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Slow paced breathing via heart rate variability (HRV) biofeedback stimulates vagus-nerve pathways that counter noradrenergic stress and arousal pathways that can influence production and clearance of Alzheimer's disease (AD)-related proteins. Thus, we examined whether HRV biofeedback intervention affects plasma Αβ40, Αβ42, total tau (tTau), and phosphorylated tau-181 (pTau-181) levels. We randomized healthy adults (N = 108) to use slow-paced breathing with HRV biofeedback to increase heart rate oscillations (Osc+) or to use personalized strategies with HRV biofeedback to decrease heart rate oscillations (Osc-). They practiced 20-40 min daily. Four weeks of practicing the Osc+ and Osc- conditions produced large effect size differences in change in plasma Aβ40 and Aβ42 levels. The Osc+ condition decreased plasma Αβ while the Osc- condition increased Αβ. Decreases in Αβ were associated with decreases in gene transcription indicators of β-adrenergic signaling, linking effects to the noradrenergic system. There were also opposing effects of the Osc+ and Osc- interventions on tTau for younger adults and pTau-181 for older adults. These results provide novel data supporting a causal role of autonomic activity in modulating plasma AD-related biomarkers.Trial registration: NCT03458910 (ClinicalTrials.gov); first posted on 03/08/2018.

Previous research suggests that higher heart rate variability (HRV) is associated with better cognitive function. However, since most previous findings on the relationship between HRV and cognitive function were correlational in nature, it is unclear whether individual differences in HRV play a causal role in cognitive performance. To investigate whether there are causal relationships, we used a simple breathing manipulation that increases HRV through a 5-week HRV biofeedback intervention and examined whether this manipulation improves cognitive performance in younger and older adults (N = 165). The 5-week HRV biofeedback intervention did not significantly improve inhibitory control, working memory and processing speed across age groups. However, improvement in the Flanker score (a measure of inhibition) was associated with the amplitude of heart rate oscillations during practice sessions in the younger and older intervention groups. Our results suggest that daily practice to increase heart rate oscillations may improve inhibitory control, but future studies using longer intervention periods are warranted to replicate the present finding.

Acute stress activates the brain's locus coeruleus (LC)-noradrenaline system. Recent studies indicate that a magnetic resonance imaging (MRI)-based measure of LC structure is associated with better cognitive outcomes in later life. Yet despite the LC's documented role in promoting physiological arousal during acute stress, no studies have examined whether MRI-assessed LC structure is related to arousal responses to acute stress. In this study, 102 younger and 51 older adults completed an acute stress induction task while we assessed multiple measures of physiological arousal (heart rate, breathing rate, systolic and diastolic blood pressure, sympathetic tone, and heart rate variability, HRV). We used turbo spin echo MRI scans to quantify LC MRI contrast as a measure of LC structure. We applied univariate and multivariate approaches to assess how LC MRI contrast was associated with arousal at rest and during acute stress reactivity and recovery. In older participants, having higher caudal LC MRI contrast was associated with greater stress-related increases in systolic blood pressure and decreases in HRV, as well as lower HRV during recovery from acute stress. These results suggest that having higher caudal LC MRI contrast in older adulthood is associated with more pronounced physiological responses to acute stress. Further work is needed to confirm these patterns in larger samples of older adults.

The last decade has seen significant progress in identifying sleep mechanisms that support cognition. Most of these studies focus on the link between electrophysiological events of the central nervous system during sleep and improvements in different cognitive domains, while the dynamic shifts of the autonomic nervous system across sleep have been largely overlooked. Recent studies, however, have identified significant contributions of autonomic inputs during sleep to cognition. Yet, there remain considerable gaps in understanding how central and autonomic systems work together during sleep to facilitate cognitive improvement. In this article we examine the evidence for the independent and interactive roles of central and autonomic activities during sleep and wake in cognitive processing. We specifically focus on the prefrontal-subcortical structures supporting working memory and mechanisms underlying the formation of hippocampal-dependent episodic memory. Our Slow Oscillation Switch Model identifies separate and competing underlying mechanisms supporting the two memory domains at the synaptic, systems, and behavioral levels. We propose that sleep is a competitive arena in which both memory domains vie for limited resources, experimentally demonstrated when boosting one system leads to a functional trade-off in electrophysiological and behavioral outcomes. As these findings inevitably lead to further questions, we suggest areas of future research to better understand how the brain and body interact to support a wide range of cognitive domains during a single sleep episode.

A century-long debate on bodily states and emotions persists. While the involvement of bodily activity in emotion physiology is widely recognized, the specificity and causal role of such activity related to brain dynamics has not yet been demonstrated. We hypothesize that the peripheral neural control on cardiovascular activity prompts and sustains brain dynamics during an emotional experience, so these afferent inputs are processed by the brain by triggering a concurrent efferent information transfer to the body. To this end, we investigated the functional brain–heart interplay under emotion elicitation in publicly available data from 62 healthy subjects using a computational model based on synthetic data generation of electroencephalography and electrocardiography signals. Our findings show that sympathovagal activity plays a leading and causal role in initiating the emotional response, in which ascending modulations from vagal activity precede neural dynamics and correlate to the reported level of arousal. The subsequent dynamic interplay observed between the central and autonomic nervous systems sustains the processing of emotional arousal. These findings should be particularly revealing for the psychophysiology and neuroscience of emotions.

There is a continuing debate concerning "adjustments" to heart period variability [i.e., heart rate variability (HRV)] for the heart period [i.e., increases inter-beat-intervals (IBI)]. To date, such arguments have not seriously considered the impact a demographic variable, such as gender, can have on the association between HRV and the heart period. A prior meta-analysis showed women to have greater HRV compared to men despite having shorter IBI and higher heart rate (HR). Thus, it is plausible that men and women differ in the association between HRV and HR/IBI. Thus, the present study investigates the potential moderating effect of gender on the association between HRV and indices of cardiac chronotropy, including both HR and IBI. Data from 633 participants (339 women) were available for analysis. Cardiac measures were assessed during a 5-min baseline-resting period. HRV measures included the standard deviation of inter-beat-intervals, root mean square of successive differences, and autoregressive high frequency power. Moderation analyses showed gender significantly moderated the association between all HRV variables and both HR and IBI (each p

Stress-related exhaustion symptoms have a high prevalence which is only likely to increase further in the near future. Understanding the physiological underpinnings of exhaustion has important implications for accurate diagnosis and the development of effective prevention and intervention programs. Given its integrative role in stress-regulation, the parasympathetic branch of the autonomic nervous systems has been a valid starting point in the exploration of the physiological mechanisms behind exhaustion. The aim of the present study was to examine the directionality and specificity of the association between exhaustion symptoms and vagally-mediated heart rate variability (vmHRV), a relatively pure measure of parasympathetic tone. Exhaustion symptoms and vmHRV were measured at four annually assessment waves (2015-2018) of the Dresden Burnout Study. A total sample of N = 378 participants who attended at least two of the four annual biomarker measurements were included in the present analyses. Cross-lagged multi-level panel modelling adjusting for various covariates (e.g., age, sex, BMI) revealed that vmHRV was meaningfully predictive of exhaustion symptoms and not vice versa. In addition, these effects were specific for exhaustion symptoms as no effect was shown for the other burnout sub-dimensions, or for depressive symptoms. Our findings indicate a clear link between exhaustion symptoms and vmHRV which may hold great potential for both enhancing the diagnosis and treatment of exhaustion symptoms.

Worry is a central process in a wide range of psychopathological and somatic conditions. Three studies (N = 856) were used to test whether a subscale composed of five items of the most commonly used trait anxiety questionnaire, Spielberger's State Trait Anxiety Inventory-Trait version (STAI-T), is appropriate to measure worry. Results showed that the subscale, named the Brief Worry Scale (BWS), had excellent internal consistency and temporal stability. Convergent and divergent validity were supported by correlation analyses using worry questionnaires and measures of anxious arousal and depression. The BWS was a particularly good predictor of the pathogenic aspects of worry, including worry perseveration in daily life (study 1), measures of clinical worry (study 2) and the uncontrollability of experimentally induced worry (study 3). Taken together, these studies demonstrate that the BWS might be a valuable scale for pathological worry, for which many researchers already have data., Author(s): Bart Verkuil [sup.1] , Briana N. Brownlow [sup.2] , Michael W. Vasey [sup.2] , Jos F. Brosschot [sup.3] , Julian F. Thayer [sup.2] [sup.4] Author Affiliations: (1) grid.5132.5, 0000 [...]

In recent clinical practice, a biomarker of vagal neuroimmunomodulation (NIM), namely the ratio of vagally-mediated heart rate variability (vmHRV) and CRP, was proposed to index the functionality of the cholinergic anti-inflammatory pathway. This study aims to transfer and extend the previous findings to two general population-based samples to explore the hypothesis that NIM-ratio is associated with all-cause mortality. Two large population studies (MIDUS 2: N = 1255 and Whitehall II wave 5: N = 7870) with complete data from a total of N = 3860 participants (36.1% females; average age = 56.3 years; 11.1% deaths, last exit 18.1 years post inclusion) were available. NIM indices were calculated using the vagally-mediated HRV measure RMSSD divided by measures of CRP (NIMCRP) or IL-6 (NIMIL6). The NIM-ratios were quartiled and entered into age, ethnicity and body mass index adjusted Cox proportional hazards models. For NIMIL6 the lowest quartile was 45% more likely to die during the observed period (max. 18 years follow-up) compared to the highest quartile (HR = 0.55 CI 0.41-0.73; p

Recent studies have shown higher resting-state vagally-mediated heart rate variability (vmHRV) to be related to greater memory retrieval. Research has not yet linked resting vmHRV with memory encoding and retrieval, as both are thought to play an important role in correctly distinguishing between true and false memories. The current study investigated this possible link in n = 71 undergraduate students. VmHRV was assessed during a 5-minute resting baseline period. Participants then completed the Deese-Roediger-McDermott (DRM) task, where they first viewed 6 word lists (12 words per list), and were later asked to identify previously shown words (true memories) and reject non-presented words. Results showed that participants with lower resting vmHRV were less able to discriminate true from false items. These data extend previous work on resting vmHRV and memory suggesting that resting vmHRV represents a psychophysiological pathway involved in both the proper encoding and retrieval of memories.

PurposePhysical activity has been associated with several individual dimensions of sleep. However, the association between physical activity and sleep health, a construct that emphasizes the multidimensional nature of sleep, has not been explored. This analysis examined the relationship between physical activity and a composite measure of sleep health.MethodsA total of 114 adults (66% female, 60.3 ± 9.2 years) were included in the analyses. Participants reported daily light-intensity physical activity (LPA) and moderate- and vigorous-intensity physical activity (MVPA) via diary, while wearing a pedometer (Omron HJ-720ITC) to measure daily steps. Sleep health was measured using the RU_SATED questionnaire, which addresses regularity of sleep patterns, satisfaction with sleep, daytime alertness, and sleep timing, efficiency, and duration. Multiple linear regression, binary logistic regression, and analysis of covariance (ANCOVA) were utilized for analyses.ResultsMean sleep health score was 9.6 ± 2.4 (0 [poor]-12 [good]). Participants reported 62.9 ± 66.0 and 51.2 ± 51.2 min/day of LPA and MVPA, respectively, and took 5585.5 ± 2806.7 steps/day. Greater MVPA was associated with better sleep health (β = 0.27, P = 0.005) and sleep health scores differed between those reporting

Multiple studies have demonstrated low vagally-mediated heart rate variability (HRV) being associated with a range of risk factors for heart disease and stroke, including inflammation, hyperglycemia, hyperlipidemia, and hypertension. Yet, no cut point exists that indicates elevated risk. In the present study we sought to identify a cut point-value for HRV that is associated with elevated risk across a range of known risk factors. METHODS:A total of 9550 working adults from 19 study sites took part in a health assessment that included measures of inflammation, hyperglycemia, hyperlipidemia, and hypertension and vagally-mediated HRV (Root mean square of successive differences between normal heartbeats (RMSSD)). Multiple age and sex adjusted logistic regressions were calculated per risk factor (normal versus clinical range), with RMSSD being entered in binary at different cut points ranging from 15-39 msec with a 2 msec increment. RESULTS:For daytime RMSSD, values below 25 ± 4 indicated elevated risk (odds ratios (OR) 1.5-3.5 across risk factors). For nighttime RMSSD, values below 29 ± 4 indicated elevated risk (OR 1.2-2.0). CONCLUSION:These results provide the first evidence that a single value of RMSSD may be associated with elevated risk across a range of established cardiovascular risk factors and may present an easy to assess novel marker of cardiovascular risk.

Reduced high-frequency heart rate variability (HF-HRV) is associated with a greater risk for cardiovascular disease (CVD). Although African Americans (AA) are at greater risk for CVD, they show greater HF-HRV compared to European Americans (EA). Previous studies suggest that differences in the association between regional cerebral blood flow (CBF) and HF-HRV in AA and EA may explain this surprising pattern of findings, termed the Cardiovascular Conundrum. Here we pooled data from a total of n = 452 EA and n = 102 AA, investigating differences in the association between CBF in 8 regions of interest (ROI), including the cingulate (anterior, mid, posterior), insula (anterior, posterior), and amygdala (basolateral, centromedial, superfical), with HF-HRV, mean heart rate (HR) and their Coefficient of Variation (CoV). Bayesian statistics illustrate that CBF - in particular in the anterior cingulate cortex (ACC) - is positively associated with HF-HRV and CoV in EA, but negatively associated in AA. Exploring the association between HF-HRV and CBF with self-reports of affect and affect regulation showed some differences as a function of ethnicity. The association between greater habitual use of reappraisal only showed a positive correlation with HF-HRV in AA. Similar, greater suppression or non-expression of angry emotions was associated with greater HF-HRV whereas greater outward direction of anger was associated with lower HF-HRV in AA only. Given the importance of the ACC in emotion and emotion regulation, we suggest that increased HF-HRV may serve a compensatory role in AA. Implications from these findings and suggestions for future studies are discussed.

IntroductionBurnout symptomatology is associated with various negative health consequences; however, the mechanisms underlying these associations remain unclear. One potential pathway involves alterations in the acute stress response. The aims of the present study were to examine burnout-associated alterations in stress-reactivity patterns, during a standardized social stressor compared to a control condition, as well as to examine whether effects associated with greater burnout symptomatology were distinct from other, conceptually overlapping indicators of chronic stress (i.e. depressive symptomatology and elevated hair cortisol concentration [HCC]).Materials and methodsIn a randomized two-factor design a total of 70 employed males with varying burnout symptoms but without evidence of physical or psychiatric disease were exposed to the Trier Social Stress Test for Groups (TSST-G) or a non-stressful control condition. Acute stress reactivity was assessed using self-report stress measures and non-invasive biomarkers. Associations among acute stress reactivity, burnout and depressive symptoms (assessed with self-report measures), as well as HCC were analysed using repeated measure ANCOVAs and moderation analysis.ResultsBurnout symptomatology was associated with elevated stress perception independent of the experimental condition. In addition, depressive symptomatology was associated with enhanced anticipatory appraisal, whereas HCC was not related to any subjective stress measure. On a physiological level, burnout and depressive symptomatology, as well as HCC were associated with a pattern of blunted cardiovascular reactivity, however the timing of this effect varied.ConclusionOur results indicate burnout-associated modulations in stress reactivity, which diverge, at least partly, from other indicators of chronic stress.

Purpose of the reviewIn the present paper, we overview emerging research examining the autonomic nervous system (ANS), especially the parasympathetic nervous system as indexed by heart rate variability (HRV), and the impact of psychosocial factors on hypertension-related disease in African Americans.Recent findingsA growing corpus of studies has shown that (1) usual patterns of compensatory sympathetic-parasympathetic regulation differ between African Americans and European Americans; (2) despite their enhanced cardiovascular disease risk profile, African Americans tend to exhibit higher HRV relative to European Americans; and (3) racial discrimination and other forms of psychosocial stress are associated with diminished HRV among African Americans. Significant disparities in hypertension-related disease exist such that African Americans have greater risk. The underlying factors associated with this increased risk are, to date, not fully understood. The present review provides evidence for a unique pattern of ANS regulation in African Americans and shows that psychosocial factors such as racial discrimination may contribute to this paradoxical situation.

Increased vascular reactivity to stress has been suggested to contribute to the greater risk for developing hypertension in African Americans. Here, we examined the way (hemodynamic profile) and the extent to which (compensation deficit) cardiac output and total peripheral resistance compensate for each other in determining blood pressure responses to a physical (orthostasis) and a mental (anger recall) stress task, in normotensive African American (AA, n = 30) and European American (EA, n = 48) college students. Blood pressure stress reactivity did not differ as a function of race. However, AAs showed a prominent vascular hemodynamic profile and a significant compensation deficit in response to both tasks, while EAs showed no hemodynamic response to orthostasis and a mixed profile in response to anger recall. The present findings demonstrate a more prominent vascular hemodynamic reactivity to stress in AAs, which could contribute to the pathogenesis of hypertension in this ethnic group.

Recently, we reported on the unusual "switch-off" of respiratory sinus arrhythmia (RSA) by analyzing heart rate (HR) beat-to-beat interval (RRI) signals and respiration in five subjects during a potentially anxiety-provoking first-time functional magnetic resonance imaging (fMRI) scanning with slow spontaneous breathing waves (Rassler et al., 2018). This deviation from a fundamental physiological phenomenon is of interest and merits further research. Therefore, in this study, the interplay between blood-oxygen level-dependent (BOLD) activity in the cerebellum/brain stem, RRI, and respiration was probed. Both the cardiovascular and the respiratory centers are located in the medulla oblongata and pons, indicating that dominant slow rhythmic activity is present in the brain stem. The recording of BOLD signals provides a way to investigate associated neural activity fluctuation in the brain stem. We found slow spontaneous breathing waves associated with two types of slow BOLD oscillations with dominant frequencies at 0.10 and 0.15 Hz in the brain stem. Both BOLD oscillations were recorded simultaneously. One is hypothesized as vessel motion-based phenomenon (BOLDv) associated with the start of expiration; the other one as pattern associated with neural activity (BOLDn) acting as a driving force for spontaneous inspiration and RRI increase (unusual cessation of RSA) about 2-3 s after BOLDv. This time delay of 2-3 s corresponds to the neurovascular coupling time.