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. Author manuscript; available in PMC: 2026 Aug 20.
Published in final edited form as: J Affect Disord. 2025 Feb 6;376:454–462. doi: 10.1016/j.jad.2025.02.011

Stressor-evoked heart rate, perceived physiological arousal, and anxiety symptoms in young adults

Taryn E Cook a,*, Thomas A Fergus a, Danielle A Young a, Sarah E Williams b, Annie T Ginty a
PMCID: PMC13488176  NIHMSID: NIHMS2202144  PMID: 39922291

Abstract

Background:

Acute psychological stress is associated with increases in heart rate (HR) and state anxiety. Stressor-evoked perceived HR changes relate more strongly to state anxiety than actual HR reactivity. However, research has yet to examine these associations in the context of general anxiety symptoms.

Methods:

Participants (N = 160) completed a resting baseline period followed by a standardized acute psychological stress task; HR was recorded throughout. After the stress task, participants rated their perceived stressor-evoked physiological arousal and anxiety intensity. Participants also completed a general anxiety symptoms measure ~17 days later.

Results:

The a priori hypothesized model demonstrated a good fit to the data, χ2 (59) = 93.15, p = .003; CFI = .94; TLI = .91; SRMR = .05; RMSEA = .06 (90% CI = .04 - .08). After controlling for covariates, perceived physiological arousal was positively related to both cognitive and somatic anxiety. In turn, only somatic anxiety was positively associated with general anxiety symptoms . Perceived physiological arousal was related to general anxiety symptoms through state somatic anxiety. HR reactivity was not statistically significantly associated with either cognitive or somatic anxiety.

Limitations:

The study was correlational, which limits the ability to determine causation.

Conclusions:

Perceived HR, rather than actual HR, is more closely associated with anxiety intensity during acute psychological stress. Stressor-evoked perceived HR and general anxiety symptoms are related indirectly through stressor-evoked somatic anxiety intensity. The findings have implications for elucidating the mechanisms of the stress-anxiety relationship.

Introduction

Epidemiological surveys estimate one-third of the population is impacted by an anxiety disorder at some point during their life (e.g., Bandelow & Michaelis, 2015; Szuhany & Simon, 2022). Young adults have among the highest prevalence rates of anxiety disorders (Calling et al., 2017; Copeland et al., 2014; Jacobi et al., 2014). While the etiology of anxiety disorders is multi-factorial, vulnerability for anxiety disorders has partially been attributed to high levels of general anxiety symptoms, which are characterized by a tendency to view situations as threatening or uncertain (Andrews, 1991; Eysenck, 2013; Knowles & Olatunji, 2020; Mishra & Varma, 2023; Rachman et al., 2000; Ree et al., 2008).

Psychological stress is related to the development and maintenance of general anxiety symptoms (Faravelli & Pallanti, 1989; Francis et al., 2012; Mineka & Zinbarg, 2006; Phillips et al., 2015). Indeed, experimental laboratory research using standardized acute psychological stress task protocols has demonstrated that individuals with high levels of general anxiety symptoms have increased levels of stressor-evoked state anxiety (i.e., stressor-evoked feelings of worry, nervousness, arousal, and tension; de Rooij et al., 2010; Grossman et al., 2001; Mauss et al., 2004; Ree et al., 2008). While evidence suggests that state anxiety and general anxiety symptoms are associated with both chronic and acute stress, the underlying mechanisms driving the acute stress-anxiety relationship are not fully understood.

Influential theories proposed a connection between the mind and the body, such that there is an association between increases in heart rate (HR) and higher levels of state anxiety (Damasio et al., 1996; Mallorquí-Bagué et al., 2016; Schachter & Singer, 1962). This can also be extended to clinical manifestations of general anxiety symptoms. Awareness of physiological symptoms, sometimes referred to as excessive body vigilance or somatosensory amplification, is associated with increases in feelings of state anxiety and increases in general anxiety symptoms (Barsky et al., 1990; Fergus & Valentiner, 2009; Gerlach et al., 2004; Lang & McTeague, 2009; Olatunji et al., 2007; Wild et al., 2008). However, meta-analytic evidence has suggested the association between self-reported state anxiety and physiological responses to acute stress is relatively small (Campbell & Ehlert, 2012; Feldman et al., 1999). Feldman et al. (1999) reported that acute psychological stress increased both negative affect and cardiovascular activity, but that the association between these two variables accounted for little variance (i.e., 2-12%). Campbell and Ehlert (2012) reported that a significant association between physiological responses and psychological responses to the Trier Social Stress Task was only present in approximately 25% of studies.

The extant literature suggests individuals prone to general anxiety symptoms report greater perceived arousal than is objectively measured via HR reactivity during acute stressors (Anderson & Hope, 2009; Edelmann & Baker, 2002; Hoehn-Saric & McLeod, 2000). Adams et al. (2022) speculated that although general anxiety symptoms may not be associated with interoceptive accuracy (e.g., an individual’s ability to accurately perceive their own heartbeat), general anxiety symptoms may be linked with other aspects of interoceptive awareness, including increased interoceptive attention and heightened perceived intensity of interoceptive states. This aligns with hypotheses explaining the discrepancy between perceived and actual physiological arousal in individuals with higher levels of general anxiety symptoms (McLeod & Hoehn-Saric, 1993). One hypothesis, the variability hypothesis, suggests that individuals are more attuned to physiological changes, rather than the absolute level of their physiological arousal. Thus, frequent fluctuations in physiological arousal, as seen in individuals with general anxiety symptoms, result in higher self-report levels of perceived physiological arousal (Hoehn-Saric & McLeod, 2000). A second hypothesis, known as the attention hypothesis, proposes that individuals with higher levels of general anxiety symptoms pay more attention to their internal states, and this increased attention amplifies their perception of their physiological arousal (McLeod & Hoehn-Saric, 1993). This hypothesis aligns with a body of literature indicating the presence of attentional biases in anxiety disorders, where individuals with anxiety disorders detect threat more often and also fail to shift their attention away from threat (Armstrong & Olatunji, 2012; Cisler & Koster, 2010; Fox et al., 2001; Mogg & Bradley, 1998; Weierich et al., 2008). Previous research has also found that individuals with higher levels of general anxiety symptoms interpret physiological sensations as more harmful and distressing (Olatunji et al., 2007; Wild et al., 2008). Taken together, it is possible that because individuals with increased general anxiety symptoms experience more frequent changes in physiological arousal and are more likely to view physiological arousal as threatening, they pay more attention to their perceived physiological arousal and struggle to shift their attention away from their perceived physiological arousal. This may result in the discrepancy between perceived and objectively measured physiological arousal.

Building on this research and theoretical foundation, a study aimed to extend this work in a sample not recruited for clinical anxiety. In two independent samples (Study 1: 100% males; Study 2: 100% females), Trotman et al. (2019) examined how both objectively measured physiological arousal (i.e., HR reactivity) and perceptions of physiological responses predicted state anxiety levels in response to an acute psychological stressor. Results indicated that perceived physiological changes, not actual HR reactivity, were associated with state somatic anxiety following the stressor in males and females (Trotman et al., 2019). Interestingly, perceived physiological changes were related to stressor-evoked state cognitive anxiety in males, but not females. This suggests possible gender differences in the association between state anxiety and self-reported arousal (Trotman et al., 2019). However, it should be noted that slightly different scales were used to assess perceived HR in the two studies, making it unclear if the differences between males and females were confounded by type of measurement used to assess perceived HR changes (Trotman et al., 2019).

As reviewed, previous research indicates potential associations between physiological arousal and state anxiety during acute stressors. Namely, that perceived HR, rather than objectively assessed physiological arousal relates to stressor-evoked state anxiety. However, to our knowledge, research has yet to examine the associations between perceptions of physiological arousal, actual physiological arousal, and state anxiety in relation to general anxiety symptoms in a non-clinical sample using robust statistical analysis techniques. Generalized anxiety symptom severity is dimensional (Marcus et al., 2014; Ruscio et al., 2001), which supports an examination of a full range of symptom severity. Examining a sample not recruited for clinical anxiety allows for a continuum of generalized anxiety symptoms to be explored. That approach reduces the likelihood of range restriction and has the potential to elucidate the stress-anxiety relationship by identifying possible pathways through which perceptions of physiology are related to symptoms of stressor-evoked state anxiety and general anxiety symptoms.

The present study aimed to use standardized acute stressors to examine the relationship between perceived physiology, anxiety in response to a stressor, and general anxiety symptoms. More specifically, the study addressed the aforementioned limitations by 1) including both males and females in a single model; 2) utilizing a comprehensive model with all variables included and accounted for; and 3) measuring levels of general anxiety symptoms outside the laboratory at a later laboratory testing session to avoid potential confounds of the stress task. As displayed in Figure 1, based on the findings of Trotman et al. (2019), it was hypothesized that perceived physiological arousal, not objectively measured physiological arousal, in response to an acute psychological stressor, would be associated with increased levels of stressor-evoked anxiety. Furthermore, it was hypothesized that greater levels of stressor-evoked state anxiety would be associated with higher levels of general anxiety symptoms outside of the laboratory measured at a later laboratory visit, and that perceived physiological arousal would therefore be indirectly associated with general anxiety symptoms through the stressor-evoked anxiety in response to the acute psychological stress task. In summary, we hypothesized that perceived physiological arousal (rather than HR reactivity) will be related to general anxiety symptoms, and that this relationship will be explained through state somatic and cognitive anxiety.

Figure 1. Hypothesized Model Examining the Extent to Which Perceived Physiological Arousal and Heart Rate (HR) Reactivity Relate to State Cognitive and Somatic Anxiety, Which in Turn Relate to General Anxiety Symptoms.

Figure 1

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Note. Dashed boxes indicate an event that occurred during the acute psychological stressor. + symbol indicates an expected positive relationship. For simplicity, race, ethnicity, gender, and effort covariates are not depicted. HR = heart rate. Cognitive and Somatic Anxiety measured via IAMS. General Anxiety Symptoms measured via anxiety subscale of HADS.

Method

Participants

Participants were 160 young adults from the Southwestern United States and data collection took place from March 2020 to August 20211. Initial inclusion criteria included: being between the ages of 18-30 years, having no current illness or infection, and having no history of cardiovascular disease or traumatic brain injury. Participants were asked to refrain from consuming alcohol or engaging in vigorous exercise for 12 hours and to avoid consuming caffeine, food, or other drinks (excluding water) for 2 hours prior to the laboratory visits. Informed consent was obtained from participants prior to data collection. Participants received $50 for completing the study.

Laboratory Procedure

Upon arrival in the laboratory, participants provided informed consent. Following collection of anthropomorphic measurements, electrocardiogram electrodes were placed in a 3-spot configuration. Participants engaged in a 10-minute adaptation period, where they were in a seated position and no physiological measures were taken. This was followed by a 10-minute baseline period during which heart rate (HR) was continuously recorded. Participants were provided instructions for the acute psychological stress task and engaged in a brief practice of the task to ensure they understood the instructions. Following successful completion of a practice attempt, participants completed the Stroop and Multi-Source Interference Task (presented in a counterbalanced order). HR was recorded continuously throughout the baseline and stress task phases. After the task, participants immediately completed questions rating their perceived physiological arousal during the task and their cognitive and somatic anxiety (via the Immediate Anxiety Measures Scale) during the task. Cardiovascular equipment was then removed from the participants. Next, participants completed a series of demographic questionnaires. Participants returned to the laboratory, on average, approximately 17 days later (M = 17.01, SD = 14.24 days) for a neuroimaging laboratory visit during which they reported their general anxiety symptoms (via the Hospital Anxiety Depression Scale).

Measures

Cardiovascular Measurements

HR was measured continuously with a 3-spot electrode configuration using a mobile electrocardiography (ECG) device (MindWare Technologies LTD, Westerville, OH). BioLab, a Mindware software platform utilized for data acquisition and integration, was used to collect the raw ECG data at a sampling frequency of 500 Hz. MindWare’s HR/HRV analysis software was then utilized to automatically detect R-peaks and manually remove artifacts. The data was then uploaded to Kubios HRV. Averages were created for each participant for baseline and for stress. Cardiovascular reactivity was calculated for each participant as: average HR during stress – average HR during baseline. HR reactivity was used as the measure of actual biological responses to the acute psychological stress task (i.e., stressor-evoked arousal).

Perceived Physiological Arousal

Following the acute psychological stress task, participants were asked to rate their perception of physiological arousal during the stress task. The item stated: “Physiological arousal refers to how activated your body’s biological systems are (e.g., heart rate, adrenaline). How physiologically aroused were you during the task?”. Participants responded on a 7-point Likert scale (1 = not at all, 7 = extremely), with a higher score reflecting greater perceived physiological arousal. In the present study, this was the measure of perceived physiological arousal during the acute psychological stress task.

Cognitive and Somatic Anxiety Intensity

Following the acute psychological stress task, participants were asked to rate how cognitively and somatically anxious they felt during the task with the first section of the Immediate Anxiety Measures Scale (IAMS; Thomas et al., 2002). Using a 7-point Likert scale (1 = not at all, 7 = extremely), participants rated the intensity of their cognitive (e.g., thoughts such as concerns or worries) and somatic anxiety (e.g., symptoms such as physical nervousness) separately, where a higher score indicated a higher level of anxiety for each dimension. The items are: “To what extent are you experiencing cognitive anxiety (i.e., what level)?” and “To what extent are you experiencing somatic anxiety (i.e., what level)?”. The IAMS has demonstrated adequate validity and reliability (Thomas et al., 2002) and has been used to assess anxiety following an acute laboratory based stress task (Ginty, Oosterhoff, et al., 2022; Trotman et al., 2019; Williams et al., 2021). The cognitive anxiety and somatic anxiety subscales of the IAMS represent measures of state anxiety in response to the acute psychological stress task.

Hospital Anxiety Depression Scale

General anxiety symptoms were measured using the anxiety subscale of the Hospital Anxiety and Depression Scale (HADS), which consists of 7 items (Zigmond & Snaith, 1983). Example items include: “I feel tense or wound up” and “Worrying thoughts go through my mind”. Participants rated their feelings on a 4-point Likert scale (0-3), with three indicating greater anxiety (except in the case of reverse scored items, such as “I still enjoy the things I used to enjoy.”). Scores were added together to create an anxiety subscale score (possible range of scores = 0 - 19). The HADS has demonstrated good concurrent validity, test-retest reliability, and internal reliability (Bramley et al., 1988; Herrmann, 1997). In the present study, the Cronbach’s alpha coefficient for the anxiety subscale was = .82.

Acute Psychological Stress Tasks

Two psychological stress tasks, a Multi-Source Interference Task (MSIT) and a Stroop task, completed in a counter-balanced order were used (Rasero et al., 2024; Sheu et al., 2012). Each task lasted 9 minutes and 20 seconds, where 52-60 second blocks of congruent conditions were interwoven with 52-60 second blocks of incongruent conditions and each block was preceded by a 10-17 second fixation period. For both tasks during the incongruent tasks, accuracy was held to 50% by adjusting the length of the intertrial intervals, where accurate performance led to shorter intervals and inaccurate performance led to longer intervals. Lastly, to account for motor response differences between congruent and incongruent conditions, the two conditions were yoked, where the incongruent block was presented first and then the congruent block was presented with its trials appearing at the mean inter-trial interval of the incongruent block. To increase social evaluation, participants were told that they were 1) being video recorded and independent body language experts would assess the video in order to judge their body language and rate their anxiety levels during the task and 2) in competition with other members of the study with an artificial score board of performance placed prominently in the room (Ginty, Tyra, et al., 2022).

During the MSIT, participants were shown 4 numbers and instructed to select the number different from the others (i.e., the target number) by pressing the button corresponding to that number. In the congruent conditions, the target number was in a position matching the order of the buttons (e.g., the numbers presented were “1 3 3 3”, the target number is 1, is in the first position, and the correct response is to push the first button). In the incongruent conditions, the target number was not in a position matching the order of the buttons (e.g., the numbers presented were “3 3 1 3”, the target number is 1, but is in the third position, and the correct response is to push the first button). During the Stroop task, participants were shown a target word and instructed to select the color of that word by pressing the button corresponding to the identifying word of the correct color. The order of the buttons corresponds to the order of the colors (e.g., button 1 corresponds to the word on the left). In the congruent Stroop condition, the target word is in the target color and the identifying words are in the same color as the target. For example, the word “blue” is presented in a blue color (i.e., the target word is in the target color). Below that word are the identifying words “green”, “yellow”, “red”, and “blue” and all words are the color blue (i.e., identifying words are the same color as the target). To answer correctly, the participant would need to hit the fourth button, as it corresponds to the correct identifying word (e.g., blue). In the incongruent Stroop condition, the target word is not in the target color and the identifying words are not in the target color. For example, the word “red” is presented in a green color (i.e., the target word is not the target color). Below that word are the identifying words “green” in a blue color, “yellow” in a green color, “red” in a yellow color, and “blue” in a red color (i.e., the identifying words are not in the target color). To answer correctly, the participant would need to hit the first button, as it corresponds to the correct identifying word (e.g., green). Both the Stroop task and MSIT have demonstrated good retest reliability and have been shown to perturb the cardiovascular system (Gianaros et al., 2002; Ginty, Gianaros, et al., 2013; Rasero et al., 2024; Sheu et al., 2012)

Data Analysis

Statistical analysis was completed using SPSS (IBM, Version 26) and AMOS (IBM, Version 26). Data were analyzed for outliers. Box plots indicated one outlier three standard deviations from the mean for HR reactivity. Data were analyzed with and without the participant, however, results remained unchanged. Thus, the participant was retained for the final analyses. Descriptive means and standard deviations were calculated for HR reactivity, perceived physiological arousal, cognitive anxiety intensity, somatic anxiety intensity, and general anxiety symptoms. To ensure the stress task perturbed the cardiovascular system, a one-way ANOVA was run to compare baseline HR and average stress task HR. Multicollinearity between main variables of interest was checked via Pearson’s correlation coefficients, variance inflation factor, and eigenvalues.

Remaining analyses were conducted in AMOS. Aligning with the two-step approach to SEM, the factor structure of the HADS anxiety subscale was examined before the hypothesized model depicted in Figure 1 was tested, controlling for gender, race, and ethnicity during the acute psychological stress task. Based on previous research examining the relationship between perceived physiological arousal, cardiovascular reactivity, and anxiety (Trotman et al., 2019), the hypothesized model was created.

The chi-squared (χ2) likelihood ratio was employed to test the model’s overall goodness of fit, where smaller and nonsignificant values indicate a good fit (Jöreskog & Sörbom, 1993). However, in practice, small, nonsignificant χ2 values are rarely observed and, thus, additional fit indices were calculated (Hu & Bentler, 1999). First, the standardized root mean square residual (SRMR) demonstrates absolute fit index by calculating the average difference between sample variances and covariances and estimated population variances and covariances. Second, two supplementary fit indices were used to compare the estimated model to an independent model: the Comparative Fit Index (CFI) and the Tucker-Lewis index (TLI; Bentler, 1990; Bollen, 1989). Lastly, the root mean square error of approximation (RMSEA) was used to determine how well the model represents the data by examining the model’s estimated lack of fit to a population covariance matrix. While there are varied views on the different cut-off values to indicate good vs adequate vs poor model fit, we used the suggestions provided by Hu and Bentler (1999). Consequently, an SRMR value close to 0.08 was used to indicate an good fit (Hu & Bentler, 1999), CFI and TLI values close to .90 and .95 represented adequate and good model fits respectively (Hu & Bentler, 1998), and an RMSEA value less than or equal to 0.06 indicated an adequate fit (Hu & Bentler, 1999). Although these criteria are still commonly reported values, various other factors can influence these indicators of model fit and, as such, caution should be used when interpreting the model fit.

Path analysis was also employed to test the usefulness of competing pathways. First, the hypothesized model was freed by including direct effects between perceived physiological arousal and general anxiety symptoms and HR reactivity and general anxiety symptoms. Next, the hypothesized model was fixed such that the effects of perceived physiological arousal and HR reactivity were mediated through cognitive and somatic anxiety. A χ2 difference comparison was done, where a significant χ2 difference indicates that freeing the direct effects improves fit.

Mardia’s coefficient demonstrated the data did not display multivariate normality (Mardia’s multivariate kurtosis = 3.48). Therefore, a bootstrapping technique was employed using 2,000 samples with 90% confidence intervals. Correlations between variables were checked for multicollinearity. After checking the model fit, direct effects were examined before checking for the indirect effects between variables.

Results

Descriptive Statistics

The final sample consisted of 160 participants (Mage = 21.52, SD = 2.97, range 18-30 years); for detailed participant characteristics, please see Table 1. Mean scores for HR reactivity, perceived physiological arousal, cognitive anxiety intensity, somatic anxiety intensity, and general anxiety symptoms are reported in Table 2.

Table 1.

Participant Characteristics

Characteristic Frequency
Gender
 Female 81 (50.6%)
 Male 78 (48.8%)
 Prefer not to answer 1 (0.6%)
Race
 American Indian or Alaska Native 3 (1.9%)
 Asian 30 (18.7%)
 Black or African American 21 (13.1%)
 Mixed/Other 12 (7.5%)
 White 94 (58.8%)
Ethnicity
 Hispanic or Latino 34 (21.3%)
 Not Hispanic or Latino 126 (78.7%)
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Table 2.

Means and Standard Deviations for Reactivity, Perceived Physiological Arousal, State Anxiety and General Anxiety Symptoms Measures

Variable Mean (SD) Range
Baseline HR (bpm) 78.04 (11.74) 48.51 – 107.83
MSIT HR (bpm) 80.43 (11.95) 49.10 – 112.62
Stroop HR (bpm) 82.66 (13.06) 48.08 – 117.39
Change from baseline HR (bpm)a 3.93 (6.06) −10.82 – 34.85
Perceived Physiological Arousal 4.0 (1.3) 1 – 7
State Cognitive Anxiety Intensity 4.4 (1.5) 1 – 7
State Somatic Anxiety Intensity 3.7 (1.4) 1 – 7
General Anxiety Symptoms 7.6 (4.1) 0 - 19
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Note. HR = heart rate; cognitive and somatic anxiety are subscales from the IAMS; general anxiety symptoms is the anxiety subscale of the HADS. Perceived physiological arousal, cognitive anxiety intensity and somatic anxiety intensity are averaged across the two stress tasks.

a

average stress HR – baseline HR.

Manipulation Checks

A one-way repeated measures ANOVA (baseline, stress) demonstrated the acute psychological stress task statistically significantly perturbed HR (F [1,159] = 67.33, p < .001, pη2 = .29; baseline HR: M = 77.61 bpm [SD = 11.74 bpm], stress HR: M = 81.54 bpm [SD = 12.11 bpm]).

The confirmation factor analysis for the factor structure of the HADS anxiety subscale revealed a good fit to the data, χ2(14) = 26.579, p = .022, CFI = .958, TLI = .937, SRMR = .048, RMSEA = .075 (90% CI = .028, .118), supporting use of the 7 items as indicators of the general anxiety symptoms construct.

Multicollinearity between the variables was checked via Pearson’s correlation coefficient. All correlations were less than .70 except the absolute value of the correlation coefficient between perceived physiological arousal and somatic anxiety intensity (r = .76) so further checks were completed to ensure independence (Woo, 2012). First, the variance inflation factor (VIF) between perceived physiological arousal and somatic anxiety (VIF = 1.00) did not exceed 5, indicating an absence of multicollinearity (Hair et al., 2011; Shrestha, 2020). Next, the condition index (CI), which is a function of eigenvalues, was investigated. A CI greater than 15 indicates evidence of multicollinearity (Shrestha, 2020). The CI between perceived physiological arousal and somatic anxiety was equal to 6.13, again indicating an absence of multicollinearity. Thus, both variables were retained in the model.

Hypothesized Model Path Analysis

To test the a priori hypothesized model in predicting general anxiety symptoms, regression paths were drawn from perceived physiological arousal and HR reactivity to cognitive and somatic anxiety intensity. Regression paths were then drawn from both cognitive and somatic anxiety intensity to general anxiety symptoms. Additionally, due to the relationship between cognitive and somatic anxiety, a coefficient was also included between their variances similar to prior research (Williams & Cumming, 2016). The hypothesized model is displayed in Figure 1. The hypothesized structural equation model demonstrated an adequate fit to the data, χ2 (59) = 93.15, p = .003; CFI = .94; TLI = .91; SRMR = .05; RMSEA = .06 (90% CI = .04 - .08).

To further examine if the pattern of interrelations are best modeled as having the impact of perceived physiological arousal on general anxiety symptoms going through state anxiety, direct regression paths were drawn from perceived physiological arousal and HR reactivity to general anxiety symptoms (χ2 (57) = 92.32, p = .002; CFI = .94; TLI = .91; SRMR = .05; RMSEA = .06 (90% CI = .04 - .09)). This path analysis did not result in a significant difference between the models, (Δχ2(2) = .83, p = .661), suggesting that freeing those direct effects does not improve model fit. As a result, these findings support the retention of the more parsimonious Figure 1.

Figure 2 contains the final model and all standardized direct effects. With the exception of biological sex sharing significant direct effects with general anxiety symptoms (β = .26, p = .004) and state cognitive anxiety (β = .26, p = .010), none of the other direct effects involving the covariates were significant. Perceived physiological arousal was positively related to state cognitive anxiety and state somatic anxiety. In turn, cognitive and somatic anxiety were positively associated with general anxiety symptoms, but only the relationship between somatic anxiety and general anxiety symptoms was statistically significant. HR reactivity was not statistically significantly associated to either state cognitive or state somatic anxiety.

Figure 2. Final Model Depicting the Direct Associations between Perceived Physiological Arousal and Heart Rate (HR) Reactivity, Cognitive and Somatic Anxiety Intensity, and General Anxiety Symptoms.

Figure 2

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Perceived physiological arousal was positively related to state cognitive and state somatic anxiety. In turn, somatic anxiety was positively associated with general anxiety symptoms. There was no statistically significant associations between HR reactivity with state cognitive or somatic anxiety, nor between state cognitive anxiety and general anxiety symptoms.

Note. Dashed boxes indicate an event that occurred during the acute psychological stressor. For simplicity, race, ethnicity, gender, and effort covariates are not depicted. Regression weights are standardized. HR = heart rate. Cognitive and Somatic Anxiety measured via IAMS. General Anxiety Symptoms measured via anxiety subscale of HADS.

As part of the review process, the model was re-run to include interval between visits (number of days) as an additional covariate in the analyses. Results indicated that although β values slightly changed, there were no differences in what was statistically significant for any of the pathways. Similarly, the model fit remained relatively unchanged. Thus, the original model was retained. Removal of the non-significant pathways from the model improved the model fit further. However, this model trimming approach was not undertaken to prevent the reported β values of significant pathways becoming overinflated from the removal of non-significant pathways which likely account for some of the variance in the predicted variables.

Indirect Effects

Collectively, the results of the direct pathways between the model variables suggests that perceived physiological arousal (rather than HR reactivity) is related to general anxiety symptoms, and that this relationship operates indirectly through state somatic anxiety. This indirect finding was confirmed by the statistically significant indirect effect between perceived physiological arousal and general anxiety symptoms (β = .27, p < .001 (90% CI = .18 - .38)). The indirect effect between HR reactivity and general anxiety symptoms was not significant (β < .01, p = .748 (90% CI = −.02 - .03)).

Discussion

The present study examined whether stressor-evoked arousal (perceived and objective) was related to general anxiety symptoms via stressor-evoked state anxiety. As hypothesized, in response to laboratory stress tasks, perceived physiological reactivity, but not HR reactivity, was associated with stressor-evoked cognitive and somatic anxiety. However, only somatic anxiety was associated with general anxiety symptoms outside of the laboratory. Therefore, perceived physiological reactivity was associated with general anxiety symptoms via somatic anxiety. The present study extends prior work by examining the associations between perceived and actual physiological arousal and state anxiety in response to acute psychological stress with general anxiety symptoms.

The results are partially in line with a previous two study paper that found perceived physiological changes, not actual HR reactivity, were associated with stressor-evoked state somatic and cognitive anxiety in males (Study 1, N = 71, 100% males) and stressor-evoked state somatic anxiety in females (N = 70, 100% females; Trotman et al., 2019). The present study included both males and females in a single model and found that perceived physiological changes in response to the acute stress task were associated with both state somatic and state cognitive anxiety after adjusting for gender. Additionally, the present study extended Trotman et al.'s (2019) work by examining general anxiety symptoms outside the laboratory at a later time point. Examining general anxiety symptoms at a different timepoint than the acute laboratory stress task visit may possibly reduce artificially elevated levels of reported general anxiety symptoms due to increased levels of state anxiety caused by the acute laboratory stress task (Leal et al., 2017). Although there was an indirect relationship between perceived physiological arousal and general anxiety symptoms via state somatic anxiety, contrary to our hypothesis, the same indirect relationship did not operate through state cognitive anxiety. Perceived physiological arousal was positively associated with state cognitive anxiety (as hypothesised), but this state anxiety was not subsequently related to general anxiety symptoms. While the HADS is a widely-used, valid measure of general anxiety symptoms, the anxiety subscale items of the HADS may have a higher proportion of items related to somatic symptoms of anxiety (e.g., “I get a sort of frightened feeling like butterflies in the stomach”, “I get sudden feelings of panic”, “I feel tense or ‘wound up’”) than items related to cognitive symptoms of anxiety (e.g., “Worrying thoughts go through my mind”). Indeed, prior work has demonstrated the HADS is associated with increased somatic symptoms (Carlehed et al., 2017; Haug et al., 2004). However, factor analyses have demonstrated that the HADS is separate from measures of physical somatic symptoms (Johnston et al., 2000). Future research should utilize alternate measures of general anxiety symptoms (e.g., the State-Trait Inventory for Cognitive and Somatic Anxiety; Ree et al., 2008) that separately assess the cognitive and somatic dimensions of general anxiety symptoms.

Results also align with previous meta-analyses, which reported a general discordance between stressor-evoked physiological responses and emotional responses to stress (Campbell & Ehlert, 2012; Feldman et al., 1999). Campbell and Ehlert (2012) found that out of twelve studies examining cardiovascular reactivity and subjective stress during a laboratory stress task, eight studies did not find statistically significant associations. Notable findings include a non-statistically significant association between anxiety ratings and HR changes (Cohen et al., 2000) and a lack of correlation between pre- versus post-task changes in anxiety and HR (Ditzen et al., 2007). Similarly, a meta-analysis by Feldman et al. (1999) examining the relationship between negative emotional responses and cardiovascular responses to an acute laboratory stressor across nine separate studies found that stressor-evoked negative emotion accounted for limited variability in cardiovascular stress reactivity. Further, they found a weak association between anxiety and cardiovascular responses. Similar to these two meta-analyses, the present study did not find a statistically significant association between objectively measured HR reactivity and state anxiety in response to the stress tasks.

In the present study, higher levels of perceived physiological arousal were associated with higher levels of stressor-evoked cognitive and somatic anxiety and, in turn, higher levels of somatic anxiety were associated with increased general anxiety symptoms. Research focusing on individuals with anxiety disorders has demonstrated that those with anxiety disorders report higher perceived physiological activation during acute psychological stress paradigms than is measured (e.g., Anderson & Hope, 2009; Edelmann & Baker, 2002; Hoehn-Saric & McLeod, 2000). Indeed, it has been demonstrated that individuals with higher levels of general anxiety symptoms may pay excessive attention to body sensations and interpret these sensations as more threatening than they are (Barsky et al., 1990; Olatunji et al., 2007). Similarly, individuals with higher levels of general anxiety symptoms often report increased distress over their symptoms (Wild et al., 2008). While research has indicated an association between perceptions of bodily sensations, psychological stress and general anxiety, the underlying processes connecting them is not well understood. Our results indicate that somatic state anxiety may be a potential mechanism through which perceived physiological activation relates to general anxiety symptoms. In this way, our results identify a mechanism of behavior change (e.g., reappraising perceived physiological arousal), aligning with the National Institutes of Health Science of Behavior change approach, that future research should examine as an intervention target in an effort to reduce state anxiety intensity and assist with the reinterpretation of perceived physiological arousal symptoms during stress as facilitative (Stoeckel et al., 2023).

A distinct, but related line of experimental research involving manipulated HR feedback has also illuminated a connection between perceived physiological arousal and anxiety. In studies where participants listened to either their own heartbeat or an altered (e.g., faster or slower) heartbeat, the findings indicated that informing participants their HR was higher than actually recorded resulted in participants altering their subjective ratings of various tasks. For example, when told their HR was higher than recorded, participants rated the perceived emotional intensity of neutral faces higher (Gray et al., 2007), their effort on a cycling task higher (Iodice et al., 2019), and their anxiety related to heart problems higher (Rietveld et al., 2004). While the present study did not provide feedback on stressor-evoked HR changes, we demonstrated that higher perceptions of physiological arousal were associated with greater levels of state anxiety supporting previous research suggesting that perceptions of physiological arousal may be a potent predictor of emotional responses to challenging tasks. The findings of the present study may also be relevant to research examining the relationship between cardiovascular events (e.g., sudden cardiac arrest), post-traumatic stress disorder (PTSD), and cardiac anxiety. Previous work suggests that following a cardiac event, most individuals display symptoms of cardiac anxiety (e.g., excessive monitoring of HR, fears of chest sensations; Argarwal et al., 2022; Edmondson, 2014; von Känel et al., 2022). Further, the enduring somatic threat model of PTSD suggests that after a cardiovascular event, patients who become sensitized to somatic cues of threat experience the most distress (Meli et al., 2019). Future research could explore interoceptive exposures as an intervention, where individuals are exposed to physiological arousal, with the goal of increasing distress towards the somatic sensations of state anxiety in service of reducing overall general anxiety symptoms (Boettcher et al., 2016).

Lastly, our findings demonstrating no statistically significant direct association between general anxiety symptoms and physiological stress reactivity are at odds with some work examining physiological responses to stress and anxiety. A recent systematic review and meta-analysis examining the association between test anxiety and physiological arousal (Roos et al., 2021) found that 68% of studies analyzed indicated a positive significant association between self-reported test anxiety and physiological arousal. However, for a study to be included in the review, the study had to include measurements of state anxiety in regards to an examination/test which may be different than most standardized laboratory stress tasks. Some research examining the association between trait levels of anxiety and cardiovascular responses to standardized laboratory stressor has demonstrated that higher levels of anxiety are associated with lower cardiovascular responses to stress (de Rooij et al., 2010; Krämer et al., 2012; Liu et al., 2023; Lü et al., 2022; Young et al., 1998), while other work has shown no association in response to stress/differences between anxious and non-anxious groups (Fisher & Newman, 2013; Pointer et al., 2012). Further, it has been demonstrated that the specific type of anxiety may impact physiological responses to acute stress (Lü et al., 2022; Tolin et al., 2021). Future studies should consider more multidimensional measures of anxiety and methods such as ecological momentary assessment to further untangle the association between stress in every day life, anxiety, and physiological arousal.

While the present study has notable strengths, it is not without limitations. First, a single-item question was used to assess perceived physiological arousal. However, this item has been used in several previous studies (Beevor et al., 2024; Ginty, Oosterhoff, et al., 2022; Trotman et al., 2019) and has demonstrated utility in predicting outcomes associated with stress. Second, some may consider perceived physiological arousal and somatic anxiety to be measuring the same thing. However, tests of multicollinearity demonstrated that they were independent measures. Third, while the present study included gender as a covariate, the study did not analyze potential moderating effects of gender on the pathways between perceived physiological arousal, stressor-evoked anxiety, and general anxiety symptoms. Future research in a larger population should aim to examine whether the same model is supported in both males and females via multi-group path analysis invariance testing. Third, the HADS was used to assess general anxiety symptoms outside of the laboratory. The scope of the HADS is limited as it only asks about feelings of anxiety during the past week and is not a formal clinical diagnosis of an anxiety disorder (e.g., Generalized Anxiety Disorder). However, the HADS is a well-recognized, frequently used scale in research that has been shown to be a clinically meaningful assessment of anxiety symptom severity and to predict psychosocial outcomes (Bjelland et al., 2002; Ginty, Carroll, et al., 2013; Herrmann, 1997). Lastly, laboratory stressors may not evoke the same physiological response as real-world stressors. However, the Stroop task and MSIT have been shown to adequately perturb the cardiovascular system and demonstrate good test-retest reliability (Ginty, Gianaros, et al., 2013; Sheu et al., 2012). In the present study, there were individual differences in HR reactivity, which is in line with previous work (e.g., Whittaker et al., 2021). Overall, there was a statistically significant increase in response to acute psychological stress in HR, compared to baseline values, across the sample. Additionally, previous research has found that physiological responses to laboratory psychological stressors predict physiological reactivity to more naturalistic stressors (e.g., public speaking; Johnston et al., 2008; Kamarck & Lovallo, 2003). Future research should include ecological measures of perceived physiology, stress, and general anxiety symptoms to investigate physiological responses to life stressors in real time (for guidelines on ecological measures examining the association between physiology and stress, see Rodrigues et al., 2015).

In summary, perceived physiological arousal, but not objectively measured HR reactivity, during a laboratory stress task was associated with stressor-evoked cognitive and somatic anxiety and, in turn, stressor-evoked somatic anxiety was associated with general anxiety symptoms outside of the laboratory. The present study provides a potential path through which stressor-evoked perceived physiological arousal may relate to subsequent general anxiety symptoms. Future research should examine this association longitudinally to elucidate the directionality of the relationship and should examine potential interventions for anxiety that address the discordance between perceived and actual physiological reactivity.

Highlights.

  • Mechanisms behind the acute stress-anxiety relationship are not fully understood.

  • Perceived HR, not actual HR, is related to stressor-evoked anxiety.

  • Somatic anxiety mediated the relationship between perceived HR and general anxiety symptoms.

  • Findings highlight the need for anxiety interventions that address perceived HR.

Acknowledgements

The authors would like to thank the undergraduate research assistants in the Baylor Behavioral Medicine Laboratory for their assistance with data collection.

Funding

This research was funded by the National Institutes of Health (K01HL145021).

Declaration of interests

The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:

Dr. Annie Ginty reports financial support was provided by National Heart Lung and Blood Institute. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

1

The first two participants were tested on March 2, 2020 and March 3, 2020. Then, the next participant was not tested until September 10, 2020 due to the COVID-19 pandemic. All testing taking place after March 3, 2020 included full COVID-19 precautions: temperature taken for all participants and research assistants before entering the main laboratory and completing a symptom check list. If participants had a fever or reported symptoms, they were not permitted to participate. All research assistants wore appropriate personal protection equipment during testing. The results with and without the two participants tested before COVID-19 was declared a pandemic were virtually identical and so it was decided to include them in the study.

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