Thermoregulation, metabolism, and stages of sleep in cold-exposed men

1986 ◽  
Vol 61 (3) ◽  
pp. 940-947 ◽  
Author(s):  
J. W. Palca ◽  
J. M. Walker ◽  
R. J. Berger
Keyword(s):  
Ambient Temperature ◽  
Rem Sleep ◽  
Sleep Stage ◽  
Sleep Onset ◽  
O2 Consumption ◽  
Peripheral Vasoconstriction ◽  
Stage 2 Sleep

Four naked men, selected for their ability to sleep in the cold, were exposed to an ambient temperature (Ta) of 21 degrees C for five consecutive nights. Electrophysiological stages of sleep, O2 consumption (VO2), and skin (Tsk), rectal (Tre), and tympanic (Tty) temperatures were recorded. Compared with five nights at a thermoneutral Ta of 29 degrees C, cold induced increased wakefulness and decreased stage 2 sleep, without significantly affecting other stages. Tre and Tty declined during each condition. The decrease in Tre was greater at 21 degrees C than at 29 degrees C, whereas Tty did not differ significantly between conditions. Increases in Tty following REM sleep onset at 21 degrees C were negatively correlated with absolute Tty. VO2 and forehead Tsk also increased during REM sleep at both TaS, whereas Tsk of the limb extremities declined at 21 degrees C. Unsuppressed REM sleep in association with peripheral vasoconstriction and increased Tty and VO2 in cold-exposed humans, do not signify an inhibition of thermoregulation during this sleep stage as has been observed in other mammals.

scholarly journals 0746 Dynamics of Sleep Stage Transitions in Patients with Narcolepsy and Other Hypersomnias

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A283-A284
Author(s):  
A Kishi ◽  
T Kitajima ◽  
R Kawai ◽  
M Hirose ◽  
N Iwata ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Transition Probabilities ◽  
Sleep Stage ◽  
Sleep Onset ◽  
Sleep Stages ◽  
Subsequent Stage ◽  
Dynamic Features ◽  
Survival Curves ◽  
Transition Analysis ◽  
Sleep Transition

Abstract Introduction Narcolepsy is a chronic sleep disorder characterized by excessive daytime sleepiness and abnormal REM sleep phenomena. Narcolepsy can be distinguished into type 1 (NT1; with cataplexy) and type 2 (NT2; without cataplexy). It has been reported that sleep stage sequences at sleep-onset as well as sleep-wake dynamics across the night may be useful in the differential diagnosis of hypersomnia. Here we studied dynamic features of sleep stage transitions during whole night sleep in patients with NT1, NT2, and other types of hypersomnia (o-HS). Methods Twenty patients with NT1, 14 patients with NT2, and 35 patients with o-HS underwent overnight PSG. Transition probabilities between sleep stages (wake, N1, N2, N3, and REM) and survival curves of continuous runs of each sleep stage were compared between groups. Transition-specific survival curves of continuous runs of each sleep stage, dependent on the subsequent stage of the transition, were also compared. Results The probability of transitions from N1-to-wake was significantly greater in NT1 than in NT2 and o-HS while that from N1-to-N2 was significantly smaller in NT1 than in NT2 and o-HS. The probability of transitions from N2-to-REM was significantly smaller in NT1 than in o-HS. Wake and N1 were significantly more continuous in NT1 than in NT2; specifically, N1 followed by N2 was significantly more continuous in NT1 than in NT2 and o-HS. N2 was significantly less continuous in NT1 and NT2 than in o-HS; this was specifically confirmed for N2 followed by N1/wake. REM sleep was significantly less continuous in NT1 than in NT2 and o-HS; specifically, REM sleep followed by wake was significantly less continuous in NT1 than in o-HS. Continuity of N3 did not differ significantly between groups. Conclusion Dynamics of sleep stage transitions differed between NT1, NT2, and o-HS. Dynamic features of sleep such as sleep instability, persistency of wake/N1, and REM fragmentation may differentiate NT1 from NT2, while N2 continuity may differentiate narcolepsy from o-HS. The results suggest that sleep transition analysis may be of clinical utility and provide insights into the underlying pathophysiology of hypersomnia and narcolepsy. Support JSPS KAKENHI (18K17891 to AK).

Consolidation enhancement: Which stages of sleep for which tasks?

2005 ◽  
Vol 28 (1) ◽  
pp. 83-84
Author(s):  
Carlyle T. Smith
Keyword(s):  
Rem Sleep ◽  
Sleep Stage ◽  
Procedural Learning ◽  
Future Research ◽  
Stage 2 Sleep

The Walker model raises a number of questions, particularly about the nature of the sleep states involved in consolidation enhancement. While REM sleep, Stage 2 sleep, and Stage 3/4 sleep have been implicated in procedural learning, we still do not understand which types of learning are involved with specific sleep states. Several possible ideas for future research are suggested.

Sleep-Related Deglutition in Children

2007 ◽  
Vol 116 (10) ◽  
pp. 747-753 ◽  
Author(s):  
Kiminori Sato ◽  
Tadashi Nakashima
Keyword(s):  
Rem Sleep ◽  
Total Sleep Time ◽  
Sleep Stage ◽  
Sleep Time ◽  
Vital Function ◽  
Stage 4 ◽  
Stage 2 Sleep ◽  
Normal Human ◽  
The Mean ◽  
Stage 1

Objectives: Clearance of the pharynx by deglutition is important in protecting the airway. The pattern of deglutition during sleep was investigated in children. Methods: Ten normal human children (8.6 ± 2.9 years) were examined via time-matched recordings of polysomnography and of surface electromyography (EMG) of the thyrohyoid and suprahyoid muscles. Results: During sleep, deglutition was episodic, and it was absent for long periods. The mean number of swallows per hour (±SD) during the total sleep time was 2.8 ± 1.7 per hour. The mean period of the longest absence of deglutition was 59.7 ± 20.3 minutes. Most deglutition occurred in association with spontaneous electroencephalographic arousal in rapid eye movement (REM) and non-REM sleep. Deglutition was related to sleep stage. The mean number of swallows per hour was 27.4 ± 27.4 during stage 1 sleep, 3.1 ± 3.5 during stage 2 sleep, 2.8 ± 3.3 during stage 3 sleep, and 0.9 ± 0.8 during stage 4 sleep. The deeper the sleep stage became, the lower the mean deglutition frequency became. The mean number of swallows per hour was 2.2 ± 2.1 during REM sleep. The EMG amplitude dropped to the lowest level of recording during REM sleep. Conclusions: Deglutition, a vital function, is infrequent during sleep in children.

Spectral and Topographic Microstructure of Brain Alpha Activity During Drowsiness at Sleep Onset and REM Sleep

2000 ◽  
Vol 14 (3) ◽  
pp. 151-158 ◽  
Author(s):  
José Luis Cantero ◽  
Mercedes Atienza
Keyword(s):  
Rem Sleep ◽  
Spectral Component ◽  
Sleep Onset ◽  
Quantitative Information ◽  
Maximum Energy ◽  
Alpha Activity ◽  
The Other ◽  
Classification Algorithms ◽  
Microstructural Properties ◽  
Brain States

Abstract High-resolution frequency methods were used to describe the spectral and topographic microstructure of human spontaneous alpha activity in the drowsiness (DR) period at sleep onset and during REM sleep. Electroencephalographic (EEG), electrooculographic (EOG), and electromyographic (EMG) measurements were obtained during sleep in 10 healthy volunteer subjects. Spectral microstructure of alpha activity during DR showed a significant maximum power with respect to REM-alpha bursts for the components in the 9.7-10.9 Hz range, whereas REM-alpha bursts reached their maximum statistical differentiation from the sleep onset alpha activity at the components between 7.8 and 8.6 Hz. Furthermore, the maximum energy over occipital regions appeared in a different spectral component in each brain activation state, namely, 10.1 Hz in drowsiness and 8.6 Hz in REM sleep. These results provide quantitative information for differentiating the drowsiness alpha activity and REM-alpha by studying their microstructural properties. On the other hand, these data suggest that the spectral microstructure of alpha activity during sleep onset and REM sleep could be a useful index to implement in automatic classification algorithms in order to improve the differentiation between the two brain states.

024 Quiescent Wakefulness: Characterising the Impact of Oxytocin on Sleep-Wake Behaviour in Male and Female Rats

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A11-A11
Author(s):  
Joel Raymond ◽  
Nicholas Everett ◽  
Anand Gururajan ◽  
Michael Bowen
Keyword(s):  
Rem Sleep ◽  
Sleep Onset ◽  
Conscious State ◽  
Positive Control ◽  
Female Rats ◽  
Male And Female ◽  
Routes Of Administration ◽  
Male And Female Rats ◽  
Competing Hypotheses ◽  
The Impact

Abstract Introduction Oxytocin is a versatile hypothalamic neuropeptide involved in diverse neurobehavioural processes. Since oxytocin can elicit anxiolytic and serenic effects, one could hypothesise that oxytocin should prime the brain for sleep and promote hypnogenesis. However, based on the social salience hypothesis—that oxytocin promotes prosocial behaviour and directs attention toward social stimuli—one could also posit that oxytocin should promote wakefulness. At present, little research has comprehensively characterised the effect of oxytocin on sleep-wake behaviour and no explanation to reconcile these two seemingly competing hypotheses has been proposed. Methods This study investigated the effects of oxytocin on sleep-wake outcomes using radiotelemetry-based polysomnography in adult male and female Wistar rats. Oxytocin was administered via the intraperitoneal (IP; 0.1, 0.3 and 1 mg/kg) and intranasal (IN; 0.06, 1, 3 mg/kg) routes. Caffeine (IP and IN; 10 mg/kg) was also administered as a wake-promoting positive control. Additionally, pre-treatment with the oxytocin receptor (OTR) antagonist L-368,899 (IP; 5 mg/kg) and vasopressin 1a receptor (V1aR) antagonist SR49059 (IP; 1 mg/kg) followed by oxytocin (IP; 1 mg/kg) was conducted to determine which receptor(s) mediated sleep-wake effects of oxytocin. Results In both male and female rats, IP oxytocin produced dose-dependent effects on sleep-wake behaviour. Specifically, oxytocin initially promoted quiescent wakefulness (a restful but conscious state) at the cost of reducing both active wakefulness and sleep. Throughout the 1.5-hour period post-administration, oxytocin delayed REM sleep onset and reduced the proportion of both NREM and REM sleep. Conversely, IN oxytocin did not significantly alter any sleep-wake parameters at any dose tested. Caffeine demonstrated wake-promoting effects under both the IP and IN routes of administration. The involvement of OTR and V1aR binding in oxytocin-induced effects on sleep-wake outcomes will be discussed. Conclusion These findings appear to reconcile the two competing hypotheses: in rats, IP oxytocin appears to promote a state of quiescent wakefulness—one of calm and rest, but also of conscious responsivity to environmental stimuli. IN oxytocin demonstrated little to no effect on sleep-wake behaviour, which is a crucial finding given the escalating use of IN oxytocin as a therapeutic for conditions with comorbid disordered sleep. Support (if any) None.

Ambient temperature-dependent thermoregulatory role of REM sleep

2012 ◽  
Vol 37 (5) ◽  
pp. 392-396
Author(s):  
Deependra Kumar ◽  
Velayudhan Mohan Kumar ◽  
Hruda Nanda Mallick
Keyword(s):  
Ambient Temperature ◽  
Rem Sleep ◽  
Temperature Dependent

Sleep-stage sequencing of sleep-onset REM periods in MSLT predicts treatment response in patients with narcolepsy

2015 ◽  
Vol 25 (2) ◽  
pp. 203-210 ◽  
Author(s):  
Panagis Drakatos ◽  
Kishankumar Patel ◽  
Chiraag Thakrar ◽  
Adrian J. Williams ◽  
Brian D. Kent ◽  
...  
Keyword(s):  
Treatment Response ◽  
Sleep Stage ◽  
Sleep Onset

Sleep Stage Assessment Using Power Spectral Indices of Heart Rate Variability With a Simple Algorithm

2012 ◽  
Vol 15 (3) ◽  
pp. 264-272 ◽  
Author(s):  
Keiko Tanida ◽  
Masashi Shibata ◽  
Margaret M. Heitkemper
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Sleep Stage ◽  
Sleep Onset ◽  
Low Frequency ◽  
Simple Algorithm ◽  
Sleep Stages ◽  
Spectral Indices ◽  
Current Form ◽  
Power Spectral

Clinical researchers do not typically assess sleep with polysomnography (PSG) but rather with observation. However, methods relying on observation have limited reliability and are not suitable for assessing sleep depth and cycles. The purpose of this methodological study was to compare a sleep analysis method based on power spectral indices of heart rate variability (HRV) data to PSG. PSG and electrocardiography data were collected synchronously from 10 healthy women (ages 20–61 years) over 23 nights in a laboratory setting. HRV was analyzed for each 60-s epoch and calculated at 3 frequency band powers (very low frequency [VLF]-hi: 0.016–0.04 Hz; low frequency [LF]: 0.04–0.15 Hz; and high frequency [HF]: 0.15–0.4 Hz). Using HF/(VLF-hi + LF + HF) value, VLF-hi, and heart rate (HR) as indices, an algorithm to categorize sleep into 3 states (shallow sleep corresponding to Stages 1 & 2, deep sleep corresponding to Stages 3 & 4, and rapid eye movement [REM] sleep) was created. Movement epochs and time of sleep onset and wake-up were determined using VLF-hi and HR. The minute-by-minute agreement rate with the sleep stages as identified by PSG and HRV data ranged from 32 to 72% with an average of 56%. Longer wake after sleep onset (WASO) resulted in lower agreement rates. The mean differences between the 2 methods were 2 min for the time of sleep onset and 6 min for the time of wake-up. These results indicate that distinguishing WASO from shallow sleep segments is difficult using this HRV method. The algorithm's usefulness is thus limited in its current form, and it requires additional modification.

Dysthymic Disorder and Rheumatic Pain Modulation Disorder (Fibrositis Syndrome): A Comparison of Symptoms and Sleep Physiology

1986 ◽  
Vol 31 (7) ◽  
pp. 608-616 ◽  
Author(s):  
Madhulika A. Gupta ◽  
Harvey Moldofsky
Keyword(s):  
Rem Sleep ◽  
Sleep Onset ◽  
High Amplitude ◽  
Depressive Illness ◽  
Pain Modulation ◽  
Dysthymic Disorder ◽  
Systematic Evaluation ◽  
Onset Latency ◽  
Rheumatic Pain ◽  
Sleep Physiology

It has been suggested that “fibrositis” or rheumatic pain modulation disorder (RPMD) is a varient of depressive illness. Both disorders are associated with abnormalities in sleep physiology. Since the clinical features of RPMD do not meet all the criteria for a major depressive disorder, the symptoms and sleep phsyiology in subjects with dysthmic disorder (DSM III criteria) (N = 6), and RMPD (N = 6) were compared, in order to determine the similarity between the two groups. The sleep physiology in dysthymic disorder was first examined over three consecutive nights since a systematic evaluation of the sleep physiology in this group of disorders has not yet been reported. All dysthymic patients showed episodic bursts of high-amplitude (75–150 microvolts) theta (3–5 Hz) bursts in stage 2 sleep, and REM onset latency was abbreviated only on night 2. The theta bursts have not been previously reported, and may be an early marker of disorganization of non-REM sleep in the dysthymic subjects. The comparison of the two groups revealed that RPMD subjects reported more pre- and post-sleep pain (p < 0.01), lighter sleep (p < 0.01), and more physical ailments during sleep (p < 0.01), and had more alpha (7–11.5 Hz) in non-REM sleep (p < 0.01). The dysthymic subjects who reported deeper sleep (p < 0.01), had a greater sleep continuity disturbance with longer stage 2 onset latency (p < 0.05), fewer hours of sleep (p < 0.05), more wakefulness after sleep onset (p < 0.05), more awakenings per hour of sleep (p < 0.01) and more stage changes per hour of sleep (p < 0.01), and showed theta bursts in stage 2 (p < 0.01). The distinctive symptoms and sleep physiologies in the two groups suggest that the two disorders are not related.

Effects of topical anesthesia on upper airway resistance during wake-sleep transitions

2005 ◽  
Vol 99 (2) ◽  
pp. 549-555 ◽  
Author(s):  
Liam S. Doherty ◽  
Philip Nolan ◽  
Walter T. McNicholas
Keyword(s):  
Sleep Onset ◽  
Upper Airway ◽  
Significant Rise ◽  
Topical Anesthesia ◽  
Reflex Response ◽  
Stage 2 Sleep ◽  
Normal Humans ◽  
Stage 1 ◽  
Sleep Transition ◽  
Stable Stage

Deformation of the upper airway (UA) by negative transmural pressure alters the activity of UA mechanoreceptors, causing a reflex increase in UA muscle activity. Topical anesthesia of the UA mucosa, which greatly reduces this reflex response, causes an increase in UA resistance during stage 2 sleep. We hypothesized that topical anesthesia of the UA mucosa would predispose to UA instability at sleep onset and, therefore, examined the effect of UA anesthesia on pharyngeal resistance (Rph) in stage 1 sleep. Eleven normal, healthy volunteers were instrumented to record standard polysomnographic variables, respiratory airflow, and UA pressure at the nasal choanae and the epiglottis. Subjects were permitted to sleep until stable stage 2 sleep was reached and were then awoken. This procedure was repeated three times to obtain reproducible wake-sleep transitions. The UA mucosa was then anesthetized with 10% lidocaine to the oropharynx and laryngopharynx, and the pharyngeal mechanics were studied during the subsequent wake-sleep transition. Three subjects were excluded because of failure to resume sleep postanesthesia. Rph was significantly higher after anesthesia during stage 1 sleep [2.88 ± 0.77 cmH2O·l−1·s (mean ± SE)] compared with control (0.95 ± 0.35 cmH2O·l−1·s; P < 0.05), but there was no difference during wakefulness. Furthermore, there was a significant rise in Rph at wake-to-sleep transitions and a significant fall in Rph at sleep-to-wake transitions after anesthesia ( P < 0.05) but not in the control condition. We conclude that sensory receptors in the UA mucosa contribute to the maintenance of UA patency at wake-sleep transition in normal humans.

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