bronco944 said:
i knew there had to be a downside. now if you were on cycle though the test reduction would not be a problem. the main question i have is is the gh release significant enough to cause any positive effects and would the cortisol release be a problem even while on cycle? dont certain Anabolic Androgenic Steroids (AAS) decrease cortisol release?
Elijah, i agree with everything you said and was not trying to say to take slin the way i do. the point i was trying to get across was that fat intake is not the biggest problem, its the total number of cals that make you get fat. most people overdo the number of carbs post shot. If fat gain is a concern, one should work there carb intake down post shot as they get more comfortable with slin, as this would reduce the total number of cals. you obviously dont want to reduce the protein and assuming fat intake is at a minimal carb reduction is the only way to cut calories post injection to prevent gaining fat.
Increased cortisol & PRL, and lowered test are not important while on AAS.
Your androgen/cortisol ratio is really high while on...
Is GH release significant enough to cause any positive effects ?
I'm not sure..
Your GH/IGF-1 will be significantly increased while on cycle so I don't know how much will the insulin induced hypoglycemia contribute....
The GH release induced by hypoglycemia is definitely significant, though.
The influence of insulin on circulating ghrelin.
Flanagan DE, Evans ML, Monsod TP, Rife F, Heptulla RA, Tamborlane WV, Sherwin RS.
Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Ghrelin is a novel peptide that acts on the growth hormone (GH) secretagogue receptor in the pituitary and hypothalamus. It may function as a third physiological regulator of GH secretion, along with GH-releasing hormone and somatostatin. In addition to the action of ghrelin on the GH axis, it appears to have a role in the determination of energy homeostasis. Although feeding suppresses ghrelin production and fasting stimulates ghrelin release, the underlying mechanisms controlling this process remain unclear. The purpose of this study was to test the hypotheses, by use of a stepped hyperinsulinemic eu- hypo- hyperglycemic glucose clamp, that either hyperinsulinemia or hypoglycemia may influence ghrelin production. Having been stable in the period before the clamp, ghrelin levels rapidly fell in response to insulin infusion during euglycemia (baseline ghrelin 207 +/- 12 vs. 169 +/- 10 fmol/ml at t = 30 min, P < 0.001). Ghrelin remained suppressed during subsequent periods of hypoglycemia (mean glucose 53 +/- 2 mg/dl) and hyperglycemia (mean glucose 163 +/- 6 mg/dl).
Despite suppression of ghrelin, GH showed a significant rise during hypoglycemia (baseline 4.1 +/- 1.3 vs. 28.2 +/- 3.9 microg/l at t = 120 min, P < 0.001). Our data suggest that insulin may suppress circulating ghrelin independently of glucose, although glucose may have an additional effect. We conclude that the GH response seen during hypoglycemia is not regulated by circulating ghrelin.
Variable plasma growth hormone (GH)-releasing hormone and GH responses to clonidine, L-dopa, and insulin in normal men
P Tapanainen, M Knip, P Lautala and J Leppaluoto
Department of Pediatrics, University of Oulu, Finland.
The effects of synthetic GHRH-(1-44) (1 microgram/kg, iv), clonidine (0.15 mg/m2, orally), L-dopa (0.5 g, orally), and insulin (0.1 IU/kg, iv) on plasma immunoreactive (ir) GHRH and GH levels were determined in normal men, aged 31-46 yr (n = 4-8). In addition, plasma ir-GHRH and GH concentrations were determined before and after the administration of clonidine in six younger men, aged 19-25 yr. GHRH was extracted from plasma using Sep-Pak C18 cartridges and measured with a mid-portion- specific GHRH antiserum. The mean plasma ir-GHRH and GH levels ranged from 9-11 ng/L and 0.5-1.5 microgram/L, respectively, in the older men during a 2-h control study. After GHRH administration, the mean plasma ir-GHRH concentration increased to a peak of 512.5 ng/L at 3 min and GH to a peak of 9.2 micrograms/L at 10 min. Clonidine resulted in a significant increase in mean plasma GH levels (P less than 0.05) in the younger men, but not in the older men. Plasma ir-GHRH concentrations did not change after clonidine. L-Dopa increased plasma ir-GHRH at 60 min (P less than 0.05) and GH at 60-120 min (P less than 0.05).
Insulin- induced hypoglycemia increased plasma GH levels (to a mean of 23.8 micrograms/L at 60 min; P less than 0.001), whereas plasma ir-GHRH levels did not change. We conclude that the mechanisms of the various GH stimulation tests differ. Some GH responses, including those induced by insulin, do not appear to be mediated by GHRH.
Exercise can increase your GH more than 10 fold from baseline, but IGFBP-1 goes up also...