Sleep Loss Results in an Elevation of Cortisol Levels the Next Evening

TLDR

Sleep curtailment is common in industrialized societies and is generally thought to affect mood and performance rather than physiological functions, yet no evidence exists for prolonged or delayed effects on the hypothalamo‑pituitary‑adrenal axis. The study aimed to assess how acute partial or total sleep deprivation influences the nighttime and daytime cortisol profile. Researchers measured plasma cortisol over a 32‑hour period in healthy young men under three conditions—normal sleep, partial sleep deprivation (0400‑0800), and total sleep deprivation—to capture circadian changes. Cortisol elevations were observed only in the evening after sleep deprivation, with 37–45 % higher levels on day 2 versus day 1 and a delayed onset of the quiescent period, indicating that even partial acute sleep loss impairs HPA recovery and may compromise stress resilience and metabolic/cognitive health.

Abstract

Sleep curtailment constitutes an increasingly common condition in industrialized societies and is thought to affect mood and performance rather than physiological functions. There is no evidence for prolonged or delayed effects of sleep loss on the hypothalamo-pituitary-adrenal (HPA) axis. We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels. Plasma cortisol profiles were determined during a 32-hour period (from 1800 hours on day 1 until 0200 hours on day 3) in normal young men submitted to three different protocols: normal sleep schedule (2300-0700 hours), partial sleep deprivation (0400-0800 hours), and total sleep deprivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sleep, plasma cortisol levels over the 1800-2300-hour period were similar on days 1 and 2. After partial and total sleep deprivation, plasma cortisol levels over the 1800-2300-hour period were higher on day 2 than on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss delays 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 the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess.