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Background: Disrupted sleep quality is one of the proposed mechanisms through which chronic stress may lead to depression. However, there exist significant individual differences in sleep reactivity, which is the extent to which one experiences sleep disturbances in response to stress., Purpose: The aim of the current study was to investigate whether low high-frequency heart rate variability (HRV), as a psychophysiological marker of poor emotional and physiological arousal regulation, predicts stress-related sleep disturbances associated with greater risk of depression symptoms., Methods: Using a chronic caregiving stress model, 125 mothers of adolescents with developmental disorders and 97 mothers of typically developing adolescents had their resting HRV and HRV reactivity recorded and completed a measure of depressive symptoms, as well as a 7 day sleep diary to assess their sleep quality. A moderated mediation model tested whether sleep quality mediated the association between chronic stress exposure and depressive symptoms and whether HRV moderated this mediation., Results: After controlling for participant age, body mass index, ethnicity, socioeconomic status, and employment status, poor sleep quality mediated the association between chronic stress and depressive symptoms. Resting HRV moderated this indirect effect such that individuals with lower HRV were more likely to report poorer sleep quality in the context of chronic stressor exposure, which, in turn, was related to greater depressive symptoms., Conclusions: Lower HRV, a potential biomarker of increased sleep reactivity to stress, is associated with greater vulnerability to stress-related sleep disturbances, which, in turn, increases the risk for elevated depressive symptoms in response to chronic stress., (© Society of Behavioral Medicine 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Depression is a major risk factor for cardiovascular disease. An important risk factor for cardiovascular disease, low heart rate variability, often has been found in depressed patients and has been associated with impulsivity. The present study investigated whether experimental lowering of serotonin would decrease heart rate variability and increase impulsivity in remitted depressed patients, in particular in those patients with disturbed impulse control., Methods: Nineteen patients in remission from depression received high-dose and low-dose acute tryptophan depletion in a randomized, counterbalanced, double-blind crossover design. Heart rate variability and impulsivity were assessed during each acute tryptophan depletion session and during a baseline session. Suicidal ideation during past depression was used as an index for individual differences in impulse control., Results: High-dose acute tryptophan depletion led to a larger increase in depressive symptoms than did low-dose acute tryptophan depletion. High-dose acute tryptophan depletion decreased heart rate variability and increased impulsivity and anxiety, but only in patients with a history of suicidal ideation. Symptom effects of high-dose acute tryptophan depletion correlated with low heart rate variability at baseline., Conclusions: Depressed patients who have problems with controlling impulsivity might be more at risk for developing cardiovascular disease, possibly related to increased vulnerability to impaired 5-hydroxytryptamine function.

ABSTRACT Background: In laboratory animals, environmental stressors markedly activate the mesocortical dopamine system. The present study tested whether this occurs in humans. Methods: The effects of a laboratory psychological stressor (Montreal Imaging Stress Task, MIST) on mesocortical dopamine release in healthy young adults (11 males, mean age ± SD, 20.6 ± 2.4 years) was measured using positron emission tomography and [18F]fallypride. Each subject was scanned in two separate days in counterbalanced order: one with the MIST and one with the control task. Binding potential (BPND) maps of the whole brain were calculated for each scan, using a simplified reference tissue compartmental model. Then BPND was compared between subjects. Heart rate, galvanic skin response, and salivary cortisol level were measured during the scans. Results: The psychological stressor significantly decreased [18F]fallypride binding values in the dorsal part of the medial prefrontal cortex (dmPFC), corresponding to the rostal part of the cingulate motor zone. The greater the stress-induced decrease in [18F]fallypride binding in the dmPFC, the greater the stress-induced increases in heart rate. Conclusions: The present study provides evidence of stress-induced dopamine release in the mPFC in humans, in vivo. Synapse 67:821-830, 2013. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]