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Friday, October 16, 2009

Sleep deprivation effects on the activity of the hypothalamic–pituitary–adrenal and growth axes: potential clinical implications

Sleep deprivation effects on the activity of the hypothalamic–pituitary–adrenal and growth axes: potential clinical implications

Alexandros N. Vgontzas , George Mastorakos , Edward O. Bixler , Anthony Kales , Philip W. Gold & George P. Chrousos

1 Sleep Research and Treatment Center, Department of Psychiatry, Pennsylvania State University, Hershey, USA, 2 Endocrine Unit, Evgenidion Hospital, Athens University, Athens, Greece, 3 Clinical Neuroendocrinology Branch, National Institute of Mental Health, Bethesda, USA, 4 Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, USA

Correspondence to: Dr Alexandros N. Vgontzas Sleep Research and Treatment Center, Department of Psychiatry Pennsylvania State University, College of Medicine, 500 University Drive, Hershey, PA 17033, USA. Fax: +1 (717) 531 6491.
Copyright 1999 Blackwell Science Ltd

ABSTRACT

OBJECTIVES

Although several studies have shown that sleep deprivation is associated with increased slow wave sleep during the recovery night, the effects of sleep deprivation on cortisol and growth hormone (GH) secretion the next day and recovery night have not been assessed systematically. We hypothesized that increased slow wave sleep postsleep deprivation is associated with decreased cortisol levels and that the enhanced GH secretion is driven by the decreased activity of the HPA axis.

DESIGN AND SUBJECTS

After four consecutive nights in the Sleep Laboratory, 10 healthy young men were totally deprived of sleep during the fifth night, and then allowed to sleep again on nights six and seven. Twenty-four hour blood sampling was performed serially every 30 minutes on the fourth day, immediately following the previous night of sleep and on the sixth day, immediately after sleep deprivation.

MEASUREMENT

Eight-hour sleep laboratory recording, including electroencephologram, electro-oculogram and electromyogram. Plasma cortisol and GH levels using specific immunoassay techniques.

RESULTS

Mean plasma and time-integrated (AUC) cortisol levels were lower during the postdeprivation nighttime period than on the fourth night (P < class="invisible-anchor" name="h005">

CONCLUSION

We conclude that sleep deprivation results in a significant reduction of cortisol secretion the next day and this reduction appears to be, to a large extent, driven by the increase of slow wave sleep during the recovery night.

We propose that reduction of CRH and cortisol secretion may be the mechanism through which sleep deprivation relieves depression temporarily.

Furthermore, deep sleep has an inhibitory effect on the HPA axis while it enhances the activity of the GH axis. In contrast, sleep disturbance has a stimulatory effect on the HPA axis and a suppressive effect on the GH axis.

These results are consistent with the observed hypocortisolism in idiopathic hypersomnia and HPA axis relative activation in chronic insomnia.

Finally, our findings support previous hypotheses about the restitution and immunoenhancement role of slow wave (deep) sleep.

http://www3.interscience.wiley.com/journal/118881160/abstract?CRETRY=1&SRETRY=0



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