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

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

Evidence against a role for the growth hormone-releasing peptide axis in human slow-wave sleep regulation

1998 ◽  
Vol 274 (5) ◽  
pp. E779-E784 ◽  
Author(s):  
Rodrigo Moreno-Reyes ◽  
Myriam Kerkhofs ◽  
Mireille L’Hermite-Balériaux ◽  
Michael O. Thorner ◽  
Eve Van Cauter ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Growth Hormone Releasing Hormone ◽  
Sleep Regulation ◽  
Healthy Men ◽  
Intravenous Injections ◽  
Late Night ◽  
The Third ◽  
Upper Limit

A complex interrelationship exists between sleep and somatotropic activity. In humans, intravenous injections of growth hormone-releasing hormone (GHRH) given during sleep consistently stimulate slow-wave (SW) sleep, particularly when given in the latter part of the night. In the present study, the possible somnogenic effects induced under similar conditions by GH-releasing peptide (GHRP) were investigated in seven young healthy men. Bolus intravenous injections of GHRP-2 (1 μg/kg body wt) or saline, in randomized order, were given after 60 s of the third rapid-eye-movement period. All GHRP injections were immediately followed by transient prolactin elevations and by GH pulses of a magnitude within or around the upper limit of the physiological range. Except for a nonsignificant tendency to increased amounts of wakefulness during the 1st h after the injection, no effects of GHRP-2 administration on sleep were detected. There was in particular no enhancement of SW sleep. Thus, in contrast to GHRH, late-night single injections of GHRP-2 at a dosage resulting in similar GH elevations have no stimulatory effects on SW sleep. The present data provide evidence against the involvement of the GHRP axis in human SW sleep regulation.

Suppression of nocturnal growth hormone secretion in epilepsy with continuous spike-waves during slow-wave sleep

1999 ◽  
Vol 41 (2) ◽  
pp. 192-194 ◽  
Author(s):  
Kuniaki Iyoda ◽  
Hitoshi Tobiume ◽  
Susumu Kanzaki ◽  
Syouko Takano2 And Yoshiki Seino
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion

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.

PHYSIOLOGICAL GROWTH HORMONE SECRETION DURING SLOW-WAVE SLEEP IN SHORT PREPUBERTAL CHILDREN

1987 ◽  
Vol 27 (3) ◽  
pp. 355-361 ◽  
Author(s):  
P. ADLARD ◽  
F. BUZI ◽  
J. JONES ◽  
R. STANHOPE ◽  
M. A. PREECE
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Prepubertal Children

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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