Abstract
Upon perception of a stimulus as stressful, the human brain reacts with the activation of the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS), to mobilize energy resources to better cope with the stressor. Since the perception of the stressor is the initial stimulus, a synchronicity between the subjective perception of stress and the physiological stress reactivity should be expected. However, according to a recent meta-analysis, these associations are weak and inconsistent. The goal of the current study was to investigate the interaction between the SNS, HPA and subjective stress perceptions, by introducing an experimental manipulation of this interaction. For this purpose, we combined the SNS inhibitor propranolol with the Trier Social Stress Test, and measured endocrinological and psychological responses to the stressor. Thirty healthy male participants were recruited and randomly assigned to either a propranolol (PROP; n = 15) or placebo (PLC; n = 15) group. All subjects were administered 80 mg of propranolol 60 minutes prior to exposure to psychosocial stress. Salivary cortisol and alpha amylase (sAA), heart rate, blood pressure and subjective stress responses were assessed throughout the study. We observed significantly reduced sAA levels and heart rate increases in the PROP group in response to stress, with no effects of the drug on systolic or diastolic blood pressure changes. In line with previous studies, a significant increase in cortisol was seen in response to the stress exposure. Importantly, the cortisol increase was significantly higher in the PROP group. A typical increase in subjective stress could be seen in both groups, with no significant group differences emerging. Complementing previous work, this study further demonstrates a significant interaction between the HPA and the SNS during acute stress. The HPA activity was found to be elevated in the presence of a suppressed SNS in reactivity to the TSST.
Highlights
The physiological and endocrine stress response is considered necessary and adaptive, allowing the individual to mobilize energy resources to overcome a threat, chronic and excessive activation is associated with numerous physiological and psychological disease states like increased risk for diabetes and cardiovascular disease, burnout, depression and chronic fatigue [1]
These results suggest that both groups were comparable on these factors, and that they were unlikely to have contributed to endocrinological and cardiovascular differences between the groups
To further explore the interaction and main effects, we performed a Tukey honestly significant difference (HSD) post hoc test. This analysis revealed significantly higher cortisol levels at samples 5 and 6 in the PROP group compared to the PLC group, both p
Summary
The physiological and endocrine stress response is considered necessary and adaptive, allowing the individual to mobilize energy resources to overcome a threat, chronic and excessive activation is associated with numerous physiological and psychological disease states like increased risk for diabetes and cardiovascular disease, burnout, depression and chronic fatigue [1]. Two main systems in the human body are activated, the hypothalamus-pituitary-adrenal (HPA) axis, and the sympathetic nervous system (SNS). Upon perception of a stimulus as stressful, the hypothalamus secretes corticotrophinreleasing hormone (CRH), which stimulates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary. This is released into the bloodstream and eventually binds to receptors in the adrenal cortex, which releases cortisol into the bloodstream [2]. In addition to the HPA, the SNS is activated during a stress response In the brain, this system induces the release of its effectors, epinephrine (E) and norepinephrine (NE), from the locus coeruleus via stimulation from the brainstem [4,5,6]. The SNS can be assessed in various ways, for example, measuring NE and E levels, galvanic skin response, heart rate, blood pressure, or salivary alpha-amylase (sAA) levels [7,8]
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