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By Wesley James
I'm hopeful that these random bits of research data will be useful to the reader in developing their own ideas about how they may use GH releasers and/or HgH in their training efforts.
Hormones of the GH Cycle
GHRH Prolactin Somatotropin (STH) Luteinizing Hormone Somatostatin Follicle Stimulating Hormone Somatocrinin Thyroid Stimulating Hormone Somatomedin Thyroxine - Thyroid Hormone
Two factors may be relevant to the action of GH: Absolute GH level and GH to Insulin Ratio.
Low levels of GH and high levels of Insulin are both associated with obesity (Bray 1983).
Lactic Acid may be the trigger substrate for GHRH.
GH levels generally and peak GH levels particularly drop 40% from age twenty-thirty and another 40% from age thirty-forty. There is a further drop beyond this with increasing age.
All GH levels, especially exercise induced GH release, decline rapidly through the thirties (Bazzare 1975, Prinz 1976, Zadik 1985).
GH blocks Insulin activity, stopping Glucose uptake into muscle cells.
High Glycemic Carbs block GH releasers.
It is GH's similarity to Insulin that causes fat loss by blocking Insulin's conversion of Glucose to fat.
GH encourages the use of fat for energy (Murad 1980).
Both GH and Insulin are required for muscle growth.
10 Grams of oral Arginine powder 1 Hour (1.5 Hours for capsules) produces GH release sufficient for fat burning and muscle growth when coupled with peak output exercise. (Individuals over 200 lbs probably need 12 Grams of Arginine.)
While Thyroid Stimulating Hormone may release GH, Thyroid Hormone itself (Thyroxine) does not.
The Hypothalamus produces GHRH which causes the Pituitary to release STH. There may be a number of intermediary and/or supplementary hormone secretions from various glands We are unaware of any definitive research on which hormones trigger or block other hormone secretions and in what order or at what levels. Among the secretions affected, in addition to GH, are Prolactin, Luteinizing Hormone, Follicle Stimulating Hormone, Thyroid Stimulating Hormone and, as previously mentioned, Insulin. The point is that while the muscle press applauded GH releasers and has now become almost dismissive of them and is now dealing with Insulin in somewhat the same way, the picture is far more complex then any of these journals have reported. As an example, to insure GH releaser effectiveness, a five hour time window is necessary, 3 hours before and two hours after. This window can be manipulated through the use of other substrates. Niacin, for example can be used to more rapidly reduce blood sugar levels but careful attention to dosage levels and timing are absolutely essential to the use of GH releasing nutrients. Moreover, this was made clear by Pearson and Shaw when they first introduced the idea to the bodybuilding world. (Though the Baryology (weight-control) research community had been aware of it for some time before.)
The GH release effect of Arginine is through Acetyl-Choline release. Acetyl-Choline levels must be kept high if GH release efforts are to be successful.
Low Potassium levels (as from diuretics), block GH release.
Phenylalanine and/or Tyrosine do not cause GH release but are involved in CCK production and thus appetite control.
Ornithine is twice as effective as Arginine in causing GH release.
Since Arginine causes an Insulin release, even in the absence of raised blood sugar levels, it produces a form of reactive hypoglycemia which accounts for a small portion of its GH Release action. This portion of the Arginine generated GH release is less affected by the proximity of dose administration to other protein intake.
The use of Melatonin may encourage GH release through the same mechanism as Tryptophan, the increase in serotonin levels at night.
The use of B-6 (pyridoxine) to augment exercise-induced GH release may work in individuals over age 30. If it does, it would require a 600 Mg oral dose 45 minutes before exercise. There are two problems with this approach: If it is used frequently, peripheral neuralgia may develop. Even occassional use can produce psychological depression which may last for days afterward.
Growth Hormone - The Multi-Pathway Theory
It is reasonably clear that GH releasers are not anabolic in the same way as Testosterone or the anabolic Steroids. At the same time, they are clearly ergogenic-- using the term loosely. It is also fairly apparent that the use of Human Growth Hormone (HgH), even the synthetic stuff, is anabolic, though not as much so as many Steroids. These observations started me searching the literature for an explanation. How is this possible? What is the mechanism through which GH releasers work? Is the pathway for HgH different from GH releasers?
The answer seems to be "yes". The reason may rest in the sequence in which the group of growth hormones are released and the balance between them. Synthetic HgH appears to the body to be Somatotropin. Somatotropin it appears is the anabolic member of the GH family. It is, however, only anabolic to the extent that it exceeds the levels of Somatostatin. The role of Somatomedin and Somatocrinin is less clear. Let us look a bit more closely at the interaction between these and the other related hormones.
It appears from the research that Somatotropin and Somatostatin, in effect, "neutralize" each other in a process common in the body. They seek to maintain stasis. The net result being no increase in muscle size. When one injects HgH, Somatotropin levels rise rapidly but since the normal pathway has not been triggered there is no corresponding level in Somatostatin. Under these conditions, until the body can produce a balancing level of Somatostatin the anabolic drive is triggered and muscle growth is stimulated. Unfortunately, so is bone and possibly organ growth in the viscera. This can lead to Acromegaly and Liver and/or Kidney damage with potentially fatal consequences.
These health risks are much reduced by age, Older individuals, having lower natural GH secretion levels, are likely to derive far more benefit from the use of exogenous HgH. This explains why a number of medical spas in Mexico and Europe are helping to reverse the the apparent signs of aging through the use of HgH.
Much more needs to be learned about the use of HgH for all types of individuals from young to old but it seems clear at this point that HgH does have an anabolic as well as ergogenic effect, albeit a risky one for most bodybuilders.
Our exploration now turns to the use of GH releasers. There are many substances that have been found to raise serum GH levels. What is rarely looked at in studies of the substrates or combinations of substrates is which hormone's levels are being raised and what ratios these elevated levels have to the other members of the group. It would appear that most GH releasing metabolites raise Somatotropin levels but with a corresponding increase in Somatostatin levels. This seems to produce a net wash in terms of anabolic drive but not in lipolytic drive. It is the observation of this phenomenon that leads me to strongly suspect that it is the action of another of the GH family that triggers the lipolytic effect. Strong suspicion falls to Somatomedin or Somatocrinin or more likely the balance between them.
Look at it this way, the ratio between Somatotropin and Somatostatin regulates the anabolic effect while the ratio between Somatomedin and Somatocrinin regulate the lipolytic effect. If this is true, and research will be required to prove it, then GH releasing combinations might be optimized for the desired effect. In the months to come, I'll be describing combinations of Over-the-Counter (OTC) supplements that will stimulate different GH ratios. This will be done in a novel way designed to allow us, together, to develop data that may clarify this poorly understood area of supplementation.Copyright © 1996 Physique Tools and Wesley James
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