2025/03/04 by Christoph Geißler, Christian Frings, Gregor Domes · 1 voice · 1 citation
Medicine · Neuroscience · #Heart Rate Variability and Autonomic Control #Optical Imaging and Spectroscopy Techniques #Stress Responses and Cortisol
paper · pdf · doi:10.1080/10253890.2025.2472067
openalex publication_date 2025/03/04 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/31
Acute stress causes a shift from executive to automated behavior. A key executive function suffering from this shift is working memory. Working memory is mainly negatively affected in the first 10 and more than 25 minutes after acute stress. These phases coincide with increased central levels of noradrenaline and cortisol. Increased levels of both hormones can cause a relative deactivation in prefrontal areas related to working memory processing. However, so far, there is little research that investigates the complete relationship between acute stress and resulting changes in stress hormones, neural activation, and working memory processing, over time. In this study, we used functional near-infrared spectroscopy to measure prefrontal activity during an nback task in a stress (28 subjects, 7 female/21 male) and a control group (28 subjects, 10 female/18 male) once (20 minutes) before and twice (4 and 24 minutes) after a socially evaluated cold pressor test or a warm water control condition. Additionally, we regularly measured changes in salivary cortisol and α-amylase (a correlate of central noradrenaline) during the experiment. While salivary cortisol was increased starting 14 minutes after acute stress, no effect of stress on salivary α-amylase or working memory performance was found. On a neural level, we found a marginally stronger decline in 3-back-related prefrontal activity from the first to the third measurement point in the stress than in the control group. These results present tentative evidence for a negative effect of acute stress on working-memory-related prefrontal processing mediated by central cortisol levels.