The Sleep of Older Subjects Fifteen Years Later

1982 ◽  
Vol 50 (1) ◽  
pp. 11-14 ◽  
Author(s):  
Wilse B. Webb
Keyword(s):  
Slow Wave ◽  
Scoring System ◽  
Slow Wave Sleep ◽  
Sleep Stages ◽  
Extended Time ◽  
Older Subjects

The EEG sleep of 5 subjects originally recorded in their early 50s was recorded 15 yr. later in their mid-60s. Increased within-sleep awakenings were present and shorter sleep stages. A modified slow wave scoring system resulted in an increased amount rather than the previously established decline in slow wave sleep with aging. Interpretive cautions necessary in extended-time studies are noted. Reliability of awakening measures across time was seen.

nCPAP Treatment of Obstructive Sleep Apnea Increases Slow Wave Sleep in Prefrontal EEG

2007 ◽  
Vol 38 (3) ◽  
pp. 148-154 ◽  
Author(s):  
Veera Eskelinen ◽  
Toomas Uibu ◽  
Sari-Leena Himanen
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Treatment Period ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Sleep Eeg ◽  
Sleep Stages ◽  
Obstructive Sleep ◽  
Sleep Stage Scoring

According to standard sleep stage scoring, sleep EEG is studied from the central area of parietal lobes. However, slow wave sleep (SWS) has been found to be more powerful in frontal areas in healthy subjects. Obstructive sleep apnea syndrome (OSAS) patients often suffer from functional disturbances in prefrontal lobes. We studied the effects of nasal Continuous Positive Airway Pressure (nCPAP) treatment on sleep EEG, and especially on SWS, in left prefrontal and central locations in 12 mild to moderate OSAS patients. Sleep EEG was recorded by polysomnography before treatment and after a 3 month nCPAP treatment period. Recordings were classified into sleep stages. No difference was found in SWS by central sleep stage scoring after the nCPAP treatment period, but in the prefrontal lobe all night S3 sleep stage increased during treatment. Furthermore, prefrontal SWS increased in the second and decreased in the fourth NREM period. There was more SWS in prefrontal areas both before and after nCPAP treatment, and SWS increased significantly more in prefrontal than central areas during treatment. Regarding only central sleep stage scoring, nCPAP treatment did not increase SWS significantly. Frontopolar recording of sleep EEG is useful in addition to central recordings in order to better evaluate the results of nCPAP treatment.

scholarly journals Strengthening sleep–autonomic interaction via acoustic enhancement of slow oscillations

SLEEP ◽  
2019 ◽  
Vol 42 (5) ◽  
Author(s):  
Daniela Grimaldi ◽  
Nelly A Papalambros ◽  
Kathryn J Reid ◽  
Sabra M Abbott ◽  
Roneil G Malkani ◽  
...  
Keyword(s):  
Slow Wave ◽  
Cardiovascular Health ◽  
Autonomic Function ◽  
Slow Wave Sleep ◽  
The Body ◽  
Parasympathetic Activity ◽  
Sleep Stages ◽  
Physiological Processes ◽  
Main Pathway ◽  
Positive Effect

Abstract Slow-wave sleep (SWS) is important for overall health since it affects many physiological processes including cardio-metabolic function. Sleep and autonomic nervous system (ANS) activity are closely coupled at anatomical and physiological levels. Sleep-related changes in autonomic function are likely the main pathway through which SWS affects many systems within the body. There are characteristic changes in ANS activity across sleep stages. Notably, in non-rapid eye-movement sleep, the progression into SWS is characterized by increased parasympathetic activity, an important measure of cardiovascular health. Experimental manipulations that enhance slow-wave activity (SWA, 0.5–4 Hz) can improve sleep-mediated memory and immune function. However, effects of SWA enhancement on autonomic regulation have not been investigated. Here, we employed an adaptive algorithm to deliver 50 ms sounds phase-locked to slow-waves, with regular pauses in stimulation (~5 s ON/~5 s OFF), in healthy young adults. We sought to determine whether acoustic enhancement of SWA altered parasympathetic activity during SWS assessed with heart rate variability (HRV), and evening-to-morning changes in HRV, plasma cortisol, and blood pressure. Stimulation, compared with a sham condition, increased SWA during ON versus OFF intervals. This ON/OFF SWA enhancement was associated with a reduction in evening-to-morning change of cortisol levels and indices of sympathetic activity. Furthermore, the enhancement of SWA in ON intervals during sleep cycles 2–3 was accompanied by an increase in parasympathetic activity (high-frequency, HRV). Together these findings suggest that acoustic enhancement of SWA has a positive effect on autonomic function in sleep. Approaches to strengthen brain–heart interaction during sleep could have important implications for cardiovascular health.

Correlation between ventilation and brain blood flow during hypoxic sleep

1986 ◽  
Vol 60 (1) ◽  
pp. 295-298 ◽  
Author(s):  
T. V. Santiago ◽  
J. A. Neubauer ◽  
N. H. Edelman
Keyword(s):  
Blood Flow ◽  
Tidal Volume ◽  
Slow Wave ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Maxillary Artery ◽  
Brain Blood Flow ◽  
Ventilatory Depression

Ventilation and brain blood flow (BBF) were simultaneously measured during carbon monoxide (CO) inhalation in awake and sleeping goats up to HbCO levels of 40%. Unilateral BBF, which was continuously measured with an electromagnetic flow probe placed around the internal maxillary artery, progressively increased with CO inhalation in the awake and both sleep stages. The increase in BBF with CO inhalation during rapid-eye-movement (REM) sleep (delta BBF/delta arterial O2 saturation = 1.34 +/- 0.27 ml X min-1 X %-1) was significantly greater than that manifested during wakefulness (0.87 +/- 0.14) or slow-wave sleep (0.92 +/- 0.13). Ventilation was depressed by CO inhalation during both sleep stages but was unchanged from base-line values in awake goats. In contrast to slow-wave (non-REM) sleep, the ventilatory depression of REM sleep was primarily due to a reduction in tidal volume. Since tidal volume is more closely linked to central chemoreceptor function, we believe that these data suggest a possible role of the increased cerebral perfusion during hypoxic REM sleep. Induction of relative tissue alkalosis at the vicinity of the medullary chemoreceptor may contribute to the ventilatory depression exhibited during this sleep period.

Sleep-electroencephalography and the secretion of cortisol and growth hormone in normal controls

1987 ◽  
Vol 116 (1) ◽  
pp. 36-42 ◽  
Author(s):  
A. Steiger ◽  
T. Herth ◽  
F. Holsboer
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Onset ◽  
Cell Activity ◽  
Cortisol Concentration ◽  
Sleep Stages ◽  
Sleep Structure ◽  
Endocrine Activity ◽  
Normal Controls

Abstract. Sleep-electroencephalography, and the nocturnal secretion of cortisol and GH were investigated simultaneously in a sample of 25 male normal controls (27.1 ± 1.3 years) in order further to examine interaction between sleep structure and concurrent endocrine activity. Slow wave sleep activity was increased during the first part of the night, whereas cortisol concentration was low and GH output reached maximal levels. The second half of the night was characterized by a relative preponderance of REM-sleep, low GH-concentration, and an increase in cortisol. However, no distinct reciprocal interaction between cortisol and GH concentration was noted. In all subjects, a pronounced GH surge between 22.00 and 02.00 h was recorded which occurred independently of the presence of slow wave sleep. Six out of the 25 subjects showed nocturnal GH increases even before sleep onset. These data indicate that somatotropic cell activity during night is less dependent upon the sleeping state or specific conventially defined sleep stages than originally reported.

Time course of EEG power density during long sleep in humans

1990 ◽  
Vol 258 (3) ◽  
pp. R650-R661 ◽  
Author(s):  
D. J. Dijk ◽  
D. P. Brunner ◽  
A. A. Borbely
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Sleep Regulation ◽  
Recovery Sleep ◽  
Electroencephalogram Eeg

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

scholarly journals A Modified Method for Scoring Slow Wave Sleep of Older Subjects

SLEEP ◽  
1982 ◽  
Vol 5 (2) ◽  
pp. 195-199 ◽  
Author(s):  
Wilse B. Webb ◽  
Lewis M. Dreblow
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Modified Method ◽  
Older Subjects

scholarly journals Blockade of endogenous growth hormone-releasing hormone receptors dissociates nocturnal growth hormone secretion and slow-wave sleep

2004 ◽  
pp. 561-566 ◽  
Author(s):  
SK Jessup ◽  
BA Malow ◽  
KV Symons ◽  
AL Barkan
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Hormone Receptors ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Nrem Sleep ◽  
Temporal Association ◽  
Sleep Stages ◽  
Sleep Study

OBJECTIVES: A temporal association between non-rapid eye movement (NREM) sleep stages 3 and 4 and nocturnal augmentation of GH release was found long ago, yet the precise mechanism for this association has not been identified. It has been shown, however that pulsatile GHRH administration increases both slow-wave sleep (SWS) and GH. Based on these data, a role for GHRH as an inducer of SWS was proposed. To test this hypothesis, we have performed the corollary experiment whereby the action of endogenous GHRH has been antagonized. DESIGN: Healthy men (20-33 years old) had an infusion of GHRH antagonist ((N-Ac-Tyr(1), D-Arg(2)) GHRH-29 (NH(2))) or saline for a 12-h period, between 2100 and 0900 h. An i.v. bolus of GHRH was given at 0700 h and GH samples were drawn from 0700 to 0900 h to document the efficacy of GH suppression by the GHRH antagonist. METHODS: A limited montage sleep study was recorded from 2300 to 0700 h during each admission. Plasma GH concentrations were analyzed by the use of a sensitive chemiluminometric assay. RESULTS: Effectiveness of the GHRH antagonist was validated in all subjects by demonstrating 93+/-1.8% (P=0.012) suppression of GH response to a GHRH bolus. Polysomnography demonstrated that the percentage of SWS was not different when saline and GHRH antagonist nights were compared (P=0.607); other quantifiable sleep parameters were also unchanged. CONCLUSIONS: We conclude that endogenous GHRH is indispensable for the nocturnal augmentation of GH secretion, but that it is unlikely to participate in the genesis of SWS.

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