Augmentation of growth hormone secretion during puberty: Evidence for a pulse amplitude-modulated phenomenon

The augmentation of GH secretion that occurs during puberty has been attributed to changes in sex steroid levels that enhance the frequency and amplitude of GH pulses. To investigate the specific GH pulse characteristics responsible for such augmentation we analyzed the serum GH concentration profiles of 10 boys in Tanner stages I−II of sexual development (group A; aged 10 5/12−15 1/12 yr) and compared their GH pulse characteristics with those of 5 boys at Tanner stages IV−V of development (group B; aged 14 8/12−15 1/12 yr). We also reanalyzed previously reported data from 5 prepubertal boys (group C; aged 13 6/12−15 5/12 yr) before and after 10 weeks of treatment with testosterone enanthate (100 mg/4 weeks, im). Using a pulse detection algorithm that constrains the false positive pulse detection rate to less than 5% (Cluster), we found that group B boys had a significantly higher mean serum GH pulse amplitude compared to group A boys (17.1 ± 2.6 vs. 8.6 ± 1.7 ng/mL; P = 0.012), but both groups had the same mean GH pulse frequency (group B, 5.4 ± 0.5 pulses/24 h vs. group A, 5.5 ± 0.4 pulses/24 h; P > 0.05). Similar changes were found in group C boys before and after testosterone therapy; there was no significant change in GH pulse frequency (6.6 ± 0.9 before vs. 7.6 ± 0.5 pulses/24 h after treatment; P > 0.05), but there was a significant increase in the GH pulse amplitude after therapy (6.8 ± 1.6 before vs. 15.4 ± 2.4 ng/mL after treatment; P = 0.04). When the 24-h GH concentration profiles were analyzed using a mathematically distinct method for the estimation of pulse amplitudes, namely the Fourier expansion time series, we confirmed a significant increase in GH pulse amplitude with later stages of puberty and androgen treatment. We conclude that the augmentation in GH secretion that occurs during either spontaneous puberty or exogenous testosterone therapy is an amplitude-modulated phenomenon, relatively independent of changes in pulse frequency. Such an effect may be secondary to the action of sex steroid hormones modulating either the responsivity of somatotrophs to endogenous GH-releasing hormone, the amount of GH-releasing hormone secreted, or the tonic inhibitory tone of somatostatin.