Blunted cardiovascular reactions in response to acute psychological stress are predictive of future health risk. A large body of research has identified depression as an influential factor associated with blunted cardiovascular reactivity. Separately, there has been a resurgence in focus on anhedonia as a key feature of depression, responsible for poor treatment responses to non-improvement in cardiac event-free survival. In a re-analysis of a previously published study that found depression to be associated with blunted systolic blood pressure (SBP) and heart rate responses (HR), we used cross-sectional network models to examine if anhedonia symptoms were key drivers of this observation. Healthy young adults (N = 180) completed measures of depression symptoms (Hospital Anxiety and Depression Scale (HADS)) and had their blood pressure and heart rate monitored throughout a standardized stress testing protocol. Using network analysis, a Walktrap algorithm identified two clusters of depressive symptoms: anhedonia and non-anhedonia. These anhedonia symptoms of depression, but not the non-anhedonia symptoms, were associated with blunted SBP and HR reactivity, such that those scoring higher on HADS-D items capturing anhedonia displayed more blunted cardiovascular response profiles. Moreover, these findings were robust to adjustment for several covariates. This study adds greater clarity on the depression-cardiovascular reactivity to stress association, by demonstrating that anhedonia is a key driver of this observation.

Lower cardiovascular reactivity is a proposed marker of motivational dysregulation and is related to a range of adverse behavioural and health outcomes. Social participation is a form of motivated behaviour and represents the frequency in which an individual engages in social activities. Low social participation has recently been linked to lower cardiovascular responses to acute psychological stress. With recent work emphasizing the importance of assessing adaptation of the cardiovascular response to recurrent stress, the aim of the current study is to build on previous work by examining the relationship between social participation and cardiovascular stress response adaptation. This study utilised data from the Pittsburgh Cold Study 3 (PCS 3). Two hundred and thirteen participants (M = 30.13; SD = 10.85) completed a social participation measure and had their systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) monitored across two separate standardized stress testing sessions. The testing sessions consisted of a 20-minute baseline and a 15-minute stress task. Results indicated that higher levels of social participation were associated with greater blood pressure habituation to recurrent stress, extending previous work identifying that social participation was associated with higher cardiovascular responses to stress. The present study identifies that those reporting greater levels of social participation may show enhanced stress tolerance when exposed to recurrent stress.

There is considerable evidence documenting associations between tobacco smoking, including initiation, maintenance, and relapse of addiction, with diminished cardiovascular responses to acute psychological stress. However, less is known about how smokers respond to repeated stress across time. The current study examined patterns of cardiovascular reactivity and adaptation to recurrent stress among 24-h abstinence smokers, smokers who continued to smoke at their normal rate, and non-smokers. Smokers were randomly assigned to one of two groups; ad libitum (n = 42), or 24 h abstinence (n = 61); non-smokers (n = 43) provided comparative referencing. Across the two laboratory sessions, participants (n = 149) were asked to complete a modified version of the trier social stress test, while monitoring systolic and diastolic blood pressure, and heart rate activity. Results showed that while non-smokers had elevated cardiovascular reactivity to begin with, they showed a greater capacity to habituate to recurrent stress across sessions. The data also suggest that smokers displayed lower cardiovascular reactivity to acute psychological stress and showed little habituation to repeated stress. In adjusted models, smokers exhibited less systolic blood pressure habituation to stress. This response profile in smokers may be a potential mechanism that leads to further cardiotoxic effects on health.

OBJECTIVES:Blunted cardiovascular reactivity is associated with a distinct behavioural profile of greater exposure to early life adversity, coupled with higher levels of behavioural disengagement and symptoms of depression. The present study sought to extend on this work by investigating if behavioural clusters with distinct patterns of reactivity were related to health and behavioural outcomes at baseline and at a 4-year follow-up. METHODS:Hierarchical cluster analyses were conducted using longitudinal data drawn from the Midlife Development in the United States (MIDUS 2) Biomarker Project and the MIDUS 3 follow-up 4 years later. During MIDUS, 2 participants (N = 513) underwent a standardized stress testing protocol and had their blood pressure and heart rate monitored throughout. In addition, hierarchical cluster analyses were conducted on responses from measures of early life adversity, behavioural disengagement and depression. Binary logistic regressions were conducted to determine whether cluster membership was related to health and behavioural outcomes which were taken at both time points. RESULTS:Three behavioural clusters emerged with statistically different blood pressure reactivity patterns. The cluster characterized by greater exposure to early life adversity, higher levels of behavioural disengagement and depressive symptoms, had relatively lower blood pressure reactivity patterns compared with both the exaggerated reactivity cluster and the cluster similar to the sample mean. In fully adjusted models, this cluster was associated with hypertension (p = .050) and depressed affect (p = .033), while Cluster 1 characteristic of an exaggerated blood pressure reactivity profile was associated with depressed affect (p < .001). Cluster membership did not significantly predict future health status. CONCLUSION:This study extends research on behavioural clusters characteristic of reactivity profiles to demonstrate how they relate to health and behavioural outcomes during MIDUS 2.

Objective This study examines if Type D personality is (1) associated with cardiovascular reactivity to acute stress in a healthy sample, and (2) has predictive utility for cardiovascular reactivity above its individual subcomponents (negative affect; NA, social inhibition; SI), as well as anxiety and depression. Design Undergraduate students (n = 173) competed a standardised cardiovascular reactivity experimental protocol consisting of resting baseline and stressor phase (mental arithmetic), with systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) monitored throughout. Main Outcome Measures The main outcome measures were cardiovascular reactivity to the stressor, which was operationalised as the difference between resting baseline and the stressor phase for SBP, DBP and HR. Results The continuous Type D interaction term (NA x SI) significantly predicted lower SBP reactivity to the mental arithmetic stressor amongst women, independent of NA, SI and confounding variables. Moreover, this remained significant after adjustment for anxiety and depressive symptoms. Depression, NA and SI were also significant independent predictors of SBP reactivity amongst women. Conclusion Type D personality is associated with lower SBP reactivity to acute stress in women, which may be indicative of blunted cardiovascular reactivity. This association was independent of NA, SI, Anxiety and Depression.

Diminished cardiovascular reactivity is a proposed marker of motivational dysregulation and is related to a range of adverse behavioural and health outcomes. Social participation represents the frequency an individual engages in social activities, is a form of motivated behaviour, and has been recently linked to lower cardiovascular responses to acute psychological stress. With recent work emphasizing the importance of assessing adaptation of the cardiovascular response to recurrent stress, the aim of the current study is to build on previous work by examining the relationship between social participation and cardiovascular stress response adaptation. Analyses were conducted using a general linear model and previously obtained data from the Pittsburgh Cold Study 3 (PCS 3). Two hundred and thirteen participants (M = 30.13; SD = 10.85) completed a social participation measure and had their systolic and diastolic blood pressure (SBP, DBP) and heart rate (HR) monitored across two separate standardized stress testing sessions. In line with previous research, lower social participation was related to lower cardiovascular responses to stress. Findings also indicate that higher levels of social participation were associated with greater blood pressure habituation to recurrent stress. Given that cardiovascular habituation to recurrent stress signifies good health, the implications of these findings are discussed. Key words: social participation, cardiovascular reactivity, cardiovascular habituation, blood pressure, Pittsburgh Cold Study.

ABSTRACT Objective The pathways underlying the early life adversity and cardiovascular reactivity association remain unclear. The current study examined the role of current depressive symptoms on this relationship. Methods Mediation analyses were conducted using data from 639 participants drawn from the Midlife Development in the United States 2 Biomarker Project. Responses were derived from the Childhood Trauma Questionnaire and Center for Epidemiologic Studies Depression Scale. Participants had their systolic and diastolic blood pressure (SBP, DBP) and heart rate monitored throughout a standardized stress testing protocol. Results The association between early life adversity and reactivity was mediated by current depressive symptoms; all adversity factors were linked to higher levels of current depressive symptoms, which, in turn, were associated with lower cardiovascular reactivity. For emotional abuse, this was noted for SBP (β = −0.06 [95% confidence interval {CI}, −0.13 to −0.01]) and DBP (β = −0.04 [−0.07 to −0.01]), physical abuse (SBP: β = −0.05 [−0.11 to −0.01]; DBP: β = −0.03 [−0.06 to −0.01]), sexual abuse (SBP: β = −0.04 [−0.09 to −0.01]; DBP: β = −0.02 [−0.05 to −0.01]), emotional neglect (SBP: β = −0.04 [−0.09 to −0.01]; DBP: β = −0.02 [−0.05 to −0.01]), physical neglect (SBP: β = −0.09 [−0.17 to −0.02]; DBP: β = −0.05 [−0.09 to −0.02]), and total Childhood Trauma Questionnaire score (SBP: β = −0.02 [−0.03 to −0.00]; DBP: β = −0.01 [−0.02 to −0.00]). Conclusions The present findings extend research and demonstrate that depression is an underlying mechanism linking early life adversity and blunted cardiovascular reactivity.

Background There is considerable evidence documenting associations between early life adversity, behavioral disengagement, and depression with blunted cardiovascular reactivity to acute psychological stress. However, while often examined as independent predictors, it is also likely that a combination of these factors uniquely relate to cardiovascular reactivity. Purpose The present study employed multivariate cluster analysis to examine if distinct combinations of these outcomes relate to cardiovascular stress reactivity. Methods Participants (N = 467) were predominantly female (60.6%) with a mean age of 19.30 years (SD = 0.82). Measures of early life adversity, behavioral disengagement, and depression were completed; in addition, participants had their blood pressure and heart rate monitored throughout a standardized stress testing session. Cardiovascular reactivity was calculated as the difference between mean stress and mean baseline cardiovascular values. Results Analyses revealed two clusters with distinct patterns of exposure to early life adversity, levels of behavioral disengagement and depression, uniquely related to cardiovascular reactivity. In unadjusted models, Cluster 1 that was characterized by greater exposure to early life adversity, higher levels of behavioral disengagement and depression, was associated with lower systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) reactivity. Cluster 2 was characterized by reactivity values similar to the sample means. In fully adjusted models, Cluster 1 predicted heart rate reactivity to stress. Conclusions The present study identifies a behavioral cluster that is characteristic of a blunted heart rate reactivity profile, significantly extending the research in this area.

Tobacco smoking has been associated with lower cardiovascular reactivity to psychological stress in middle-aged samples, but its impact on cardiovascular reactivity to stress in young adults remains unclear. The present study examined whether young healthy adults showed differing cardiovascular stress reaction profiles depending on their smoking status. Across two laboratory studies (N = 64 and N = 114), we asked participants to complete cognitive stress-tasks while undergoing continuous hemodynamic monitoring. In both studies, there was not a statistically signification association between systolic blood pressure, diastolic blood pressure, or heart rate reactivity to stress (all ps > .05). However, examination of the underlying hemodynamic profile of the stress response suggested differences between non-smokers and smokers in both studies. In Study 1, non-smokers exhibited the expected myocardial response to the active stress-task; however, smokers exhibited a mixed hemodynamic profile. In Study 2, smokers evidenced a weaker myocardial profile to the active stress-tasks compared to non-smokers. However, the examination of the continuous hemodynamic profile score (HP) did not identify statistical differences. These results highlight that any level of the smoking habit is associated with an altered hemodynamic profile in response to stress in smokers, which may have important implications for long-term cardiovascular health. The findings also suggest that controlling for smoking behavior in reactivity research examining blood pressure and heart rate responses to stress in young adults is not necessary.

The psychological pathways linking depression to blunted cardiovascular reactivity (CVR) are still being elucidated. The purpose of the present study was to test whether the association between eveningness, a diurnal/ sleep-wake preference and CVR would be mediated by depressive symptoms. One hundred and eighty-two healthy young adults completed measures of morningness/eveningness (the Morningness-Eveningness Questionnaire; MEQ-SA), depressive symptoms (Hospital Anxiety and Depression Scale; HADS) and had their blood pressure and heart rate monitored throughout a standardised stress testing protocol. Results indicated that depressive symptoms were negatively associated with systolic blood pressure (SBP) but not diastolic blood pressure (DBP) or heart rate (HR) reactions to the stress task. Eveningness was also negatively associated with both SBP and DBP, but not HR. As such, those who reported increased depressive symptomology, and higher scores on eveningness displayed a more blunted cardiovascular response. Furthermore, the latter relationship was mediated by depressive symptoms such that those reporting higher scores on eveningness also reported increased depressive symptomology and this resulted in blunted CVR for SBP. These findings withstood adjustment for several confounding factors including time of testing. In conclusion, the present findings highlight the importance of considering eveningness when looking at the depression-blunted CVR relationship.

Recent theoretical developments in cardiovascular reactivity research suggest the association between depression and blunted reactions to stress is linked to motivational factors. Thus, the present study aimed to test whether the association between depressive symptoms and cardiovascular reactivity to acute stress was mediated by motivation; be it intrinsic or extrinsic motivation. One hundred and eighty-two healthy young adults completed measures of motivation (Global Motivation Scale; GMS), and depression (Hospital Anxiety and Depression Scale; HADS) and had their blood pressure and heart rate monitored throughout a standardised stress testing protocol. Results indicated that depression was negatively associated with both systolic blood pressure (SBP) and heart rate (HR) reactions to the stress task (all ps < .05), such that those who reported higher depressive symptomology displayed a blunted response. Furthermore this relationship was mediated by intrinsic, but not extrinsic motivation; the blunted responses were less pronounced through intrinsic motivation. The present findings add extensively to existing research and confirm that motivation is an underlying mechanism linking depression and cardiovascular reactivity.