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BackgroundEvidence suggests a link between sedentary behaviours and depressive symptoms. Mechanisms underlying this relationship are not understood, but inflammatory processes may be involved. Autonomic and inflammatory responses to stress may be heightened in sedentary individuals contributing to risk, but no study has experimentally investigated this.AimsTo examine the effect of sedentary time on mood and stress responses using an experimental design.MethodForty-three individuals were assigned to a free-living sedentary condition and to a control condition (usual activity) in a cross-over, randomised fashion and were tested in a psychophysiology laboratory after spending 2 weeks in each condition. Participants completed mood questionnaires (General Health Questionnaire and Profile of Mood States) and wore a motion sensor for 4 weeks.ResultsSedentary time increased by an average of 32 min/day (P = 0.01) during the experimental condition compared with control. Being sedentary resulted in increases in negative mood independent of changes in moderate to vigorous physical activity (ΔGHQ = 6.23, ΔPOMS = 2.80). Mood disturbances were associated with greater stress-induced inflammatory interleukin-6 (IL-6) responses (β = 0.37).ConclusionsTwo weeks of exposure to greater free-living sedentary time resulted in mood disturbances independent of reduction in physical activity. Stress-induced IL-6 responses were associated with changes in mood.

BackgroundPsychosocial stress is a risk factor for coronary heart disease (CHD). The mechanisms are incompletely understood, although dysfunction of the hypothalamic pituitary adrenal (HPA) axis might be involved. We examined the association between cortisol responses to laboratory-induced mental stress and the progression of coronary artery calcification (CAC).Methods and ResultsParticipants were 466 healthy men and women (mean age = 62.7±5.6 yrs), without history or objective signs of CHD, drawn from the Whitehall II epidemiological cohort. At the baseline assessment salivary cortisol was measured in response to mental stressors, consisting of a 5-min Stroop task and a 5-min mirror tracing task. CAC was measured at baseline and at 3 years follow up using electron beam computed tomography. CAC progression was defined as an increase >10 Agatston units between baseline and follow up. 38.2% of the sample demonstrated CAC progression over the 3 years follow up. There was considerable variation in the cortisol stress response, with approximately 40% of the sample responding to the stress tasks with an increase in cortisol of at least 1 mmol/l. There was an association between cortisol stress reactivity (per SD) and CAC progression (odds ratio = 1.27, 95% CI, 1.02–1.60) after adjustments for age, sex, pre-stress cortisol, employment grade, smoking, resting systolic BP, fibrinogen, body mass index, and use of statins. There was no association between systolic blood pressure reactivity and CAC progression (odds ratio per SD increase = 1.03, 95% CI, 0.85–1.24). Other independent predictors of CAC progression included age, male sex, smoking, resting systolic blood pressure, and fibrinogen.ConclusionResults demonstrate an association between heightened cortisol reactivity to stress and CAC progression. These data support the notion that cortisol reactivity, an index of HPA function, is one of the possible mechanisms through which psychosocial stress may influence the risk of CHD.

Psychosocial factors, such as chronic mental stress and mood, are recognized as an important predictor of longevity and wellbeing. In particular, depression is independently associated with cardiovascular disease and all-cause mortality, and is often comorbid with chronic diseases that can worsen their associated health outcomes. Regular exercise is thought to be associated with stress reduction and better mood, which may partly mediate associations between depression, stress, and health outcomes. The underlying mechanisms for the positive effects of exercise on wellbeing remain poorly understood. In this overview we examine epidemiological evidence for an association between physical activity and mental health. We then describe the exercise withdrawal paradigm as an experimental protocol to study mechanisms linking exercise, mood, and stress. In particular we will discuss the potential role of the inflammatory response as a central mechanism.

African American cigarette smokers have lower rates of cessation than Whites and live in communities with a higher number of tobacco advertisements. Exposure to smoking cues may promote smoking and undermine cessation. It may be possible to reduce attention to smoking cues (“attentional bias”). In this study, we investigated the effect of Attentional re-training (AR) on attentional bias and smoking in African-American smokers. Non-treatment seeking African American smokers (N = 64) were randomly assigned to an AR or Control condition. Participants were given a mobile device for 2 weeks and prompted to complete up to three AR (or control) trainings per day. Participants completed assessments of attentional bias, craving, and smoking both in the lab and in the field. Participants in the AR and Control conditions completed an average of 29.07 AR (SD = 12.48) and 30.61 control training tasks (SD = 13.07), respectively. AR reduced attentional bias assessed in the laboratory, F (1,126) = 9.20, p = .003, and field, F (1, 374) = 6.18, p = .01. This effect generalized to new stimuli, but not to new tasks. AR did not significantly reduce craving or biological measures of smoking. Smoking assessed on the mobile device declined over days in the AR group, F (1, 26) = 10.95, p = .003, but not in the Control group, F (1, 27) = 0.02, p = .89. Two weeks of AR administered on a mobile device reduced attentional bias in African American smokers and had mixed effects on smoking.

Dispositional optimism may confer benefits to the individual through attenuated hypothalamic-pituitary-adrenal axis response to waking in everyday life. However, no evidence emerged for an association between optimism and cortisol laboratory stress responses, which suggests that other compensatory mechanisms might play a role.

Cardiovascular (CV) responses to mental stress are prospectively associated with poor CV outcomes. The association between CV responses to mental stress and reaction times (RTs) in aging individuals may be important but warrants further investigation. The present study assessed RTs to examine associations with CV responses to mental stress in healthy, older individuals using robust regression techniques. Participants were 262 men and women (mean age = 63.3 ± 5.5 years) from the Whitehall II cohort who completed a RT task (Stroop) and underwent acute mental stress (mirror tracing) to elicit CV responses. Blood pressure, heart rate, and heart rate variability were measured at baseline, during acute stress, and through a 75‐min recovery. RT measures were generated from an ex‐Gaussian distribution that yielded three predictors: mu‐RT, sigma‐RT, and tau‐RT, the mean, standard deviation, and mean of the exponential component of the normal distribution, respectively. Decreased intraindividual RT variability was marginally associated with greater systolic (B = −.009, SE = .005, p = .09) and diastolic (B = −.004, SE = .002, p = .08) blood pressure reactivity. Decreased intraindividual RT variability was associated with impaired systolic blood pressure recovery (B = −.007, SE = .003, p = .03) and impaired vagal tone (B = −.0047, SE = .0024, p = .045). Study findings offer tentative support for an association between RTs and CV responses. Despite small effect sizes and associations not consistent across predictors, these data may point to a link between intrinsic neuronal plasticity and CV responses.

SUMMARYThe purpose of this study was to discover whether greater sleep problems are associated with reduced heart rate variability during working hours and at night, and to determine whether this association is in part mediated by experienced affective states. This study involved 199 working women with a mean age of 33.8 years. Sleep problems were assessed with the Jenkins Sleep Problems Scale, and the Day Reconstruction Method was used to measure positive affect and stress on the evening before and during the working day. Heart rate variability was indexed by the mean square root of the successive standard difference in heart period. Disturbed sleep was inversely related to heart rate variability during the working day (P = 0.022), independently of demographic and behavioural confounders. Additional adjustment for positive affect and stress did not lead to further reductions in the association between sleep problems and reduced heart rate variability over the work day. Sleep problems were not predictive of reduced nighttime heart rate variability. This report extends the findings from experimental studies and clinical samples, and suggests that disturbed sleep might impair heart rate variability in real life settings, in particular during working hours. Reduced heart rate variability might be a potential pathway linking sleep problems with cardiovascular disease. Based on the current data there was little evidence that the inverse associations between sleep problems and heart rate variability were mediated by experienced affective states.