A general enhancement of autonomic and cortisol responses during social evaluative threat.
OBJECTIVE
To examine the Social Self Preservation Theory, which predicts that stressors involving social evaluative threat (SET) characteristically activate the hypothalamic-pituitary-adrenal (HPA) axis. The idea that distinct psychosocial factors may underlie specific patterns of neuroendocrine stress responses has been a topic of recurrent debate.


METHODS
Sixty-one healthy university students (n = 31 females) performed a challenging speech task in one of three conditions that aimed to impose increasing levels of SET: performing the task alone (no social evaluation), with one evaluating observer, or with four evaluating observers. Indices of sympathetic (preejection period) and parasympathetic (heart rate variability) cardiac drive were obtained by impedance- and electrocardiography. Salivary cortisol was used to index HPA activity. Questionnaires assessed affective responses.


RESULTS
Affective responses (shame/embarrassment, anxiety, negative affect, and self-esteem), cortisol, heart rate, sympathetic and parasympathetic activation all differentiated evaluative from nonevaluative task conditions (p < .001). The largest effect sizes were observed for cardiac autonomic responses. Physiological reactivity increased in parallel with increasing audience size (p < .001). An increase in cortisol was predicted by sympathetic activation during the task (p < .001), but not by affective responses.


CONCLUSIONS
It would seem that SET determines the magnitude, rather than the pattern, of physiological activation. This potential to perturb broadly multiple physiological systems may help explain why social stress has been associated with a range of health outcomes. We propose a threshold-activation model as a physiological explanation for why engaging stressors, such as those involving social evaluation or uncontrollability, may seem to induce selectively cortisol release.
School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK. j.a.bosch@bham.ac.uk
Jos A
JA
Bosch
Eco J C
EJ
de Geus
Douglas
D
Carroll
Annebet D
AD
Goedhart
Leila A
LA
Anane
Jet J Veldhuizen
JJ
van Zanten
Eva J
EJ
Helmerhorst
Kate M
KM
Edwards
D000328:Adult; D001007:Anxiety / Q000523:psychology*; D001341:Autonomic Nervous System / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D002307:Cardiography, Impedance; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D006854:Hydrocortisone / Q000032:analysis* / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D007398:Interpersonal Relations; D008016:Life Change Events; D010913:Pituitary-Adrenal System / Q000502:physiology; D012463:Saliva / Q000737:chemistry; D012649:Self Concept; D012752:Shame; D013060:Speech / Q000502:physiology; D013315:Stress, Psychological / Q000523:psychology*; D011795:Surveys and Questionnaires
D006854:Hydrocortisone