Homeostatic sleep regulation in habitual short sleepers and long sleepers

1996 ◽  
Vol 270 (1) ◽  
pp. R41-R53 ◽  
Author(s):  
D. Aeschbach ◽  
C. Cajochen ◽  
H. Landolt ◽  
A. A. Borbely
Keyword(s):  
Rem Sleep ◽  
Process Model ◽  
Sleep Latency ◽  
Spectral Power ◽  
Spectral Power Density ◽  
Sleep Time ◽  
Sleep Regulation ◽  
Sleep Episode ◽  
Rem Density ◽  
Electroencephalogram Eeg

Homeostatic sleep regulation in habitual short sleepers (sleep episode < 6 h, n = 9) and long sleepers (> 9 h, n = 7) was investigated by studying their sleep structure and sleep electroencephalogram (EEG) during baseline conditions and after prolonging their habitual waking time by 24 h. In each sleep episode, total sleep time was > 3 h longer in the long sleepers than in the short sleepers. Sleep deprivation decreased sleep latency and rapid eye movement (REM) density in REM sleep more in long sleepers than in short sleepers. The enhancement of EEG slow-wave activity (SWA; spectral power density in the 0.75-4.5 Hz range) in non-REM sleep after sleep loss was larger in long sleepers (47%) than in short sleepers (19%). This difference in the SWA response was predicted by the two-process model of sleep regulation on the basis of the different sleep durations. The results indicate that short sleepers live under a higher “non-REM sleep pressure” than long sleepers. However, the two groups do not differ with respect to the homeostatic sleep regulatory mechanisms.

scholarly journals The truncated TrkB receptor influences mammalian sleep

2015 ◽  
Vol 308 (3) ◽  
pp. R199-R207 ◽  
Author(s):  
Adam J. Watson ◽  
Kyle Henson ◽  
Susan G. Dorsey ◽  
Marcos G. Frank
Keyword(s):  
Rem Sleep ◽  
Knockout Mice ◽  
Psychiatric Illness ◽  
Sleep Latency ◽  
Sleep Time ◽  
Sleep Regulation ◽  
Trkb Receptor ◽  
Adult Mice ◽  
The Relationship

Brain-derived neurotrophic factor (BDNF) is a neurotrophin hypothesized to play an important role in mammalian sleep expression and regulation. In order to investigate the role of the truncated receptor for BDNF, TrkB.T1, in mammalian sleep, we examined sleep architecture and sleep regulation in adult mice constitutively lacking this receptor. We find that TrkB.T1 knockout mice have increased REM sleep time, reduced REM sleep latency, and reduced sleep continuity. These results demonstrate a novel role for the TrkB.T1 receptor in sleep expression and provide new insights into the relationship between BDNF, psychiatric illness, and sleep.

scholarly journals Regular Caffeine Intake Delays REM Sleep Promotion and Attenuates Sleep Quality in Healthy Men

2021 ◽  
pp. 074873042110139
Author(s):  
Janine Weibel ◽  
Yu-Shiuan Lin ◽  
Hans-Peter Landolt ◽  
Christian Berthomier ◽  
Marie Brandewinder ◽  
...  
Keyword(s):  
Sleep Quality ◽  
Rem Sleep ◽  
Sleep Time ◽  
Caffeine Intake ◽  
Sleep Regulation ◽  
Caffeine Consumption ◽  
Subjective Sleep Quality ◽  
Placebo Condition ◽  
Double Blind ◽  
Sleep Episode

Acute caffeine intake can attenuate homeostatic sleep pressure and worsen sleep quality. Caffeine intake—particularly in high doses and close to bedtime—may also affect circadian-regulated rapid eye movement (REM) sleep promotion, an important determinant of subjective sleep quality. However, it is not known whether such changes persist under chronic caffeine consumption during daytime. Twenty male caffeine consumers (26.4 ± 4 years old, habitual caffeine intake 478.1 ± 102.8 mg/day) participated in a double-blind crossover study. Each volunteer completed a caffeine (3 × 150 mg caffeine daily for 10 days), a withdrawal (3 × 150 mg caffeine for 8 days then placebo), and a placebo condition. After 10 days of controlled intake and a fixed sleep-wake cycle, we recorded electroencephalography for 8 h starting 5 h after habitual bedtime (i.e., start on average at 04:22 h which is around the peak of circadian REM sleep promotion). A 60-min evening nap preceded each sleep episode and reduced high sleep pressure levels. While total sleep time and sleep architecture did not significantly differ between the three conditions, REM sleep latency was longer after daily caffeine intake compared with both placebo and withdrawal. Moreover, the accumulation of REM sleep proportion was delayed, and volunteers reported more difficulties with awakening after sleep and feeling more tired upon wake-up in the caffeine condition compared with placebo. Our data indicate that besides acute intake, also regular daytime caffeine intake affects REM sleep regulation in men, such that it delays circadian REM sleep promotion when compared with placebo. Moreover, the observed caffeine-induced deterioration in the quality of awakening may suggest a potential motive to reinstate caffeine intake after sleep.

scholarly journals Regular caffeine intake attenuates REM sleep promotion and sleep quality in healthy men

2020 ◽  
Author(s):  
Janine Weibel ◽  
Yu-Shiuan Lin ◽  
Hans-Peter Landolt ◽  
Christian Berthomier ◽  
Marie Brandewinder ◽  
...  
Keyword(s):  
Sleep Quality ◽  
Rem Sleep ◽  
Sleep Time ◽  
Caffeine Intake ◽  
Sleep Regulation ◽  
Caffeine Consumption ◽  
Subjective Sleep Quality ◽  
Placebo Condition ◽  
Double Blind ◽  
Sleep Episode

AbstractAcute caffeine intake can attenuate homeostatic sleep pressure and worsen sleep quality. Besides, caffeine intake – particularly in high doses and close to bedtime – may also affect circadian-regulated REM sleep promotion, an important determinant of subjective sleep quality. However, it is not known whether such changes persist under chronic caffeine consumption during daytime. Twenty male caffeine consumers (26.4 ± 4 years old, habitual caffeine intake 478.1 ± 102.8 mg/day) participated in a double-blind crossover study. Each volunteer completed a caffeine (3 × 150 mg caffeine daily), a withdrawal (3 × 150 mg caffeine for eight days then placebo), and a placebo condition. After ten days of controlled intake and a fixed sleep-wake cycle, we recorded 8 h of electroencephalography starting 5 h after habitual bedtime (i.e., start on average at 04:22 am which is around the peak of circadian REM sleep promotion). A 60 min evening nap preceded each sleep episode and reduced high sleep pressure levels. While total sleep time and sleep architecture did not significantly differ between the three conditions, REM latency was longer after daily caffeine intake compared to both placebo and withdrawal. Moreover, the accumulation of REM sleep proportion was slower, and volunteers reported more difficulties at awakening after sleep and feeling more tired upon wake-up in the caffeine condition compared to placebo. Our data indicate that besides acute also regular daytime caffeine intake affects REM sleep regulation in men. We have evidence that regular caffeine intake during daytime weakens circadian sleep promotion when compared to placebo. Moreover, the observed caffeine-induced deterioration in the quality of awakening may suggest a potential motive to reinstate caffeine intake after sleep.

scholarly journals Dreaming and Insomnia: Link between Physiological REM Parameters and Mentation Characteristics

2020 ◽  
Vol 10 (6) ◽  
pp. 378
Author(s):  
Fee Benz ◽  
Dieter Riemann ◽  
Bernd Feige
Keyword(s):  
Rem Sleep ◽  
Multivariate Analyses ◽  
Spectral Power ◽  
Group Differences ◽  
Alpha Power ◽  
Insomnia Disorder ◽  
Rem Density ◽  
Power Prior ◽  
High Level ◽  
Objectively Measured

(1) Background: An unresolved phenomenon of insomnia disorder is a discrepancy between objectively measured sleep and subjective complaints. It has been shown that rapid eye movement (REM) sleep might be especially vulnerable to an altered perception. The present work aimed to investigate the link between physiological REM parameters and mentation characteristics in REM sleep. (2) Methods: 22 patients with insomnia and 23 good sleepers indicating at least one REM mentation within an awakening study were included. Multivariate analyses of variance (MANOVAs) were calculated to examine group differences and effects of mentation characteristics on number of arousals, REM density, and spectral power prior to awakenings. (3) Results: Increased perceived wakefulness was related to lower delta, theta, and alpha power in the minute prior to the REM awakenings. Nevertheless, no group differences regarding spectral power were found. With respect to number of arousals and REM density, no significant effects of mentation characteristics and no group differences were found. (4) Conclusions: Our results suggest that spectral power in REM sleep is linked with altered sleep perception. Reduced delta, theta, and alpha power might be a signature of this modified REM sleep associated with a high level of perceived wakefulness. Future awakening studies are necessary to further explore the link between physiological REM parameters and sleep perception.

scholarly journals The European starling (Sturnus vulgaris) shows signs of NREM sleep homeostasis but has very little REM sleep and no REM sleep homeostasis

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Eye Movement ◽  
Rem Sleep ◽  
Spectral Power ◽  
Nrem Sleep ◽  
Sleep Time ◽  
European Starling ◽  
Dark Phase ◽  
Rapid Eye Movement ◽  
Sleep Homeostasis

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.

Sleep and hibernation in ground squirrels (Citellus spp): electrophysiological observations

1977 ◽  
Vol 233 (5) ◽  
pp. R213-R221 ◽  
Author(s):  
J. M. Walker ◽  
S. F. Glotzbach ◽  
R. J. Berger ◽  
H. C. Heller
Keyword(s):  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Dark Period ◽  
Total Sleep Time ◽  
Brain Temperature ◽  
Sleep Time ◽  
Light Period ◽  
Ground Squirrels ◽  
Sleep Stages ◽  
Electroencephalogram Eeg

Electroencephalogram (EEG), electrooculogram, electromyogram, and electrocardiogram were recorded from ground squirrels (Citellus beldingi and C. lateralis) during the summer and also during the hibernation season. Summer recordings revealed that the animals spent an average of 66% of the 24-h period asleep (49% of the 12-h light period and 84% of the 12-h dark period); 19% of the total sleep time (TST) consisted of rapid-eye-movement (REM) sleep, and 81% of TST consisted of slow-wave sleep (SWS). Recordings obtained during the hibernation season showed that hibernation was entered through sleep, but the distribution of sleep states was different than in euthermic sleep. During the early entrance when brain temperature (Tbr) was between 35 and 25 degrees C, the animals were asleep 88% of the time, but only 10% of the TST was spent in REM sleep. The EEG amplitude declined with decreased Tbr so that classical sleep stages could not be identified below a Tbr of 25 degrees C. The frequency of the EEG increased as Tbr decreased; but activity in the 0–4 cycles/s band occupied the majority of the record even at a Tbr of 10 degrees C. Below a Tbr of 10 degrees C the EEG was isoelectric except for intermittent bursts of spindles. It was concluded from these and other results that the entrance into hibernation represents an extension of the thermoregulatory adjustments that occur during SWS.

scholarly journals An Asymmetrical Hypothesis for the NREM-REM Sleep Alternation—What Is the NREM-REM Cycle?

2021 ◽  
Vol 15 ◽  
Author(s):  
Olivier Le Bon
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Refractory Period ◽  
High Variability ◽  
Oscillator Model ◽  
Rapid Eye Movement ◽  
Sleep Regulation ◽  
Short Term ◽  
Sleep Episode ◽  
Sleep Homeostasis

Since the discovery of rapid eye movement (REM) sleep (Aserinsky and Kleitman, 1953), sleep has been described as a succession of cycles of non-REM (NREM) and REM sleep episodes. The hypothesis of short-term REM sleep homeostasis, which is currently the basis of most credible theories on sleep regulation, is built upon a positive correlation between the duration of a REM sleep episode and the duration of the interval until the next REM sleep episode (inter-REM interval): the duration of REM sleep would therefore predict the duration of this interval. However, the high variability of inter-REM intervals, especially in polyphasic sleep, argues against a simple oscillator model. A new “asymmetrical” hypothesis is presented here, where REM sleep episodes only determine the duration of a proportional post-REM refractory period (PRRP), during which REM sleep is forbidden and the only remaining options are isolated NREM episodes or waking. After the PRRP, all three options are available again (NREM, REM, and Wake). I will explain why I think this hypothesis also calls into question the notion of NREM-REM sleep cycles.

I. Time course of interventions and recovery sleep

2002 ◽  
Vol 283 (2) ◽  
pp. R521-R526 ◽  
Author(s):  
Esther Werth ◽  
Kimberly A. Cote ◽  
Eva Gallmann ◽  
Alexander A. Borbély ◽  
Peter Achermann
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Time Course ◽  
Early Morning ◽  
Adult Males ◽  
Sleep Regulation ◽  
Rem Sleep Deprivation ◽  
Sleep Episode ◽  
Recovery Sleep ◽  
Sleep Propensity

Although repeated selective rapid eye movement (REM) sleep deprivation by awakenings during nighttime has shown that the number of sleep interruptions required to prevent REM sleep increases within and across consecutive nights, the underlying regulatory processes remained unspecified. To assess the role of circadian and homeostatic factors in REM sleep regulation, REM sleep was selectively deprived in healthy young adult males during a daytime sleep episode (7–15 h) after a night without sleep. Circadian REM sleep propensity is known to be high in the early morning. The number of interventions required to prevent REM sleep increased from the first to the third 2-h interval by a factor of two and then leveled off. Only a minor REM sleep rebound (11.6%) occurred in the following undisturbed recovery night. It is concluded that the limited rise of interventions during selective daytime REM sleep deprivation may be due to the declining circadian REM sleep propensity, which may partly offset the homeostatic drive and the sleep-dependent disinhibition of REM sleep.

scholarly journals Bright morning light advances the human circadian system without affecting NREM sleep homeostasis

1989 ◽  
Vol 256 (1) ◽  
pp. R106-R111 ◽  
Author(s):  
D. J. Dijk ◽  
D. G. Beersma ◽  
S. Daan ◽  
A. J. Lewy
Keyword(s):  
Rem Sleep ◽  
Process Model ◽  
Sleep Onset ◽  
Light Condition ◽  
Bright Light ◽  
Circadian Pacemaker ◽  
Sleep Regulation ◽  
Plasma Melatonin ◽  
Sleep Homeostasis ◽  
Dim Light

Eight male subjects were exposed to either bright light or dim light between 0600 and 0900 h for 3 consecutive days each. Relative to the dim light condition, the bright light treatment advanced the evening rise in plasma melatonin and the time of sleep termination (sleep onset was held constant) for an average approximately 1 h. The magnitude of the advance of the plasma melatonin rise was dependent on its phase in dim light. The reduction in sleep duration was at the expense of rapid-eye-movement (REM) sleep. Spectral analysis of the sleep electroencephalogram (EEG) revealed that the advance of the circadian pacemaker did not affect EEG power densities between 0.25 and 15.0 Hz during either non-REM or REM sleep. The data show that shifting the human circadian pacemaker by 1 h does not affect non-REM sleep homeostasis. These findings are in accordance with the predictions of the two-process model of sleep regulation.

scholarly journals The Statin Target HMG-Coenzyme a Reductase (Hmgcr) Regulates Sleep Homeostasis in Drosophila

2022 ◽  
Vol 15 (1) ◽  
pp. 79
Author(s):  
Ahmed M. Alsehli ◽  
Sifang Liao ◽  
Mohamed H. Al-Sabri ◽  
Lukas Vasionis ◽  
Archana Purohit ◽  
...  
Keyword(s):  
Sleep Disturbances ◽  
Coenzyme A ◽  
Sleep Latency ◽  
Statin Treatment ◽  
Sleep Regulation ◽  
Sleep Behavior ◽  
Sleep Episode ◽  
Sleep Homeostasis ◽  
The Impact ◽  
Coenzyme A Reductase

Statins, HMG Coenzyme A Reductase (HMGCR) inhibitors, are a first-line therapy, used to reduce hypercholesterolemia and the risk for cardiovascular events. While sleep disturbances are recognized as a side-effect of statin treatment, the impact of statins on sleep is under debate. Using Drosophila, we discovered a novel role for Hmgcr in sleep modulation. Loss of pan-neuronal Hmgcr expression affects fly sleep behavior, causing a decrease in sleep latency and an increase in sleep episode duration. We localized the pars intercerebralis (PI), equivalent to the mammalian hypothalamus, as the region within the fly brain requiring Hmgcr activity for proper sleep maintenance. Lack of Hmgcr expression in the PI insulin-producing cells recapitulates the sleep effects of pan-neuronal Hmgcr knockdown. Conversely, loss of Hmgcr in a different PI subpopulation, the corticotropin releasing factor (CRF) homologue-expressing neurons (DH44 neurons), increases sleep latency and decreases sleep duration. The requirement for Hmgcr activity in different neurons signifies its importance in sleep regulation. Interestingly, loss of Hmgcr in the PI does not affect circadian rhythm, suggesting that Hmgcr regulates sleep by pathways distinct from the circadian clock. Taken together, these findings suggest that Hmgcr activity in the PI is essential for proper sleep homeostasis in flies.

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