Timing of human sleep: recovery process gated by a circadian pacemaker

1984 ◽  
Vol 246 (2) ◽  
pp. R161-R183 ◽  
Author(s):  
S. Daan ◽  
D. G. Beersma ◽  
A. A. Borbely
Keyword(s):  
Sleep Deprivation ◽  
Sleep Onset ◽  
Recovery Process ◽  
Bed Rest ◽  
Circadian Pacemaker ◽  
Phase Dependence ◽  
Circadian Phase ◽  
Sleep Timing ◽  
Human Sleep ◽  
Partial Sleep Deprivation

A model for the timing of human sleep is presented. It is based on a sleep-regulating variable (S)--possibly, but not necessarily, associated with a neurochemical substance--which increases during wakefulness and decreases during sleep. Sleep onset is triggered when S approaches an upper threshold (H); awakening occurs when S reaches a lower threshold (L). The thresholds show a circadian rhythm controlled by a single circadian pacemaker. Time constants of the S process were derived from rates of change of electroencephalographic (EEG) power density during regular sleep and during recovery from sleep deprivation. The waveform of the circadian threshold fluctuations was derived from spontaneous wake-up times after partial sleep deprivation. The model allows computer simulations of the main phenomena of human sleep timing, such as 1) internal desynchronization in the absence of time cues, 2) sleep fragmentation during continuous bed rest, and 3) circadian phase dependence of sleep duration during isolation from time cues, recovery from sleep deprivation, and shift work. The model shows that the experimental data are consistent with the concept of a single circadian pacemaker in humans. It has implications for the understanding of sleep as a restorative process and its timing with respect to day and night.

scholarly journals 0289 What is the Optimal Duration to Sleep in on Weekends?

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A109-A109
Author(s):  
J E Stone ◽  
F Cheong ◽  
A J Phillips
Keyword(s):  
Rise Time ◽  
Free Choice ◽  
Sleep Onset ◽  
Timing Constraints ◽  
Circadian Phase ◽  
Late Night ◽  
Sleep Timing ◽  
Sleep Debt ◽  
Wake Patterns ◽  
Night Condition

Abstract Introduction Most individuals in the workforce exhibit differing sleep/wake patterns between work days and weekends. Work days are typically characterized by shorter and earlier sleep. On weekends, sleep debt is repaid by sleeping later and longer, often due to evening events. While social jet-lag (the mismatch in work vs. free sleep timing) is associated with poor health outcomes, repaying sleep debt is beneficial to health. The degree to which individuals should sleep in on weekends is currently unknown. Methods We used a mathematical model of human sleep/wake timing, which has been validated for predicting sleep/wake patterns in a variety of field/lab conditions. Sleep timing constraints are inputs, and the model generates predicted sleep/wake patterns and alertness levels. We simulated a traditional 7-day work week, with 7am rise times on week days. Inter-individual differences in chronotype were modeled by varying intrinsic circadian period. The model was applied to two conditions: (i) free choice of sleep onset times on weekends; or (ii) late nights on weekends (2am bedtime). Weekend rise time was systematically varied to optimize predicted daytime alertness. Results Optimal weekend rise times varied as a function of chronotype. With free choice sleep onset times, the model predicted optimal rise time was later for late types than early types, ranging from 7:20 to 8:40am across individuals. Sleeping later than optimal was associated with poorer performance due to misaligned circadian phase. The same trend was observed in the late-night condition, but with later optimal rise times, ranging from 8:30 to 9:50am. Conclusion Although individuals should maintain a consistent sleep/wake pattern on all days of the week, they often do not, due to work or social commitments. Within real-world constraints, we provided the first objective recommendations for sleep timing on the weekend, finding a compromise between repaying sleep debt and avoiding circadian misalignment. Support N/A

School Schedules Affect Sleep Timing in Children and Contribute to Partial Sleep Deprivation

2014 ◽  
Vol 8 (4) ◽  
pp. 169-174 ◽  
Author(s):  
Tâmile Stella Anacleto ◽  
Taísa Adamowicz ◽  
Laura Simões da Costa Pinto ◽  
Fernando Mazzilli Louzada
Keyword(s):  
Sleep Deprivation ◽  
Sleep Timing ◽  
School Schedules ◽  
Partial Sleep Deprivation

Sleep in western culture

2018 ◽  
Author(s):  
Roger Ekirch
Keyword(s):  
Nineteenth Century ◽  
Sleep Deprivation ◽  
Industrial Revolution ◽  
Sleep Onset ◽  
Western Culture ◽  
The Past ◽  
Predominant Form ◽  
Artificial Illumination ◽  
Illness Anxiety

Although a universal necessity, sleep, as the past powerfully indicates, is not a biological constant. Before the Industrial Revolution, sleep in western households differed in a variety of respects from that of today. Arising chiefly from a dearth of artificial illumination, the predominant form of sleep was segmented, consisting of two intervals of roughly 3 hours apiece bridged by up to an hour or so of wakefulness. Notwithstanding steps taken by families to preserve the tranquillity of their slumber, the quality of pre-industrial sleep was poor, owing to illness, anxiety, and environmental vexations. Large portions of the labouring population almost certainly suffered from sleep deprivation. Despite the prevalence of sleep-onset insomnia, awakening in the middle of the night was thought normal. Not until the turn of the nineteenth century and sleep’s consolidation did physicians view segmented sleep as a disorder requiring medication.

086 Sleep midpoint after job loss predicts breakfast skipping patterns

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A36-A36
Author(s):  
Leah Callovini ◽  
Gaby Gubka ◽  
Candace Mayer ◽  
Darlynn Rojo-Wissar ◽  
David Glickenstein ◽  
...  
Keyword(s):  
Job Loss ◽  
Activity Patterns ◽  
Sleep Onset ◽  
Daily Routine ◽  
Cross Sectional ◽  
Circadian Phase ◽  
Breakfast Skipping ◽  
Occupational Transitions ◽  
The Relationship ◽  
Significant Covariates

Abstract Introduction Few studies have examined circadian phase after job loss, an event that upends daily routine. It is common that a daily routine begins with the consumption of breakfast, and breakfast behavior may contribute to health status in adults. Therefore, we sought to examine whether a later midpoint of sleep was associated with breakfast skipping among adults whose schedules were no longer dictated by employment. Methods Data were obtained from the Assessing Daily Activity Patterns Through Occupational Transitions (ADAPT) study. The sample of 155 participants had involuntarily lost their jobs in the last 90 days. Both cross-sectional and 18-month longitudinal analyses assessed the relationship between sleep midpoint after job loss and current and later breakfast skipping. Assessment periods were 14 days. Sleep was measured via actigraphy, and breakfast skipping was measured via daily diary (1 = had breakfast; 0 = did not have breakfast). The midpoint of sleep was calculated as the circular center based on actigraphy sleep onset and offset times. Results The midpoint of sleep at baseline was negatively associated with breakfast consumption at baseline (B = -.09, SE = .02, p = .000). Also, a later midpoint was associated with breakfast skipping over the next 18 months (estimate = -.08; SE = .02; p = .000). Prospective findings remained significant when adjusting for gender, ethnicity, age, perceived stress, body mass index (BMI), education, and reemployment over time. Education (estimate = 14.26, SE = 6.23, p < .05) and BMI (estimate = -.51, SE = .25, p < .05) were the only significant covariates. No other sleep indices predicted breakfast behavior cross-sectionally or prospectively. Conclusion Consistent with research in adolescents, unemployed adults with a later circadian phase are more likely to skip breakfast more often. Breakfast skipping was also associated with higher BMI. Taken together, these findings provide support for the future testing of sleep/wake scheduling interventions to modify breakfast skipping and potentially mitigate weight gain after job loss. Support (if any) #1R01HL117995-01A1

Partial sleep deprivation to prevent 48-hour mood cycles

1990 ◽  
Vol 81 (4) ◽  
pp. 398-399 ◽  
Author(s):  
C. M. Churchill ◽  
S. C. Dilsaver
Keyword(s):  
Sleep Deprivation ◽  
Partial Sleep Deprivation

The Link Between Sleep, Stress and BDNF

2017 ◽  
Vol 41 (S1) ◽  
pp. S282-S282 ◽  
Author(s):  
A. Eckert ◽  
S. Karen ◽  
J. Beck ◽  
S. Brand ◽  
U. Hemmeter ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Serum Levels ◽  
Bdnf Expression ◽  
Depressed Patients ◽  
Level Increase ◽  
Stress Experience ◽  
Partial Sleep Deprivation ◽  
Competing Interest ◽  
Fast Increase ◽  
Serum Bdnf

The protein brain derived neurotrophic factor (BDNF) is a major contributor to neuronal plasticity. There is numerous evidence that BDNF expression is decreased by experiencing psychological stress and that accordingly a lack of neurotrophic support causes depression. The use of serum BDNF concentration as a potential indicator of brain alteration is justified through extensive evidence. Recently, we reported, for the first time, a relationship between BDNF and insomnia, since we could show that reduced levels of serum BDNF are correlated with sleep impairment in control subjects, while partial sleep deprivation was able to induce a fast increase in serum BDNF levels in depressed patients. Using a bi-directional stress model as an explanation approach, we propose the hypothesis that chronic stress might induce a deregulation of the HPA system leading in the long term to sleep disturbance and decreased BDNF levels, whereas acute sleep deprivation, can be used as therapeutical intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial sleep deprivation (PSD) induced a very fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase. Moreover, we revealed that stress experience and subjective sleep perception interact with each other and affect serum BDNF levels. We identified sleep as a mediator of the association between stress experience and serum BDNF levels.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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