Growth hormone
Pulsatile pituitary GH secretion
Also searched as Pulsatile pituitary GH secretion.
You do not take this; you earn it. Its biggest pulse of the day arrives about an hour after you fall asleep, and it answers to sleep, exercise and fasting. Note the catch on the pathway below: more growth hormone does not automatically mean more IGF-1, because the liver has to be listening.
In depth
Growth hormone — released in pulses from the pituitary, largest during deep sleep, and the signal that drives IGF-1 production.
What drives it
Growth factor reduces it.
10.3389/fendo.2024.1456195 — It is a thermostat, not a one-way pathway. doi 10.3389/fendo.2024.1456195
Sleep increases it.
GH release is pulsatile and sleep is named among the principal physiological regulators of GH secretion alongside food, exercise, fasting, age and body composition (Endotext NBK279056). Peak release occurs during slow-wave sleep; roughly two-thirds of daily GH output occurs at night, with about 70 percent of that in the first slow-wave episode.
Training load increases it.
Exercise is one of the named physiological regulators of GH secretion; peak release occurs during slow-wave sleep and in response to exercise, fasting and physiological stress (Endotext NBK279056).
Hunger hormone increases it.
10.3389/fendo.2021.636403 — Ghrelin is a growth hormone secretagogue - the receptor is named GHS-R for that reason. doi 10.3389/fendo.2021.636403
What it drives
It increases Growth factor.
IGF-1 is how most of growth hormone's message is delivered: GH is secreted by the anterior pituitary and acts on peripheral organs to stimulate IGF-1 production, with the liver supplying about 75% of circulating IGF-I; the Igf1 gene is a principal target of GH activation (PMC4075164, Endotext NBK279056). More GH does not automatically mean more IGF-1. Direction depends on the endpoint. PMC4075164
It increases Muscle.
Named among the core mechanisms across six sarcopenia reviews: protein metabolism, mitochondrial dysfunction, chronic inflammation, and neuromuscular junction degeneration, with regulation of inflammation primarily targeting inhibition of NF-kB signaling and elevated PGC-1-alpha OR PAX7 expression reversing mitochondrial OR satellite cell dysfunction. doi 10.3390/ijms26146740 · PMC13074595
It increases Recovery.
10.3803/EnM.2020.35.2.272 — Recovery is assembled from the sarcopenia and VO2max literatures; none of the papers cited studied recovery itself. doi 10.3803/EnM.2020.35.2.272
It increases Wound healing.
The one measured finding among them is the periodontal-anemia link: a meta-analysis of sixteen studies on hemoglobin and iron metabolism in periodontitis, whose authors call the association still controversial and ask for larger cohorts. doi 10.1152/japplphysiol.00971.2016 · PMC7005133
It increases Releases stored fat.
10.1210/er.2008-0027 — the full STIMULATOR list, named together in the arabic reference and nowhere else in this evidence set: 'هناك مجموعة من الهرمونات داخل جسم الإنسان التي تقوم بتحفيز تحلل الدهن مثل أدرينالين ونورإبينفرين وغريلين وتستوستيرون وكورتيزول بالإضافة إلى هرمون النمو. تعمل هذه الهرمونات على إطلاق المستقبلات المقترنة بالبروتين ج، والتي بدورها تفعّل محلقة الأدينيليل' = epinephrine, norepinephrine, ghrelin, testosterone, cortisol and growth hormone all stimulate fat release, acting through G-protein-coupled receptors that activate adenylate cyclase (ar.wikipedia.org — تحلل الدهن (arabic)). Three of those six had NO connection drawn to fat release at all before this. The practical point: the body has six ways to open this door, and several of them ARE things a person controls — sleep, training and fasting raise growth hormone; an empty stomach raises ghrelin. And one of the six is cortisol, which is also a stress hormone: the same signal that opens this door carries costs elsewhere. doi 10.1210/er.2008-0027
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.