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This Committee Report provides methodological, interpretive, and reporting guidance for researchers who use measures of heart rate (HR) and heart rate variability (HRV) in psychophysiological research. We provide brief summaries of best practices in measuring HR and HRV via electrocardiographic and photoplethysmographic signals in laboratory, field (ambulatory), and brain-imaging contexts to address research questions incorporating measures of HR and HRV. The Report emphasizes evidence for the strengths and weaknesses of different recording and derivation methods for measures of HR and HRV. Along with this guidance, the Report reviews what is known about the origin of the heartbeat and its neural control, including factors that produce and influence HRV metrics. The Report concludes with checklists to guide authors in study design and analysis considerations, as well as guidance on the reporting of key methodological details and characteristics of the samples under study. It is expected that rigorous and transparent recording and reporting of HR and HRV measures will strengthen inferences across the many applications of these metrics in psychophysiology. The prior Committee Reports on HR and HRV are several decades old. Since their appearance, technologies for human cardiac and vascular monitoring in laboratory and daily life (i.e., ambulatory) contexts have greatly expanded. This Committee Report was prepared for the Society for Psychophysiological Research to provide updated methodological and interpretive guidance, as well as to summarize best practices for reporting HR and HRV studies in humans., (© 2024 The Authors. Psychophysiology published by Wiley Periodicals LLC on behalf of Society for Psychophysiological Research.)

Resting heart rate may confer risk for cardiovascular disease (CVD) and other adverse cardiovascular events. While the brainstem's autonomic control over heart rate is well established, less is known about the regulatory role of higher level cortical and subcortical brain regions, especially in humans. This study sought to characterize the brain networks that predict variation in prevailing heart rate in otherwise healthy adults. We used machine learning approaches designed for complex, high-dimensional data sets, to predict variation in instantaneous heart period (the inter-heartbeat-interval) from whole-brain hemodynamic signals measured by fMRI. Task-based and resting-state fMRI, as well as peripheral physiological recordings, were taken from two data sets that included extensive repeated measurements within individuals. Our models reliably predicted instantaneous heart period from whole-brain fMRI data both within and across individuals, with prediction accuracies being highest when measured within-participants. We found that a network of cortical and subcortical brain regions, many linked to visceral motor and visceral sensory processes, were reliable predictors of variation in heart period. This adds to evidence on brain-heart interactions and constitutes an incremental step toward developing clinically applicable biomarkers of brain contributions to CVD risk., (© 2024 The Author(s). Psychophysiology published by Wiley Periodicals LLC on behalf of Society for Psychophysiological Research.)

Understanding the association between autonomic nervous system [ANS] function and brain morphology across the lifespan provides important insights into neurovisceral mechanisms underlying health and disease. Resting-state ANS activity, indexed by measures of heart rate [HR] and its variability [HRV] has been associated with brain morphology, particularly cortical thickness [CT]. While findings have been mixed regarding the anatomical distribution and direction of the associations, these inconsistencies may be due to sex and age differences in HR/HRV and CT. Previous studies have been limited by small sample sizes, which impede the assessment of sex differences and aging effects on the association between ANS function and CT. To overcome these limitations, 20 groups worldwide contributed data collected under similar protocols of CT assessment and HR/HRV recording to be pooled in a mega-analysis (N = 1,218 (50.5% female), mean age 36.7 years (range: 12-87)). Findings suggest a decline in HRV as well as CT with increasing age. CT, particularly in the orbitofrontal cortex, explained additional variance in HRV, beyond the effects of aging. This pattern of results may suggest that the decline in HRV with increasing age is related to a decline in orbitofrontal CT. These effects were independent of sex and specific to HRV; with no significant association between CT and HR. Greater CT across the adult lifespan may be vital for the maintenance of healthy cardiac regulation via the ANS-or greater cardiac vagal activity as indirectly reflected in HRV may slow brain atrophy. Findings reveal an important association between CT and cardiac parasympathetic activity with implications for healthy aging and longevity that should be studied further in longitudinal research., (© 2020 The Authors. Psychophysiology published by Wiley Periodicals LLC on behalf of Society for Psychophysiological Research.)

Stressor-evoked cardiovascular reactivity, trait positive emotionality, and negative emotionality are all associated with cardiovascular disease. It is unknown, however, whether cardiovascular reactivity may constitute a pathway by which trait positive or negative emotionality relates to disease risk. Accordingly, this study modeled the cross-sectional relationships between trait positive and negative emotionality, stressor-evoked cardiovascular reactivity, and severity of a subclinical vascular marker of cardiovascular risk, carotid artery intima-media thickness (CA-IMT). The sample consisted of healthy, midlife adults free from clinical cardiovascular disease (N = 286; ages 30-54; 50% female). Trait positive and negative emotionality were measured by three questionnaires. Heart rate and blood pressure reactivity were assessed across three stressor tasks. CA-IMT was assessed by ultrasonography. Latent factors of positive and negative emotionality, blood pressure reactivity, heart rate reactivity, and CA-IMT were created using structural equation modeling. Greater negative emotionality was marginally associated with more CA-IMT (β = .21; p = .049), but lower blood pressure reactivity (β = -.19; p = .03). However, heightened blood pressure (β = .21; p = .03), but not heart rate reactivity (β = -.05; p = .75), associated with greater CA-IMT. Positive emotionality was uncorrelated with cardiovascular reactivity (blood pressure: β = -.04; p = .61; heart rate: β = .16; p = .11) and CA-IMT (β = .16; p = .07). Although trait negative emotionality associates with a known marker of cardiovascular disease risk, independent of positive emotionality, it is unlikely to occur via a stressor-evoked cardiovascular reactivity pathway., (© 2020 Society for Psychophysiological Research.)

Metrics of heart period variability are widely used in the behavioral and biomedical sciences, although somewhat confusingly labeled as heart rate variability (HRV). Despite their wide use, HRV metrics are usually analyzed and interpreted without reference to prevailing levels of cardiac chronotropic state (i.e., mean heart rate or mean heart period). This isolated treatment of HRV metrics is nontrivial. All HRV metrics routinely used in the literature exhibit a known and positive relationship with the mean duration of the interval between two beats (heart period): as the heart period increases, so does its variability. This raises the question of whether HRV metrics should be "corrected" for the mean heart period (or its inverse, the heart rate). Here, we outline biological, quantitative, and interpretive issues engendered by this question. We provide arguments that HRV is neither uniformly nor simply a surrogate for heart period. We also identify knowledge gaps that remain to be satisfactorily addressed with respect to assumptions underlying existing HRV correction approaches. In doing so, we aim to stimulate further progress toward the rigorous use and disciplined interpretation of HRV. We close with provisional guidance on HRV reporting that acknowledges the complex interplay between the mean and variability of the heart period., (© 2018 The Authors Psychophysiology published by Wiley Periodicals, Inc. on behalf of Society for Psychophysiological Research.)

Exaggerated cardiovascular reactivity to acute psychological stress is associated with an increased risk of developing cardiovascular disease. The amygdala and hippocampus have been implicated in centrally mediating stressor-evoked cardiovascular reactivity. However, little is known about the associations of amygdala and hippocampus morphology with stressor-evoked cardiovascular reactivity. Forty (M age = 19.05, SD = 0.22 years) healthy young women completed two separate testing sessions. Session 1 assessed multiple parameters of cardiovascular physiology at rest and during a validated psychological stress task (Paced Auditory Serial Addition Test), using electrocardiography, Doppler echocardiography, and blood pressure monitoring. In Session 2, 1 year later, structural MRI was conducted. Brain structural volumes were computed using automated segmentation methods. Regression analyses, following Benjamini-Hochberg correction, showed that greater heart rate and cardiac output reactivity were associated with reduced amygdala and hippocampus gray matter volume. Systolic blood pressure reactivity was associated with reduced hippocampus volume. In contrast, no associations between diastolic blood pressure, mean arterial blood pressure, stroke volume, or total peripheral resistance reactivity with amygdala or hippocampus volumes were apparent. Comparison analyses examining insula volume found no significant associations. Some indicators of greater stressor-evoked cardiovascular reactivity associate with reduced amygdala and hippocampus gray matter volume, but the mechanisms of this association warrant further study., (© 2018 The Authors. Psychophysiology published by Wiley Periodicals, Inc. on behalf of Society for Psychophysiological Research.)

Resting high-frequency heart rate variability (HF-HRV) relates to cardiac vagal control and predicts individual differences in health and longevity, but its functional neural correlates are not well defined. The medial prefrontal cortex (mPFC) encompasses visceral control regions that are components of intrinsic networks of the brain, particularly the default mode network (DMN) and the salience network (SN). Might individual differences in resting HF-HRV covary with resting state neural activity in the DMN and SN, particularly within the mPFC? This question was addressed using fMRI data from an eyes-open, 5-min rest period during which echoplanar brain imaging yielded BOLD time series. Independent component analysis yielded functional connectivity estimates defining the DMN and SN. HF-HRV was measured in a rest period outside of the scanner. Midlife (52% female) adults were assessed in two studies (Study 1, N = 107; Study 2, N = 112). Neither overall DMN nor SN connectivity strength was related to HF-HRV. However, HF-HRV related to connectivity of one region within mPFC shared by the DMN and SN, namely, the perigenual anterior cingulate cortex, an area with connectivity to other regions involved in autonomic control. In sum, HF-HRV does not seem directly related to global resting state activity of intrinsic brain networks, but rather to more localized connectivity. A mPFC region was of particular interest as connectivity related to HF-HRV was shared by the DMN and SN. These findings may indicate a functional basis for the coordination of autonomic cardiac control with engagement and disengagement from the environment., (© 2015 Society for Psychophysiological Research.)

We examined the neural correlates of resting cardiac vagal activity in a sample of 432 participants (206 male; 61 African American; mean age 42 years). Pulsed arterial spin labeling was used to quantify whole brain and regional cerebral blood flow at rest. High-frequency heart rate variability (HF-HRV) was used to measure cardiac vagal activity at rest. The primary aim was to determine whether brain regions implicated in regulating cardiac vagal reactions were also related to cardiac vagal activity at rest, and whether these associations varied by sex or race. Brain areas previously related to vagal reactivity were related to resting HF-HRV. Directionality of relationships differed between overall and regional flows. Some relationships were only observed in women and African Americans. There appears to be communality between brain regions associated with task-induced vagal reactivity and those associated with resting cardiac vagal activity., (© 2014 Society for Psychophysiological Research.)

The neurovisceral integration hypothesis suggests in part that cerebral control of autonomic function conveys comparable control of executive function and, hence, correlation among vagally determined high frequency heart rate variability (HF-HRV), executive function, and regional cerebral blood flow (CBF). In 440 middle-aged men and women, resting HF-HRV was related to regional CBF derived from a resting arterial spin-labeled MRI scan and to seven neuropsychological tests of executive function. Despite some intercorrelations, regression modeling failed to support integrated central control of HF-HRV and executive function. Integration between autonomic and cognitive control appears more circumscribed than the general integration suggested by the neurovisceral integration hypothesis., (© 2014 Society for Psychophysiological Research.)

The present study compared neural activity in participants with blunted (N = 9) or exaggerated (N = 8) cardiac stress reactions. Neural activity was recorded with fMRI while participants performed a validated stress task and control task. Exaggerated reactors exhibited significant increases in heart rate from control to stress task, whereas blunted reactors had no change in heart rate. Blunted reactors also had reduced activation in the anterior midcingulate cortex and insula compared to exaggerated reactors during the stress condition, and a greater deactivation in the amygdala and posterior cingulate. The biological differences between groups in response to the stress task could not be explained by subjective measures of engagement, stressfulness, or difficulty. This study supports the notion that blunted peripheral physiological stress reactivity may be a marker of a corresponding under-recruitment of brain systems during behavioral states requiring motivated action., (Copyright © 2013 Society for Psychophysiological Research.)

We examined the reliability of measures of fMRI, subjective, and cardiovascular reactions to standardized versions of a Stroop color-word task and a multisource interference task. A sample of 14 men and 12 women (30-49 years old) completed the tasks on two occasions, separated by a median of 88 days. The reliability of fMRI BOLD signal changes in brain areas engaged by the tasks was moderate, and aggregating fMRI BOLD signal changes across the tasks improved test-retest reliability metrics. These metrics included voxel-wise intraclass correlation coefficients (ICCs) and overlap ratio statistics. Task-aggregated ratings of subjective arousal, valence, and control, as well as cardiovascular reactions evoked by the tasks showed ICCs of 0.57 to 0.87 (ps < .001), indicating moderate-to-strong reliability. These findings support using these tasks as a battery for fMRI studies of cardiovascular reactivity., (Copyright © 2012 Society for Psychophysiological Research.)

Objective: To evaluate the impact of acute stress and relationship-focused imagery on cardiac vagal control, as indicated by levels of respiratory sinus arrhythmia (RSA), in depressed and nondepressed women. Impairment in cardiac parasympathetic (vagal) control may confer risk for cardiac mortality in depressed populations., Methods: Electrocardiogram and respiratory rate were evaluated in 15 nonmedicated depressed women and 15 matched controls during two laboratory conditions: 1) a relationship-focused imagery designed to elicit vagal activation; and 2) a speech stressor designed to evoke vagal withdrawal., Results: As expected, the relationship-focused imagery increased RSA (F(3,66) = 3.79, p = .02) and the speech stressor decreased RSA (F(3,66) = 4.36, p = .02) across women. Depressed women exhibited lower RSA during the relationship-focused imagery, and this effect remained after control for respiratory rate and trauma history (F(1,21) = 5.65, p = .027). Depressed women with a trauma history exhibited the lowest RSA during the stress condition (F(1,22) = 9.61, p = .05). However, after controlling for respiratory rate, Trauma History × Task Order (p = .02) but not Trauma History × Depression Group (p = .12) accounted for RSA variation during the stress condition., Conclusion: Depression in women is associated with lower RSA, particularly when women reflect on a close love relationship, a context expected to elicit vagal activation and hence increase RSA. In contrast, depression-related variation in stressor-evoked vagal activity seems to covary with women's trauma history. Associations between vagal activity and depression are complex and should be considered in view of the experimental conditions under which vagal control is assessed, as well as physiological and behavioral factors that may affect vagal function.

Objective: To assess depression, anxiety, and anger as well as the variance that these emotions share (conceptualized as negative affect) in relationship to high-frequency heart rate variability (HF-HRV), a specific indicator of parasympathetic cardiac autonomic function related to premature cardiovascular morbidity and mortality. Although individual trait negative emotions have been studied in relation to risk for coronary heart disease (CHD) as well as biological mechanisms leading to CHD end points (e.g., autonomic nervous system [ANS] dysfunction), the degree to which a general tendency to experience negative emotions may account for these relations is not known., Methods: The sample included 653 community volunteers (51.0% female; 15.8% Black) aged 30 to 54 years (mean +/- standard deviation = 43.8 +/- 7.1 years). Latent constructs of depression, anxiety, and anger were each measured by three scales from well-validated self-report questionnaires. Resting HF-HRV was derived from 5-minute segments of continuous electrocadiographs recorded during both unpaced and paced respiration conditions., Results: Structural equation models (SEM) of the individual trait emotions showed depression and anxiety related inversely to HF-HRV and anger unrelated to HF-HRV. SEM also showed negative affect related inversely to HF-HRV. All associations were present after covariate adjustment for traditional cardiovascular risk factors, including age, sex, race, education, body mass index, smoking status, and blood pressure., Conclusions: Negative affect as a common pathway between depression, anxiety, and anger and impairments in cardiac autonomic function was supported, suggesting negative affect may be the unifying and potentially toxic element linking individual trait negative emotions to ANS dysregulation.

Objective: To examine whether high-frequency heart rate variability, an indirect measure of parasympathetic (vagal) control over variations in heart rate, is associated with immune reactivity to an in vitro inflammatory challenge. Convergent evidence from the animal literature shows that the autonomic nervous system plays a key role in regulating the magnitude of immune responses to inflammatory stimuli. Signaling by the parasympathetic system inhibits the production of proinflammatory cytokines by activated monocytes/macrophages and thus decreases local and systemic inflammation. As yet, no direct human evidence links parasympathetic activity to inflammatory competence., Methods: We examined the relationship of variations in heart rate, recorded during paced respiration, to lipopolysaccharide-induced production of the inflammatory cytokines interleukin (IL)-1beta, IL-6, tumor necrosis factor (TNF)-alpha, and IL-10 among a community sample of 183 healthy adults (mean age = 45 years; 59% male; 92% White, 7% African-American)., Results: Consistent with animal findings, higher derived estimates of vagal activity measured during paced respiration were associated with lower production of the proinflammatory cytokines TNF-alpha and IL-6 (r = -.18 to -.30), but were not related to production of the anti-inflammatory cytokine IL-10. These associations persisted after controlling for demographic and health characteristics, including age, gender, race, years of education, smoking, hypertension, and white blood cell count., Conclusions: These data provide initial human evidence that vagal activity is inversely related to inflammatory competence, raising the possibility that vagal regulation of immune reactivity may represent a pathway linking psychosocial factors to risk for inflammatory disease.

The aim of the present study was to characterize the functional relationships between behaviorally evoked regional brain activation and cardiac autonomic activity in humans. Concurrent estimates of regional cerebral blood flow (rCBF; obtained by positron emission tomography), heart period, and high-frequency heart period variability (HF-HPV; an indicator of cardiac parasympathetic activity) were examined in 93 adults (aged 50-70 years) who performed a series of increasingly difficult working-memory tasks. Increased task difficulty resulted in decreased heart period (indicating cardioacceleration) and decreased HF-HPV (indicating decreased cardiac parasympathetic activity). Task-induced decreases in heart period and HF-HPV were associated with concurrent increases and decreases in rCBF to cortical and subcortical brain regions that are speculated to regulate cardiac autonomic activity during behavioral processes: the medial-prefrontal, insular, and anterior cingulate cortices, the amygdala-hippocampal complex, and the cerebellum. These findings replicate and extend a small number of functional neuroimaging studies that suggest an important role for both cortical and subcortical brain systems in human cardiac autonomic regulation.

In response to the COVID‐19 pandemic, prior studies have modified the Trier Social Stress Test to be conducted remotely. The current study aimed to extend these studies to test whether a remote Trier Social Stress Test (rTSST) can elicit (a) affective, (b) blood pressure, and (c) heart rate responses relative to a control condition and whether these responses were reliable when assessed 1 week later. Participants (N = 99, 19.7 ± 3.5 years, 55% female) were randomized to a control or stress condition. Participants received blood pressure monitors in person. Controls completed easier versions of the tasks with a single, friendly researcher. Stress participants performed more difficult versions of the task in front of two judges who participants believed were rating their performance. Blood pressure and heart rate were measured every 2 min throughout, while affect was assessed at baseline, after the final task, and following recovery. The rTSST was feasible to administer with minimal technical issues reported. Participants reported lower positive affect and higher negative affect during the tasks in the stress condition relative to controls. Similarly, stress participants had higher cardiovascular responses during the tasks relative to controls, except that blood pressure was not elevated during mental arithmetic in stress participants relative to controls. Cardiovascular responses demonstrated good test–retest reliability when assessed 1 week later, especially when computed using area under the curve methods. Overall, a rTSST can be used to elicit affective and cardiovascular reactivity and provides an opportunity to increase the accessibility of research participation among diverse populations. We demonstrate that the Trier Social Stress Test can evoke both affective and cardiovascular (heart rate and blood pressure) responses when delivered online and remotely. This protocol can be administered during the COVID‐19 pandemic and could be used to include underserved and other populations that may have less accessibility to participate in research protocols. [ABSTRACT FROM AUTHOR]

The ventromedial prefrontal cortex (vmPFC) integrates sensory, affective, memory‐related, and social information from diverse brain systems to coordinate behavioral and peripheral physiological responses according to contextual demands that are appraised as stressful. However, the functionality of the vmPFC during stressful experiences is not fully understood. Among 40 female participants, the present study evaluated (a) functional connectivity of the vmPFC during exposure to and recovery following an acute psychological stressor, (b) associations among vmPFC functional connectivity, heart rate, and subjective reports of stress across individuals, and (c) whether patterns of vmPFC functional connectivity were associated with distributed brain networks. Results showed that psychological stress increased vmPFC functional connectivity with individual brain areas implicated in stressor processing (e.g., insula, amygdala, anterior cingulate cortex) and decreased connectivity with the posterior cingulate cortex and thalamus. There were no statistical differences in vmPFC connectivity to individual brain areas during recovery, as compared with baseline. Spatial similarity analyses revealed stressor‐evoked increased connectivity of the vmPFC with the so‐called dorsal attention, ventral attention, and frontoparietal networks, as well as decreased connectivity with the default mode network. During recovery, vmPFC connectivity increased with the frontoparietal network. Finally, individual differences in heart rate and perceived stress were associated with vmPFC connectivity to the ventral attention, frontoparietal, and default mode networks. Psychological stress appears to alter network‐level functional connectivity of the vmPFC in a manner that further relates to individual differences in stressor‐evoked cardiovascular and affective reactivity. Although the ventromedial prefrontal cortex (vmPFC) is purported to coordinate behavioral and peripheral physiological responses according to contextual demands that are appraised as stressful, the functionality of the vmPFC during stressful experiences is not fully understood. We extended previous research by demonstrating stressor‐evoked increases vmPFC functional connectivity with areas of the brain implicated in stressor processing and decreased connectivity with the posterior cingulate and thalamus. Spatial similarity analyses linking patterns of vmPFC connectivity to distributed brain networks revealed stressor‐evoked increased connectivity with the dorsal attention, ventral attention, and frontoparietal networks, as well as decreased connectivity with the default mode network. [ABSTRACT FROM AUTHOR]

The integration of behavioral processes with changes in vagally-controlled heart rate has been the focus of our investigations. A series of studies is reviewed showing that central and peripheral response inhibition is a primary source of transient, vagally-induced cardiac slowing during information processing. Individual differences in such responses are then shown to relate to the amplitude of cardiovascular responses to stressors. Overall, the specificity and sensitivity of vagal responses to higher level cortical function is supported by our research. [Copyright &y& Elsevier]