SLEEP LOSS RESULTS IN AN ELEVATION OF CORTISOL-LEVELS THE NEXT EVENING

Citation
R. Leproult et al., SLEEP LOSS RESULTS IN AN ELEVATION OF CORTISOL-LEVELS THE NEXT EVENING, Sleep, 20(10), 1997, pp. 865-870
Citations number
31
Categorie Soggetti
Behavioral Sciences","Clinical Neurology
Journal title
SleepACNP
ISSN journal
01618105
Volume
20
Issue
10
Year of publication
1997
Pages
865 - 870
Database
ISI
SICI code
0161-8105(1997)20:10<865:SLRIAE>2.0.ZU;2-9
Abstract
Sleep curtailment constitutes an increasingly common condition in indu strialized societies and is thought to affect mood and performance rat her than physiological functions. There is no evidence for prolonged o r delayed effects of sleep loss on the hypothalamo-pituitary-adrenal ( HPA) axis. We evaluated the effects of acute partial or total sleep de privation on the nighttime and daytime profile of cortisol levels. Pla sma cortisol profiles were determined during a 32-hour period (from 18 00 hours on day 1 until 0200 hours on day 3) in normal young men submi tted to three different protocols: normal sleep schedule (2300-0700 ho urs), partial sleep deprivation (0400-0800 hours), and total sleep dep rivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sl eep, plasma cortisol levels over the 1800-2300-hour period were simila r on days 1 and 2. After partial and total sleep deprivation, plasma c ortisol levels over the 1800-2300-hour period were higher on day 2 tha n on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), a nd the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss de lays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation. Sleep loss could thus affect the resiliency of t he stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess.