Maximum
Human Growth Hormone for Dummies
by L.
Rea
Growth hormone (GH) has been surrounded by a cloud of mystique for many years carried by whispered hushes of freak status and a shot at the Mr. O for those who venture its use. Warnings of facial disfigurement and hopes of sexual appendage elongation alike have accompanied the strange tales of this hormone’s power. Wow, get a life!
The truth is that GH works very well indeed…if it is properly employed. If An athlete has trained and eaten correctly (many do not of course) the net gain in lean tissue mass can be as much as a 14% increase in total lean mass in a matter of weeks with a similar corresponding loss in adipose (fat) tissue. But the effects are far positive effects of a GH protocol can be far reaching in that the protocol allows continued progress where none has been realized for quite some time. Many lose much of the potential possible progress during the actual GH protocol and almost all give up the long-term gains that they could have realized by simply understanding a few facts of reality concerning GH use. Employment of these facts usually results in realizing the 14% net gain possible and keeping them post-protocol while adding a few more freaky pounds. Been there done that.
There are several hormones, hormone-like substances, and a few supplements that act anabolically enough to result in an increase in lean muscle mass without any degree of androgenic activity. Many of these substances are highly anti-catabolic as well. If an athlete’s goal is to make continuous progress either an anabolic or anti-catabolic environment must be maintained without creating uncontrolled negative reactions to the intended anabolic or anti-catabolic action. In the case of Absolute Anabolics this means that the anabolic signaling method must be phased or cycled in the appropriate time frames as well as utilization of the correct products to aid an athlete in working with instead of against their bodies. We will first discuss the hormone and then discuss OTC products that either positively affect them or those that mimic their activity.
Growth
Hormone (GH)
GH is
probably the best known of the hormones we refer to as Absolute Anabolics. GH
is often heralded to be a fountain of youth for the aging and a mandatory addition
to the drug protocols of the elite competitive athlete. It is also naturally produced
within the body.
The average healthy adult produces between 0.5-1.5 iu (international units) of GH daily. This is not to say that the body cannot produce a great deal more GH, only that this is all the body wants to produce for our declining post-adolescent years. (Which really sucks) After all, we are past our hormonal prime as males at age 18-25 (yet we are not in our muscular prime for well over a decade after).
A growing child produces 4-7 GH pulses of about 2iu each for 4-5 days but not necessarily on consecutive days. This amounts to as much as 70iu of GH entering the circulatory system in a rather brief period. (Gee, and I wonder why I have to buy clothes for my kid about every other week?)
As we have discussed in earlier
books and articles, the two types of muscle proteins capable of growth are structural
and contractile proteins. Contractile proteins are called actin and myosin. Their
job is to induce body movement through contractions that result in the shortening
of the muscle fibers. This is quite similar to a ratcheting effect in action.
The structural proteins hold the entire muscle and connective tissue complex together.
Both proteins add to total muscle mass, strength potential and density. GH has
a profound positive effect upon structural protein anabolism while providing a
degree of increased protein synthesis within contractile proteins. Additionally,
GH use results in a very powerful anticatabolic effect. By increasing total structural
protein content we realize a very obvious increase in lean muscle mass and strength
potential while benefiting actual structural integrity. This is important when
considering long-term potential and results. Structural integrity can be a dramatic
limiting factor or growth stimulus. The lack of supporting tissues obviously also
limits potential training weight-loads for the affected muscle groups. Therefore
a greater degree of structural protein synthesis results in an increase in contractile
protein synthesis due to adaptation to a greater weight-load. (Gee, ya think so?
Duh)
Consider this aspect of structural integrity: Would you try to
do bar squats on loose sand? Of course not! And the reason is due to a lack of
structural integrity. So why would anyone seeking to build the perfect beast disregard
the necessity of a complete musculature?
Yes,
there are a few other benefits to increased GH levels to consider…
*Increased lean mass tissue *Improved memory
*Increased strength
*Improved stamina
*Increased Libido *Stronger bones
*Lower blood pressure
*Lower bodyfat percentage
*Increased rate of recovery and regeneration of
tissues
*Regeneration of skin proteins and improved skin elasticity
*Anticatabolic/lean
tissue sparing during calorie restricted periods
*Increased use of fat stores
as an energy source.
Some older athlete’s have reported an increase in hair growth on the pate and a decrease in gray hair.
Many of the effects of GH can be attributed to the known 8 growth factors resulting from its elevation in the circulatory system. Of these the most noted growth factor in the sports community is IGF-1, and less so FGF. Many who have used GH with poor results simply did not realize the chain of events that GH use induces and therefore missed the long-term gains that they had at their finger-tips. Of course some simply totally screwed up the protocol.
Okay, Science Geek Time!
I realize that reading through the science behind a given subject can be as boring as watching mold grow on a kitchen sink (actually had to do this in a biology class years ago…had two very hot lab partners though) but the ability to create protocols of specific intent with a known out come requires some degree of knowledge relating to the Action/Reaction Factors that effect it…and therefore us.
There are immature cells that sit out-side of, but joined to, muscle fibers called satellite-cells or stem-cells. These are metabolically active cells that do not have the capacity to (yet) join in with all of the other muscle cells and fibers to produce contractile force. They also lack fiber-type and much of a growth capacity (duh!). So picture this as a sort of muscle cell nursery. The proliferation/multiplication of these satellite-cells is induced by FGF (Fibroblast Growth Factor) when it merges/binds with existing cell receptors. The result is an up-regulation in satellite-cell count and production (more cells).
The mature satellite-cells sit around the muscle cell nursery stealing food from the immature satellite-cells and pretty much do nothing. (Like most adolescents. Gee I miss those days). Some type of (there are several) an Action Factor occurs that results in the production/release of IGF-1 (Insulin-Like Growth Factor-1). When IGF-1 binds to its satellite-cell receptor the inclusion process of that cell into its adjoined muscle fiber results. The eventual out come is more muscle cells and fibers. These two events are called hyperplasia.
Now that the mature satellite-cells have become muscle cells, it is time to get a job. In the presence of high circulatory androgen/testosterone levels, massive muscle cell androgen receptor/testosterone binding occurs. The result is that, at the expense of type-I muscle fibers, an increase in type-II muscle fiber count occurs. The second Reaction Factor that happens is increased muscle cell contractile protein synthesis (anabolism/growth). This is called hypertrophy because each affected cell is getting larger. If anyone missed the point, this means that we can change low growth potential type-I fibers into high growth potential type-II muscle fibers.
Insulin binding with its cell receptor
initiates a series of events that results in increased cellular up-take of glucose
(from carbohydrates), fatty-acids (from fats), amino acids (from proteins), and
micro-nutrients. This means that insulin has the ability to increase cellular
growth nutrient up-take to a point of triggering anabolism/growth/hypertrophy.
Unfortunately supraphysiological insulin levels result in the up-take of only
about half of the necessary amino acids for cell growth. (Which sucks, but the
process is yet unfinished)
When GH binds to its healthy muscle cell receptor,
several good things happen:
The cell increases IGF-1 production.
The cell
switches to favoring fat as a main energy source.
An increase in structural
protein synthesis occurs (anabolism)
The up-take of the other half of the
necessary amino acids for cell growth significantly increases.
Thyroid
Hormones regulate the body’s metabolic rate. That is:
The rate at which
cells absorb and utilize calories.
The rate of protein synthesis occurs.
The rate at which fat is oxidized (burned).
*The liver readily forms circulatory IGF-1 in the presence of GH and Insulin. Metabolically active cells secrete IGF-1 as a result of meeting up with GH, estrogens, or as a result of a chemical cascade originating from cellular and tissue elongation (stretching).
The human body is an amazingly adaptive
organism that is basically lazy. In short it fights change by doing as little
as possible. The body prefers to slowly degrade into mediocrity through preservation
of homeostasis. Homeostasis simply means a state of no change. Yup: Weenie status.
Anytime the hormone ratio/profile that supports this slide in the oblivion is
altered the body either attempts to shut down the offending organ or gland, or
inhibits the effect at the cellular level. Obviously GH and its growth factor
substrates are no different in this aspect.
Control Of The GH/IGF-1 Axis
There
are two recognized peptide hormones known to regulate the body’s GH levels.
When the hypothalamus secretes GHRH (growth hormone releasing hormone) it contacts
its receptors of the pituitary gland resulting in a pulsitile release of GH. If
there were no inhibiting hormone, or negative feed-back loop, the levels of circulatory
GH and resulting IGF-1 would reach a very profound measure indeed (Oh darn). Somatostatin
is the hormone that tells the pituitary to decrease or stop GH secretion. But
of course it does not stop there. Somatostatin triggers GH/IGF-1 receptor down-regulation
and a decrease in sensitivity as well as acting to decrease the secretion of TSH
(thyroid stimulating hormone). The result is a decrease in metabolic rate and
a reduction in net anabolism. Sucks, huh? Ya, so does the correlating decrease
in calorie expenditure from fat stores and an increase in muscle catabolism (fat
dude status). So, all we have to do is decrease or stop the somatostatin release
and shredded freak status will soon be ours…right?
There is a second inhibitive pathway to regulate GH levels is called a negative feed-back loop. When circulatory GH or Somatostatin makes its way back to the hypothalamus and/or the pituitary gland the over abundance of either will shut down its own respective receptors as well.
Bottom-Line
When an athlete administers supraphysiological dosages of GH for a prolonged period
of time without correctly anticipating and responding to Action/Reaction Factors
the pituitary and hypothalamus respond to the increasing negative feed-back loop
by shutting down first GHRH release and second shutting off the GH supply. So
GH release is suppressed on two levels. Next the release of Somatostatin gradually
increases to beyond normal levels to further inhibit what the body assumes to
be pituitary release of GH. Of course the GH/IGF-1 receptors are beaten up pretty
bad by the chronic elevation of Somatostatin and the dosages of GH administered
are required to increase to match. During the protocol this means higher dosages
with fewer returns and post protocol it means suppressed endogenous GH secretion
and a great deal of lean tissue loss. Not bad enough? How about the fat accumulation
and loss of long term results? Like 2 steps forward and 1.5 back, huh?
The body does not respond by totally shutting down the GH/IGF-1 axis simply because an individual administers a couple of iu of GH. In fact the body fails to “significantly” suppress GH release on a long-term basis until after more than 2 weeks of continuous multiple daily injections are administered. So what is a wanna-be freak suppose to do? There is always the option of winning the Mr. O and investing your winnings and endorsement money into BioTech stocks such as Genentech for non-stop administration protocols, or work with, instead of against, the body’s Action/Reaction Factors.
For Every Action There Is A Profitable
Reaction
The human physiology commonly begins a significant multi-level
fight for homeostasis against exogenous GH use at just over the 14 day continuous
administration period. This is due to an increase in Somatostatin and a down-regulation
of GHRH release. The result is a decrease in GH/IGF-1 receptor sensitivity and
a shut-down in GH secretion by the pituitary respectively.
Estrogens promote cellular and hepatic IGF-1 secretion and pituitary release of
GH. Though it seems that most high androgens can inhibit this process to some
extent, those that foster its formation tend to promote it…as do certain
blood meds employed to control the elevation in blood pressure realized from estrogen
induced water retention.
A few chemicals called GH secretagogues have
shown the unique ability to restore the GH/IGF-1 Axis to normal function. In fact
some of these drugs have been clinically documented to elicit GH release levels
as much as 40 times normal with consecutive dosages realizing nearly the same
degree of elevation…multiple times daily. The down fall of GH secretagogues
drugs like MK-677, Hexarelin and GHRP-2 is that the body begins to react to them
as well after a bout 2 weeks with a decrease in GH secretion of about 40%.
(Come on now, you had to have seen this coming)
Maximum GH/IGF-1 For
Dummies…and Me Example Protocol
(With AAS)
Day
1. Testosterone
Propionate 150-200mg/GHRP-2 4xd
2. Testosterone Propionate 100-150mg/GHRP-2
4xd
3. Testosterone Propionate 100-150mg/Clonidine 0.5mg 2xd/GHRP-2 4xd
4. Trenbolone Acetate 75-100mg/Clonidine 0.5mg 2xd/GHRP-2 4xd
5. GH 4iu 2xd/Trenbolone
Acetate 75-100mg/Clonidine 0.5mg 2xd
6. GH 4iu 2xd/Trenbolone Acetate 75-100mg
7. GH 4iu 2xd/Testosterone Propionate 150-200mg
8. Testosterone Propionate
100-150mg/GHRP-2 4xd
9. Testosterone Propionate 100-150mg/GHRP-2 4xd
10.
Testosterone Propionate 100-150mg/Clonidine 0.5mg 2xd/GHRP-2 4xd
11. Trenbolone
Acetate 75-100mg/Clonidine 0.5mg 2xd/GHRP-2 4xd
12. GH 4iu 2xd/Trenbolone
Acetate 75-100mg/Clonidine 0.5mg 2xd
13. GH 4iu 2xd/Trenbolone Acetate 75-100mg
14. GH 4iu 2xd/Testosterone Propionate 150-200mg
15. Testosterone Propionate
100-150mg/GHRP-2 4xd
16. Testosterone Propionate 100-150mg/GHRP-2 4xd
17. Testosterone Propionate 100-150mg/Clonidine 0.5mg 2xd/GHRP-2 4xd
18. Trenbolone
Acetate 75-100mg/Clonidine 0.5mg 2xd/GHRP-2 4xd
19. GH 4iu 2xd/Trenbolone
Acetate 75-100mg/Clonidine 0.5mg 2xd
20. GH 4iu 2xd/ Trenbolone Acetate 75-100mg
21. GH 4iu 2xd/Testosterone Propionate 150-200mg
22. Testosterone Propionate
100-150mg/GHRP-2 4xd
23. Testosterone Propionate 100-150mg/GHRP-2 4xd
24. Testosterone Propionate 100-150mg/Clonidine 0.5mg 2xd/GHRP-2 4xd
25. Trenbolone
Acetate 75-100mg/Clonidine 0.5mg 2xd/GHRP-2 4xd
26. GH 4iu 2xd/Trenbolone
Acetate 75-100mg/Clonidine 0.5mg 2xd
27. GH 4iu 2xd/Trenbolone Acetate 75-100mg
28. GH 4iu 2xd/Testosterone Propionate 150-200mg
*Nolvadex 20mg 2xd
*GHRP-2
is continued for 7 days post-cycle and the protocol is repeated
*10g L-Arginine
AM/PM on exogenous GH days
*Optional: Add methandrostenolone 30mg on Testosterone
days and oxandrolone on trenbolone days.
Testosterone aromatizes
to estrogens thus promoting GH/IGF-1 release and formation. With the synergistic
effect of increase pituitary release of GH resulting from clonidine and GHRP-2
administration, GH/IGF-1 levels are Significant. This structure allows an over-lapping
effect during exogenous GH administration periods evolving into an additive effect
(endogenous + exogenous = A lot of GH).
So why the intermittent use of
GH? As I explained prior the human body has an amazing ability to adapt. Consider
the amount of growth that occurs from the intermittent GH pulses natural to children
and the results that transpire. Nature can be highly effective, huh?
By utilizing the fast-acting and brief half-life qualities of testosterone propionate and non-aromatizing trenbolone acetate the protocol allows for near immediate response and a high androgenic environment to maximize the value of GH use.
There are other options for the replacement of GHRP-2 that I will list, but considering the fact that there is an over the counter product that contains it available. (Intragrowth).
Pyridostigmine: A cholinergic agonist that decreases hypothalamic somatostatin has been effective at a dose of 120mg/d
MK-677: A GH secretagogue has been effective at 50mg/d
Hexarelin: A GH secretagogue has been effective at a dosage of 2mcg/kg of bodyweight 3xd.
Train
hard, eat big and grow. Enough said.
Author L. Rea is the genius behind
the book "Chemical Muscle Enhancement." a quantum leap forward in the
practical application of anabolic pharmacology. Readers wishing to purchase
this book can do so at 1supplement.com or Rock Body Nutrition stores: 866-808
BODY.
Reference and Reading Materials:
Different effects of pyridostigmine on growth hormone (GH) response
to GH-releasing hormone in endogenous and exogenous hypercortisolemic patients
Borges, M. H. S., Castro, R. C., Kater, C. E., Lengyel, A. M. J.
BRAZILIAN
JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH , 26(11):1191 1993
Clonidine
Potentiates the Growth Hormone Response to a Growth Hormone Releasing Hormone
Challenge in Hypothalamic Growth Hormone Releasing Hormone Deficient Rats
Arce, V., Garcia Barros, M., Vara, E., Lima, L.
NEUROENDOCRINOLOGY , 61(5):552
1995
The effect of four weeks of supraphysiological growth
hormone administration on the insulin-like growth factor axis in women and men.
Bengtsson, B. A., Basset, E. E., Sacca, L., Napoli, R., Sonksen, P. H., Dall,
R., Cuneo, R. C., Boroujerdi, M. A., Baxter, R. C., Ehrnborg, C., Keay, N., Cittadini,
A., Longobardi, S., Rosen, T., Jorgensen, J. O. L., Christiansen, J. S.
JOURNAL
OF CLINICAL ENDOCRINOLOGY & METABOLISM, THE , 85(11):4193-4200 2000
Androgen
Receptor Blockade with Flutamide Enhances Growth Hormone Secretion in Late Pubertal
Males: Evidence for Independent Actions of Estrogen and Androgen
Metzger,
D. L., Kerrigan, J. R.
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM,
THE , 76(5):1147 1993
Exogenous growth hormone administration
does not inhibit the growth hormone response to hexarelin in normal men
Cappa,
M., Setzu, S., Bernardini, S., Carta, D., Federici, G., Grossi, A., Loche, S.
JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION , 18(10):762-766 1995
Physiological
levels of growth hormone fail to suppress growth hormone releasing hormone (1-29)
NH2-stimulated growth hormone secretion in man
Brain, C., Thakrar, D. N.,
Hindmarsh, P. C., Brook, C. G. D.
JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
, 16(1):15 1993
Bellone J, Bartolotta E, Sgattoni C, et al. J Endocrinol Invest 1998 Sep;21(8):494-500.