Why the study?
The study aimed to investigate whether acute stress enhances cardiac interoceptive attention and how activation of the sympatho-adrenomedullary and hypothalamic-pituitary-adrenocortical stress axes contributes to this potential effect.
Does acute stress induced by SECPT enhance cardiac interoceptive attention in young, healthy individuals?
Does acute stress induced by SECPT enhance cardiac interoceptive attention in young, healthy individuals?
Acute stress selectively enhances cardiac interoceptive attention as measured by heartbeat-evoked potentials 40 minutes post-stress, without affecting interoceptive accuracy.
Acute stress selectively enhances cardiac interoceptive attention (HEPs) without affecting accuracy; extends RCT evidence on stress effects in healthy adults.
Previous findings suggest that acute stress enhances attention focused on heartbeats, which is the definition of the construct cardiac "interoceptive attention" (IAt). The difference of heartbeat-evoked potentials (HEPs) assessed while performing a heartbeat counting task (HCT) versus a distraction task is considered an indicator of cardiac IAt. The aim of this study was to investigate whether acute stress enhances cardiac IAt and how activation of the sympatho-adrenomedullary (SAM) and the hypothalamic-pituitary-adrenocortical (HPA) stress axis contributes to this potential effect. Sixty-six young, healthy individuals were randomly assigned to a stress (socially evaluated cold pressor test/SECPT; n = 32) or a control group (n = 34), and underwent a HCT and a distraction task once before and three times (+0, +20, +40 min) after the intervention (SECPT/control). The SECPT effectively increased heart rate, systolic/diastolic blood pressure, and cortisol release. Cardiac interoceptive accuracy based on the HCT was unaffected by stress. Individuals in the SECPT group showed an increase in HEPs (R-wave +455-595 ms) assessed during the HCT 40 min after the intervention (at F8, Cz, C4, CP6, P8). These findings suggest that acute stress may selectively enhance cardiac IAt. Its primarily right-hemispheric topography suggests the involvement of insular activity in mediating this effect. Exploratory analyses in the stress group showed that the responsiveness of HEPs to the stressor (+40 min vs. before) was negatively correlated with stress responsiveness in systolic blood pressure and pain intensity/unpleasantness. Future studies should clarify whether this late effect of acute stress on IAt is due to parasympathetic deactivation during stress recovery, and if their underlying neural networks (e.g., cardiac parasympathetic afferents) play a role in mediating IAt.
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Schulz et al. (2025) studied this question.
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