First cycle using HGH and or IGF-1 for hight and muscle growth

[SlimmerMe]

I never knew that! I thought that exogenous/endogenous GH has a short pulse and that you can bypass any "negative feedback" using these compounds. I guess this applies to peptides as well? Please, could you share a reference or source to this information?

Here is something Marcus 300 posted awhile back so hope this helps:

Like many hormones which are triggered by the HPTA have a negative feedback
loop, which simply means when levels are to high it will blunt the release
of any further hgh. HGH isnt just produced at night while in REM it pulses
throughout the day but the main the release is at night so taking HGH can
blunt some of the normal pulses throughout the day or night depending when
you take it. Ive read an article by Red Baron stating using exogenous HGH
will create this negative feedback on your HPTA for about 4 hours

[Sworder]

SlimmerMe, thank you very much for taking the time to explain it and refer to Marcus300. Now I won't comment on Marcus' post besides stating that I have never heard of hGH being mentioned along with the Hypothalamus-Pituitary-Testicular Axis. It's a united front, so to speak, if you mention specific pituitary functions that don't reflect in feedback loop of the testes. Making it wrong to say that hGH will create a negative feedback loop on the HPTA. I respectfully believe that your conclusions are wrong. It will create a short suppression but nothing worth mentioning to the degree that you did.

Thank you very much for taking the time. I sincerely appreciate it and sorry for playing hard-ball. I hate being an a$$hole, but I hate seeing wrongful information being put out even more.

Recovery of growth hormone release from suppression by exogenous insulin-like growth factor I (IGF-I): evidence for a suppressive action of free rather than bound IGF-I.
http://www.ncbi.nlm.nih.gov/pubmed/9709956

Abstract

To determine the time course of recovery of GH release from insulin-like growth factor I (IGF-I) suppression, 11 healthy adults (18-29 yr) received, in randomized order, 4-h i.v. infusions of recombinant human IGF-I (rhIGF-I; 3 microg/kg-h) or saline (control) from 25.5-29.5 h of a 47.5-h fast. Serum GH was maximally suppressed within 2 h and remained suppressed for 2 h after the rhIGF-I infusion; during this 4-h period, GH concentrations were approximately 25% of control day levels [median (interquartile range), 1.2 (0.4-4.0) vs. 4.8 (2.8-7.9) microg/L; P < 0.05]. A rebound increase in GH concentrations occurred 5-7 h after the end of rhIGF-I infusion [7.6 (4.6 -11.7) vs. 4.3 (2.5-6.0) microg/L; P < 0.05]. Thereafter, serum GH concentrations were similar on both days. Total IGF-I concentrations peaked at the end of the rhIGF-I infusion (432 +/- 43 vs. 263 +/- 44 microg/L; P < 0.0001) and remained elevated 18 h after the rhIGF-I infusion (360 +/- 36 vs. 202 +/- 23 microg/L; P = 0.001). Free IGF-I concentrations were approximately 140% above control day values at the end of the infusion (2.1 +/- 0.4 vs. 0.88 +/- 0.3 microg/L; P = 0.001), but declined to baseline within 2 h after the infusion. The close temporal association between the resolution of GH suppression and the fall of free IGF-I concentrations, and the lack of any association with total IGF-I concentrations suggest that unbound (free), not protein-bound, IGF-I is the major IGF-I component responsible for this suppression. The rebound increase in GH concentrations after the end of rhIGF-I infusion is consistent with cessation of an inhibitory effect of free IGF-I on GH release.