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Background  Acute stress can have an effect on pain sensitivity, yet the direction of the effect – whether it is hypoalgesic or hyperalgesic – is mixed across studies. Moreover, which part of the stress response influences pain sensitivity is still unclear. In the current experimental study, we aim to examine the effect of acute stress on heat pain thresholds and pain tolerance levels in healthy participants, while taking into account individual differences in stress responses.    Methods  Forty‐two healthy participants were randomly assigned to either a well‐validated stress paradigm: the Maastricht Acute Stress Task ( MAST ; combining physical and psychological stressors) or to a nonstressful version of the task. Heat pain thresholds and tolerance levels were assessed at three times: prior to the  MAST , immediately after the  MAST  during the presumed sympatho‐adrenal medullary ( SAM ) response, and 15 min after  MAST  to cover the presumed hypothalamus–pituitary–adrenal ( HPA ) axis response. Stress responses were assessed both subjectively and physiologically.    Results  We observed that the acute stress induction led to increased heat pain thresholds, an effect that was present only in participants showing a cortisol response following stress induction and only in the presumed  HPA  axis time window. The strength of this hypoalgesic effect was further predicted by the change in cortisol and by fear of pain levels.    Conclusions  Our findings indicate that the  HPA  axis – and not the autonomic – stress response specifically underlies this stress‐induced hypoalgesic effect, having important implications for clinical states with  HPA  axis dysfunctions.    Significance  This experimental study shows that an acute stress induction – that combines physical and psychological stressors – increases heat pain thresholds, but not tolerance in healthy participants. Furthermore, the magnitude of this stress‐induced hypoalgesic effect is predicted by cortisol reactivity and fear of pain, revealing specific involvement of the  HPA  axis stress system and interactions with pain‐related psychosocial aspects.

Fear of pain and cortisol reactivity predict the strength of stress‐induced hypoalgesia