I ended up having my slin and fruit smoothie about 2 hours after my previous meal. I had my serving of pre workout and a home made scone and left for the gym. I trained back, calves and hams and finished with 10 mins of intense cardio. I trained for about 2 1/2 hours and pushed it. Probably about 40 sets for back... I was dripping with sweat the entire time. The pump I got from the slin and pre workout was insane. It effected my grip strength as my forearms/bi-ceps (and the rest of me) got so pumped up. I made good use of my lifting wraps tonight.
I had 1 serving of secret sauce post workout in the sauna and that went down well (tastes great). When I got home I shot 150mcg cjc no dac and ghrp-2... 15 mins later 2IU hgh. The pep combo made me go hypo bad... I started cooking my post workout meal after the pep shots. I could feel it so I had a yoghurt whilst I cooked. By the time I done the rice and chicken and plated up I probably left it a few mins too much. The sweat was dripping off me, hands were shaking and my legs felt like jelly. People say peps (ghrh/ghrp) can't make you go hypo and it's the ghrelin release but trust me this was hypo. I started to feel better once I ate my meal... I drizzled honey on top of the chicken to speed up the process.
I have never done too much research on this subject but I know GH has an effect on various bodily systems that can cause hypo and hyperglycemia. This was definitely hypoglycemia though. I have just researched the subject and found these studies:
Nat Clin Pract Endocrinol Metab. 2007 Mar;3(3):302-10.
Mechanisms of disease: metabolic effects of growth hormone and insulin-like growth factor 1.
LeRoith D1, Yakar S.
Abstract
Insulin-like growth factor (IGF) 1 is a member of a family that is involved in growth, development, cell differentiation, and metabolism. IGF1, IGF2 and insulin act primarily through tyrosine-kinase-linked receptors--the IGF1 receptor (IGF1R) and insulin receptor (IR). The IGF1R binds IGF1 and IGF2 with high affinity and the IR binds insulin with high affinity; however, since both receptors share a high degree of structural and functional homology, the IGF1R can bind insulin and the IR can bind the IGFs with reduced affinity. These two receptors can, moreover, form heterodimers, which bind both ligands. Upon binding to the receptors, cascades of tyrosine and serine kinases are stimulated to facilitate growth or metabolism. The IGF2 receptor is a scavenger receptor, and is, therefore, not involved in mediation of growth or metabolic effects of the IGF family and will not be discussed in the current article. IGF1 is a major gene target of growth hormone and its product mediates many of the actions of growth hormone on growth and development; however, IGF1 has actions distinct from those of growth hormone in carbohydrate, lipid, and protein metabolism. For example, excess growth hormone causes insulin resistance and hyperglycemia, whereas IGF1 has insulin-like effects that reduce blood glucose levels and has been used experimentally to treat both type 1 and type 2 diabetes.
PMID: 17315038 [PubMed - indexed for MEDLINE]
Endocr J. 2010;57(7):639-44. Epub 2010 Apr 17.
Concordant and discordant adrenocorticotropin (ACTH) responses induced by growth hormone-releasing peptide-2 (GHRP-2), corticotropin-releasing hormone (CRH) and insulin-induced hypoglycemia in patients with hypothalamopituitary disorders: evidence for direct ACTH releasing activity of GHRP-2.
Kimura T1, Shimatsu A, Arimura H, Mori H, Tokitou A, Fukudome M, Nakazaki M, Tei C.
Abstract
The insulin-induced hypoglycemia test (insulin tolerance test: ITT) and corticotropin-releasing hormone (CRH) test are used to examine the activities of the hypothalamo-pituitary-adrenal (HPA) axis. Growth hormone-releasing peptide-2 (GHRP-2), a potent GH secretagogue, also stimulates adrenocorticotropin (ACTH) secretion. To evaluate the role of GHRP-2 in assessing the HPA axis, we examined 6 patients with various hypothalamo-pituitary disorders, and measured ACTH and cortisol responses during provocative tests (ITT, CRH, and GHRP-2 test). None of the 6 patients showed any significant ACTH or cortisol responses to ITT, but significant ACTH release was observed during CRH and GHRP-2 tests. These findings suggest GHRP-2 may directly stimulate ACTH secretion in patients with hypothalamo-pituitary disorders.
PMID: 20431231 [PubMed - indexed for MEDLINE]
Metabolism. 1981 Oct;30(10):996-1000.
Hypoglycemia stimulates ACTH secretion through a direct effect on the basal hypothalamus.Aizawa T, Yasuda N, Greer MA.
Abstract
The primary site of action of insulin hypoglycemia to induce ACTH secretion was investigated in rats with medial basal hypothalamic ablation (MBHA), medial basal hypothalamic deafferentation (MBHD), and chlorpromazine-morphine-pentobarbital (C-M-P) treatment. Plasma corticosterone (B) concentration was used as an index of ACTH secretion. Hypoglycemia failed to provoke ACTH secretion in MBHA and C-M-P treated animals, while it stimulated ACTH secretion in MBHD animals to the same extent as in controls. The rise in plasma B induced by synthetic lysine-vasopressin injection was not significantly different between MBHA and control animals, indicating pituitary ACTH reserve was not affected by the operation. Our data indicate that hypoglycemia stimulates ACTH secretion through a primary effect in the medial basal hypothalamus and not in the extrahypothalamic CNS or adenohyphophysis.
PMID: 6268929 [PubMed - indexed for MEDLINE]
Cell Metab. 2013 Oct 1;18(4):596-607. doi: 10.1016/j.cmet.2013.09.002.
Profiling of Glucose-Sensing Neurons Reveals that GHRH Neurons Are Activated by Hypoglycemia.
Stanley S1, Domingos AI, Kelly L, Garfield A, Damanpour S, Heisler L, Friedman J.
Abstract
Comprehensive transcriptional profiling of glucose-sensing neurons is challenging because of low expression levels of glucokinase (Gck) and other key proteins that transduce a glucose signal. To overcome this, we generated and validated transgenic mice with a neuronal/endocrine-specific Gck promoter driving cre expression and mated them to mice with cre-dependent expression of an EGFP-tagged ribosomal protein construct (EEF1A1-LSL.EGFPL10) that can be used to map and profile cells. We found significant Gck expression in hypothalamic and limbic regions in cells that are activated following administration of glucose or 2-deoxyglucose. Transcriptional profiling from Gck-cre/EEF1A1-LSL.EGFPL10 mice enriched known and previously unknown glucose-sensing populations including neurons expressing growth hormone releasing hormone (GHRH). Electrophysiological recordings show that hypoglycemia activates GHRH neurons, suggesting a mechanistic link between hypoglycemia and growth hormone release. These studies provide a means for mapping glucose-sensitive neurons and for generating transcriptional profiles from other cell types expressing cre in a cell-specific manner.
Copyright © 2013 Elsevier Inc. All rights reserved.
PMID: 24093682 [PubMed - indexed for MEDLINE]
I will do more research on the subject when I have time. Regardless I am feeling good and looking forward to training 2moro night. I am thinking shoulders, arms and quads.