the detection of MSIMI. We sought to identify response patterns that would predict the development of MSIMI. Participants were 211 patients with documented CAD. Mental stress testing was performed using a public speaking task. Rest-stress myocardial perfusion imaging was the gold standard for ischemia detection. PAT responses were assessed during the 2 phases of the stressful task (stress anticipation and the task performance) and were calculated as a ratio of stress to the resting pulse wave amplitude. Vascular response during the stress anticipation period (speech preparation) was more pronounced than during the actual speaking task (the mean preparation index was 0.64 +/- 0.53; the mean speech index was 0.72 +/- 0.60; P < 0.001). PAT response during speech preparation had modest accuracy for predicting MSIMI (area under the curve [AUC] was 0.63; 95% confidence interval [CI]: 0.53-0.74, P = 0.015). A PAT index < or = 0.52 was identified as the best cut off value for detecting MSIMI with a sensitivity of 76% and a specificity of 56%. We identified a pattern of peripheral arterial response to mental stress that has a relatively modest accuracy in predicting MSIMI. Further research is needed to validate the findings of this study.

A prepared speech in front of a pre-recorded audience: Subjective, physiological, and neuroendocrine responses to the Leiden Public Speaking Task

This study describes a new public speaking protocol for youth. The main question asked whether a speech prepared at home and given in front of a pre-recorded audience creates a condition of social-evaluative threat. Findings showed that, on average, this task elicits a moderate stress response in a community sample of 83 12- to 15-year-old adolescents. During the speech, participants reported feeling more nervous and having higher heart rate and sweatiness of the hands than at baseline or recovery. Likewise, physiological (heart rate and skin conductance) and neuroendocrine (cortisol) activity were higher during the speech than at baseline or recovery. Additionally, an anticipation effect was observed: baseline levels were higher than recovery levels for most variables. Taking the anticipation and speech response together, a substantial cortisol response was observed for 55% of participants. The findings indicate that the Leiden Public Speaking Task might be particularly suited to investigate individual differences in sensitivity to social-evaluative situations.

Tryptophan depletion affects the autonomic stress response in generalized social anxiety disorder

In generalized social anxiety disorder (gSAD), serotonergic dysfunctions are found, as well as abnormalities of the autonomic nervous system (ANS) in basal conditions and of the hypothalamic pituitary adrenal (HPA) axis in response to psychological challenges. These findings raise the question whether these phenomena are interrelated. Therefore we designed a study in which two groups with nine pair wise age and gender matched gSAD patients (total of 10 men and 8 women), who were successfully treated with a selective serotonin reuptake inhibitor (SSRI), underwent a tryptophan depletion challenge (TD) or a placebo condition. A TD procedure temporarily decreases serotonergic neurotransmission. In order to activate the stress system the TD/placebo challenge was combined with a public speaking task. We assessed ANS responses, as measured with the promising new marker salivary alpha-amylase (sAA), and HPA-axis responses, as measured with salivary cortisol. The most important result was that the TD group showed a significant larger sAA response to the public speaking task as compared to the placebo group, reflecting hyperresponsivity of the ANS in this group, whereas no differences were seen in cortisol responses. This suggests that in gSAD there is a vulnerability of the ANS more than the HPA-axis.

High-frequency heart rate variability and cortico-striatal activity in men and women with social phobia

Identifying brain systems that regulate or modulate autonomic nervous system functions may identify pathways through which psychosocial factors can influence health and disease. Reduced high-frequency heart rate variability (HF-HRV) characterizes anxiety disordered patients and is predictive of adverse myocardial events. Sex differences in the prevalence of anxiety disorders and cardiac diseases implicate the possibility of sex specific neural regulation of HF-HRV. We investigated the correlation between HF-HRV and regional cerebral blood flow (rCBF) in 28 subjects (15 women) with social phobia undergoing a stressful public speaking task. Regional CBF was measured with [15O] water positron emission tomography. Stress induced rCBF correlated positively with HF-HRV in the right supra genual anterior cingulate cortex Brodmann's area (BA) 32, the right head of the caudate nucleus and bilaterally in the medial prefrontal cortex (BA10), extending into the dorsolateral prefrontal cortex (BA46) in the left hemisphere. Men showed larger positive co-variation in the caudate than women. These findings underscore the importance of the emotional division of the anterior cingulate cortex, the prefrontal cortex and the striatum in cardiovagal activity. The study replicates and extends results from published functional neuroimaging studies on cardioregulatory or modulatory areas in healthy subjects to men and women with social phobia. Moreover, caudate functions, possibly related to dopaminergic neurotransmission, have sexually dimorphic effects on vagal modulation of the heart.

Differences in hypothalamic–pituitary–adrenal axis functioning among children with ADHD predominantly inattentive and combined types

Some evidence suggests that the HPA axis may be dysfunctional in children with attention-deficit/hyperactivity disorder (ADHD). The aim of this study was to investigate whether a different pattern of HPA axis activity is found between the inattentive (I) and combined (C) subtypes of ADHD, in comparison with healthy control children. A total of 100 prepubertal subjects [52 children with ADHD combined type (ADHD-C), 23 children with ADHD predominantly inattentive type (ADHD-I), and 25 healthy control subjects] were studied. The effects of stress were studied by comparing cortisol responses to a psychosocial stressor, consisting of a public speaking task. Children with ADHD-I showed an elevated cortisol response to the psychosocial stressor, in contrast to children with ADHD-C who showed a blunted cortisol response to the psychosocial stressor. When a distinction was made between responders and non-responders (a subject was classified as a responder when there was an increase in cortisol reactivity), hyperactivity symptoms were clearly related to a lower cortisol reactivity to stress. The results indicate that a low-cortisol responsivity to stress may be a neurobiological marker for children with ADHD-C, but not for those with ADHD-I. Directions for future research and clinical implications are discussed.

Interoceptive Sensitivity Modulates Anxiety During Public Speaking

This study explored the relationship between interoceptive sensitivity and the experience of public-speaking anxiety. We compared participants with high and low interoceptive sensitivity concerning self-report and behavioral measures of anxiety and concerning physiological variables before, during, and after a public-speaking task. Participants with high interoceptive sensitivity reported significantly less state anxiety before and after performing a public speech as well as less habitual public-speaking anxiety. No significant differences in behavioral or physiological measures were observed. We assume that individuals with high interoceptive sensitivity, to whom physiological signals are more easily accessible, experience less uncertainty during public speaking and can thus adjust their emotional processes more adequately. This finding appears in line with Damasio’s somatic marker hypothesis, which suggests that reasoning, decision-making, and social behavior are optimized by body-related signals in complex situations.

A Link between Serotonin-Related Gene Polymorphisms, Amygdala Activity, and Placebo-Induced Relief from Social Anxiety

Placebo may yield beneficial effects that are indistinguishable from those of active medication, but the factors underlying proneness to respond to placebo are widely unknown. Here, we used functional neuroimaging to examine neural correlates of anxiety reduction resulting from sustained placebo treatment under randomized double-blind conditions, in patients with social anxiety disorder. Brain activity was assessed during a stressful public speaking task by means of positron emission tomography before and after an 8 week treatment period. Patients were genotyped with respect to the serotonin transporter-linked polymorphic region (5-HTTLPR) and the G-703T polymorphism in the tryptophan hydroxylase-2 (TPH2) gene promoter. Results showed that placebo response was accompanied by reduced stress-related activity in the amygdala, a brain region crucial for emotional processing. However, attenuated amygdala activity was demonstrable only in subjects who were homozygous for the long allele of the 5-HTTLPR or the G variant of the TPH2 G-703T polymorphism, and not in carriers of short or T alleles. Moreover, the TPH2 polymorphism was a significant predictor of clinical placebo response, homozygosity for the G allele being associated with greater improvement in anxiety symptoms. Path analysis supported that the genetic effect on symptomatic improvement with placebo is mediated by its effect on amygdala activity. Hence, our study shows, for the first time, evidence of a link between genetically controlled serotonergic modulation of amygdala activity and placebo-induced anxiety relief.

Effects of Neonatal Dexamethasone Treatment on the Cardiovascular Stress Response of Children at School Age

The goal was to investigate cardiovascular responses to a psychosocial stressor in school-aged, formerly premature boys and girls who had been treated neonatally with dexamethasone or hydrocortisone because of chronic lung disease. We compared corticosteroid-treated, formerly preterm infants with formerly preterm infants who had not been treated neonatally with corticosteroids (reference group). Children performed the Trier Social Stress Test for Children, which includes a public speaking task and a mental arithmetic task. Blood pressure was recorded continuously before, during, and after the stress test. Plasma norepinephrine levels were determined before the test, directly after the stress task, and after recovery. Overall, in response to stress, girls had significantly larger changes in systolic blood pressure and mean arterial pressure and in stroke volume and cardiac output, compared with boys. Boys exhibited larger total peripheral resistance responses, compared with girls. The hydrocortisone group did not differ significantly from the reference group in any of the outcome measures. However, dexamethasone-treated children had smaller stress-induced increases in systolic and mean arterial blood pressure than did hydrocortisone-treated children. In addition, the dexamethasone group showed smaller increases in stroke volume and blunted norepinephrine responses to stress, compared with children in the reference group. Correction for gender did not affect these results. The differences in cardiovascular stress responses between girls and boys are consistent with known gender differences in adult cardiovascular stress responses. Our data demonstrate that neonatal treatment with dexamethasone has long-term consequences for the cardiovascular and noradrenergic stress responses; at school age, the cardiovascular stress response was blunted in dexamethasone-treated children. Hydrocortisone-treated children did not differ from the reference group, which suggests that hydrocortisone might be a safe alternative to dexamethasone for treating chronic lung disease of prematurity.