Insulin and Bodybuilding; Growth Hormone Releasing Peptides
by Author L. Rea
Publication Date: December 11, 2002 Nothing in this article is intended to take the place of advice from a licensed health professional. Consult a physician before taking any medication.
For note I am a national level competitor. Here are my questions that I would like you to help with:
Is taking GH a good idea at say 3iu 3x/day or will it be released as a consequence of mechanisms to a far greater degree naturally through this program and therefore not necessary as exo?
Can you eat as much fat as you wish due to the extra calorie expenditure (like with DNP) or is there a limit--I was eating about 4800 calories last bulking phase with minimum fat gain so if I ate about 800g protein how much fat is optimal with this plan, also would try to use 'good' fats predominantly like omegas, olive, walnuts, CLA, GLA, fish?
Obvioulsy in this plan am I correct to assume you CAN have slin and fat in system simultaneously or is that still best to try to avoid?
The table in the article shows that slin and test suspension are taken EOD each is this correct?
I see perhaps slin best to do EOD for the reason of sensitivity maintenance perhaps, but is it not best to have the most consistent levels of Test and use an oil based suspension either ED or 2xED?
BTW, I would likely do this with 150-200 ED or a tren base/Test base mix, maybe some d-bol for IGF-1 increase how does one eat in the off/no slin days if that is what is implied, less calories or stay the same? Have you read Oliver Starr's program and have any comments on his differing points like ED slin usage? Thank you for all your help... I want to do this as best as possible! A: Thank you for taking the time to not only read but to think about my article Big Fat Bastards and Insulin, Eric. First let me say that the use of insulin without proper medical supervision is quite dangerous in itself and I do not advise anyone to do so otherwise. The principal behind the protocol is the utilization of two growth facilitating Action/Reaction Factors of the body that simultaneously reduce adipose tissue synthesis and increase lean tissue mass: Insulin and IGF-1. When there are reasonably brief supraphysiological increases in circulatory insulin levels in the presence of hyperaminoacidemia (lots of extra amino acids in the circulatory system) and the absence of significant carbohydrate derived glucose, the result is an increase in the release of IGF-1 (both liver and cell derived). Additionally the cross over stimulation of insulin upon IGF-1 receptors becomes excessive. The result is a storing effect of nutrients focussed upon muscle tissue instead of adipose tissue or a division of the two. This is why athlete’s prosper through increase lean mass tissue as a result of GH use in the presence of carbohydrate derived glucose. The GH short cuts the series of metabolic Action/Reaction Factors facilitated by the Big Fat Bastard discussion protocol by inducing a very similar hormonal and enzymic environment. So the benefits of adding GH would be comparatively minimal and a waste of a perfectly primed alternative growth environment for the most part. Additionally you should realize that the idea behind protocol phasing is to allow the various anabolic pathways and receptor mechanisms a regeneration period for improved long term results. I will however add that if this were utilized during a calorie deficit period such as pre-contest the added anti-catabolic value of GH would be of value. This would also be effective in a few other specific intent protocols, but as I said prior…why waste a perfectly primed alternative growth environment? This obviously leads us to an expanded bit of information regarding diet. If an individual normally made good lean tissue progress with minimal fat accumulation during bulking phases employing a mixed macronutrient diet allowing for 5000 calories then the alterations are simple. The amount of protein necessary to support maximum growth and gluconeogenesis is calculated (Please refer to the Big Fat Bastards article) and the rest is calculated in fat calories plus 10%. This means calories are increased 10% or to 5500 calories daily. Fat sources are highly important. The addition of fish or hemp seed oil is a necessary consideration so as to off-set the potential for omega-6 vs. omega-3 EFA dominance. In short the excessive production of certain prostaglandins over others can be growth and health inhibitive due to an excess of their production substrates (omega-6 EFAs) being available at the wrong times. The use of CLA is mandatory during insulin employment and increased calorie consumption for a greater reduction in the possibility of adipose tissue augmentation. (Most actually lean out rather quickly considering the calorie intake) As a rule athletes have been told that the practice of having exogenous insulin and fat in the circulatory system simultaneously will lead to increased adipose tissue stores and other anti-growth events. In truth this is so when one employs a more common mixed diet that allows enough excess carbohydrate intake to elevate triglycerides significantly. Without going into a multi-page nutrient Action/Reaction chart let it be said that diets that foster ketosis and/or gluconeogenesis fail to result in this situation. Instead we realize an increase in fatty acid use as an energy source but a decrease in the enzyme process that allows for fat storage. A wiser individual would however have glucose tabs and a glucagon kit handy for emergencies. The every other day protocol structure employed for testosterone suspension and insulin out-lined in the Big Fat Bastard discussion protocol is designed to best utilize the alternating of both insulin and non-insulin mediated glucose/amino acid up-take mechanisms by muscle cells. Additionally the estrogen spikes and pits facilitate the natural release of GH and subsequently IGF-1 in a pulsitile fashion that compliments the opposing spikes and pits of exogenously administered insulin. Since the hepatic manufacture and release of IGF-1 is dependent upon these opposing activities it seems obvious that the protocol as designed was done so with this intent in mind. And in truth it has worked quite well in the past while remaining economical. It should be noted that even though the administration active-life of testosterone suspension is only about a day, its metabolites and plasma values exceed this. An example is that the DHT realized from a single administration of testosterone suspension will remain active for an additional day after the testosterone administration active-life has elapsed. This is a plus in that, like most variations of 5a-reductase androgens, DHT promotes glucose up-take by muscle cells and increased training intensity. This acts synergistically with the increase in estrogens to trigger growth mechanisms not insulin dependant. (Glucose derived from gluconeogenesis I should add) The by-line on this is that it is the sea-saw effect of alternating high plasma concentrations of insulin and testosterone in this properly timed sequence that results in a highly anabolic environment to muscle via multiple pathways. This in turn allows a so-called resting period for each pathway as the other is initiated. Personally I prefer the long term goal value of saving the trenbolone and D-ball for other protocols that they fit better into. Though I should add the note that the addition of both on the testosterone suspension administration days would produce greater short term results. I often find myself in a position where athletes simply are not aware of the fact that it is the proper use of phases, not simply cycles, that allows the most amazing potential for alterations in the project we call ourselves. Mister Rea
What do you know of the use of growth hormone releasing peptides in bodybuilding? Can growth hormone releasing peptides (GHRHP-2/GHRHP-6/hexarelin etc) lead to increase in muscles/ muscle sparing during caloric restriction? Would it be more efficient to take before bed, or before workout? Has anyone tried combining with androgens and or high dose arginine, low dose t3? How long is the increase in growth hormone? I hope these are not to many questions to ask, but thanks in advance! K. Boden A: I see that you have done some home-work on the subject, Lad. Knowledge leads to the ability to make better choices and in return predictable progress of a specific intent. As a drug administered in the absence of others for the purpose of muscular augmentation the GH secretagogues pretty much just suck. Let me babble for a bit and explain this to some extent. All of the chemicals you ask about including the amino acid arginine fall into a class called Growth Hormone Secretagogues (GHS). A GHS is just a chemical that by Action or Reaction aids in increasing the secretion or release of GH. If you recall several supplement companies were mass selling arginine and ornithine amino acid based products as the great steroid replacement supplements claiming that the huge increase in GH release would add 20 LBS of rock hard muscle in a short period of time…while you sleep! How did that work out for you? Like the rest of us, it didn’t. The claims were based upon a study that involved intravenous transfusions of 30 grams of arginine given to test subjects in a fasted state before sleep. Do the oral amino acid product’s work as well as the intravenous transfusions? (Quit laughing) No. But they can help in the right environment.Endogenous GH ReleaseBefore anyone can grasp the value of the effects (positive or negative) any chemical may or may not offer it seems obviously necessary to have a fundamental understanding of its origin and regulatory Action/Reaction Factors. In the case of GH secretagogues and related substances it is rather easy to explain. As is the case with other hormones and hormone–like substances, the body regulates GH secretion and activity by way of a series of checks and balances. Through chemical messengers your body is able to increase or decrease the release and activity of other substances. This is like sending an E-mail or letter with a set of instructions for the receiver while trying to avoid spamming. The two primary regulatory pep-tide hormones for GH originate at the hypothalamus. Growth Hormone Releasing Hormone (GHRH): Acts as a stimulator of GH release by binding with pituitary gland receptors thus triggering secretion of GH into the vascular system. When circulatory GH and IGF-1 levels are low the hypothalamus releases pulses of GHRH to go play nice with the pituitary gland. Somatostatin (SS): Acts as an inhibitor of GH release by binding with pituitary gland receptors and shutting down the GH secretion cascade. SS also inhibits cellular GH and IGF-1 interaction. When circulatory GH and/or IGF-1 Levels are high a negative feed-back loop occurs by the two hormones themselves merging with hypothalamic receptors that in turn trigger the up-regulation of SS release and shut down the goodies production. *Of course there are other functions dependent upon SS such as thyroid activity but that is not our point of interest here. So how do the chemicals you asked about act as GHS? Arginine and ornithine act as SS inhibitors and the pep-tides act as GHRH stimulators or analogs. Oddly enough these GHRH analogs are not structurally similar to GHRH and likely act upon other receptors (yet unidentified) than those of the GHRH origin. (Simple enough?) The important fact here is that some pep-tides have been documented to increase GH secretion by as much as 4000% over normal base-line for brief periods of time. The idea of a 4000% increase in endogenous GH secretion certainly sounds as if it would elicit a correlating increase in lean tissue growth. Studies on hexarelin, the most effective secretagogue tested so far, have shown a 40% decrease in action by the second week of administration and a 12% decrease each week after. This strongly suggests that there is a negative feed-back loop in play other than the shut-down of GHRH release by SS since the prior has been endogenously introduced in replacement. The progressive decline in GH release realized from hexarelin administration may appear trivial in the face of a 4000% increase but the data is misleading in this respect. The 4000% increase was based upon individuals who were nearly devoid of endogenous GH release and 400 times next to nothing is still nothing special. Sorry, my goal was to point out how the appearance of effectiveness can be misunderstood. So how do the chemicals you asked about work in the real world? In a well structured study called: "Arginine and growth hormone-releasing hormone restore the blunted growth hormone-releasing activity of hexarelin in elderly subjects" by Arvat E; Gianotti L; Grottoli S; Imbimbo BP; Lenaerts V; Deghenghi R; Camanni F; Ghigo E. performed at the Department of Clinical Pathophysiology, University of Turin, Italy and reported in the J Clin Endocrinol Metab 1994 Nov; 79(5):1440-3 we find useful answers. In this study researchers compared the GH responses to hexarelin, GHRH, and the combined administration of hexarelin and GHRH or arginine in young and elderly subjects. Thirteen young (24 to 30 years old) and 16 elderly (65 to 84 years old) average healthy males were divided into 2 test groups. The first group had 7 young and 8 elderly subjects who received the following as single iv injections during 3 different treatment sessions: hexarelin 2mcg/kg, GHRH 2mcg/kg, or hexarelin 2mcg/kg plus GHRH 2mcg/kg. The second group consisted of 6 young and 8 elderly subjects who were administered single iv injections of hexarelin 2mcg/kg or hexarelin 2mcg/kg plus arginine 0.5g/kg during 2 different treatment sessions. In both groups basal IGF-I levels in the elderly were lower than those in young subjects with a comparison value of 114.5 +/- 18.7 vs. 211.5 +/- 19.1mcg/L; P 0.001. In the first group the GH response to hexarelin was greater in young test subjects when compared to elderly subjects (area under the curve from 0-120 = 4849 +/- 601 vs. 2112 +/- 683 mcg.min/L; P 0.001). Interesting is that GHRH elicited a lower GH response than that induced by hexarelin in both young (1455 +/- 102mcg/h.L ; P 0.02) and elderly subjects (563 +/- 87mcg/min. L; P 0.02). GHRH potentiated the somatotrope response to hexarelin in both young (7725 +/- 503 micrograms/min. L; P 0.02) and elderly subjects (3895 +/- 612 micrograms/min. L; P 0.02), but to a lesser extent in the latter (P 0.001). In the second group, the GH response induced by hexarelin was also higher in young subjects than in elderly subjects (4819 +/- 668 vs. 1649 +/- 459 micrograms/min. L; P 0.001). The GH response to hexarelin was potentiated by arginine in elderly (4139 +/- 1057 micrograms/min. L; P 0.001), but not in young subjects (4743 +/- 774 micrograms/min. L) due to the lower SS release realized by younger males. This study shows that the maximal effective dose of hexarelin releases more GH than the maximal effective dose of GHRH in both young and elderly healthy test subjects. The effect of hexarelin on GH secretion is age dependent, and the GH response to the combined administration of hexarelin and GHRH was significantly higher in young subjects compared to elderly subjects. Arginine does not potentiate the GH response to hexarelin in young subjects, whereas it significantly enhances it in normal elderly test subjects. As most readers know by now the amount of IGF-1 produced as a result of an increase in circulatory GH is the reason an increase in muscle protein synthesis occurs. Therefore it is also a prime indicator as to the potential value of any chemical intended to increase circulatory GH levels. By this guidelines we see that there is actually a possible increase in IGF-1 of 250-1000% plus through administration of these secretagogues. Now that I had you suffer through some science geek stuff to make sure that everyone was on the same page, so to speak, we need to get to the part most are curious about: Do the drugs work? I looked for any studies on the use of secretagogues in relation to wasting diseases or athletics since both apply to the goal of increased protein synthesis and/or decreased catabolism of lean tissue mass. Sorry, none of any value. From personal experiences I can tell you that as a stand- alone chemical intended for any anabolic or anti-catabolic effect the substances have little value. However, they have shown a degree of regenerative value for suppressed endogenous GH release concerns originating from prolonged exogenous GH administration most have yet to consider. Or another point of interest is… The idea of utilizing drugs such as hexarelin and arginine during periods of calorie restriction has a great deal of potential value in relation to an improved biochemical profile most favorable to adipose tissue oxidation. One of the problems an individual faces when dieting for fat loss is the down-regulation of thyroid stimulating hormone (TSH) that begins at about 2 weeks and subsequent decrease in T-4 to T-3 conversion. This means that metabolic rate and specific uncoupling proteins decrease resulting in an increase in the amount of lean tissue mass lost with the intended fat (Yikes!). The reason TSH decreases is in part due to an increase in SS that inhibits its synthesis signal. So a substance that inhibits SS while promoting the release and effects of GH/IGF-1 would allow for less suppression of thyroid hormones and the all important uncoupling proteins related to their activity. Simply replacing the lost thyroid hormone with Cytomel or another T-3 drug does not allow for the entire synergistic hormone cascade to occur that is most favorable for fat loss and lean tissue retention during calorie restricted periods. The goal would therefore be to prolong the natural cascade for as long as possible or create protocols that regenerate the process intermittently similar to what is done with the HPTA and "The Boys". But that is another science geek lesson. |
