The physiological response to Trier Social Stress Test relates to subjective measures of stress during but not before or after the test.

The Trier Social Stress Test (TSST) is an effective psychosocial laboratory protocol for inducing stress in humans and has been used in numerous research studies. The stressor leads to a physiological response of the hypothalamus-pituitary-adrenal axis (HPAA) and the autonomous nervous system (ANS). Common biomarkers are cortisol levels and heart rate. In addition to the physiological stress response, the TSST also triggers a psychological response such as an increase in perceived stress, anxiety and emotional insecurity. Whereas HPA and ANS measures can easily be obtained for the TSST period itself, psychological measures are usually determined prior to (baseline) and after the TSST. This may exclude information of the stressful event itself. In the present study, we assessed perceived stress, anxiety and emotional insecurity before, during and after the TSST using visual analogue scales. In addition, cortisol levels and heart rates were assessed. Data of 260 healthy non-smoking males aged 16-60 yrs were used for analyses. Our results show that stress perception, anxiety and emotional insecurity were significantly higher during the TSST as compared to post-TSST ratings. Furthermore, our results suggest a covariance of the psychological stress response during the TSST and the physiological stress responses (cortisol and heart rate) for stress perception though the explained variance was small. This observation was not found for pre- and post-TSST ratings suggesting that assessing psychological stress measures during the stressor itself present a more informative measure of the stress response.

Attenuation of the hypothalamic-pituitary-adrenal axis responsivity to the Trier Social Stress Test by the benzodiazepine alprazolam.

Little is known about effects of commonly used anxiolytic drugs on psychologically evoked responses of two major stress systems, the hypothalamic-pituitary-adrenal (HPA) and the sympathetic-adrenal-medullary (SAM) axis. The purpose of the present study was to assess effects of the anxiolytic alprazolam on responses of the HPA and the SAM axes to a standardized psychosocial stress protocol, the Trier Social Stress Test (TSST). Forty-six healthy, non-smoking, non-medicated males, aged between 18 and 45 years, were invited once to the laboratory and received a single oral dose of 1mg alprazolam or placebo, respectively, 1h prior to the TSST. The secretion of ACTH, cortisol, epinephrine, norepinephrine as well as changes in heart rate, blood pressure, and psychological states (anxiety, wakefulness, good mood, calmness) in response to the TSST were measured. Subjects pre-treated with alprazolam showed a strongly blunted response of ACTH as well as total and free cortisol to the TSST. Whereas alprazolam-treated subjects displayed significantly lower systolic blood pressure immediately before the TSST, neither the secretion of epinephrine, norepinephrine nor changes of heart rate in response to the stress test differed from placebo-treated subjects. Regarding psychological parameters, alprazolam clearly decreased subjective ratings on the questionnaire scale "wakefulness" and increased ratings on the scale "good mood", whereas ratings on scales assessing "state anxiety" or "agitation" were not affected. In healthy subjects, we observed a dissociation of the effects of alprazolam on the endocrine and the autonomic response to psychosocial stress. The psychological responses seemed to be masked by sedative properties of alprazolam.

A new view on hypocortisolism.

Low cortisol levels have been observed in patients with different stress-related disorders such as chronic fatigue syndrome, fibromyalgia, and post-traumatic stress disorder. Data suggest that these disorders are characterized by a symptom triad of enhanced stress sensitivity, pain, and fatigue. This overview will present data on the development, mechanisms and consequences of hypocortisolism on different bodily systems. We propose that the phenomenon of hypocortisolism may occur after a prolonged period of hyperactivity of the hypothalamic-pituitary-adrenal axis due to chronic stress as illustrated in an animal model. Further evidence suggests that despite symptoms such as pain, fatigue and high stress sensitivity, hypocortisolism may also have beneficial effects on the organism. This assumption will be underlined by some studies suggesting protective effects of hypocortisolism for the individual.