0187 STRESSOR REACTIVITY IN SLEEP-DEPRIVED NORMAL SLEEPERS AND SLEEP-ONSET INSOMNIACS

Abstract

Exposure to stressors increases physiological arousal through the hypothalamic-pituitary-adrenal (HPA) axis. Sleep deprivation has been reported to potentiate HPA axis stressor reactivity in healthy adults. Insomnia has been linked with hyperarousal and chronic HPA activation, which may also potentiate HPA axis stressor reactivity. In a highly standardized study protocol, we measured responses to psychosocial and physical stressors in normal sleepers and sleep-onset insomniacs while well-rested or exposed to acute total sleep deprivation (TSD). Twenty adults (9 sleep-onset insomniacs, 11 healthy normal sleepers; ages 22–39; 14 females) completed a 5-day (4-night) in-laboratory study. After an adaptation day and a baseline day (each 10h time in bed (TIB); 22:00-08:00), subjects were assigned to a 38h TSD condition (6 sleep-onset insomniacs, 6 healthy controls) or a matching control condition (10h TIB; 3 sleep-onset insomniacs, 5 healthy controls). After 36h TSD, subjects underwent the 10min Maastricht Acute Stress Test (MAST). This test involved 5 cold pressor trials, requiring subjects to submerge their non-dominant hand in cold water (0°C) for 60-90s. Between cold pressor trials, subjects performed a socially evaluated, difficult, mental arithmetic task. Salivary cortisol was measured just before and every 15 min after the MAST from 20:00 until 21:15, and at 21:45. Salivary cortisol was also collected at baseline 24 hours earlier. Cortisol levels, expressed relative to baseline, increased immediately following the MAST, peaked 30min later, and then gradually returned to pre-MAST levels (F=7.31, P<0.001). Relative to well-rested normal sleepers, the cortisol peak was dampened in the sleep-onset insomniacs and in the TSD condition, although this dampening did not reach statistical significance. The MAST psychosocial and physical stressors elicited an HPA axis response in both normal sleepers and sleep-onset insomniacs and in both TSD and control conditions. However, the results did not support the idea that sleep deprivation and/or insomnia potentiate HPA axis stressor reactivity. ONR grant N00014-13-C-0063.