Tired as hell on HGH

[Muscle_4_Hire]

I'm running 8 iu 6 days on, 1 day off of blue top HGH. I'm also doing this without insulin. As expected, I shoot in and I feel tired but I didn't know I'd be this tired. It feels like the morning after sleeping pills kinda thing. I take the HGH and it seriously knocks me on my ass where I'll sleep for 3 hours even if I slept 10 that night.
What could the problem be? I'm thinking it has something to do with insulin sensitivity since I'm not running slin with it. I'm thinking of 300 mg ALA and 300 mcgs of chromium piccinolate ED to increase sensitivity as Red Baron suggested.
Any thoughts on this?

[perfectbeast2001]

I doubt the slin issue is causing fatigue although it is a good idea to supp with those things if you are consuming GH near carbs.
Are you using any thyroid drugs. GH blunts the release of these in the body which can lead to feelings of lethargy. Try 100mcg of t4 every night.

[fred9]

Melanin-concentrating hormone (MCH [?]), a 19-amino acid orexigenic (appetite-stimulating) hypothalamic peptide, is an important regulator of energy homeostasis. It is cleaved from its precursor prepro-MCH (ppMCH) along with several other neuropeptides whose roles are not fully defined. Because pituitary hormones such as growth hormone (GH), ACTH, and thyroid-stimulating hormone affect body weight and composition, appetite, insulin sensitivity, and lipoprotein metabolism, we investigated whether MCH [?] exerts direct effects on the human pituitary to regulate energy balance using dispersed human fetal pituitaries (21-22 wk gestation) and cultured GH-secreting adenomas. We found that MCH receptor-1 [?] (MCH-R1 [?]), but not MCH receptor-2, is expressed in both normal (fetal and adult) human pituitary tissues and in GH cell adenomas. MCH [?] (10 nM) stimulated GH release from human fetal pituitary cultures by up to 62% during a 4-h incubation (P < 0.05). Interestingly, neuropeptide EI (10 nM), which is also cleaved from ppMCH, increased human GH secretion by up to 124% in fetal pituitaries. A milder, albeit significant, induction of GH secretion by MCH [?] (20%) was seen in cultured GH-secreting pituitary adenomas. A comparable stimulation of GH secretion was seen when cultured mouse pituitary cells were treated with MCH [?]. Treatment of cultured GH adenoma cells with MCH [?] (100 nM) induced extracellular signal-regulated kinases 1 and 2 phosphorylation, suggesting activation of MCH-R1 [?]. In aggregate, these data suggest that MCH [?] may regulate pituitary GH secretion and imply a potential cross-talk mechanism between appetite-regulating neuropeptides and pituitary hormones.

[perfectbeast2001]

Melanin-concentrating hormone (MCH [?]), a 19-amino acid orexigenic (appetite-stimulating) hypothalamic peptide, is an important regulator of energy homeostasis. It is cleaved from its precursor prepro-MCH (ppMCH) along with several other neuropeptides whose roles are not fully defined. Because pituitary hormones such as growth hormone (GH), ACTH, and thyroid-stimulating hormone affect body weight and composition, appetite, insulin sensitivity, and lipoprotein metabolism, we investigated whether MCH [?] exerts direct effects on the human pituitary to regulate energy balance using dispersed human fetal pituitaries (21-22 wk gestation) and cultured GH-secreting adenomas. We found that MCH receptor-1 [?] (MCH-R1 [?]), but not MCH receptor-2, is expressed in both normal (fetal and adult) human pituitary tissues and in GH cell adenomas. MCH [?] (10 nM) stimulated GH release from human fetal pituitary cultures by up to 62% during a 4-h incubation (P < 0.05). Interestingly, neuropeptide EI (10 nM), which is also cleaved from ppMCH, increased human GH secretion by up to 124% in fetal pituitaries. A milder, albeit significant, induction of GH secretion by MCH [?] (20%) was seen in cultured GH-secreting pituitary adenomas. A comparable stimulation of GH secretion was seen when cultured mouse pituitary cells were treated with MCH [?]. Treatment of cultured GH adenoma cells with MCH [?] (100 nM) induced extracellular signal-regulated kinases 1 and 2 phosphorylation, suggesting activation of MCH-R1 [?]. In aggregate, these data suggest that MCH [?] may regulate pituitary GH secretion and imply a potential cross-talk mechanism between appetite-regulating neuropeptides and pituitary hormones.

and the point of this is?????

[znak]

and the point of this is?????

He is checking our vocabulary and his own ability to cut and paste.

[Booz]

Melanin-concentrating hormone (MCH [?]), a 19-amino acid orexigenic (appetite-stimulating) hypothalamic peptide, is an important regulator of energy homeostasis. It is cleaved from its precursor prepro-MCH (ppMCH) along with several other neuropeptides whose roles are not fully defined. Because pituitary hormones such as growth hormone (GH), ACTH, and thyroid-stimulating hormone affect body weight and composition, appetite, insulin sensitivity, and lipoprotein metabolism, we investigated whether MCH [?] exerts direct effects on the human pituitary to regulate energy balance using dispersed human fetal pituitaries (21-22 wk gestation) and cultured GH-secreting adenomas. We found that MCH receptor-1 [?] (MCH-R1 [?]), but not MCH receptor-2, is expressed in both normal (fetal and adult) human pituitary tissues and in GH cell adenomas. MCH [?] (10 nM) stimulated GH release from human fetal pituitary cultures by up to 62% during a 4-h incubation (P < 0.05). Interestingly, neuropeptide EI (10 nM), which is also cleaved from ppMCH, increased human GH secretion by up to 124% in fetal pituitaries. A milder, albeit significant, induction of GH secretion by MCH [?] (20%) was seen in cultured GH-secreting pituitary adenomas. A comparable stimulation of GH secretion was seen when cultured mouse pituitary cells were treated with MCH [?]. Treatment of cultured GH adenoma cells with MCH [?] (100 nM) induced extracellular signal-regulated kinases 1 and 2 phosphorylation, suggesting activation of MCH-R1 [?]. In aggregate, these data suggest that MCH [?] may regulate pituitary GH secretion and imply a potential cross-talk mechanism between appetite-regulating neuropeptides and pituitary hormones.

lol FRED English please...............................

[fred9]

He is checking our vocabulary and his own ability to cut and paste.

lol...sorry, i just woke up when i pasted it..wasnt in the mood to type something more about it....i just checked a little about it last week...found some info about ghrelin, melanin and energy with gh-administration...

gh decreases ghrelin and melanin..which in turn influence energy balance in our bodies...didnt research any further, but those two are some important thiings with energy production / gh administration

here two more readable article:
Energy homeostasis – the balance of energy intake, expenditure, and storage – is controlled by autonomic regulation originating in the hypothalamus and the brain stem, which receive input from the periphery. Upon receiving signals from the periphery, centres in the central nervous system (CNS) react through endocrine or neuronal responses to maintain a steady balance. Growth hormone (GH) and melanin-concentrating hormone (MCH) act in the CNS to influence the energy balance and may be connected to the peripheral signals ghrelin and leptin. The overall aim of this thesis was to investigate how these different hormonal systems interact. To investigate the metabolic role of GH in the CNS, transgenic mice that overexpress bovine GH in the CNS (GFAP-bGH) were studied. GFAP-bGH mice have higher food intake and body weight and are obese compared with wild-type (WT) mice. Moreover, GFAP-bGH mice had hyperinsulinemia, pancreas islet hyperplasia, and dyslipidemia, but no changes in energy expenditure were observed. Thus, GH is an orexigenic signal in the CNS that leads to obesity and alters insulin and blood lipid profiles. Mice deficient in the gene encoding GHr (GHr KO) were injected in the CNS with ghrelin to study whether the orexigenic signal from ghrelin is dependent on functional GH signalling. The stimulatory effect of ghrelin on food intake was blunted in GHr KO mice, which suggests that the effects of ghrelin on food intake involve the central GH/GHr system. Furthermore, GHr KO mice were growth retarded and obese with higher leptin and corticosterone levels, low insulin and glucose levels and altered circulating lipids. Functional GH signalling is thus required for normal carbohydrate metabolism and lipid biology. The orexigenic neuropeptide MCH may also be involved in ghrelin-induced food intake and GH secretion. Food intake of mice that were deficient in the gene encoding MCHr (MCHr KO) and were injected in the CNS with ghrelin was similar to that of ghrelin injected WT mice, which suggests that MCHr is not required for the stimulating effect of ghrelin on food intake. But ghrelin had no effect on pituitary GH expression in MCHr KO mice, which suggests that MCHr is involved in ghrelin-mediated GH expression. Furthermore, MCHr is important for the acute effect of intracerebroventricular ghrelin on serum insulin but not on corticosterone levels. Thus, functional MCHr is required for the effects of ghrelin on GH expression and insulin secretion. Since leptin and MCH act in common pathways in the hypothalamus to regulate energy balance, leptin-deficient MCHr KO (MCHr KO ob/ob) mice were studied to investigate the importance of MCHr on the phenotype of ob/ob mice. MCHr KO ob/ob mice were similar to ob/ob mice concerning body weight, food intake, hepatic steatosis, blood lipid profile, and energy expenditure. But normal glucose tolerance and markedly reduced insulin levels were observed in MCHr KO ob/ob mice, indicating improved insulin sensitivity. MCHr KO ob/ob mice had higher locomotor activity, improved core body temperature regulation, and reduced corticosterone levels. Thus, MCHr may be involved in direct or secondary signalling cascades that lead to changes in insulin sensitivity, locomotor activity, and blood serum parameters. In conclusion, GH and MCHr play important roles in the CNS in regulating energy balance, including effects on food intake, body weight, obesity, and circulating endocrine signals.

Ghrelin: a hormone regulating food intake and energy homeostasis

--------------------------------------------------------------------------------
Mercedes Gil-Camposa1, Concepción María Aguileraa2, Ramón Cañetea1 and Angel Gila2 c1



a1 Unit of Paediatric Endocrinology Cordoba, Reina Sofia University Hospital, Spain

a2 Institute of Nutrition and Food Technology, Department of Biochemistry and Molecular Biology Campus de Cartuja 18071, University of Granada, Granada, Spain


Article author query


Gil-Campos M [PubMed] [Google Scholar]
Aguilera CM [PubMed] [Google Scholar]
Cañete R [PubMed] [Google Scholar]
Gil A [PubMed] [Google Scholar]


Abstract
Regulation of energy homeostasis requires precise coordination between peripheral nutrient-sensing molecules and central regulatory networks. Ghrelin is a twenty-eight-amino acid orexigenic peptide acylated at the serine 3 position mainly with an n-octanoic acid, which is produced mainly in the stomach. It is the endogenous ligand of the growth hormone secretagogue (GHS) receptors. Since plasma ghrelin levels are strictly dependent on recent food intake, this hormone plays an essential role in appetite and meal initiation. In addition, ghrelin is involved in the regulation of energy homeostasis. The ghrelin gene is composed of four exons and three introns and renders a diversity of orexigenic peptides as well as des-acyl ghrelin and obestatin, which exhibit anorexigenic properties. Ghrelin stimulates the synthesis of neuropeptide Y (NPY) and agouti-related protein (AgRP) in the arcuate nucleus neurons of the hypothalamus and hindbrain, which in turn enhance food intake. Ghrelin-expressing neurons modulate the action of both orexigenic NPY/AgRP and anorexigenic pro-opiomelanocortin neurons. AMP-activated protein kinase is activated by ghrelin in the hypothalamus, which contributes to lower intracellular long-chain fatty acids, and this appears to be the molecular signal for the expression of NPY and AgRP. Recent data suggest that ghrelin has an important role in the regulation of leptin and insulin secretion and vice versa. The present paper updates the effects of ghrelin on the control of energy homeostasis and reviews the molecular mechanisms of ghrelin synthesis, as well as interaction with GHS receptors and signalling. Relationships with leptin and insulin in the regulation of energy homeostasis are addressed.

[Muscle_4_Hire]

fred your posts dont have a summary so we cant make out what youre saying. beast do you really think t4 is the solution here? never thought it would be my thyroid

[IGOTJUICE007]

are you taking it all in one dose? My typical wake up is 8am (i know im lucky), so what I do is around 5am I wake up take a leak, and shoot my dose, that way when I get lethargic I am sleeping. When I wake up, I am good to go.

[Muscle_4_Hire]

I take all 8 iu in one dose and my inj time is 9AM since I wake up at 8 AM to get a shower etc... I work out of my home so being lethargic is manageable since I just put on some metal and it keeps me up.

I'm seeing that T4 converts into T3 in the body so wouldn't it be best to take T3? It would be a lot easier for me to get T3.

[Expat]

I'm running 8 iu 6 days on, 1 day off of blue top HGH. I'm also doing this without insulin. As expected, I shoot in and I feel tired but I didn't know I'd be this tired. It feels like the morning after sleeping pills kinda thing. I take the HGH and it seriously knocks me on my ass where I'll sleep for 3 hours even if I slept 10 that night.
What could the problem be? I'm thinking it has something to do with insulin sensitivity since I'm not running slin with it. I'm thinking of 300 mg ALA and 300 mcgs of chromium piccinolate ED to increase sensitivity as Red Baron suggested.
Any thoughts on this?

I also had that problem immediatley after starting growth in Feb 06. I finally went to the Doc and was diagnosed w/Mono. So you might want to have some labs done, to eliminate possible underlying medical issues. I have just begun recently feeling well enougth to start working out again. (I never stopped doing growth and continue to.>Good Luck

[jerseyboy]

I always felt dead tired and lethargic when doing morning injects. To make it worse your doing all 8iu's in the AM so it's no wonder your tired. Yes you can use T3. I do but it gives me a racing heart rate and anxiety. Now I take all 10iu's of my GH IM PWO with slin and IGF. For me it works out much better eliminating daytime drowsiness. Next week my work schedule is changing so I may be able to go back to early morning injects.

[perfectbeast2001]

http://www.anthony-roberts.com/th_gh.html

reason to take t4 instead of t3

[longhorn814]

I take all 8 iu in one dose and my inj time is 9AM since I wake up at 8 AM to get a shower etc... I work out of my home so being lethargic is manageable since I just put on some metal and it keeps me up.

I'm seeing that T4 converts into T3 in the body so wouldn't it be best to take T3? It would be a lot easier for me to get T3.

trying taking your shot about a hour or so before you actually get up