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Archive: Insulin The Anabolic Substance
Posted on Sunday, March 07 @ 12:00:00 MST
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Diet For Killer Abs
How to get ripped, six pack abs
Bodybuilder reveals his secrets - Guaranteed!
www.burnthefat.com
Written by: L. Rea
Ask any of the elite who has become truly massive beasts which anabolic
substance has had the most profound effect upon their physique and the
answer from the largest mammals will unanimously be insulin.
Though GH has
brought to the forefront of competitive stages the well retained lean
muscle mass tissue displayed beneath an onion skin exterior of today, it
is the symbiotic relationship insulin has with all other physical
enhancement chemistry that has made beasts what they are in the new
millenium.
Insulin is predominantly a storage hormone in that it initiates a
cascade of cellular events that result in up-regulation of cellular
nutrient content. It obviously goes without saying then that
supraphysiological plasma levels of insulin result in supraphysiological
cellular levels of nutrients. This in itself allows for a highly anabolic
effect known as an osmotic response. A cellular osmotic response is
nothing more than an increase in water and growth potentiating nutrients
intracellularly that has a effect similar to increasing the amount of air
in a balloon. More air in the balloon means a larger balloon. More water
and proportionate growth nutrients means a larger cell. Interesting enough
is the fact that this also triggers another survival mechanism that tells
the stretched cell wall to increase in thickness to accommodate the
osmotic response. This is due to an up-regulation in localized IGF-1 and
MGF production and the synergistic response initialize. Oh ya. That is
anabolism in the form of hypertrophy. Unfortunately, insulin is quite
anabolic to fat cells too.
Since insulin is the body’s main "storage" hormone it should come as no
surprise to the reader that many diabetics and would-be beasts alike have
become horribly fat as a result of improper insulin use and misguided
dietary habits. Many bodybuilders have employed the 10-15 grams of
carbohydrates per IU of insulin administered protocol with a great deal of
success in spite of the inherent dangers of non-medical insulin use.
However many, who have either become insulin resistant/insensitive or are
genetically predisposed to inordinate adipose (fat) tissue accumulation,
have endured a greater anabolism of adipose tissue than muscle. Some have
foolishly put on more covering clothing and simply accepted this as a
necessary side effect endured for the greater eventual goal. Others have
added the additional potential negative side effects of heart
arrhythmia/tachycardia, diabetes, and other not so fun stuff as well.
As I have pointed out many times before, adipose tissue is a major site
for aromatase enzyme activity which in itself compounds the Big Fat
Bastard problem. Many AAS (anabolic/androgenic steroids) are susceptible
to the effects of aromatase enzyme conversion to estrogens as is
endogenously produced (made inside the body) androgens such as
testosterone. Obviously the greater the volume and activity of this enzyme
that exists in the body, the greater the chance and degree of
aromatization that occurs. Estrogen is directly anabolic to a minor degree
to muscle tissue. Both fortunately and unfortunately it is highly anabolic
to adipose tissue. Since estrogen is the hormone that induces female
pattern fat deposits it is fortunate because a nice rack is a thing of
beauty. Unfortunately I have as of yet not noted a single male bodybuilder
who looked good or happy with boobs or any other fatty female attributes.
So a greater degree of adipose tissue accumulation from insulin
administration results in a compounded adipose tissue storage effect from
aromatase enzyme susceptible AAS employment.
In some instances the result of this vicious cycle is bodybuilders who
fail to ingest adequate calories during AAS protocols as a means of
decreasing adipose tissue accumulation. Unless you are from another planet
you realize this also limits muscular growth potential as well.
Before we discuss all of the interesting facts concerning the means of
becoming a big fat bastard, it is necessary to have a fundamental
understanding of the macronutrient product glucose.
GLUCOSE
Glucose is the body’s preferred energy substrate. Though the brain’s
nutrient make-up is nearly 1/3 omega-3 fatty acids it is glucose that is
without fail mandatory for continued sentience. So carb up a little and
read closely as we learn a few things about the body we have been
entrusted to play nice with.
When we ingest food stuffs in the form of the three macronutrients
protein, carbohydrates, and fats the GI track introduces a series of
chemical Action/Reaction Factors that result in the break-down of these
nutrients to metabolic substrates.
- Proteins = amino acids
- Carbohydrates = glucose
- Fats = fatty acids
It appears simple on the surface but in fact glucose can be converted
to triglycerides and adipose tissue or lean tissue glycogen stores and
toilet tinkle. Like wise fatty acids can be stored as fat or utilized as
an energy substrate by the body’s tissues but it cannot be converted to
glucose. This is interesting when one considers the fact that
carbohydrates can become glucose or fat, but fat cannot become glucose
(though the cellular mitochondria can use fatty acids as an energy
substrate as a keto response). Protein is ultimately destined to become
amino acids employed for cellular repair and growth or intimate moments
with the bathroom. But certain amino acids called gluconeogenic amino
acids can be converted to glucose too. This can be disastrous for a
bodybuilder who hopes to be a beast one day since lean muscle mass is
predominantly made up of protein in the form of amino acids and a complete
spectrum is necessary. We will get to this later. For now simply accept
that glucose is necessary for life and bodybuilding progress alike.
The average circulatory value for glucose allows for about only 4 grams
of glucose. It is actually uncommon for blood glucose levels to rise
beyond an additional 1.5-2.0 grams or to drop below the 4 gram mark. A
healthy individual who ingests a meal containing 50-150g of mixed
carbohydrates will realize the normal increase in circulatory glucose for
only about an hour. Interesting thing here is that endogenous (made by the
body) insulin secretion will remain elevated for an additional 2 hours
after glucose clearing. When the same individual ingests 300g of carbs
(Fat Bastard) at one time the resulting insulin secretion levels will be
300% above normal for an additional 7 hours after blood glucose clearing.
This is clearly a highly anabolic environment, but after tissue glycogen
stores reach maximum levels a grotesque amount of the excess glucose finds
its way to adipose tissue. And don’t worry. If all of the existing fat
cells are full, the body is way to happy to make new ones to secrete lots
of aromatase enzyme. And herein awaits the key to greater lean mass tissue
and a decrease in adipose tissue.
GLUCONEOGENESIS
Gluconeogenesis is the biosynthesis of new glucose. This means that
glucose is synthesized from other substrates than carbohydrates or
glycogen stores. Obviously since the only source of fuel for the brain,
testes, kidneys, and erythrocytes is glucose the body in its amazing
adaptive manner can manufacture glucose from other materials. Those who
are up on keto diets are aware of the fact that the body can derive energy
from ketone bodies (which are converted into acetyl-CoA). But that is an
entire different topic for now. In short the body utilizes the carbon
structures within substrates to create energy in the eventual form of ATP
(adenosine triphosphate). ATP is cellular energy that, as readers are
aware, is the body’s only energy currency. In the case of gluconeogenesis
the carbon structures can come from other sources.
Triglycerides are structures consisting of three fatty acids adjoined
by a glycerol molecule. By cleaving the fatty acids away from the glycerol
molecule the body can utilize the freed glycerol molecule to make glucose
through a series of conversions and subsequent carbon utilization.
With the exception of lysine and leucine all 20 (or 22 if you are of
that school of thought) amino acids can be turned into TCA cycle
intermediates which in turn allows for the carbon skeletons of the amino
acids to be converted to pyruvate. The newly formed pyruvate can then be
utilized by the gluconeogenic pathway to create glucose by way of another
series of metabolic pathways. Let me explain that a little better. When
glycogen stores in the liver and muscle are depleted the
working/recovering muscles, brain and organs need another energy source.
Catabolism of muscle tissue proteins to amino acids becomes the main
source of carbon skeletons for the maintenance of mandatory blood glucose.
As you will recall the body can clear 50 –150 grams of carbohydrates in
only a few hours.
So how much muscle do you think the gluconeogenic adaptive process can
munch in the same period of inadequate nutrient supply from diet? By the
way, the amino acid Alanine is the favorite gluconeogenic snack with
Arginine and Glutamine coming in as close seconds.
THINK ABOUT IT
In the presence of circulatory insulin elevation gluconeogenesis in the
liver and muscle tissue decreases. During periods of circulating
supraphysiological levels of amino acid muscle catabolism decreases. In
the presence of both protein synthesis occurs.
So it would seem that the two choices a wanna-be beast faces is 300
grams of carbohydrates to induce a sufficient prolonged insulin spike and
a Big Fat Bastard pose down or non-stop keto diets and declarations of
"Hey, I may look like a weenie but I am really cut" for life.
- The obvious solution is an elevation in both circulatory insulin and
a corrected amino acid pool rendered highly efficient by design and not
by chance.
Insulin administration is nothing new to the larger beasts of the
bodybuilding world. Unfortunately neither is Big Fat Bastard status in the
brief off-season. So it should come as no surprise to those who have
entered the realm of the chemically enhance athlete to learn that insulin
can make even the best genetically predisposed individual fat. It has been
my experience that this is simply not necessary.
Insulin forces excessive amounts of amino acids into muscle cells when
an adequate supply exists at the time of insulin exposure. Insulin also
triggers increased muscle cell glycogen synthesis by way of positively
effecting the rate limiting enzyme glycogen synthase. We also know the
positive effects correct application of supraphysiological insulin levels
has had upon the most catabolic pathway there is that affects muscle mass
from reading my two prior books. Add to this the fact that insulin is
synergistic to and with all other chemicals of muscular enhancement and
realize the potential.
In relationship to goals it would seem evident that a protocol
employing the attributes of insulin would necessitate the symbiotic
relationship the hormone has with macronutrients as it applies to lean
muscle mass tissue.
- Muscle is more than 80% protein by dry weight.
- ATP is the energy currency of muscular contractions, repair, and
growth.
- Glucose is the prime source substrate for ATP synthesis and
mandatory for proper brain and organ function (yes, that one also).
- Excess blood glucose will result in excess adipose tissue
accumulation.
The Protocol
Diet
When this protocol was created its intent was rapid accumulation of
lean mass tissue without an increase in adipose tissue deposits. Since the
foundation of the diet was structured for efficient gluconeogenic
dependant upon a correct ratio and amount of amino acids, a great deal of
protein was consumed daily. The most effective protein intake minimum was
the equivalent of 3 grams of protein per pound of bodyweight daily divided
into at least 6 meals. Using a 200 pound individual as an example it was
possible to reduce this slightly by simply eating 4 whole food meals daily
providing 50 grams of whole protein each and sipping on whey protein
drinks in water throughout the day
providing the remaining 400 grams of protein. I preferred whey protein
simply because it is one of the only two drinkable products I am aware of
that allows for actual hyperaminoacid response in the circulatory system.
Casein, egg, and (some people still use it) soy proteins fail to clear the
GI track at a rate significant enough to induce the necessary
supraphysiological amino acid concentrations for the protocol. The fact
that whey protein is easily oxidized by the liver should be the first clue
to the reason why results are superior. By the way, the other is Human
Profile by Hazardous Materials (it is nearly 100% absorbed)
So here is the kicker. Though fat intake could be quite high, total
daily carbohydrate intake could not exceed 0.5 grams per 25 pounds of
bodyweight daily. The reason is simple: The goal was to force the body to
employ the gluconeogenic pathway as a means of energy production. Any
degree of actual glycogen regeneration resulted in the body returning to
the glycosis pathway which allows for adipose tissue accumulation. The
reason this worked so well was simplistic in nature. The making of ATP
through amino acid gluconeogenesis is very inefficient thus allowing for a
huge calorie expenditure similar to what occurs during DNP utilization.
During calorie expenditure the body does not store fat but it does undergo
protein anabolism. When enough protein was ingested the result was always
a net increase in lean body mass of 5-8 pounds by the end of a two week
protocol. Not bad for an experienced beasts, huh?
Additional Supplements
Since exogenous insulin was utilized during this protocol and, as
mentioned prior, the gluconeogenic energy pathway loves certain amino
acids it is easy to realize that the normal ratio of amino acids derived
from whey protein and whole foods was not likely adequate. A mixture of 4
parts Alanine, 2 parts Glutamine, 2 parts Arginine and 1 part Taurine was
created and capsulated. The dosage ingested was 1 gram of the supplemental
mix per I.U. of insulin administered daily divided into 2 post
administration dosages.
The preparation for this protocol required a liver glycogen depletion
period of 24 hours prior to initial insulin administration. This was done
to initiate the gluconeogenic pathway prior to protocol onset thus
preventing any loss of lean tissue growth potential.
Though only a total idiot would ever assume that non-medical exogenous
insulin use was safe, the utilization of a fast acting insulin was the
better choice for this protocol. The first reason of course being that
short acting chemistry also means shorter periods of potential exposure to
negative side effects like a coma. Second is the fact that it was
necessary due to the relevance in liver capacity for glucose manufacture
by way of gluconeogenesis. Running out of adequate glucose reserves would
introduce a series of potential negative side effects that would have
required the ingestion of dextrose to inhibit.
EXAMPLES OF INSULIN
| Name of Insulin |
Start Activity |
Highest Activity |
Ends Activity |
Low BS |
| Very short-acting (Humalog)
|
10 minutes |
1.5 hours |
3 hours |
2-4 hours |
| Short-acting (Regular/-R) |
20 minutes |
3-4 hours |
8 hours |
3-7 hours |
| Intermediate acting (Nor L) |
1.5-2 hours |
4-15 hours |
22-24 hours |
6-13 hours |
| Long-acting (Ultra Lente) |
4 hours |
10-24 hours |
36 hours |
12-28 hours |
| Combination: 70% N/30% R |
0-1 hour |
3-13 hours |
12-20 hours |
3-12 hours |
| Combination: 50% N/50% R |
0-1 hour |
3-12 hours |
12-20 hours |
3-12 hours |
- Humalog was administered about 15 minutes before an appropriate meal
- Regular Type-R was administered 30 minutes before an appropriate
meal
- Low BS = Low blood sugar (Glucose).
As the reader can see when viewing the examples of insulin above, the
employment of Humalog allowed for a total of 4 daily administrations of
10-15iu each and Humulin-R (Short-acting) only allowed for 3 daily
administrations. This is not to say some have not increased the dosage or
chose different insulin analogs, but it is to say that under these
circumstances it was not necessary or more effective.
When looking at the following example consider these facts:
- Testosterone suspension has an active-life of about 24 hours tough
plasma androgen levels remain elevated for about an additional 24 hours.
- Sex hormones such as testosterone and estrogens are inactive when
bound by SHBG (sex hormone binding globulin) and free or active when
not.
- Insulin is a powerful SHBG inhibitor.
- Insulin increases muscle glucose transporters and androgen receptors
Protocol Example
| Day |
Protocol |
Day |
Protocol |
| 1. |
Testosterone Sus. 150mg |
15. |
Testosterone Sus. 150mg |
| 2. |
Humalog 10iu 4xd |
16. |
Humalog 10iu 4xd |
| 3. |
Testosterone Sus. 150mg |
17. |
Testosterone Sus. 150mg |
| 4. |
Humalog 10iu 4xd |
18. |
Humalog 10iu 4xd |
| 5. |
Testosterone Sus. 150mg |
19. |
Testosterone Sus. 150mg |
| 6. |
Humalog 10iu 4xd |
20. |
Humalog 10iu 4xd |
| 7. |
Testosterone Sus. 150mg |
21. |
Testosterone Sus. 150mg |
| 8. |
Humalog 10iu 4xd |
22. |
Humalog 10iu 4xd |
| 9. |
Testosterone Sus. 150mg |
23. |
Testosterone Sus. 150mg |
| 10. |
Humalog 10iu 4xd |
24. |
Humalog 10iu 4xd |
| 11. |
Testosterone Sus. 150mg |
25. |
Testosterone Sus. 150mg |
| 12. |
Humalog 10iu 4xd |
26. |
Humalog 10iu 4xd |
| 13. |
Testosterone Sus. 150mg |
27. |
Testosterone Sus. 150mg |
| 14. |
Humalog 10iu 4xd |
28. |
Humalog 10iu 4xd |
Testosterone Sus. = testosterone suspension
150mg of testosterone suspension created a great deal of estrogen since
it originates as a non-esterfied AAS. Estrogen up-regulated the muscle
cells glucose transporters called GLUT-4 and increased androgen receptor
sensitivity. This also meant that the administered testosterone was free
or unbound from its inactivating protein SHBG. A great deal of the hormone
entering the circulatory system was quickly bound, though not before a
serious degree of anabolism occurred. But there is a portion left bound
and in reserve.
Insulin inhibited SHBG resulting in a synergistic pro-anabolic
response. By freeing the remaining prior days administered testosterone
from SHBG an increase in androgenic activity was realized. Since SHBG is
also estrogens binding protein the excretion of estrogens was dramatically
accelerated. This resulted in rapid estrogen clearing and a notable
increase in GH secretion which was amplified by the lack of the inhibitory
effect normally caused by excess glucose. As most readers are aware, GH
and insulin must both be present in the liver to produce IGF-1.
The end result was adequate glucose regeneration at the expense of
adipose tissue with a profound degree of lean tissue protein synthesis and
growth. No more Big Fat Bastard!
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