Anxiety sensitivity moderates the subjective experience but not the physiological response to psychosocial stress

International Journal of Psychophysiology 141 (2019) 76–83

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International Journal of Psychophysiology journal homepage: www.elsevier.com/locate/ijpsycho

Full Length Article

Anxiety sensitivity moderates the subjective experience but not the physiological response to psychosocial stress

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Travis A. Wearnea,b, , Abbie Luciena, Emily M. Trimmera,b, Jodie A. Logana,b, JacquelineA. Rushbya,b, Emily Wilsona,b, Michaela Filipčíkováa,b, Skye McDonalda,b a b

School of Psychology, University of New South Wales, Sydney, NSW, Australia Moving Ahead Centre for Research Excellence in Brain Recovery, Australia

A R T I C LE I N FO

A B S T R A C T

Keywords: Anxiety sensitivity Trier social stress test Psychosocial stress Physiology Heart rate variability Autonomic nervous system Emotion

The ability to regulate emotional reactions is a complex process that incorporates both physiological and psychological components. Anxiety sensitivity is a construct associated with the negative and often misinterpretation of bodily sensations, with previous findings suggesting that anxiety sensitivity may regulate an individual's physiological response to an acute stress response. The aim of the current study, therefore, was to identify whether anxiety sensitivity moderates the physiological and subjective experience of acute psychosocial stress. Fifty-eight undergraduate students high and low on anxiety sensitivity (as indexed by the Anxiety Sensitivity Index – Third Edition) had their physiology recorded during a widely-used psychosocial stress induction procedure; the Trier Social Stress Test (TSST). Heart rate and skin conductance, together with selfreported anger and tension on the Profile of Mood States questionnaire, significantly increased in response to the TSST. Conversely, high-frequency heart rate variability (HF-HRV) decreased in response to the TSST. We found that anxiety sensitivity moderated the subjective experience of the TSST, such that those who had greater anxiety sensitivity self-reported elevated tension in response to the TSST compared to those with low anxiety sensitivity. Anxiety sensitivity did not moderate any of the physiological outcomes of the TSST. Consequently, this study provides a physiological profile on how the autonomic nervous system responds to stress. Additionally, these findings suggest that beliefs about body sensations specifically affects the interpretation of stressful experiences rather than augmenting physiological reactions themselves. This may provide insights into how biases subserve the development and maintenance of dysregulated emotional experience.

1. Introduction Regulating emotion in response to situational demands is vital for successful interaction with one's environment, well-being, and social functioning (Gross, 2001). Emotional regulation to stress, in particular, refers to the transient adaptive response to everyday threats and involves the regulation of responses across hormonal, physiological and other biological levels (Campbell and Ehlert, 2012). However, there is considerable variability in how individuals regulate themselves when faced with stress. As such, understanding how individual physiological and psychological mechanisms interact with stressors is important to understanding negative emotional states and dysregulated emotional experience. Anxiety sensitivity, in particular, is a psychological construct that describes one's fear of the physical symptoms that accompany anxiety, where more anxiety sensitive individuals perceive and misinterpret autonomic sensations as dangerous (Reiss et al., 1986). As

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such, anxiety sensitivity may well exacerbate, or otherwise influence, the actual physiological responses that occur during stress, however, this is yet to be understood. The autonomic nervous system plays a crucial role in the regulation of emotion, and arousal needs to be continually adjusted to meet the current demands of the environment. Heart rate (HR) and skin conductance (SCL) increase as a function of arousal while heart rate variability (HRV) – the beat-to-beat temporal changes in heart rate - has gained recognition as a biological index of autonomic flexibility and emotion regulation capacity. Under transient conditions of stress, the sympathetic nervous system exerts dominance to increase arousal (i.e., increased SCL and HR) while parasympathetic nervous activity is suppressed, thereby resulting in a consistently high HR and reduced variability between heart beats. For example, Delaney and Brodie (2000) observed significant reductions in HRV during a 5-minute psychological stress test. Conversely, a meta-analysis has shown that

Corresponding author at: School of Psychology, University of New South Wales, NSW 2052, Australia. E-mail address: [email protected] (T.A. Wearne).

https://doi.org/10.1016/j.ijpsycho.2019.04.012 Received 5 February 2019; Received in revised form 16 April 2019; Accepted 29 April 2019 Available online 01 May 2019 0167-8760/ © 2019 Elsevier B.V. All rights reserved.

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higher HRV correlates with increased blood flow in the amygdala and ventromedial prefrontal cortex, regions known to be important for effective emotion regulation (Thayer et al., 2012). Accordingly, HRV is frequently used as a physiological measure of emotional responding. Collectively, these physiological measures (i.e., SCL, HR, and HRV) represent a network of autonomic function and provide a useful tool for studying psychological factors in emotion regulation when responding to stress. However, an analysis of 49 studies (Campbell and Ehlert, 2012) to identify the association between physiological and psychological responses to the Trier Social Stress Test (TSST), a laboratory procedure used to induce psychosocial stress and a corresponding strong physiological stress response, revealed that only 22 examined HR, one examined SCL, and two used an HRV measure. Therefore, there are very few studies that have examined all of these physiological measures simultaneously in response to psychosocial stress. This represents a gap in the literature, as the different physiological indices (HR, SCL, and HRV) when used in combination, can offer a nuanced picture of how people anticipate, experience, and recover from a stressful event. It has also been demonstrated that psychological processes may play a significant role in regulating an individual's stress response. For example, Gaab et al. (2005) found that anticipatory cognition appraisal explained 22% of the variance in the cortisol response to the TSST, while worry, a maladaptive emotion regulation strategy, has been shown to lower HRV (Thayer et al., 1996). Of specific relevance to the current study, some research has shown that anxiety sensitivity moderates physiological arousal. For example, changes in HR and HRV were more strongly associated with anxiety in high anxiety sensitive individuals with flight phobia than those low in anxiety sensitivity (Busscher et al., 2013). Additionally, healthy participants with low anxiety sensitivity have been shown to have a higher parasympathetic response during the cold presser test compared to those with high anxiety sensitivity (Dodo and Hashimoto, 2015). Other research, however, has found that healthy participants with low and high anxiety sensitivity do not differ with respect to baseline HRV (Melzig et al., 2009). This, therefore, suggests that the interaction between anxiety sensitivity and physiology could be specific related to a stress response. To date, only one study has studied anxiety sensitivity in relation to the TSST. McCaul et al. (2017) examined the relationship between alcohol craving and stress reactivity during the TSST and found that anxiety sensitivity did not correlate with participants' stress response. However, the only stress measure used was cortisol, and therefore the moderating effect of anxiety sensitivity on other physiological indices to psychosocial stress is unknown. Furthermore, participants were all recruited on the basis that they were heavy drinkers, and therefore, the relationship between anxiety sensitivity and autonomic output in response to the TSST amongst a more general population remains to be investigated. The aim of the current study was to examine the relationship between autonomic output, subjective experience, and anxiety sensitivity in response to psychosocial stress, as indexed by the Trier Social Stress Test. While the TSST elicits a significant stress response, physiological markers of autonomic arousal have been understudied relative to hormonal responses. It was hypothesised that HR and SCL would increase while HRV would decrease in response to the TSST. An additional aim of the present study was to identify whether anxiety sensitivity moderates autonomic and subjective output in response to the TSST procedure. Given that anxiety sensitivity may predispose individuals to adopt fearful reactions as a way of managing their internal thoughts about body sensations, and in line with previous physiological research with anxiety sensitivity, it was hypothesised that those high in anxiety sensitivity would demonstrate greater physiological (i.e., increased HR and SCL with decreased HRV) and subjective output in response to the TSST compared to those with low anxiety sensitivity.

2. Materials & method 2.1. Participants Based on previous studies and power calculations using GPower (Faul et al., 2007), we found that a group size of 62 participants enabled group difference ANOVA analyses (i.e., high and low anxiety sensitivity individuals across the 5 phases of the TSST) with 85% power to detect a medium effect size of 0.3 with a type 1 error rate of 5%. Our finale sample of 58 participants enabled ANOVA analyses with 83% power to detect a medium effect size of 0.3. Sixty-two psychology undergraduate students were recruited to participate in the current study in exchange for course credit. Participants were pre-screened to ensure they were healthy adults, aged 18 to 70 years old, had normal or corrected vision, were fluent in conversational English, and did not have a history of brain injury, stroke, or a heart condition. They were asked to refrain from caffeine and tobacco for at least 2 h priors, and alcohol for at least 8 h prior to their participation, as to avoid the acute effects of psychostimulants on psychophysiological output. Two participants were excluded from the final analysis as they voluntarily withdrew from the experiment, and a further two participants were excluded as their data was > 2.5 standard deviations away from the mean across multiple outcome measures. This left a final sample of 58 participants (32 female, 26 male), with an average age of 22.24 years (range = 18 to 58 years, SEM = 0.84) and 14.27 years of education (range = 12 to 18 years, SEM = 0.20). Participants had abstained from caffeine an average of 3 h and 55 min (range = two hours to six hours), and alcohol an average of 14.5 h (range = 10 to 20 h), prior to their participation in the study. Screening at the time of the study also reveal two participants had consumed nicotine an average of 4 h prior to their participation (range = 3 to 5 h). 2.2. Measures 2.2.1. Anxiety sensitivity index – 3 (ASI-3) (Taylor et al., 2007) The ASI-3 is an 18-item questionnaire that measures the extent to which individuals fear the perceived consequences associated with feeling anxious. Using a 5-point Likert Scale, participants rate statements in terms of the extent the statements apply to them (0 = very little, 5 = very much). Reliability for the total score has been found to be excellent (α = 0.94), and the internal consistency is also good (Wheaton et al., 2012). 2.2.2. Depression anxiety and stress scale (DASS 21) (Lovibond and Lovibond, 1995) The DASS-21 is a 21 item self-report questionnaire that assesses the extent of depression, anxiety and stress-related symptoms exhibited in an individual. Participants rate statements on a 4-point Likert scale according to the frequency the statement applied to them over the previous week (0 = did not apply to me at all, 4 = applied to me very much, or most of the time). Higher scores reflect higher severity of symptoms. In a non-clinical sample, the DASS-21 has been found to have excellent internal consistency (α = 0.94 for depression, 0.87 for anxiety, and 0.91 for stress), and acceptable to excellent concurrent validity (Antony et al., 1998). For the purpose of the current study, the DASS was used as an index of general psychological distress as opposed to a measure of mood reactivity to the TSST. 2.2.3. Profile of mood states (Terry et al., 1999) Transient mood states were assessed using the 24-item Profile of Mood States – Adolescent version, which has shown to be valid for use in adults (Terry et al., 2003). Participants rate the degree to which they feel each emotion (e.g., anxious) on a 5-point Likert scale ranging from 0 (not at all) to 4 (extremely). The POMS has a six factor structure with four items each, with relevant item scores for to a potential total of 16. Higher scores indicate more anger, confusion, depression, fatigue, 77

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2.3. Procedure

tension and vigour. In this study, we were specifically interested in changes to the anger and tension subscales as measures of state mood and anxiety in response to the TSST procedure. It has good construct and criterion validity, together with strong internal consistency (Terry et al., 2003; Terry et al., 1999).

Participants completed the study individually during one session that lasted approximately 90 min. At the time of signing up for the study and upon arrival, participants were informed that the experiment would involve completing several questionnaires, the use of physiological recording equipment, and participation in a short-role playing scenario. Details of the TSST were not disclosed at this point to ensure that the participants did not ruminate over the content of the session during the baseline recording. All procedures were approved by the Human Research Ethics Committee at the University of New South Wales. Participants first completed the DASS, ASI-3 and a basic demographic and screening questionnaire to ensure they satisfied the study inclusion criteria. Participants were then fitted with the physiological equipment. The entire acclimatization period prior to recording of physiological data lasted approximately 20 min, consistent with previously published recommendations (Barry et al., 2008). Participants first completed a baseline (5 mins) recording during which they were instructed to sit upright, remain still, and keep their eyes open. Next, during the anticipation (10 min) phase, the experimenter described the details of the TSST procedure to the participant. They were informed that they would be participating in a 10-min task that comprised of a 5min speech followed by a 5-min mathematics task in front of two confederates (specific details of the TSST procedure can be found elsewhere, Kirschbaum et al., 1993). They were then given 10 min to prepare for the speech using provided writing materials during which their physiology was recorded. During the TSST Test phase (10 min), the experimenter removed the participant's notes and invited the two confederates into the room to sit at a desk opposite the participant. The confederates were instructed to behave in a cold and passive manner towards the participant in order to maximise their experience of psychosocial stress. They first asked the participant to commence the speech and if the participant was silent for > 20 s, they were prompted to continue speaking. At end of the speech, a confederate cut off the participant and instructed them to perform the mathematics task. If the participant made a mistake, they were asked to start again. At the end of the test phase, the confederates stood and left the room. During recovery, the participants were instructed to sit and relax in the same manner as they did during baseline for 20 min (this was recorded as two distinct 10 minute recovery sessions). This period was used to both obtain physiological data concerning individual recovery from exposure to psychosocial stress, but also provided participants the opportunity to calm down and ensured they did not leave the experiment in a distressed state. Participants completed the POMS questionnaire at the end of each recording and phase of the experiment (i.e., baseline, anticipation, TSST, 10 min recovery, 20 min recovery). Following the cessation of the experiment, the physiological equipment was removed and the participant were debriefed on the true purpose of the study.

2.2.4. Physiological measures Heart rate and HRV data were recorded via three ECG Ag/AgCl sensors placed on the underside of the participants' wrists, along with two similar sensors placed on the participants' second and third digits to measure skin conductance. All of the equipment was attached to a 10 channel FlexComp Infinti Encoder system. Data on these measures were acquired using BioGraph Infiniti Software 6.0 (Thought Technology Ltd., Quebec, Canada), connected to a laptop. Recordings were manually started and stopped by the experimenter at the start and end of each time point of the experiment, respectively (i.e., baseline [5 min duration], anticipation [10 min duration], TSST [10 min duration], and 10-min [10 min duration] and 20-min recovery [10 min duration]). Raw inter-beat interval (IBI) records were manually cleaned in order to reduce artefact/artificial beats and were formally analysed using CardioPro Infiniti 6.0 software (Thought Technology Ltd., Quebec, Canada). There are several methods used to evaluate HRV, and two of the most commonly used are time domain and frequency domain analyses (Malik, 1996). Time domain methods involve analyses of the normal-to-normal (NN) intervals between these complexes. For example, the standard deviation of NN intervals (SDNN) reflects overall HRV, and is a frequently used measure in the literature (Pumprla et al., 2002). Frequency domain methods, on the other hand, quantify the amount of heart rate variance occurring at different frequencies, obtained from a short-term recording of at least five minutes, by using power spectral analysis. The high frequency (HF) component occurs between 0.15 and 0.40 Hz while low frequency (LF) occurs within 0.04–0.15 Hz (Appelhans and Luecken, 2006; Malik, 1996). Both time (SDNN) and frequency domain measures (LF and HF) were included in the current study and all recordings were at least of 5 min duration. This approach is consistent with International Task Force Guidelines (Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology, 1996) and previous HRV research from our laboratory (Francis et al., 2016). Therefore, HR, SCL, together with SDDN, LF, and HF HRV were. 2.2.5. The Trier social stress test (TSST) The Trier Social Stress Test (TSST) is a reliable and frequently used stress induction procedure that combines uncontrollability with socioevaluative and cognitive elements to induce psychosocial stress (Dickerson and Kemeny, 2004). It is a highly standardised protocol that reliably leads to high activation of the hypothalamic-pituitary-adrenal (HPA) stress axis and a strong physiological stress response (Kudielka et al., 2007). For example, previous studies have shown reliable increases in saliva alpha-amylase (Kudielka et al., 2007), SCL (RomeroMartinez et al., 2013), HR (Hellhammer and Schubert, 2012), and decreases in HRV (Petrowski et al., 2017) in response to the TSST. It is comprised of an anticipation phase (10 min) and a test phase (10 min) in which the participant must deliver a speech and perform mental arithmetic in front of several people. In the current experiment, the TSST was largely administered in accordance with the original procedure detailed by Kirschbaum et al. (1993), with some exceptions. Participants were not moved between rooms, as this was logistically impractical given the setup of the physiological equipment. Also, the effect of the TSST on endocrine response is now well-established (Allen et al., 2014) and were consequently not collected in the current study. It is common practice for experimenters to alter various aspects of the TSST to suit the demands of their particular study. Many variations of the procedure have still elicited strong physiological stress responses (Engert et al., 2016; Tarbell et al., 2017; van Hedger et al., 2017), suggesting these changes were acceptable.

2.4. Statistical analyses All data are presented as means and standard error of the mean. The data was first examined to identify missing values and any missing values were replaced using imputation (< 1% of values). Skin conductance, and HRV measures (LF and HF) were log transformed due to the non-normal distributions, consistent with previously published methods (Francis et al., 2016). Given the non-normal and bi-modal distribution of anxiety sensitivity in our sample, a k-means cluster analysis was conducted with anxiety sensitivity as the defining variable to develop two clusters of those with “high” and “low” anxiety sensitivity. Independent t-tests or chi-square tests were conducted to examine group differences on demographic, clinical and baseline variables. Principal analyses involved mixed repeated measures ANOVAs for each of the dependent variables (heart rate, SCL, SDNN, LF, HF, mood) with time (5 levels: baseline, anticipation, TSST, 10 min 78

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recovery and 20 min recovery) as the within subject factor and anxiety sensitivity group (two levels; low vs high) entered as the betweensubject factor. Mauchly's test of sphericity was used to test for homogeneity of variance, and where sphericity was violated, ANOVA results were analysed using a Greenhouse-Geisser Epsilon adjustment, consistent with previously published studies examining changes across the TSST (Kirschbaum et al., 1993; van Hedger et al., 2017; Villada et al., 2016). Post-hoc comparisons were used to examine significant changes across individual time-points, with a Bonferroni correction applied to control for multiple comparisons. In the event of significant differences in baseline physiology or emotion, these were controlled for as covariates in order to determine whether changes throughout the TSST were above and beyond baseline differences between those high and low with anxiety sensitivity. Significance was held at p < .05. 3. Results 3.1. Demographic and group characteristics The low anxiety sensitivity group had an average ASI-3 score of 5.86 (SEM = 0.563, n = 22) while the high anxiety sensitivity group had an average score of 23.67 (SEM = 1.673, n = 36), p < .0005. There was no significant difference between those who scored high and low on anxiety sensitivity with respect to age (t(56) = −1.050, p = .298), years of education (t(56) = 0.109, p = .914), and distribution of sex [(χ2 (1, n = 58) = 0.594, p = .364]. However, as expected, those in the high anxiety sensitivity group reported greater symptoms of depression (p < .01, d = 0.71), anxiety (p < .005, d = 0.77) and stress (p < .0005 d = 0.95) compared to those with low anxiety sensitivity, although these scores did not indicate any severe and extremely severe levels of psychological distress as determined by cut-off scores established by the authors (Lovibond and Lovibond, 1995).

Fig. 1. Skin Conductance changes throughout the Trier Social Stress Test Procedure. Skin conductance significantly increased from baseline to anticipation and to Test. While skin conductance reduced during recovery, it was still significantly elevated compared to baseline.

3.2. Baseline physiological and emotion characteristics There was no significant difference between those who scored high and low on anxiety sensitivity with respect to baseline SCL (t (56) = −0.305, p = .762), HR (t(56) = −1.511, p = .136), and the HRV measures SDNN (t(56) = 0.811, p = .421), LF (t(56) = 1.168, p = .762), and HF (t(56) = 0.901, p = .372). However, those with high anxiety sensitivity reported elevated baseline feelings of anger (p < .05, d = 0.59), and tension (p < .0005, d = 1.15). 3.3. Physiological response to the tsst: moderation of anxiety sensitivity 3.3.1. Skin conductance The TSST elicited significant changes to SCL over time, F (2.495,139.701) = 104.720, p < .0005, partial η2 = 0.652 (Fig. 1). There was no main effect of anxiety sensitivity on SCL (F (1,56) = 0.001, p = .976) nor was there a significant interaction between the TSST and anxiety sensitivity (F(2.495, 139.701) = 0.536, p = .626). SCL significantly increased from baseline to anticipation (p < .0005) and further increased from anticipation to test (p < .0005). While skin conductance had significantly decreased from the test to both 10-min and 20-min recovery (both p < .0005), they remained significantly elevated relative to baseline (p < .0005).

Fig. 2. Heart rate changes throughout the Trier Social Stress Test Procedure. Heart rate significantly increased from baseline to anticipation and to Test. Heart rate returned to baseline levels during both 10-minute and 20-minute recovery.

3.3.2. Heart rate There was a significant main effect of time on HR, meaning that HR significantly changed throughout the course of the TSST, F(2.077, 116.318) = 53.208, p < .0005, partial η2 = 0.487 (Fig. 2). There was no main effect of anxiety sensitivity on HR (F(1,56) = 2.218, p = .142) nor was there a significant interaction between the TSST and anxiety sensitivity (F(2.077, 116.318) = 0.295, p = .754). HR significantly increased from baseline to anticipation (p < .005), further increased from anticipation to test (p < .0005), and significantly decreased from

test to recovery (p < .0005). There was no significant difference in HR between 10-min recovery and 20 min recovery (p = .654) and recovery HR was back to baseline levels (both p = 1.00).

3.3.3. Heart rate variability 3.3.3.1. SDNN. There was 79

no

main

effect

of

time

(F(1.650,

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Fig. 3. Low frequency-HRV changes throughout the Trier Social Stress Test Procedure. Low Frequency HRV did not significantly change from baseline to Test but low frequency HRV significantly increased during recovery relative to test.

Fig. 4. High frequency-HRV changes throughout the Trier Social Stress Test Procedure. High Frequency HRV significantly reduced during test and returned to baseline levels during both 10-minute and 20-minute recovery.

92.428) = 2.074, p = .140), no main effect of anxiety sensitivity (F (1,56) = 0.830, p = .366) nor was there a significant interaction between the TSST and anxiety sensitivity on SDNN (F(1.650, 92.428) = 1.330, p = .267). 3.3.3.2. Low frequency (LF). There was a significant main effect of time on LF HRV, meaning that LF significantly changed throughout the course of the TSST, F(2.763, 154.727) = 6.581, p < .0005, partial η2 = 0.105 (Fig. 3). There was no main effect of anxiety sensitivity on LF (F(1,56) = 0.845, p = .362) nor was there a significant interaction between the TSST and anxiety sensitivity (F(2.763, 154.727) = 2.132, p = .103). There were no significant differences in LF-HRV between baseline with anticipation (p = 1.00) and test (p = .125) but LF significantly increased from Test to 10 min recovery (p < .05) and 20 min recovery (p < .0005). 3.3.3.3. High frequency (HF). There was a significant main effect of time on HF HRV, meaning that HF significantly changed throughout the course of the TSST, F(2.537, 142.050) = 8.887, p < .0005, partial η2 = 0.137 (Fig. 4). There was no main effect of anxiety sensitivity on HF (F(1,56) = 0.727, p = .397) nor was there a significant interaction between the TSST and anxiety sensitivity (F(2.537, 142.050) = 0.547, p = .622). There were no significant differences in HF-HRV between baseline and anticipation (p = 1.00), but HF was significantly reduced during test relative to baseline (p < .005) and anticipation (p < .0005). HF recovered to baseline levels during 10-minute recovery (p = 1.00) and 20-minute recovery (p = 1.00).

Fig. 5. Self-report of anger throughout the Trier Social Stress Test Procedure for those high and low on anxiety sensitivity. Anger significantly increased during test and those with high on anxiety sensitivity. Those with high anxiety sensitivity self-reported significantly more anger during test compared to those with low anxiety sensitivity, controlling for baseline differences in the self-report of anger, although these differences did not survive a Bonferroni correction.

revealed that those with high anxiety sensitivity reported elevated anger compared to those with low anxiety sensitivity during the Test (F (1,55) = 5.206, p < .05) and 10 min recovery (F(1,55) = 4.123, p < .05) but not anticipation (p = .547) nor 20 min recovery (p = .08). However, these differences did not survive a Bonferroni correction for multiple comparisons (0.05/4).

3.4. Subjective response to the TSST: Moderation of anxiety sensitivity 3.4.1. Self-report of emotion: Anger There was a significant main effect of time on self-reported anger (F (2.033, 113.836) = 10.827, p < .0005, partial η2 = 0.162; Fig. 5), there was a main effect of anxiety sensitivity on self-report of anger (F (1,56) = 9.311, p < .005., partial η2 = 0.143) and was there a significant interaction between the TSST and anxiety sensitivity, F(2.033, 113.836) = 3.213, p < .05, partial η2 = 0.054). Follow-up analyses, after controlling for baseline differences in the self-report of anger,

3.4.2. Self-report of emotion: Tension There was a significant main effect of time on self-reported tension (F(2.379, 133.211) = 47.543, p < .0005, partial η2 = 0.459), there 80

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et al., 1993), with Kirschbaum et al. (1993) supporting our finding that HR was increased from baseline to anticipation and that it was even greater during the TSST. Fewer studies have reported changes in SCL in response to the TSST, although there are findings that are consistent with our results. For example, Guez et al. (2016) found that SCL increased from pre-TSST to post-TSST while Romero-Martinez et al. (2013) reported that SCL increased from rest to during the stressor tasks before deceasing at recovery. Together, these findings suggest clear autonomic arousal in response to the anticipatory effects of the task and to the stressor itself. However, interestingly, we found that while HR returned to baseline levels at recovery, SCL was still elevated at 10minute and 20-minute recovery relative to baseline. Even though it is known that SCL recovers at a slower rate than HR, the differential recovery of these physiological outcomes likely reflects distinct contributions of the autonomic nervous system in response to stress. That is, elevated SCL is uniquely controlled by the sympathetic nervous system (Boucsein, 1992) while HR reflects both sympathetic and parasympathetic influences. Therefore, reduced HR during recovery likely indicates increased parasympathetic drive as means to decelerate elevated HR to facilitate a relaxed response to environmental demands. The influence of parasympathetic drive was also mirrored in the HRV results. As expected, we found that HF-HRV significantly decreased during test relative to baseline and anticipation. HF-HRV is reflective of parasympathetic influences on the heart, with increased vagal tone resulting in elevated HF-HRV. Therefore, the reduction of HF-HRV during test indicates parasympathetic withdrawal and increased sympathetic drive. Indeed, some research has been able to demonstrate that the TSST does in fact induce robust reductions in HRV (e.g., Petrowski et al. (2017)). Conversely, we found that LF did not change throughout baseline to test but it increased during recovery. LF has been proposed to reflect both sympathetic and parasympathetic influences on cardiac activity (Appelhans and Luecken, 2006; Malik, 1996), although there is contention in the literature as to what LF is measuring, with evidence that LF gives a measure of baroreflex function rather than sympathetic drive (Goldstein et al., 2011). Thus, the increase in LF during recovery could be the result of a feedback mechanism to decelerate HR to maintain blood pressure homeostasis and as means to facilitate emotion regulation during recovery. We found no changes to HRV during anticipation compared to baseline. This is interesting as it could be hypothesised that the anticipatory period would be associated with reduced HRV in light of the stress involved in preparing for the speech task. Alternatively, the act of planning a speech during this phase could be interpreted as an active coping strategy in preparation for the speech task. In this case, normal HRV can be viewed as the biological correlate of good emotion regulation, and some research has already linked HRV with various coping variables (Laborde et al., 2015). Once the anticipation phase ended, however, and participants were engaged with the stressor, they were unable to apply the same coping strategy used in anticipation. Consequently, they exhibited a decrease in HF-HRV associated with stress and reduced emotion regulation capacity. In testing this hypothesis, future studies could experimentally manipulate this phase in order to determine if coping and emotion regulation strategies are related to HRV. For example, comparisons of maladaptive versus adaptive emotion regulation strategies during the anticipation period could help determine whether these change HRV responses. Nevertheless, collectively, these changes describe a physiological profile associated with psychosocial stress and highlight the important distinction between anticipatory and immediate stresses on physiological outcomes. This is an important consideration, as many studies of the TSST do not differentiate between the anticipation and test phases but rather assess these as a combined stress induction. These studies may therefore miss crucial information regarding psychosocial stress responses. Inconsistent with our hypotheses, we found that anxiety sensitivity did not moderate any of the physiological outcomes at baseline or in response to the TSST. These are consistent with studies that have shown

Fig. 6. Self-report of tension throughout the Trier Social Stress Test Procedure for those high and low on anxiety sensitivity. Tension significantly increased during test and those with high on anxiety sensitivity in general reported greater tension compared to low anxiety sensitivity. Those with high anxiety sensitivity self-reported significantly more tension during test compared to those with low anxiety sensitivity, controlling for baseline differences in the self-report of tension.

was a main effect of anxiety sensitivity on self-report of tension (F (1,56) = 17.051, p < .0005, partial η2 = 0.233) and there was a significant interaction between the TSST and anxiety sensitivity, F(2.379, 133.211) = 3.089, p < .05, partial η2 = 0.052; Fig. 6). Follow-up analyses, after controlling for baseline differences in the self-report of tension, revealed that those with high anxiety sensitivity reported elevated tension compared to those with low anxiety sensitivity during the Test (F(1,55) = 6.743, p < .01, partial η2 = 0.109) but not anticipation (p = .384), 10 min recovery (p = .052) nor 20 min recovery (p = .400). This difference remained significant after a Bonferroni correction for multiple comparisons (0.05/4 = 0.0125). 4. Discussion This study found that there was physiological reactivity psychosocial stress. HR and SCL increased while HF-HRV decreased in response to the TSST, and the experience of anger and tension also increased in response to stress. These results provide induced that the TSST induced physiological and subjective changes commensurate with psychosocial stress. Furthermore, the main findings of this study were that those with higher anxiety sensitivity reported elevated negative affect (i.e., anger and tension) more generally than those with lower anxiety sensitivity. Additionally, while anxiety sensitivity did not moderate the physiological response to the TSST, it did moderate the subjective reactivity to stress, such that those with higher anxiety sensitivity reported even greater feelings of tension in response to the TSST compared to those with low anxiety sensitivity. Overall, these findings suggest that while there are salient and large effects of psychosocial stress on autonomic outcomes, the construct of anxiety sensitivity specifically interacts with the subjective interpretation of these autonomic variables and does not promote heightened physiological experience. Consistent with our hypotheses, we found that arousal increased during the TSST such that HR and SCL increased throughout anticipation and the test phases of the TSST. Amongst the TSST studies that have measured HR changes, almost all have reported significant increases in HR from baseline to the TSST (Allen et al., 2014; Kirschbaum 81

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subjective interpretation of the TSST. Studies have reported significant sex differences in cortisol (Kirschbaum et al., 1992) and HR (Kudielka et al., 2004) in response to the TSST. Additionally, most studies cite the impact of hormonal factors, menstruation, and use of oral contraceptives on the female cortisol response. Accordingly, studies typically isolate the biological sex of their participants or conduct analyses differentiating between male and female responses. However, given that this study did not use a cortisol measure, these concerns were not as applicable in the current study. Furthermore, while examining males and females separately may have revealed some sex differences in stress responding across some of the physiological variables, entering sex as a covariate produced no changes to our results or any significant interactions with our outcomes (data not shown). Therefore, for the benefit of increased power, we did not include sex as a variable of interest in the current findings. While we provided a physiological profile associated with psychosocial stress, and consequently measured SCL, HR and HRV, we did not include respiration as one of our outcome measures. The reason for this is that speech and movement are two major sources of artefact in the measurement of respiration (Porges and Byrne, 1992; Wientjes, 1992). Given that this study required participants to stand and speak, a respiration belt would have recorded too much movement to reliably index breathing rate as a measure of physiological response to stress. Indeed, other TSST studies have also reported a failure to include respiration measures in their study as a limitation (e.g., Petrowski et al., 2010), highlighting that respiration is a measure of interest in the TSST paradigm, and requires further investigation. However, Hernando et al. (2015) measured respiration using a highly modified version of the TSST procedure, which included memory and storytelling tasks, in addition to the standard speech and arithmetic elements, were used to induce stress. The study reported that respiration increased during all the tasks, relative to baseline. Therefore, it may be appropriate for future studies to incorporate modified versions of the TSST in order to appropriately record respiration and profile a full physiological profile. In light of this, another limitation is the measurement of HRV in the current study was orthostatic stress. Research has found that orthostatic (standing with an erect posture) stress, induced by standing for three minutes or more, results in significant HF HRV reduction relative to sitting (Knepp and Friedman, 2008). Given that the test phase was the only phase in which participants were required to stand, it is possible that some of the observed HF HRV reductions in this phase was driven by orthostatic stress rather than psychosocial stress. Whilst the original TSST procedure (Kirschbaum et al., 1993) indicates that participants should stand for the speech and arithmetic components of the TSST, it is impossible to differentiate the effects of psychosocial stress and orthostatic stress on parasympathetic driven HRV. Future studies should attempt to control for the influence of orthostatic stress on HRV by having participants seated during the Test instead. In conclusion, this study provided empirical evidence regarding the physiological changes associated with psychosocial stress, and found that the TSST induced significant changes in HR, SCL and HF-HRV. This study was also able to provide valuable clarity regarding how autonomic output differentially changes during anticipatory stress and psychosocial stress. Finally, we found that anxiety sensitivity moderates the subjective experience of psychosocial stress. This suggests that beliefs about body sensations negatively impact the interpretation of stressful experiences in the absence of changes to physiology. This raises the importance of how anxiety-related beliefs about physiology underlie the interpretation of stress and could have useful clinical implications for targeted treatment for dysregulated emotional experience.

that anxiety sensitivity does not moderate baseline HRV or startle potentiation (Melzig et al., 2009) nor cortisol response for those with elevated alcohol craving (McCaul et al., 2017). However, anxiety sensitivity has been shown to be associated with physiological response for those experiencing anxiety with flight phobia (Busscher et al., 2013) and those with low anxiety sensitivity had a higher parasympathetic response during the cold presser test (Dodo and Hashimoto, 2015). Such differences between research studies may refer to the samples used and the specific targets of the stressor. That is, the cold presser test evokes a parasympathetic nervous response while the driving factors of the TSST is sympathetic dominance. Additionally, we used a healthy control sample as opposed to a clinical group to examine physiological response to psychosocial stress. As such, it may be that anxiety sensitivity moderates physiological outcomes only for those with clinical status, meaning that those with elevated anxiety sensitivity without psychopathology may be unlikely to be susceptible to the interaction between anxiety sensitivity and the physiological manifestations of stress. Another possibility is that the sample size used in the current study was underpowered to detect individual differences. However, the sample size calculations for our sample was adequate to detect a medium effect size, and the probabilities for the interaction between physiological outcomes and anxiety sensitivity were large, meaning that the failure to identify these relationships were not due to Type 2 errors. As such, it is likely that anxiety sensitivity does not moderate physiological outcomes for those without clinical status. Further research comparing anxiety sensitivity in clinical and healthy comparison groups would be needed to further understand the mediating role of anxiety sensitivity with the development and maintenance of clinical psychopathology. Nevertheless, we found that anxiety sensitivity moderated the subjective experience of psychosocial stress, such as those with higher anxiety sensitivity reported greater tension in response to the TSST compared to those with low anxiety sensitivity. Furthermore, these findings were evident after controlling for baseline differences in the self-report of tension for both anxiety sensitive groups, meaning that these changes were specific to psychosocial stress and not a generalised effect on emotional experience. Given the lack of moderation between anxiety sensitivity and physiology, these findings suggest that anxiety sensitivity specifically interacts with the interpretation of psychosocial stress and its associated physiological outcomes, rather than being a genuine interpretation of heightened physiological response to stress. These findings could have potential clinical implications for the treatment of altered emotion regulation to psychosocial stress. For example, autonomic reappraisal may be an effective emotion regulation strategy for participants with high anxiety sensitivity as to avoid the misinterpretation of the physical manifestations of stress, and may be an important avenue for future clinical research studies. This study has several limitations that need to be considered. First, the sample of participants was taken from an undergraduate university student population, and as a result were largely young adults. Studies have found that the degree of stress responsivity to the TSST varies as a function of age (e.g., Kudielka et al. (2004), and as such, the age of the participants used in this study limits the generalizability of the current findings across all age groups. Also, the TSST incorporates a number of stressful components simultaneously. It is possible that participants could habituate to the task as these components progress and it can also be difficult to tease apart which aspects of the stressor are causing the psychophysiological components of the stress response (e.g., social evaluation, public speaking, and mathematical ability). Additionally, while we have specifically focussed on anxiety sensitivity as a measure of moderating reactivity to psychosocial stress, other personality or anxiety-related cognitions could possibly affect these outcomes. For example, neuroticism interacts with stress responsivity (Xin et al., 2017) and previous studies have highlighted that neuroticism predicts anxiety sensitivity (Cox et al., 1999). Therefore, neuroticism could be potential mediator in the relationship between anxiety sensitivity and

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