Development of CO2 sensitivity: effects of gestational age, postnatal age, and sleep state

1981 ◽  
Vol 50 (5) ◽  
pp. 956-961 ◽  
Author(s):  
R. D. Guthrie ◽  
T. A. Standaert ◽  
W. A. Hodson ◽  
D. E. Woodrum

To determine the independent effects of sleep state, gestational age, and postnatal age on eucapnic ventilation and steady-state CO2 sensitivity, nine premature (146 +/- 3 days) and eight full-term (168 +/- 2 days) monkeys, Macaca nemestrina, from accurately timed conceptions were studied serially over the first 3 wk of life. Minute volume (VE)/kg,tidal volume (VT)/kg, and respiratory frequency were quantitated during rapid-eye-movement sleep (REM) and nonrapid-eye-movement sleep (NREM)in room air and when animals were breathing varied concentrations of cO2 in 21% O2. Eucapnic VE/kg and CO2 sensitivity [(deltaVE/kg)/delta PaCO2] increased progressively with advancing postnatal age during NREM sleep in grouped term and premature animals. CO2 sensitivity was not significantly different between REM and NREM sleep except in full-term animals at the highest postconceptual age studied (189 +/- 2 days) when [(delta VE/kg)/delta PaCO2] was lower in REM sleep than in NREM sleep (209 +/- 54 vs. 301 +/- 71 ml.min-1.kg-1.Torr-1; P less than 0.05, paired-t test). Gestational age had no measurable effect on eucapnic ventilation or CO2 sensitivity. These results support the hypothesis that REM sleep-induced depression of CO2 sensitivity develops in the neonatal monkey with advancing postconceptual age.

1980 ◽  
Vol 48 (2) ◽  
pp. 347-354 ◽  
Author(s):  
R. D. Guthrie ◽  
T. A. Standaert ◽  
W. A. Hodson ◽  
D. E. Woodrum

The effects of sleep state and postnatal maturation on steady-state CO2 sensitivity, "inspiratory drive" (VT/TI), and the inspiratory "duty cycle" (TI/Ttot) were examined in nine unanesthetized premature Macaca nemestrina in the first 3 wk of life. Minute volume (VE) in room air was less in NREM sleep than in the awake state but there were no differences in VE, VT/TI, or TI/Ttot between REM and NREM sleep. VE and VT/TI corrected for body weight increased in REM and NREM sleep with postnatal maturation whereas TI/Ttot did not vary. Concomitant with this increase in room air VE and VT/TI, an increase in CO2 sensitivity (delta V/delta Paco2) with postnatal maturation was documented in NREM sleep. CO2 sensitivity was similar between REM and NREM states at each postnatal age. The increase in VE following inhalation of 2-5% CO2 was mediated by an increase in VT/TI, whereas TI/Ttot remained constant. The differences in the effect of sleep on CO2 sensitivity between neonates and adults are discussed and possible mechanisms for the observed developmental increase in CO2 sensitivity are proposed.


1981 ◽  
Vol 51 (3) ◽  
pp. 557-564 ◽  
Author(s):  
E. Tabachnik ◽  
N. L. Muller ◽  
A. C. Bryan ◽  
H. Levison

The effect of sleep state on ventilation and the mechanics of breathing was studied in nine normal adolescents by use of a respiratory inductive plethysmograph and surface electromyogram electrodes. Minute ventilation was state dependent (P less than 0.01), decreasing by a mean of 8% from wakefulness to nonrapid-eye-movement (NREM) sleep and increasing 4% from NREM to rapid-eye-movement (REM) sleep. These changes were caused by changes in respiratory rate. Tidal volume (VT) was not affected by sleep state (P greater than 0.10). The pattern of breathing during wakefulness was similar to that of REM sleep. During NREM sleep intercostal and diaphragmatic muscle activity increased by a mean of 34% and 11%, respectively, as compared with wakefulness, indicating an increase in the respiratory work load. This was accompanied by a substantial increase in rib cage contribution to VT. REM sleep was associated with a marked decrease in intercostal muscle activity (P less than 0.05) and a diminished rib cage contribution; VT was maintained due to a mean increase of 34% in diaphragmatic muscle activity (P less than 0.05).


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Mojtaba Bandarabadi ◽  
Carolina Gutierrez Herrera ◽  
Thomas C. Gent ◽  
Claudio Bassetti ◽  
Kaspar Schindler ◽  
...  

Abstract Sleep spindle generation classically relies on an interplay between the thalamic reticular nucleus (TRN), thalamo-cortical (TC) relay cells and cortico-thalamic (CT) feedback during non-rapid eye movement (NREM) sleep. Spindles are hypothesized to stabilize sleep, gate sensory processing and consolidate memory. However, the contribution of non-sensory thalamic nuclei in spindle generation and the role of spindles in sleep-state regulation remain unclear. Using multisite thalamic and cortical LFP/unit recordings in freely behaving mice, we show that spike-field coupling within centromedial and anterodorsal (AD) thalamic nuclei is as strong as for TRN during detected spindles. We found that spindle rate significantly increases before the onset of rapid eye movement (REM) sleep, but not wakefulness. The latter observation is consistent with our finding that enhancing spontaneous activity of TRN cells or TRN-AD projections using optogenetics increase spindle rate and transitions to REM sleep. Together, our results extend the classical TRN-TC-CT spindle pathway to include non-sensory thalamic nuclei and implicate spindles in the onset of REM sleep.


2001 ◽  
Vol 91 (1) ◽  
pp. 239-248 ◽  
Author(s):  
James A. Rowley ◽  
Carrie S. Sanders ◽  
Brian R. Zahn ◽  
M. Safwan Badr

It has been proposed that the upper airway compliance should be highest during rapid eye movement (REM) sleep. Evidence suggests that the increased compliance is secondary to an increased retroglossal compliance. To test this hypothesis, we examined the effect of sleep stage on the relationship of retroglossal cross-sectional area (CSA; visualized with a fiber-optic scope) to pharyngeal pressure measured at the level of the oropharynx during eupneic breathing in subjects without significant sleep-disordered breathing. Breaths during REM sleep were divided into phasic (associated with eye movement, PREM) and tonic (not associated with eye movements, TREM). Retroglossal CSA decreased with non-REM (NREM) sleep and decreased further in PREM [wake 156.8 ± 48.6 mm2, NREM 104.6 ± 65.0 mm2( P < 0.05 wake vs. NREM), TREM 83.1 ± 46.4 mm2 ( P = not significant NREM vs. TREM), PREM 73.9 + 39.2 mm2 ( P < 0.05 TREM vs. PREM)]. Retroglossal compliance, defined as the slope of the regression CSA vs. pharyngeal pressure, was the same between all four conditions (wake −0.7 + 2.1 mm2/cmH2O, NREM 0.6 ± 3.0 mm2/cmH2O, TREM −0.2 ± 3.3 mm2/cmH2O, PREM −0.6 ± 5.1 mm2/cmH2O, P = not significant). We conclude that the intrinsic properties of the airway wall determine retroglossal compliance independent of changes in the neuromuscular activity associated with changes in sleep state.


1976 ◽  
Vol 40 (5) ◽  
pp. 688-693 ◽  
Author(s):  
E. A. Phillipson ◽  
E. Murphy ◽  
L. F. Kozar

We have examined the respiratory changes that occur during physiological sleep in three dogs with exteriorized cervical vagal loops. Sleep stage was determined by behavioral and EEG criteria. During non-REM (NREM) sleep breathing was slower (mean change, 23%),deeper (mean change, 18%), and less variable (coefficients of variation, 0.05–0.10) than during wakefulness (W); minute volume of ventilation (Ve) decreased (mean change, 14%) and alveolar CO2 pressure (PAco2) increased slightly (mean change, 1.3 mmHg). In addition, the rate of O2 consumption and ventilatory response to hypercapnia were decreased. In contrast, REM sleep was characterized by rapid, shallow, and considerably more irregular (coefficients of variation, 0.18–0.30) breathing; Ve increased markedly and PAco2 decreased (mean change, 5.2 mmHg). Blockade of both cervical vagus nerves produced comparable changes in each stage of sleep (W, NREM, REM): breathing became slower and deeper, but the differences between stages and the marked irregularity in REM sleep persisted. In contrast, the Hering-Breuer inflation reflex (HBIR) was strong in W and NREM sleep, but weak in REM sleep. The results indicate that changes in respiratory control and stability during sleep are not due to fluctuations in vagal influence despite the fact that one vagal reflex (HBIR) was sleep-state dependent.


2010 ◽  
Vol 298 (1) ◽  
pp. R34-R42 ◽  
Author(s):  
Takafumi Kato ◽  
Yuji Masuda ◽  
Hayato Kanayama ◽  
Norimasa Nakamura ◽  
Atsushi Yoshida ◽  
...  

Exaggerated jaw motor activities during sleep are associated with muscle symptoms in the jaw-closing rather than the jaw-opening muscles. The intrinsic activity of antagonistic jaw muscles during sleep remains unknown. This study aims to assess the balance of muscle activity between masseter (MA) and digastric (DG) muscles during sleep in guinea pigs. Electroencephalogram (EEG), electroocculogram, and electromyograms (EMGs) of dorsal neck, MA, and DG muscles were recorded with video during sleep-wake cycles. These variables were quantified for each 10-s epoch. The magnitude of muscle activity during sleep in relation to mean EMG activity of total wakefulness was up to three times higher for MA muscle than for DG muscle for nonrapid eye movement (NREM) and rapid-eye-movement (REM) sleep. Although the activity level of the two jaw muscles fluctuated during sleep, the ratio of activity level for each epoch was not proportional. Epochs with a high activity level for each muscle were associated with a decrease in δEEG power and/or an increase in heart rate in NREM sleep. However, this association with heart rate and activity levels was not observed in REM sleep. These results suggest that in guinea pigs, the magnitude of muscle activity for antagonistic jaw muscles is heterogeneously modulated during sleep, characterized by a high activity level in the jaw-closing muscle. Fluctuations in the activity are influenced by transient arousal levels in NREM sleep but, in REM sleep, the distinct controls may contribute to the fluctuation. The above intrinsic characteristics could underlie the exaggeration of jaw motor activities during sleep (e.g., sleep bruxism).


2015 ◽  
Author(s):  
Sudhansu Chokroverty

Recent research has generated an enormous fund of knowledge about the neurobiology of sleep and wakefulness. Sleeping and waking brain circuits can now be studied by sophisticated neuroimaging techniques that map different areas of the brain during different sleep states and stages. Although the exact biologic functions of sleep are not known, sleep is essential, and sleep deprivation leads to impaired attention and decreased performance. Sleep is also believed to have restorative, conservative, adaptive, thermoregulatory, and consolidative functions. This review discusses the physiology of sleep, including its two independent states, rapid eye movement (REM) and non–rapid eye movement (NREM) sleep, as well as functional neuroanatomy, physiologic changes during sleep, and circadian rhythms. The classification and diagnosis of sleep disorders are discussed generally. The diagnosis and treatment of the following disorders are described: obstructive sleep apnea syndrome, narcolepsy-cataplexy sydrome, idiopathic hypersomnia, restless legs syndrome (RLS) and periodic limb movements in sleep, circadian rhythm sleep disorders, insomnias, nocturnal frontal lobe epilepsy, and parasomnias. Sleep-related movement disorders and the relationship between sleep and psychiatric disorders are also discussed. Tables describe behavioral and physiologic characteristics of states of awareness, the international classification of sleep disorders, common sleep complaints, comorbid insomnia disorders, causes of excessive daytime somnolence, laboratory tests to assess sleep disorders, essential diagnostic criteria for RLS and Willis-Ekbom disease, and drug therapy for insomnia. Figures include polysomnographic recording showing wakefulness in an adult; stage 1, 2, and 3 NREM sleep in an adult; REM sleep in an adult; a patient with sleep apnea syndrome; a patient with Cheyne-Stokes breathing; a patient with RLS; and a patient with dream-enacting behavior; schematic sagittal section of the brainstem of the cat; schematic diagram of the McCarley-Hobson model of REM sleep mechanism; the Lu-Saper “flip-flop” model; the Luppi model to explain REM sleep mechanism; and a wrist actigraph from a man with bipolar disorder. This review contains 14 highly rendered figures, 8 tables, 115 references, and 5 MCQs.


1984 ◽  
Vol 57 (4) ◽  
pp. 1089-1096 ◽  
Author(s):  
A. D. Berssenbrugge ◽  
J. A. Dempsey ◽  
J. B. Skatrud

We assessed the influence of sleep state on ventilatory acclimatization to hypoxia. Ventilation, arterial O2 saturation (SaO2), and arterial acid-base status were monitored in healthy adult males during wakefulness, nonrapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep in normoxia [barometric pressure (PB) = 740 Torr] and over 4 continuous days of hypobaric hypoxia (PB = 455 Torr). The relative hypoventilation observed during sleep compared with wakefulness in normoxia was also observed during all stages of hypoxic acclimatization. The characteristic time-dependent changes associated with acclimatization to chronic hypoxia were similar during wakefulness and all sleep states: 1) arterial CO2 partial pressure (PaCO2) decreased 27–31% by night 4 with approximately half of this fall occurring acutely (0.3–3 h hypoxia); 2) minute ventilation increased progressively with duration of hypoxic exposure including increased levels of hyperventilation throughout the initial night of sleep in hypoxia; 3) SaO2 was lowest acutely and gradually increased coincident with the progressive hyperventilation; and 4) pHa increased acutely and remained unchanged despite additional hyperventilation due to a compensatory reduction in [HCO3-]a. In addition, in the acclimatized subject hyperventilation persisted following acute restoration of normoxia, and this continued hyperventilation was similar in magnitude during both wakefulness and NREM sleep. These results indicate that suprapontine influences on ventilatory control associated with the state of wakefulness are not required in the process of ventilatory acclimatization to chronic hypoxia.


1979 ◽  
Vol 47 (6) ◽  
pp. 1304-1310 ◽  
Author(s):  
C. E. Sullivan ◽  
E. Murphy ◽  
L. F. Kozar ◽  
E. A. Phillipson

Ventilatory responses to CO2 and to lung inflation were compared in four dogs during tonic and phasic segments of rapid-eye-movement (REM) sleep. Phasic REM sleep (P-REM) was identified by the presence of bursts of rapid eye movements, visible muscle twitchings, and frequent phasic discharges in the nuchal electromyogram. These features were absent during tonic REM sleep (T-REM). During P-REM the response of minute volume of ventilation (VI) to progressive hypercapnia (0.58 +/- 0.19 (l/min)/Torr, mean +/- SE) was significantly less than in slow-wave sleep (SWS) (1.40 +/- 0.14; P less than 0.05). In contrast, during T-REM the response (1.48 +/- 0.19) was similar to that in SWS. Similarly, during P-REM the duration of apnea (5.9 +/- 1.5 s) elicited by sustained inflation of the lungs with 1.0 liter of air, was significantly shorter than in SWS (25.8 +/- 0.8); in contrast, during T-REM the duration of apnea (17.8 +/- 3.6) was similar to that in SWS. The results indicate that previously described decreases in VI responses to CO2 and apneic responses to lung inflation during P-REM, compared to SWS, are related to the phasic phenomena of REM sleep, rather than to the REM sleep state per se.


1983 ◽  
Vol 55 (4) ◽  
pp. 1113-1119 ◽  
Author(s):  
F. G. Issa ◽  
C. E. Sullivan

The arousal and breathing responses to total airway occlusion during sleep were measured in 12 normal subjects (7 males and 5 females) aged 25-36 yr. Subjects slept while breathing through a specially designed nosemask, which was glued to the nose with medical-grade silicon rubber. The lips were sealed together with a thin layer of Silastic. The nosemask was attached to a wide-bore (20 mm ID) rigid tube to allow a constant-bias flow of room air from a blower. Total airway occlusion was achieved by simultaneously inflating two rubber balloons fixed in the inspiratory and expiratory pipes. A total of 39 tests were done in stage III/IV nonrapid-eye movement (NREM) sleep in 11 subjects and 10 tests in rapid-eye-movement (REM) sleep in 5 subjects. The duration of total occlusion tolerated before arousal from NREM sleep varied widely (range 0.9-67.0 s) with a mean duration of 20.4 +/- 2.3 (SE) s. The breathing response to occlusion in NREM sleep was characterised by a breath-by-breath progressive increase in suction pressure achieved by an increase in the rate of inspiratory pressure generation during inspiration. In contrast, during REM sleep, arousal invariably occurred after a short duration of airway occlusion (mean duration 6.2 +/- 1.2 s, maximum duration 11.8 s), and the occlusion induced a rapid shallow breathing pattern. Our results indicate that total nasal occlusion during sleep causes arousal with the response during REM sleep being more predictable and with a generally shorter latency than that in NREM sleep.


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