A limited number of human studies, all originating from the same group of investigators, have examined sleep quality in subjects with congenital isolated GH-deficiency and in acromegalic patients before and after treatment (90). In GH-deficient adults, a decrease in duration of SW sleep and a significant suppression in delta power were observed but there were no significant differences in REM sleep (90,91). After six months of daily treatment with 2 IU/m2 GH, the relative amount of REM sleep increased and there was a trend for an increased duration of SW sleep (92).
In untreated acromegalic patients without sleep apnea, standard polysomnography revealed a reduction in REM sleep as well as a reduction in amount of SW sleep as compared to control subjects (92). However, a more complex picture emerged when power spectral analysis of the EEG was performed (92). Indeed, though the minutes of REM and SW were decreased, the spectral energy per min spent in both REM and SW was increased, indicating that the amplitude of the EEG waves during both SW and REM sleep is higher in acromegalics than in control subjects (92). The amplitude of the EEG is the sum of the post-synaptic potentials of the cerebral cortex, and thus a higher energy presumably reflects an increased neuronal activity in the cerebral cortex. One year after adenomectomy, an important increase in REM time was observed, resulting in normal values for this age group (92). A moderate increase in SW sleep was also observed. Treatment normalized the EEG energy per minute in both SW and REM stages (92).
As will become apparent from the review given below in Effects of Exogenous GH Administration on Sleep Quality, some of the alterations of sleep quality found in patients with GH deficiency or acromegaly and the effects of treatments of these conditions are not consistent with the findings from studies on the effects of acute administration of GH or GHRH on sleep in normal subjects. However, it must be recognized that chronic pathological conditions and their correction by treatment may involve indirect effects on sleep quality in addition to those putatively mediated by the hormones of the somatotropic axis.
Rodent studies of sleep in hypothysectomized animals or in animals with lesions of the arcuate nucleus have provided conflicting observations and are difficult to interpret because neither model is specific for the somatotropic axis (reviewed in ref. 89). An association between chronic GH excess and increased sleep duration was demonstrated in giant "supermice" genetically engineered with extra GH genes (93).
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