Sleep deprivation potentiates HPA axis stress reactivity in healthy adults.

Abstract

This article describes an experiment that was designed to investigate the effects of sleep deprivation on physiological stress responses in healthy adults. 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). 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. 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.