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
2000 ◽  
Vol 279 (3) ◽  
pp. R874-R883 ◽  
Author(s):  
K. Spiegel ◽  
R. Leproult ◽  
E. F. Colecchia ◽  
M. L'Hermite-Balériaux ◽  
Z. Nie ◽  
...  

In normal men, the majority of GH secretion occurs in a single large postsleep onset pulse that is suppressed during total sleep deprivation. We examined the impact of semichronic partial sleep loss, a highly prevalent condition, on the 24-h growth hormone profile. Eleven young men were studied after six nights of restricted bedtimes (0100–0500) and after 7 nights of extended bedtimes (2100–0900). Slow-wave sleep (SWS) was estimated as the duration of stages III and IV. Slow-wave activity (SWA) was calculated as electroencephalogram power density in the 0.5- to 3-Hz frequency range. During the state of sleep debt, the GH secretory pattern was biphasic, with both a presleep onset “circadian” pulse and a postsleep onset pulse. Postsleep onset GH secretion was negatively related to presleep onset secretion and tended to be positively correlated with the amount of concomitant SWA. When sleep was restricted, both SWS and SWA were increased during early sleep. Unexpectedly, the increase in SWA affected the second, rather than the first, SWA cycle, suggesting that presleep onset GH secretion may have limited SWA in the first cycle, possibly via an inhibition of central GH-releasing hormone activity. Thus neither the GH profile nor the distribution of SWA conformed with predictions from acute sleep deprivation studies, indicating that adaptation mechanisms are operative during chronic partial sleep loss.


Life Sciences ◽  
1969 ◽  
Vol 8 (23) ◽  
pp. 1299-1307 ◽  
Author(s):  
J.F. Sassin ◽  
D.C. Parker ◽  
L.C. Johnson ◽  
L.G. Rossman ◽  
J.W. Mace ◽  
...  

1994 ◽  
Vol 3 (1) ◽  
pp. 16-25 ◽  
Author(s):  
JAMES K. WALSH ◽  
PAUL G. HARTMAN ◽  
PAULA K. SCHWEITZER

2021 ◽  
Vol 12 ◽  
Author(s):  
Geneviève Scavone ◽  
Andrée-Ann Baril ◽  
Jacques Montplaisir ◽  
Julie Carrier ◽  
Alex Desautels ◽  
...  

Sleepwalking has been conceptualized as deregulation between slow-wave sleep and arousal, with its occurrence in predisposed patients increasing following sleep deprivation. Recent evidence showed autonomic changes before arousals and somnambulistic episodes, suggesting that autonomic dysfunctions may contribute to the pathophysiology of sleepwalking. We investigated cardiac autonomic modulation during slow-wave sleep in sleepwalkers and controls during normal and recovery sleep following sleep deprivation. Fourteen adult sleepwalkers (5M; 28.1 ± 5.8 years) and 14 sex- and age-matched normal controls were evaluated by video-polysomnography for one baseline night and during recovery sleep following 25 h of sleep deprivation. Autonomic modulation was investigated with heart rate variability during participants' slow-wave sleep in their first and second sleep cycles. 5-min electrocardiographic segments from slow-wave sleep were analyzed to investigate low-frequency (LF) and high-frequency (HF) components of heart rate spectral decomposition. Group (sleepwalkers, controls) X condition (baseline, recovery) ANOVAs were performed to compare LF and HF in absolute and normalized units (nLF and nHF), and LF/HF ratio. When compared to controls, sleepwalkers' recovery slow-wave sleep showed lower LF/HF ratio and higher nHF during the first sleep cycle. In fact, compared to baseline recordings, sleepwalkers, but not controls, showed a significant decrease in nLF and LF/HF ratio as well as increased nHF during recovery slow-wave sleep during the first cycle. Although non-significant, similar findings with medium effect sizes were observed for absolute values (LF, HF). Patterns of autonomic modulation during sleepwalkers' recovery slow-wave sleep suggest parasympathetic dominance as compared to baseline sleep values and to controls. This parasympathetic predominance may be a marker of abnormal neural mechanisms underlying, or interfere with, the arousal processes and contribute to the pathophysiology of sleepwalking.


SLEEP ◽  
2021 ◽  
Author(s):  
Michelle E Stepan ◽  
Erik M Altmann ◽  
Kimberly M Fenn

Abstract Sleeping for a short period (i.e., napping) may help mitigate impairments in cognitive processing caused by sleep deprivation, but there is limited research on effects of brief naps in particular. Here, we tested the effect of a brief nap opportunity (30- or 60-min) during a period of sleep deprivation on two cognitive processes with broad scope, placekeeping and vigilant attention. In the evening, participants (N = 280) completed a placekeeping task (UNRAVEL) and a vigilant attention task (Psychomotor Vigilance Task [PVT]) and were randomly assigned to either stay awake overnight or sleep at home. Sleep-deprived participants were randomly assigned to receive either no nap opportunity, a 30-min opportunity, or a 60-min opportunity. Participants who napped were set up with polysomnography. The next morning, sleep participants returned, and all participants completed UNRAVEL and the PVT. Sleep deprivation impaired performance on both tasks, but nap opportunity did not reduce the impairment, suggesting that naps longer than those tested may be necessary to cause group differences. However, in participants who napped, more time spent in slow-wave sleep (SWS) was associated with reduced performance deficits on both tasks, effects we interpret in terms of the role of SWS in alleviating sleep pressure and facilitating memory consolidation.


1992 ◽  
Vol 263 (5) ◽  
pp. R1078-R1085 ◽  
Author(s):  
F. Obal ◽  
L. Payne ◽  
M. Opp ◽  
P. Alfoldi ◽  
L. Kapas ◽  
...  

Previous reports suggest that the hypothalamic growth hormone-releasing hormone (GHRH) promotes sleep, especially non-rapid-eye-movement sleep (NREMS). To evaluate the role of endogenous GHRH in sleep regulation, the effects of antibodies to rat GHRH (GHRH-ab) were studied on normal sleep, brain temperature (Tbr), and GH secretion in experiment I and on enhanced sleep after sleep deprivation in experiment II. In experiment I, affinity-purified GHRH-ab (50 and 200 micrograms) raised in goats and a control goat immunoglobulin G (IgG) preparation were injected intracerebroventricularly (icv) in rats 1 h before the onset of the light cycle, and sleep-wake activity and Tbr were recorded for the next 12 or 23 h. Both doses of GHRH-ab suppressed NREMS and REMS throughout the light cycle. Sleep durations at night were normal. Electroencephalographic (EEG) slow-wave activity, characterized by EEG slow-wave amplitudes, was reduced after GHRH-ab during both the light and the dark cycles. Plasma GH concentrations measured 6-12 h after injection of GHRH-ab (200 micrograms) were diminished. Both the control IgG and GHRH-ab elicited fever. In experiment II, the sleep-wake activity and Tbr of rats were recorded for 24 h in three experimental conditions: base-line with icv injection of IgG, 3-h sleep deprivation with icv IgG injection, and 3-h sleep deprivation with icv GHRH-ab (200 micrograms). After sleep deprivation (+IgG), a prompt increase in EEG slow-wave activity (power density analysis) and late increases in NREMS and REMS durations were found.(ABSTRACT TRUNCATED AT 250 WORDS)


2012 ◽  
Vol 13 (1) ◽  
pp. 96-101 ◽  
Author(s):  
Nea Kalleinen ◽  
Arho Virkki ◽  
Olli Polo ◽  
Sari-Leena Himanen ◽  
Kerttu Irjala ◽  
...  

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