This report found no effect on Gh output, I have read others where they DID find a connection. Personally I have a hard time sleeping always and any stims or anabolics make it much harder but if I take dipenhydramine it really makes me feel like I have no recovery all night. I wake up and I feel so flat and tired, but most of all I am weak in the gym. If it didnt make me feel this way I would take it every night because 8-9 hrs of sleep it just so awesome.
BTW the OP is a legit article from Journal of Clinical Endocrinology, but it is also from 1979 lol
Here is another source that has more info than you ever wanted from 1999
(Can't post links yet so heres the reference:
Physiological Reviews, Vol. 79, No. 2, April 1999, pp. 511-607
Copyright ©1999 by the American Physiological Society)
Specifically:
4. Histamine
The role of histamine on GH release in the rat is still debated, but most of the evidence points to inhibition by H1 receptors. In conscious rats, intracerebroventricular administration of histamine or a series of H1-receptor agonists reduced GH release induced by morphine; mepyramine, a H1-receptor antagonist, had no effect by itself but prevented the inhibitory action of 2-methylhistamine, a H1-receptor agonist. The H2-receptor agonists and antagonists also inhibited morphine-induced GH release but apparently with a nonspecific mechanism (776). Similarly, nanomolar intracerebroventricular doses of histamine or amodiaquine, an inhibitor of histamine catabolism, caused a dose-related suppression of pulsatile GH secretion (775).
At odds with these findings, in E2- and progesterone-primed anesthetized male rats, a H1-receptor antagonist blocked the rise in GH induced by morphine, neurotensin, and SP, with a mechanism that could not be related simply to the hypotensive properties of these substances (891).
The inhibitory effect of histamine neurotransmission on GH release has since been illustrated in neonatal and adult rats. In the former, blockade of histamine synthesis with -fluoromethylhistidine (-FMH) significantly raised plasma GH and potentiated the GH response to an enkephalin analog; GH and SS mRNA were significantly higher in -FMH-treated pups, whereas GHRH mRNA levels were unaltered. In young adult male rats, acute administration of -FMH did not change baseline GH levels but potentiated the enkephalin-induced stimulation of GH secretion. Repeated intracerebroventricular doses of -FMH did not alter the hormone levels, significantly reduced hypothalamic GHRH mRNA, and left SS and GHmRNA unchanged (439). Overall, these findings suggest an inhibitory histamine tone on GH secretion in neonatal and adult young rats, the failure of -FMH to increase GH secretion in the latter being probably due to upregulation of histamine receptors after brain histamine depletion (862).
Data in freely moving dogs point instead to a facilitatory role on GH secretion. Of the three H1-receptor antagonists used, only clemastine, which reportedly has no antiserotoninergic, antiadrenergic, and anticholinergic action, blunted hypoglycemia-induced GH release (626), whereas diphenhydramine, clemastine, and the H2-receptor antagonist cimetidine, respectively, suppressed or blunted the cGH release induced by an opioid peptide (174) or by cholinergic stimulation (100).
Basically, looks like under experimental condition H1 receptor antagonist like dipenhydramine will block GH stimulation from all sources except hypoglycemia induced secretion. I dont know which of these sources best emulates the spike of GH induced as sleep begins, but this short segment really references a lot of experiments that mostly point towards diphendydramine inhibiting GH production.
