Ventilation during early and late rapid-eye-movement sleep in normal humans

1991 ◽  
Vol 71 (4) ◽  
pp. 1201-1215 ◽  
Author(s):  
J. B. Neilly ◽  
E. A. Gaipa ◽  
G. Maislin ◽  
A. I. Pack
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Respiratory Frequency ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Rib Cage ◽  
Ventilatory Parameters ◽  
Normal Humans

Because successive rapid-eye-movement (REM) sleep periods in the night are longer in duration and have more phasic events, ventilation during late REM sleep might be more affected than in earlier episodes. Despite the increase in eye movement density (EMD) in late REM sleep, average minute ventilation was, however, not reduced compared with that in early REM sleep. Decreases in rib cage motion (mean inspiratory flow of the rib cage) in association with increasing EMD were offset by increments in respiratory frequency. Apart from expiratory time, there were no significant changes in the slopes of the relationships between EMD and specific ventilatory components, from early to late REM sleep periods. However, there was an increase in the number of episodes when ventilation was reduced during late REM sleep. Changes in ventilatory pattern during late REM sleep are due to changes in the underlying nature of REM sleep. The ventilatory response during eye movements is, however, subject specific. Some subjects exhibit large decrements in mean inspiratory flow of the rib cage and increments in respiratory frequency during bursts of eye movement, whereas other individuals demonstrate only small changes in these ventilatory parameters.

Occlusion pressure and ventilation during sleep in normal humans

1986 ◽  
Vol 61 (4) ◽  
pp. 1279-1287 ◽  
Author(s):  
D. P. White
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Nrem Sleep ◽  
Respiratory Drive ◽  
Rapid Eye Movement ◽  
System Sensitivity ◽  
Hypercapnic Ventilatory Response ◽  
Normal Humans

Previous investigation in normal humans has demonstrated reduced ventilation and ventilatory responses to chemical stimuli during sleep. Most have interpreted this to be a product of decreasing central nervous system sensitivity to the normal stimuli that maintain ventilation, whereas other factors such as increasing airflow resistance could also contribute to this reduction in respiration. To improve our understanding of these events, we measured ventilation and occlusion pressures (P0.1) during unstimulated ventilation and rebreathing-induced hypercapnia during wakefulness and non-rapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep. Eighteen subjects (10 males and 8 females) of whom seven were snorers (5 males and 2 females) were studied. Ventilation was reduced during both NREM and REM sleep (P less than 0.05), but this decrement in minute ventilation tended to be greater in snorers than nonsnorers. Unstimulated P0.1, on the other hand, was maintained or increased during sleep in all groups studied, with males and snorers showing the largest increase. The hypercapnic ventilatory response fell during both NREM and REM sleep and tended to be lower during REM than NREM sleep. However, the P0.1 response to hypercapnia during NREM sleep was well maintained at the waking level although the REM response was statistically reduced. These studies suggest that the mechanism of the reduction in ventilation and the hypercapnic ventilatory response seen during sleep, particularly NREM sleep, is likely to be multifactorial and not totally a product of decreasing central respiratory drive.

Mechanics of the respiratory system and breathing pattern during sleep in normal humans

1984 ◽  
Vol 56 (1) ◽  
pp. 133-137 ◽  
Author(s):  
D. W. Hudgel ◽  
R. J. Martin ◽  
B. Johnson ◽  
P. Hill
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Transpulmonary Pressure ◽  
Dynamic Compliance ◽  
Face Mask ◽  
Esophageal Pressure ◽  
Rapid Eye Movement ◽  
Airflow Resistance

The purposes of this investigation were to describe the changes in 1) dynamic compliance of the lungs, 2) airflow resistance, and 3) breathing pattern that occur during sleep in normal adult humans. Six subjects wore a tightly fitting face mask. Flow and volume were obtained from a pneumotachograph attached to the face mask. Transpulmonary pressure was calculated as the difference between esophageal pressure obtained with a balloon and mask pressure. At least 20 consecutive breaths were analyzed for dynamic compliance, airflow resistance, and breathing pattern during wakefulness, non-rapid-eye-movement stage 2 and rapid-eye-movement (REM) sleep. Dynamic compliance did not change significantly. Airflow resistance increased during sleep; resistance was 3.93 +/- 0.56 cmH2O X 1–1 X s during wakefulness, 7.96 +/- 0.95 in stage 2 sleep, and 8.66 +/- 1.43 in REM sleep (P less than 0.02). By placing a catheter in the retroepiglottic space and thus dividing the airway into upper and lower zones, we found the increase in resistance occurred almost entirely above the larynx. Decreases in tidal volume, minute ventilation, and mean inspiratory flow observed during sleep were not statistically significant.

GABAergic Regulation of REM Sleep in Reticularis Pontis Oralis and Caudalis in Rats

2003 ◽  
Vol 90 (2) ◽  
pp. 938-945 ◽  
Author(s):  
Larry D. Sanford ◽  
Xiangdong Tang ◽  
Jihua Xiao ◽  
Richard J. Ross ◽  
Adrian R. Morrison
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Escape Behavior ◽  
Aminobutyric Acid ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sprague Dawley ◽  
Site Specific ◽  
Guide Cannulae ◽  
Nucleus Reticularis

The nucleus reticularis pontis oralis (RPO) and nucleus reticularis pontis caudalis (RPC) are implicated in the generation of rapid eye movement sleep (REM). Work in cats has indicated that GABA in RPO plays a role in the regulation of REM. We assessed REM after local microinjections into RPO and RPC of the γ-aminobutyric acid-A (GABAA) agonist, muscimol (MUS), and the GABAA antagonist, bicuculline (BIC). Rats (90-day-old male Sprague-Dawley) were implanted with electrodes for recording electroencephalographs (EEG) and electromyographs (EMG). Guide cannulae were aimed into RPO ( n = 9) and RPC ( n = 8) for microinjecting MUS (200, 1,000.0 μM) and BIC (0.056, 0.333, 1.0, 1,000.0, and 10,000.0 μM). Animals received bilateral microinjections of saline, MUS, and BIC (0.2 μl microinjected at 0.1 μl/min) into each region followed by 6-h sleep recordings. In RPO, MUS (1,000.0 μM) suppressed REM and BIC (1,000.0 μM) enhanced REM. In RPC, MUS (200, 1,000.0 μM) suppressed REM, but BIC (1,000.0 μM and less) did not significantly affect REM. Higher concentrations of BIC (10,000.0 μM) injected into RPO ( n = 9) and RPC ( n = 4) produced wakefulness and escape behavior. The results indicate that GABA in RPO/RPC is involved in the regulation of REM and suggest site-specific differences in this regulation.

Respiratory and cardiovascular responses to increased and decreased carotid sinus pressure in sleeping dogs

1995 ◽  
Vol 78 (5) ◽  
pp. 1688-1698 ◽  
Author(s):  
K. W. Saupe ◽  
C. A. Smith ◽  
K. S. Henderson ◽  
J. A. Dempsey
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Eye Movement ◽  
Carotid Sinus ◽  
Minute Ventilation ◽  
Control Level ◽  
Cardiovascular Responses ◽  
Systemic Blood Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

The purpose of this study was to determine the effects of changing blood pressure in the carotid sinus (Pcs) on ventilatory output during wakefulness and non-rapid-eye-movement sleep in unanesthetized dogs. Eight dogs were chronically instrumented so that ventilation, heart rate, and blood pressure could be measured while pressure in the isolated carotid sinus was rapidly changed by means of an extracorporeal perfusion circuit. Raising Pcs 35–75 mmHg consistently reduced ventilation 15–40% in a dose-response fashion, with little or no further diminution in minute ventilation as Pcs was further increased > 75 mmHg above control level. This decrease in minute ventilation was immediate, due primarily to a decrease in tidal volume, and was sustained over the 20-s period of elevated Pcs. Increases in Pcs also caused immediate sustained reductions in systemic blood pressure and heart rate, both of which also fell in a dose-dependent fashion. The ventilatory and systemic cardiovascular responses to increased Pcs were the same during wakefulness and non-rapid-eye-movement sleep. Decreasing Pcs 40–80 mmHg caused a sudden carotid chemoreceptor-mediated hyperpnea that was eliminated by hyperoxia. We conclude that increasing Pcs causes a reflex inhibition of ventilation and that this reflex may play a role in sleep-disordered breathing.

Metabolic rate and breathing during sleep

1985 ◽  
Vol 59 (2) ◽  
pp. 384-391 ◽  
Author(s):  
D. P. White ◽  
J. V. Weil ◽  
C. W. Zwillich
Keyword(s):  
Metabolic Rate ◽  
Eye Movement ◽  
Sleep Stage ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Normal Subjects ◽  
Co2 Production ◽  
Sleep Stages ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

Recent investigation suggests that both ventilation (VE) and the chemical sensitivity of the respiratory control system correlate closely with measures of metabolic rate [O2 consumption (VO2) and CO2 production (VCO2)]. However, these associations have not been carefully investigated during sleep, and what little information is available suggests a deterioration of the relationships. As a result we measured VE, ventilatory pattern, VO2, and VCO2 during sleep in 21 normal subjects (11 males and 10 females) between the ages of 21 and 77 yr. When compared with values for awake subjects, expired ventilation decreased 8.2 +/- 2.3% (SE) during sleep and was associated with a 8.5 +/- 1.6% decrement in VO2 and a 12.3 +/- 1.7% reduction in VCO2, all P less than 0.01. The decrease in ventilation was a product primarily of a significant decrease in tidal volume with little change in frequency. None of these findings were dependent on sleep stage with results in rapid-eye-movement (REM) and non-rapid-eye-movement sleep being similar. Through all sleep stages ventilation remained tightly correlated with VO2 and VCO2 both within a given individual and between subjects. Although respiratory rhythmicity was somewhat variable during REM sleep, minute ventilation continued to correlate with VO2 and VCO2. None of the parameters described above were influenced by age or gender, with male and female subjects demonstrating similar findings. Ten of the subjects demonstrated at least occasional apneas. These individuals, however, were not found to differ from those without apnea in any other measure of ventilation or metabolic rate.

Partitioning of inhaled ventilation between the nasal and oral routes during sleep in normal subjects

2003 ◽  
Vol 94 (3) ◽  
pp. 883-890 ◽  
Author(s):  
Michael F. Fitzpatrick ◽  
Helen S. Driver ◽  
Neela Chatha ◽  
Nha Voduc ◽  
Alison M. Girard
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Sleep Stage ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Sleep Stages ◽  
Rapid Eye Movement ◽  
Nasal Mask ◽  
Rapid Eye Movement Sleep ◽  
Significant Difference

The oral and nasal contributions to inhaled ventilation were simultaneously quantified during sleep in 10 healthy subjects (5 men, 5 women) aged 43 ± 5 yr, with normal nasal resistance (mean 2.0 ± 0.3 cmH2O · l−1 · s−1) by use of a divided oral and nasal mask. Minute ventilation awake (5.9 ± 0.3 l/min) was higher than that during sleep (5.2 ± 0.3 l/min; P < 0.0001), but there was no significant difference in minute ventilation between different sleep stages ( P = 0.44): stage 2 5.3 ± 0.3, slow-wave 5.2 ± 0.2, and rapid-eye-movement sleep 5.2 ± 0.2 l/min. The oral fraction of inhaled ventilation during wakefulness (7.6 ± 4%) was not significantly different from that during sleep (4.3 ± 2%; mean difference 3.3%, 95% confidence interval −2.1–8.8%, P = 0.19), and no significant difference ( P = 0.14) in oral fraction was observed between different sleep stages: stage two 5.1 ± 2.8, slow-wave 4.2 ± 1.8, rapid-eye-movement 3.1 ± 1.7%. Thus the inhaled oral fraction in normal subjects is small and does not change significantly with sleep stage.

scholarly journals MATHEMATICAL PHASE MODEL OF NEURAL POPULATIONS INTERACTION IN MODULATION OF REM/NREM SLEEP

2016 ◽  
Vol 21 (6) ◽  
pp. 794-810 ◽  
Author(s):  
Paolo Acquistapace ◽  
Anna P. Candeloro ◽  
Vladimir Georgiev ◽  
Maria L. Manca
Keyword(s):  
Experimental Data ◽  
Eye Movement ◽  
Rem Sleep ◽  
Reaction Diffusion ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Neuronal Populations ◽  
Neural Populations ◽  
Cyclic Oscillation

Aim of the present study is to compare the synchronization of the classical Kuramoto system and the reaction - diffusion space time Landau - Ginzburg model, in order to describe the alternation of REM (rapid eye movement) and NREM (non-rapid eye movement) sleep across the night. These types of sleep are considered as produced by the cyclic oscillation of two neuronal populations that, alternatively, promote and inhibit the REM sleep. Even if experimental data will be necessary, a possible interpretation of the results has been proposed.

scholarly journals Rapid Eye Movement Sleep Debt Accrues in Mice Exposed to Volatile Anesthetics

2011 ◽  
Vol 115 (4) ◽  
pp. 702-712 ◽  
Author(s):  
Jeremy Pick ◽  
Yihan Chen ◽  
Jason T. Moore ◽  
Yi Sun ◽  
Abraham J. Wyner ◽  
...  
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Volatile Anesthetics ◽  
Dark Phase ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Oxygen Control ◽  
Dark Cycle ◽  
Sleep Debt ◽  
Anesthetic Exposure

Background General anesthesia has been likened to a state in which anesthetized subjects are locked out of access to both rapid eye movement (REM) sleep and wakefulness. Were this true for all anesthetics, a significant REM rebound after anesthetic exposure might be expected. However, for the intravenous anesthetic propofol, studies demonstrate that no sleep debt accrues. Moreover, preexisting sleep debts dissipate during propofol anesthesia. To determine whether these effects are specific to propofol or are typical of volatile anesthetics, the authors tested the hypothesis that REM sleep debt would accrue in rodents anesthetized with volatile anesthetics. Methods Electroencephalographic and electromyographic electrodes were implanted in 10 mice. After 9-11 days of recovery and habituation to a 12 h:12 h light-dark cycle, baseline states of wakefulness, nonrapid eye movement sleep, and REM sleep were recorded in mice exposed to 6 h of an oxygen control and on separate days to 6 h of isoflurane, sevoflurane, or halothane in oxygen. All exposures were conducted at the onset of light. Results Mice in all three anesthetized groups exhibited a significant doubling of REM sleep during the first 6 h of the dark phase of the circadian schedule, whereas only mice exposed to halothane displayed a significant increase in nonrapid eye movement sleep that peaked at 152% of baseline. Conclusion REM sleep rebound after exposure to volatile anesthetics suggests that these volatile anesthetics do not fully substitute for natural sleep. This result contrasts with the published actions of propofol for which no REM sleep rebound occurred.

scholarly journals Regulation of REM Sleep by Inhibitory Neurons in the Dorsomedial Medulla

2020 ◽  
Author(s):  
Joseph A. Stucynski ◽  
Amanda L. Schott ◽  
Justin Baik ◽  
Shinjae Chung ◽  
Franz Weber
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Gabaergic Neurons ◽  
Inhibitory Neurons ◽  
Sleep Stages ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Brain Rhythms ◽  
Slow Activity ◽  
Raphé Nuclei

ABSTRACTThe two major stages of mammalian sleep – rapid eye movement sleep (REMs) and non-REM sleep (NREMs) – are characterized by distinct brain rhythms ranging from millisecond to minute-long (infraslow) oscillations. The mechanisms controlling transitions between sleep stages and how they are synchronized with infraslow rhythms remain poorly understood. Using opto- and chemogenetic manipulation, we show that GABAergic neurons in the dorsomedial medulla (dmM) promote the initiation and maintenance of REMs, in part through their projections to the dorsal and median raphe nuclei. Fiber photometry revealed that dmM GABAergic neurons are strongly activated during REMs. During NREMs, their activity fluctuated in close synchrony with infraslow oscillations in the spindle band of the electroencephalogram, and the phase of this rhythm modulated the latency of optogenetically induced REMs episodes. Thus, dmM inhibitory neurons powerfully promote REMs, and their slow activity fluctuations may coordinate transitions from NREMs to REMs with infraslow brain rhythms.

scholarly journals REM sleep: unique associations with behavior, corticosterone regulation and apoptotic pathways in chronic stress in mice

2018 ◽  
Author(s):  
Mathieu Nollet ◽  
Harriet Hicks ◽  
Andrew P. McCarthy ◽  
Huihai Wu ◽  
Carla S. Möller-Levet ◽  
...  
Keyword(s):  
Machine Learning ◽  
Eye Movement ◽  
Chronic Stress ◽  
Rem Sleep ◽  
Chronic Mild Stress ◽  
Specific Aspect ◽  
Mild Stress ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Apoptotic Pathways

AbstractOne of sleep’s putative functions is mediation of adaptation to waking experiences. Chronic stress is a common waking experience, however, which specific aspect of sleep is most responsive, and how sleep changes relate to behavioral disturbances and molecular correlates remain unknown. We quantified sleep, physical, endocrine and behavioral variables and the brain and blood transcriptome in mice exposed to nine weeks of unpredictable chronic mild stress (UCMS). Comparing 46 phenotypical variables revealed that rapid-eye-movement sleep (REMS), corticosterone regulation and coat state were most responsive to UCMS. REMS theta oscillations were enhanced whereas delta oscillations in non-REMS were unaffected. Transcripts affected by UCMS in the prefrontal cortex, hippocampus, hypothalamus and blood were associated with inflammatory and immune responses. A machine learning approach controlling for unspecific UCMS effects identified transcriptomic predictors for specific phenotypes and their overlap. Transcriptomic predictor sets for the inter-individual variation in REMS continuity and theta activity shared many pathways with corticosterone regulation and in particular pathways implicated in apoptosis, including mitochondrial pathways. Predictor sets for REMS and anhedonia, one of the behavioral changes following UCMS, shared pathways involved in oxidative stress, cell proliferation and apoptosis. RNA predictor sets for non-NREMS parameters showed no overlap with other phenotypes. These novel data identify REMS as a core and early element of the response to chronic stress, and identify apoptotic pathways as a putative mechanism by which REMS mediates adaptation to stressful waking experiences.Significance StatementSleep is responsive to experiences during wakefulness and is altered in stress-related disorders. Whether sleep changes primarily concern rapid-eye-movement sleep (REMS) or non-REM sleep, and how they correlate with stress hormones, behavioral and transcriptomic responses remained unknown. We demonstrate using unpredictable chronic (9-weeks) mild stress that REMS is the most responsive of all the measured sleep characteristics, and correlates with deficiency in corticosterone regulation. An unbiased machine learning, controlling for unspecific effects of stress, revealed that REMS correlated with RNA predictor sets enriched in apoptosis including mitochondrial pathways. Several pathways were shared with predictors of corticosterone and behavioral responses. This unbiased approach point to apoptosis as a molecular mechanism by which REMS mediates adaptation to an ecologically relevant waking experience.

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