Repeating patterns of sleep restriction and recovery: Do we get used to it?
Despite its prevalence in modern society, little is known about the long-term impact of restricting sleep during the week and 'catching up' on weekends. This common sleep pattern was experimentally modeled with three weeks of 5 nights of sleep restricted to 4h followed by two nights of 8-h recovery sleep. In an intra-individual design, 14 healthy adults completed both the sleep restriction and an 8-h control condition, and the subjective impact and the effects on physiological markers of stress (cortisol, the inflammatory marker IL-6, glucocorticoid receptor sensitivity) were assessed. Sleep restriction was not perceived to be subjectively stressful and some degree of resilience or resistance to the effects of sleep restriction was observed in subjective domains. In contrast, physiological stress response systems remain activated with repeated exposures to sleep restriction and limited recovery opportunity. Morning IL-6 expression in monocytes was significantly increased during week 2 and 3 of sleep restriction, and remained increased after recovery sleep in week 2 (p<0.05) and week 3 (p<0.09). Serum cortisol showed a significantly dysregulated 24h-rhythm during weeks 1, 2, and 3 of sleep restriction, with elevated morning cortisol, and decreased cortisol in the second half of the night. Glucocorticoid sensitivity of monocytes was increased, rather than decreased, during the sleep restriction and sleep recovery portion of each week. These results suggest a disrupted interplay between the hypothalamic-pituitary-adrenal and inflammatory systems in the context of repeated exposure to sleep restriction and recovery. The observed dissociation between subjective and physiological responses may help explain why many individuals continue with the behavior pattern of restricting and recovering sleep over long time periods, despite a cumulative deleterious physiological effect.
Department of Psychiatry and Behavioral Sciences, 401 Quarry Rd., Stanford University School of Medicine, Stanford, CA, United States.
Norah S
NS
Simpson
Department of Neurology, Beth Israel Deaconess Medical Center/Harvard Medical School, DANA-727, 330 Brookline Ave., Boston, MA 02215, United States.
Moussa
M
Diolombi
Department of Neurology, Beth Israel Deaconess Medical Center/Harvard Medical School, DANA-727, 330 Brookline Ave., Boston, MA 02215, United States.
Jennifer
J
Scott-Sutherland
Department of Neurology, Beth Israel Deaconess Medical Center/Harvard Medical School, DANA-727, 330 Brookline Ave., Boston, MA 02215, United States.
Huan
H
Yang
Department of Neurology, Beth Israel Deaconess Medical Center/Harvard Medical School, DANA-727, 330 Brookline Ave., Boston, MA 02215, United States.
Vrushank
V
Bhatt
Department of Neurology, Beth Israel Deaconess Medical Center/Harvard Medical School, DANA-727, 330 Brookline Ave., Boston, MA 02215, United States.
Shiva
S
Gautam
Department of Neurology, Beth Israel Deaconess Medical Center/Harvard Medical School, DANA-727, 330 Brookline Ave., Boston, MA 02215, United States.
Janet
J
Mullington
Department of Neurology, Beth Israel Deaconess Medical Center/Harvard Medical School, DANA-727, 330 Brookline Ave., Boston, MA 02215, United States. Electronic address: mhaack@bidmc.harvard.edu.
Monika
M
Haack
D000293:Adolescent; D000328:Adult; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D009000:Monocytes / Q000378:metabolism; D012892:Sleep Deprivation / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D013312:Stress, Physiological; D013315:Stress, Psychological / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D055815:Young Adult
C508600:IL6 protein, human; D015850:Interleukin-6; D006854:Hydrocortisone
Cortisol; Inflammation; Sleep restriction; Stress; Subjective