Please Scroll Down to See Forums Below I've never read much about this but if you look at the model of test supplementation or even insulin for that matter then wouldn't it apply to HGH? Is there any data on this? I've heard alot of seemingly knowledgeable guys on here talk about HGH, especially willbhuge, and your input would be much appreciated...
.jpg "Research Chemical Sciences")
.png "Research Chemical Sciences")
HGH and natural HGH supression...
- Thread starter Prince77
- Start date
There once was a bloke named Ironmaster who would post here. Many considered him a fountain of hgh knowledge. You may want to search the archives for some of his posts. I think I recall him once citing studies which found that exogenous hgh administration retards your pituitary's production by only 2 days even on a long cycle. Do not take this for gospel though as I am trying to remember the verbatims of an ancient post.
Singleton
New member
I read that test will bring back your gh levels. Here's 1 study that confirms it.
Clin Endocrinol Metab. 2004 Mar;89(3):1285-90. Related Articles, Links
Click here to read
Short-term testosterone supplementation relieves growth hormone autonegative feedback in men.
Veldhuis JD, Evans WS, Iranmanesh A, Weltman AL, Bowers CY.
Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905, USA. [email protected]
The present study tests the postulate that testosterone (Te) stimulates GH secretion, in part, by attenuating autonegative feedback. To this end, 13 healthy men (ages 43-71 yr) received three consecutive weekly im injections of placebo (Pl) (n = 7) or Te (200 mg) (n = 6) in a prospectively randomized, double-blind, parallel-cohort design. An iv pulse of saline or recombinant human (rh)GH (3 micro g/kg.6 min) was infused 2 h before bolus saline or GH-releasing peptide (GHRP)-2 (1 micro g/kg) in the fasting state. Blood was withdrawn every 10 min, GH concentrations were quantitated by chemiluminometry, secretion was determined by deconvolution analysis, and outcomes were compared by ANOVA. After Pl, rhGH suppressed basal, pulsatile, and GHRP-2-stimulated GH secretion by 2.6-, 2.4-, and 2.1-fold, respectively (each P < 0.03), and truncated GHRP-2-stimulated GH secretory bursts (P < 0.005). Compared with Pl, Te: 1) stimulated basal and pulsatile GH secretion by 1.9 and 2.4-fold (P < 0.01 and P < 0.02), respectively; 2) reduced feedback on basal GH secretion (P < 0.01); 3) blunted GHRP-2-stimulation by 1.9-fold (P < 0.01); and 4) facilitated initial recovery of rhGH-suppressed GH concentrations (P < 0.005). The foregoing actions were selective, inasmuch as Te did not relieve autoinhibition of pulsatile GH secretion. In summary, short-term Te supplementation decreases rhGH-imposed negative feedback on basal GH secretion and enhances early escape of GH from autoinhibition. In principle, such actions could potentiate the renewal of high-amplitude pulses of GH in androgen-replete individuals.
Clin Endocrinol Metab. 2004 Mar;89(3):1285-90. Related Articles, Links
Click here to read
Short-term testosterone supplementation relieves growth hormone autonegative feedback in men.
Veldhuis JD, Evans WS, Iranmanesh A, Weltman AL, Bowers CY.
Division of Endocrinology and Metabolism, Department of Internal Medicine, Mayo Medical and Graduate Schools of Medicine, General Clinical Research Center, Mayo Clinic, Rochester, Minnesota 55905, USA. [email protected]
The present study tests the postulate that testosterone (Te) stimulates GH secretion, in part, by attenuating autonegative feedback. To this end, 13 healthy men (ages 43-71 yr) received three consecutive weekly im injections of placebo (Pl) (n = 7) or Te (200 mg) (n = 6) in a prospectively randomized, double-blind, parallel-cohort design. An iv pulse of saline or recombinant human (rh)GH (3 micro g/kg.6 min) was infused 2 h before bolus saline or GH-releasing peptide (GHRP)-2 (1 micro g/kg) in the fasting state. Blood was withdrawn every 10 min, GH concentrations were quantitated by chemiluminometry, secretion was determined by deconvolution analysis, and outcomes were compared by ANOVA. After Pl, rhGH suppressed basal, pulsatile, and GHRP-2-stimulated GH secretion by 2.6-, 2.4-, and 2.1-fold, respectively (each P < 0.03), and truncated GHRP-2-stimulated GH secretory bursts (P < 0.005). Compared with Pl, Te: 1) stimulated basal and pulsatile GH secretion by 1.9 and 2.4-fold (P < 0.01 and P < 0.02), respectively; 2) reduced feedback on basal GH secretion (P < 0.01); 3) blunted GHRP-2-stimulation by 1.9-fold (P < 0.01); and 4) facilitated initial recovery of rhGH-suppressed GH concentrations (P < 0.005). The foregoing actions were selective, inasmuch as Te did not relieve autoinhibition of pulsatile GH secretion. In summary, short-term Te supplementation decreases rhGH-imposed negative feedback on basal GH secretion and enhances early escape of GH from autoinhibition. In principle, such actions could potentiate the renewal of high-amplitude pulses of GH in androgen-replete individuals.
