Increased GH Release During Slow Wave Sleep

Sleep does not involve a constant state of reduced brain activity but instead an approximate 90-min oscillation between non-REM (rapid eye movement) stages and REM stages, which is normally repeated 4-6 times per night. Polygraphic sleep recordings include electroencephalograph^ (EEG), electromyographic (EMG), and electrooculographic (EOG) recordings. The so-called polysomnogram is visually scored in 20- or 30-s epochs in stages I, II, III, IV, REM, and Wake using standardized criteria (30). In the normal sequence, waking is followed by the lighter stages of non-REM sleep (i.e., stages I and II) and then within 10-20 min by so-called slow wave sleep (SWS: stages III and IV), which is maintained for nearly one hour in normal young subjects. Lighter stages of non-REM sleep then reappear and the first REM period is initiated. As the night progresses, non-REM sleep becomes more shallow, the duration of REM episodes becomes longer and the number and the duration of awakenings increase. During a normal night in normal young subjects, approx 20% of the night are spent in SW, 25% in REM, 50% in stages I and II, and 5% in wake. The upper panel of Fig. 3 shows a typical polysomnogram of a young normal subject.

An alternative, and perhaps more informative, way to analyze sleep is to submit the EEG recordings to power spectral analysis. This procedure provides a more detailed quantification of changes in EEG frequency and amplitude than sleep stage scoring but is not as standardized and may be more readily affected by artifacts. The EEG signal is digitalized and after appropriate filtering, submitted to a Fast Fourier Transform with calculation of the spectral density in standard frequency bands. The low frequency delta waves that are apparent during SWS are reflected in an increase in spectral power in the so-called delta range (0.5-3 Hz). The second panel of Fig. 3 illustrates the profile of delta power corresponding to the polysomnogram shown in the upper panel. It is noteworthy that delta activity may be present in stage II sleep and therefore precede the appearance of stages III and IV.

Already in the late sixties, well documented studies involving analyses of polygraphi-cally recorded sleep and concomitant GH levels concorded in indicating that there is a consistent relationship between the appearance of delta waves in the EEG and GH secretion during early sleep as well as during the later part of the night (3-5,31). Moreover, selective slow-wave sleep deprivation was shown to result in diminished (but not totally

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