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Published on: June 16, 2018
Acute and chronic stress effects on cardiac interoceptive accuracy and heartbeat-evoked potentials in
André Schulz1, Silja Bellingrath2, Annika Lutz3
1Clinical Psychophysiology Laboratory, Department of Behavioural and Cognitive Sciences, University of Luxembourg, Esch-sur-Alzette, Luxembourg; Institute for Cognitive and Affective Neuroscience, Trier University, Trier, Germany.
Abstract:
Acute stress affects interoception, the processing and perception of signals from inside the body. In contrast, the effects of chronic stress on interoception remain largely unknown, although chronic stress is a potential risk factor for disorders involving interoceptive alterations. This study aimed at investigating the impact of both acute and chronic stress on two key facets of interoception: interoceptive accuracy (IAc) and interoceptive attention (IAt). The study involved schoolteachers, a population at risk of experiencing moderate to high levels of chronic stress. From an initial sample of 219 schoolteachers, 80 attended the laboratory session, with 68 providing complete data sets. They completed a heartbeat counting task (HCT) and a distraction task (DT) before and after undergoing a socially-evaluated cold pressor test (SECPT) as acute stressor. Heartbeat-evoked potentials (HEPs) served as indicators of cardiac IAt. The SECPT evoked an increase in heart rate, blood pressure and salivary cortisol. Cardiac IAc was unaffected by the SECPT. HEPs were higher while performing the HCT than the DT (indicating cardiac IAt), which was intensified after the SECPT. Notably, SECPT effects on cardiac IAt were reversed in individuals with high levels of self-reported chronic stress, whereas cardiac IAc showed a negative association with cortisol/DHEA ratio in hair. Our findings suggest that acute stress increases attentional resources for processing interoceptive sensations, whereas chronic stress attenuates this effect, while simultaneously increasing the sensory threshold for their perception, which may be a mechanism of somatic symptom generation in stress-related disorders.
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