GHRP6 for bulking

[Elvia1023]

Ghrp6 is better for appetite stimulation. Ghrp2 has a stronger HGH release.

x2

They are very similar though in their effects.

Don't ever use GHRP-6 when cutting I am struggling with GHRP-2 as that can increase appetite too. After I inject it's a major struggle not to eat the entire fridge.

I think when cutting hexarelin and ipamorelin are best. GHRP-2 too if you don't get much of an appetite increase from it.

Overall GHRP-2 is probably the best all rounder.

GHRP-6 when you want lots of gh and trying to gain big weight.

 

[John Juan]

One of the first things users of ghrp6 notice is rapid strength gain.

 

[John Juan]

GHRP-6 was the first of a family of synthetic peptides discovered that will enhance the release of the Growth Hormone by the pituitary gland in a dose-dependent manner and as a chain reaction also cause a rise in IGF-1 levels in the body.

 

[Elvia1023]

One of the first things users of ghrp6 notice is rapid strength gain.

This has been mentioned by many recently. I usually dose my ghrp's pre workout . With 6 though I do it a little earlier then I have a big meal. 1 hour later I will have a light meal/snack for preworkout. Then I dose the ghrp-6 post workout and eat a massive meal full of protein and carbs.

 

[John Juan]

This has been mentioned by many recently. I usually dose my ghrp's pre workout . With 6 though I do it a little earlier then I have a big meal. 1 hour later I will have a light meal/snack for preworkout. Then I dose the ghrp-6 post workout and eat a massive meal full of protein and carbs.

One of the top amateur bodybuilders in the USA used ghrp6 to put on 60Lbs. His response to it was unreal. He weighs 285Lbs now very lean. I expect him to turn pro this year.

 

[John Juan]

Influence of sex, age and adrenergic pathways on the growth hormone response to GHRP-6.

AuthorsPeñalva A, et al. Show all Journal
Clin Endocrinol (Oxf). 1993 Jan;38(1):87-91.

Abstract

OBJECTIVE: His-dTrp-Ala-Trp-dPhe-Lys-NH2 (GHRP-6) is a synthetic compound that releases GH in a dose-related and specific manner in several species including man. To further characterize the effects of GHRP-6 on GH secretion in normal human subjects, we assessed plasma GH levels following GHRP-6 administration in normal male adult subjects, normal female adult subjects at different stages of their menstrual cycle and in normal prepubertal male and female children. We also studied the influence of adrenergic pathways on GHRP-6 induced GH secretion in normal adult male subjects.

DESIGN: In a group of eight volunteers the following tests were carried out: GHRP-6 alone (1 microgram/kg i.v. at 0 minutes); propranolol (40 mg p.o. at -30 minutes) plus GHRP-6; and prazosin (3 mg p.o. at -120 minutes) plus GHRP-6. Another group of eight volunteers were studied with GHRP-6 as above; clonidine alone (300 mg p.o. at -60 minutes); and clonidine plus GHRP-6. A group of nine women were studied with 1 microgram/kg i.v. of GHRP-6 at 0 minutes, at different stages of their menstrual cycle. Finally, 12 children were studied with GHRP-6 using the same dose and methods as above.

PATIENTS: Twenty-five normal adult subjects (16 male and nine female) and 12 normal prepubertal children (six male and six female) wer studied after giving informed consent.

MEASUREMENTS: Plasma GH levels were measured by radioimmunoassay.

RESULTS: No differences in GH responses to GHRP-6 were found between children and normal adult male or female subjects at different stages of their menstrual cycle. Administration of propranolol and clonidine did not modify the GH responses to GHRP-6 in male adults. In contrast, prazosin administration induced an increase in plasma GH levels that was statistically different from that of GHRP-6 alone (. < 0.05 between area under curve).

CONCLUSIONS: GHRP-6 exerts a potent stimulatory effect on GH secretion in adults and children. Its effects, at least at the dose studied, are independent of sex and age. Noradrenergic pathways through alpha 2 adrenergic receptors are unlikely to influence this response.

 

[John Juan]

I have my personal training client on 125mcg GHRP6 and 100mcg cjc1295 no dac, prior to each meal. He has gained 5Lbs in two weeks and his strength is exploding!

 

[John Juan]

Ablation of ghrelin receptor reduces adiposity and improves insulin sensitivity during aging by regulating fat metabolism in white and brown adipose tissues

Summary
Aging is associated with increased adiposity in white adipose tissues and impaired thermogenesis in brown adipose tissues; both contribute to increased incidences of obesity and type 2 diabetes. Ghrelin is the only known circulating orexigenic hormone that promotes adiposity. In this paper, we show that ablation of the ghrelin receptor (growth hormone secretagogue receptor, GHS-R) improves insulin sensitivity during aging. Compared to wild-type (WT) mice, old Ghsr−/− mice have reduced fat and preserve a healthier lipid profile. Old Ghsr−/− mice also exhibit elevated energy expenditure and resting metabolic rate, yet have similar food intake and locomotor activity. While GHS-R expression in white and brown adipose tissues was below detection in the young mice, GHS-R expression was readily detectable in visceral white fat and interscapular brown fat of the old mice. Gene expression profiles reveal that Ghsr ablation reduced glucose/lipid uptake and lipogenesis in white adipose tissues, but increased thermogenic capacity in brown adipose tissues. Ghsr ablation prevents age-associated decline of thermogenic gene expression of uncoupling protein 1 (UCP1). Cell culture studies in brown adipocytes further demonstrate that ghrelin suppresses the expression of adipogenic and thermogenic genes, while GHS-R antagonist abolishes ghrelin’s effects and increases UCP1 expression. Hence, GHS-R plays an important role in thermogenic impairment during aging. Ghsr ablation improves aging-associated obesity and insulin resistance by reducing adiposity and increasing thermogenesis. GHS-R antagonists may be a new means of combating obesity by shifting the energy balance from obesogenesis to thermogenesis.

 

[John Juan]

Doing a clean bulk at around 5,000 calories can be so difficult after a few weeks. You can only do so many things to make extra lean ground turkey breast and brown rice taste good. That's where ghrp6 is worth it's weight in gold! Even dog food is edible after a shot of ghrp6.

 

[Elvia1023]

The effects of GH-releasing peptide-6 (GHRP-6) and GHRP-2 on intracellular adenosine 3',5'-monophosphate (cAMP) levels and GH secretion in ovine and rat somatotrophs.

Wu D1, Chen C, Zhang J, Bowers CY, Clarke IJ.

Abstract

The mechanism of action of GH-releasing peptide-6 (GHRP-6) and GHRP-2 on GH release was investigated in ovine and rat pituitary cells in vitro. In partially purified sheep somatotrophs, GHRP-2 and GH-releasing factor (GRF) increased intracellular cyclic amp (cAMP) concentrations and caused GH release in a dose-dependent manner; GHRP-6 did not increase cAMP levels. An additive effect of maximal doses of GRF and GHRP-2 was observed in both cAMP and GH levels whereas combined GHRP-6 and GHRP-2 at maximal doses produced an additive effect on GH release only. Pretreatment of the cells with MDL 12,330A, an adenylyl cyclase inhibitor, prevented cAMP accumulation and the subsequent release of GH that was caused by either GHRP-2 or GRF. The cAMP antagonist, Rp-cAMP also blocked GH release in response to GHRP-2 and GRF. The cAMP antagonist did not prevent the effect of GHRP-6 on GH secretion whereas MDL 12,330A partially reduced the effect. An antagonist for the GRF receptor, [Ac-Tyr1,D-Arg2]-GRF 1-29, significantly diminished the effect of GHRP-2 and GRF on cAMP accumulation and GH release, but did not affect GH release induced by GHRP-6. Somatostatin prevented cAMP accumulation and GH release responses to GHRP-2, GRF and GHRP-6. Ca2+ channel blockade did not affect the cAMP increase in response to GHRP-2 or GRF but totally prevented GH release in response to GHRP-2, GRF and GHRP-6. These results indicated that GHRP-2 acts on ovine pituitary somatotrophs to increase cAMP concentration in a manner similar to that of GRF; this occurs even during the blockade of Ca2+ influx. GHRP-6 caused GH release without an increase in intracellular cAMP levels. GH release in response to all three secretagogues was reduced by somatostatin and was dependent upon the influx of extracellular Ca2+. The additive effect of GHRP-2 and GRF or GHRP-6 suggested that the three peptides may act on different receptors. In rat pituitary cell cultures, GHRP-6 had no effect on cAMP levels, but potentiated the effect of GRF on cAMP accumulation. The synergistic effect of GRF and GHRP-6 on cAMP accumulation did not occur in sheep somatotrophs. Whereas GHRP-2 caused cAMP accumulation in sheep somatotrophs, it did not do so in rat pituitary cells. These data indicate species differences in the response of pituitary somatotrophs to the GHRPs and this is probably due to different subtypes of GHRP receptor in rat or sheep.

PMID: 8699133 [PubMed - indexed for MEDLINE]