Effects of acute stress on cognitive emotion regulation and underlying neuroendocrine mechanisms

• Published in: Psychoneuroendocrinology Vol. 160; p. 106722
• Main Authors: Langer, Katja, Jentsch, Valerie L., Wolf, Oliver T.
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.02.2024
• ISSN: 0306-4530; 1873-3360
• DOI: 10.1016/j.psyneuen.2023.106722

In stressful situations, emotion regulation (ER) competencies are particularly needed protecting individuals from potentially negative consequences of chronic stress. Initial empirical work showed acute stress to either impair or improve the ability to deal with negative emotions. Besides emotional intensity and sex hormones, another moderator might be the timing of ER measurement relative to stress exposure. Whereas somewhat delayed increases in the stress hormone cortisol have been linked to regulatory improvements, rapid noradrenergic effects might impair ER attempts. In three studies, we characterized acute stress vs. cortisol effects on the ability to downregulate negative emotions via reappraisal and distraction varying the time interval between stress exposure (study I: 25min; study III: 10min) / cortisol administration (study II: 30min vs. 90min) and ER assessment. Affective ratings and pupil dilation served as an index of ER outcomes and cognitive regulatory effort. In the first study, psychosocial stress improved the effectiveness of reappraisal in men, which was positively related to cortisol increases. Seeking to mimic these effects pharmacologically in the second study, cortisol enhanced the ability to downregulate negative emotions of particularly high intensity independent of timing (+30min vs. +90min). Examining ER competencies immediately after stress exposure, the third study provided first evidence for an association between cardiovascular stress reactivity and ER impairments in women. Together, these studies document beneficial stress effects on the cognitive control of especially high intensity emotions via glucocorticoid-driven mechanisms. These effects might be opposed by rapid noradrenergic actions and critically moderated by sex.