Pulsatile release of GH in humans is a reflection of the variability in somatotrope responsivity to hypothalamic GHRH mediated by fluctuating levels of endogenous hypothalamic SRIF. Twenty-four-h studies of spontaneous GH secretion that have demonstrated large GH pulses are actually composed of multiple discreet smaller bursts of GH resolved only with more frequent (30-s) sampling (120). Electroencephalographic (EEG) monitoring during these studies identified a significant correlation of GH secretion and slow-wave sleep. A model of GH secretion has been suggested whereby specific cortical or midbrain events correlating with slow-wave sleep precedes both pituitary GH secretion and the generation of a peripheral GH secretory burst, which is influenced by hypothalamic neurons that increase GHRH release or decrease SRIF secretion (or both), thereby increasing GH secretion by the somatotropes (11).
Twenty-four-hour studies performed in healthy adult subjects using 20-min sampling intervals and an ultrasensitive immunoradiometric assay (IRMA) for GH with a detection limit of 20 ng/L identified an absolute GH nadir of 40 ng/L, well below the sensitivity of most assays (120). The ultrasensitive IRMA allowed the demonstration of an oscillatory rhythm of GH secretion, whereas GH secretion was thought to be episodic in nature (120). In addition, previous estimates of integrated GH (2.50 ^g/L in women; 2.33 ^g/L in men) may therefore be falsely elevated as a result of overestimation of GH levels below the level of assay sensitivity using standard radioimmunoassays (120). This same principle of the oscillatory rhythm likely also applies to children.
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