Abstract

Social-evaluative threat (SET) − when the self could be negatively judged by others – can cause pronounced responses in the different stress systems: threat/challenge appraisal, the sympathetic (SNS) and parasympathetic (PNS) nervous systems, experienced motivation and affect, and the hypothalamus-pituitary-adrenal (HPA) axis. Here, we utilize a four-stage stress response model to shed light on the complex associations between different stress responses, where earlier stages are hypothesized to predict later stages. Additionally, we take into account important moderators, such as biological sex (controlling for menstrual cycle phase), personality traits (neuroticism and extraversion), and baseline stress levels. Thirty-seven men and 30 women in their luteal phase participated in an impromptu public speaking task to induce SET. Stress responses in four different stages were measured using: self-reported appraisal (threat or challenge, stage 1: S1), cardiovascular measures (pre-ejection period as SNS index, respiratory sinus arrhythmia as PNS index, S2), self-reported motivation and affect (state approach motivation, state anxiety, S3) and endocrine measures (cortisol as HPA index, S4). Stress reactivity was calculated by subtracting individual peaks from baseline. Results showed that SET induced pronounced stress reactivity in stages two to four. Against expectations, self-reported appraisal (S1) or motivation and affect (S3) did not predict later stress reactivity. As hypothesized, increased SNS (but not PNS) reactivity (S2) predicted increased HPA reactivity (S4). Bayesian model comparison confirmed the absence of sex differences in stress reactivity, likely due to controlling for menstrual cycle phase and sex differences in neuroticism levels. Higher trait neuroticism predicted blunted SNS (S2) and HPA (S4) reactivity, while higher baseline stress levels predicted blunted stages two and three reactivity overall. In conclusion, this rigorously controlled experiment partly supports and partly contradicts previous findings regarding associations between stress response stages, and offers new insight into the causes of blunted HPA responses in women.

Full Text
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