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.

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.

SEASONAL PATTERNS OF SLEEP STAGES AND SECRETION OF CORTISOL AND GROWTH HORMONE DURING 24 HOUR PERIODS IN NORTHERN NORWAY

1975 ◽  
Vol 78 (1) ◽  
pp. 65-76 ◽  
Author(s):  
Elliot D. Weitzman ◽  
Andries S. deGraaf ◽  
Jon F. Sassin ◽  
Tomar Hansen ◽  
Ole B. Godtlibsen ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Plasma Cortisol ◽  
Sleep Stage ◽  
Sleep Onset ◽  
Cortisol Concentration ◽  
Sleep Stages ◽  
Seasonal Patterns ◽  
Healthy Male ◽  
Plasma Cortisol Concentration ◽  
Male Subjects

ABSTRACT A group of 7 healthy male subjects was studied in regard to sleep stages and 24 h plasma cortisol and growth hormone patterns during the 4 seasons of the year in an Arctic environment (Tromsø, Norway). No difference in total sleep or sleep stage per cents was found for any of the yearly seasons. A small but statistical significant increase in mean plasma cortisol concentration and amount secreted for 24 h was found for the autumn-winter seasons, as compared with the spring and summer. However, no difference in the circadian curve of cortisol hormonal pattern was found. All subjects secreted growth hormone shortly after sleep onset at night and no difference was found as a function of season of the year.

Secretion of growth hormone during slow-wave sleep deprivation

1987 ◽  
Vol 116 (3_Suppl) ◽  
pp. S60-S61
Author(s):  
J. BORN ◽  
R. PIETROWSKY ◽  
P. PAUSCHINGER ◽  
H. L. FEHM
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Slow Wave Sleep

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 Cerebral metabolic rate of oxygen during transition from wakefulness to sleep measured with high temporal resolution OxFlow MRI with concurrent EEG

2020 ◽  
pp. 0271678X2091928
Author(s):  
Alessandra Caporale ◽  
Hyunyeol Lee ◽  
Hui Lei ◽  
Hengyi Rao ◽  
Michael C Langham ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Cerebral Metabolism ◽  
Sleep Onset ◽  
High Temporal Resolution ◽  
Mean Values ◽  
Cerebral Metabolic Rate ◽  
Sleep Physiology ◽  
Concomitant Reduction

During slow-wave sleep, synaptic transmissions are reduced with a concomitant reduction in brain energy consumption. We used 3 Tesla MRI to noninvasively quantify changes in the cerebral metabolic rate of O2 (CMRO2) during wakefulness and sleep, leveraging the ‘OxFlow’ method, which provides venous O2 saturation (SvO2) along with cerebral blood flow (CBF). Twelve healthy subjects (31.3 ± 5.6 years, eight males) underwent 45–60 min of continuous scanning during wakefulness and sleep, yielding one image set every 3.4 s. Concurrent electroencephalography (EEG) data were available in eight subjects. Mean values of the metabolic parameters measured during wakefulness were stable, with coefficients of variation below 7% (average values: CMRO2 = 118 ± 12 µmol O2/min/100 g, SvO2 = 67.0 ± 3.7% HbO2, CBF = 50.6 ±4.3 ml/min/100 g). During sleep, on average, CMRO2 decreased 21% (range: 14%–32%; average nadir = 98 ± 16 µmol O2/min/100 g), while EEG slow-wave activity, expressed in terms of [Formula: see text]-power, increased commensurately. Following sleep onset, CMRO2 was found to correlate negatively with relative [Formula: see text]-power (r = −0.6 to −0.8, P < 0.005), and positively with heart rate (r = 0.5 to 0.8, P < 0.0005). The data demonstrate that OxFlow MRI can noninvasively measure dynamic changes in cerebral metabolism associated with sleep, which should open new opportunities to study sleep physiology in health and disease.

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.

scholarly journals Low acetylcholine during early sleep is important for motor memory consolidation

SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Samsoon Inayat ◽  
Qandeel ◽  
Mojtaba Nazariahangarkolaee ◽  
Surjeet Singh ◽  
Bruce L McNaughton ◽  
...  
Keyword(s):  
Skill Acquisition ◽  
Slow Wave ◽  
Nicotinic Acetylcholine Receptors ◽  
Memory Consolidation ◽  
Acetylcholinesterase Inhibitor ◽  
Sleep Onset ◽  
Motor Memory ◽  
Sleep Structure ◽  
Rotarod Performance ◽  
Cholinergic Tone

Abstract The synaptic homeostasis theory of sleep proposes that low neurotransmitter activity in sleep optimizes memory consolidation. We tested this theory by asking whether increasing acetylcholine levels during early sleep would weaken motor memory consolidation. We trained separate groups of adult mice on the rotarod walking task and the single pellet reaching task, and after training, administered physostigmine, an acetylcholinesterase inhibitor, to increase cholinergic tone in subsequent sleep. Post-sleep testing showed that physostigmine impaired motor skill acquisition of both tasks. Home-cage video monitoring and electrophysiology revealed that physostigmine disrupted sleep structure, delayed non-rapid-eye-movement sleep onset, and reduced slow-wave power in the hippocampus and cortex. Additional experiments showed that: (1) the impaired performance associated with physostigmine was not due to its effects on sleep structure, as 1 h of sleep deprivation after training did not impair rotarod performance, (2) a reduction in cholinergic tone by inactivation of cholinergic neurons during early sleep did not affect rotarod performance, and (3) stimulating or blocking muscarinic and nicotinic acetylcholine receptors did not impair rotarod performance. Taken together, the experiments suggest that the increased slow wave activity and inactivation of both muscarinic and nicotinic receptors during early sleep due to reduced acetylcholine contribute to motor memory consolidation.

The temporal relationship between growth hormone and slow wave sleep is weaker after menopause

2012 ◽  
Vol 13 (1) ◽  
pp. 96-101 ◽  
Author(s):  
Nea Kalleinen ◽  
Arho Virkki ◽  
Olli Polo ◽  
Sari-Leena Himanen ◽  
Kerttu Irjala ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Temporal Relationship ◽  
Slow Wave Sleep

scholarly journals Excessive Fragmentary Myoclonus: Time of Night and Sleep Stage Distributions

1993 ◽  
Vol 20 (2) ◽  
pp. 142-146 ◽  
Author(s):  
Otavio Lins ◽  
Michelle Castonguay ◽  
Wayne Dunham ◽  
Sonya Nevsimalova ◽  
Roger Broughton
Keyword(s):  
Sleep Disorders ◽  
Patient Group ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Sleep Stage ◽  
Sleep Onset ◽  
Sleep Fragmentation ◽  
New Technique ◽  
A New Technique

ABSTRACT:Excessive fragmentary myoclonus during sleep consists of high amounts of brief twitch-like movements occurring asynchronously and asymmetrically in different body areas and has been reported to occur in association with a number of sleep disorders. It was analyzed using a new technique of quantification, the fragmentary myoclonus index (FMI). The FMI exhibited high rates in all stages of sleep but with a somewhat lower frequency in slow wave sleep explaining, as well, a significantly lower rate in the first hour after sleep onset compared to later hours. There was no evidence for greater sleep fragmentation or lighter sleep compared to a matched patient group in whom it had not been noted.

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