Sleep deprivation potentiates HPA axis stress reactivity in healthy adults.

OBJECTIVE: This article describes an experiment that was designed to investigate the effects of sleep deprivation on physiological stress responses in healthy adults. METHOD: Twenty-six participants, ages 22-49, completed a 3-night laboratory experiment with randomization to one night of sleep-deprivation or a normal-sleep control condition. After a night of baseline sleep, 12 participants were sleep deprived and 14 were not. After the sleep manipulation, each participant completed the Trier Social Stress Test, a task that requires delivering a speech and performing difficult arithmetic in front of a stern, three-person panel. The stressor was administered from 5:00 p.m.-5:30 p.m. and saliva samples were collected 20 and 5 min before (baseline) and 5, 20, and 40 min after the stressor. Samples were assayed for cortisol (a biomarker for the HPA axis) and alpha-amylase (a putative biomarker for the sympatho-adrenal medullar system). RESULTS: Sleep deprivation was associated with higher cortisol levels at baseline (p < .0001) and an amplified cortisol response to the stressor relative to control participants (pinteraction = 0.0039). Alpha-amylase showed a significant main effect of the stressor (p = .0026), but there was no effect of sleep loss at baseline or in response to the stressor. CONCLUSIONS: Sleep deprivation is associated with both elevated resting cortisol release and with an exaggerated cortisol response to a stressor indicative of elevated HPA axis responses in healthy adults. Individual differences in the magnitude of this response may represent a risk factor for psychological and physical health consequences associated with heightened cortisol exposure.