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As we have seen so far, Frank was able to significantly increase his lean muscle mass as a result of chemically induced alterations in the Anabolic/Catabolic Ratio.

We know the body both gains and loses protein based tissue equal to bodyweight x 1.818 expressed in grams daily.

We have discussed two methods my beasts had utilized for altering either side of the equation in favor of increasing lean muscle mass. After a recap, we will look at a third option employed by Frank and other beast and then put it all together for maximum results.

Max Androgen Phases significantly and rapidly increased strength,

bodyweight, and lean muscle mass. They did so through an increase in anabolism or increased protein synthesis. While it is true that all AAS posses some anti-catabolic qualities, their action is predominantly the result of an alteration in the Anabolic/Catabolic ratio in favor of anabolism. This is similar to a checking account.

If we made daily deposits equal to withdrawals, we would not realize a change in balance. However, if we made daily deposits in excess of withdrawals, we would realize an increase due to addition. Unfortunately the body catches on to this alteration in normal homeostasis (balance) and begins to react with catabolic counter- measures after 2-3 weeks. As you know, these counter-measures come in the form of hormones such as cortisol, glucagon, and estrogen.

Due to a ramp type increase in cortisol, a maintained AAS threshold would no longer induce significant anabolism beyond elevating catabolism after about 6 weeks. This in turn results in a near equal anabolic/catabolic ratio. If the AAS threshold /level were decreased or discontinued, the elevated cortisol levels would overwhelm even well above normal endogenous androgen induced anabolism. Which of course would result in excessive post-cycle lean muscle mass loss. The use of AAS also resulted in another negative feed-back loop...

Estrogen Levels Elevate During AAS Protocols For 2 Reasons: (1) Almost all AAS aromatized to some extent. This reaction was obviously due to the

aromatase enzyme that converts AAS into estrogen.

(2) The body elevated estrogen biosynthesis in an attempt to re-establish the body's natural testosterone/estrogen ratio.

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In both cases, the excess estrogen caused a negative feed-back loop that told the hypothalamus to shut down endogenous androgen production. If the estrogen levels remained elevated post-cycle the inhibition of the HPTA remained significant and the athlete's body developed female pattern fat deposits. It also significantly reduced post cycle-lean mass retention.

But we know one way Frank turned these negative feed-back loops into another growth phase. Right? Frank would have been foolish to administer any AAS protocol continuously anyway. If health concerns were not reason enough to utilize brief Max Androgen Phases, long-term growth potential certainly was. Frank became a beast by the motto "Get in, grow hard, and get out before the body counter attacks."

Cortisol/Estrogen Suppression Phases increased total lean muscle mass by

altering the anabolic/catabolic ratio in favor of protein sparing. They were also a method of destruction for both elevated cortisol production/levels and HPTA negative feed-back loops induced by elevated estrogen levels. The checking account analogy applied here in reverse. If we decreased the total amount of daily withdrawls, but still maintained daily deposits, we would realize an increase in total holdings.

Therefore, Cortisol/Estrogen Suppression Phases greatly increased post-cycle lean mass retention or gains. They have also been utilized as a stand-alone means of increasing total lean mass to some degree. When layered into a Max Androgen Phase during the last 7-10 (or day #1 5 ) days of activity, Cortisol/Estrogen Suppression Phases destroyed post-cycle blues quite well. (Gee, Ya Think?) They also turned "off periods" into growth periods. Obviously, they had value when utilized during the first 7-1 5 days of a Max Androgen Phase as well. But there was a better protocol...

Absolute Anabolic Phases were constructed without the use of AAS. Though in

some cases they may have been a layer of Low Dose AAS Phases. Since Low Dose

AAS Phases did not significantly inhibit HPTA function or cause excessive cortisol and

estrogen production this was certainly quite beneficial. The functions of Absolute Anabolic Phases were:

1. Induced growth through an alteration in the Anabolic/Catabolic ratio in favor of protein synthesis.

2. Induced an increase in lean muscle mass by inhibiting cortisol and glucagon production without negatively affecting HPTA function or estrogen levels. This means they also altered the Anabolic/Catabolic ratio in favor of protein sparing.

Absolute Anabolic Phases were another method of utilizing "AAS off periods" for quality growth. It should also seem evident that they were additionally utilized as a means of destroying cortisol induced lean muscle mass loss post AAS cycle. But what if I had constructed a protocol in which Frank was to begin an Absolute Anabolic Phase at an appropriate time that would allow its last 7-15 days to layer over a Max Androgen Phase initial 7-15 days? It would have delayed his body's catabolic attack an additional 7-15 days while significantly increasing the results realized from the Max Androgen Phase.

Now, what if I had layered a Cortisol/Estrogen Suppression Phase into his Max Androgen Phase beginning the last 7-15 days of its activity? Yup, we would have only allowed Frank's body 14 days at most to mount a counter attack against new growth. Remember; it took the body 2-3 weeks to begin adequate counter measures? This means Frank would have been in a near continuous sate of growth while following a 28-30 day on/28-30 day off protocol for actual AAS use. It was simply far more logical and productive.

As a point of fact, ponder this. We know the human body both gains and loses protein based tissue equal to bodyweight x 1.818 expressed in grams daily. So a (little) 200 Ib bodybuilder both gains and loses about 363.6 grams of protein based tissue daily (200 Ib x 1.818 =383.6 g). If through whatever means we altered the Anabolic /Catabolic ratio by increasing anabolism 50% and decreasing catabolism 50

% our small 200 Ib bodybuilder would gain almost a pound in lean tissue mass daily.

Oh ya, and by the way, this near pound of growth daily would be without training. Strange, but true. Of course this would require adequate calories and obviously major protein intake. Before anyone checks into couch potato status, our 200 Ib bodybuilder would get quite fat, as well as sissy weak.

"The fat could be mediated with appropriate chemistry, but sissy status can only be over come with hard-core training, you weenie".

FIRST A BRIEF RECAP

As with any chemical muscle enhancement drugs, those out-lined in this section had Action/Reaction effects that absolutely had to be considered. All drugs and chemicals create an adaptive response within the body.

Some are growth inducing by altering the ratio of anabolism/catabolism in favor of anabolism or retention, while others have secondary reactions which will instantly put a halt to progress. Some can seriously hamper long term potential. As example, Insulin has been noted to make an athlete huge, fat, or dead.

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INSULIN

Insulin is the most anabolic hormone, yet it is anti-catabolic as well. Since this is a storage hormone, anabolism is initiated by inducing storage intracellularly of glucose, amino acids, and fats, as well as electrolytes. Remember, creatine is an amino acid structure as are several growth inducing chemicals. As well, there is a great deal of evidence that by creating a state of cellular hydration, supraphysiological insulin induces a secondary anabolism and cellular hypertrophy.

Insulin has anti-catabolic qualities simply because the presence of Insulin in the blood stream at high enough levels prevents catabolic hormones such as cortisol and glucagon from becoming elevated. This obviously creates a state in which amino acids and glucose cannot exit cells.

As noted in the treatment of type II diabetics, insulin receptor-sites can be de- sensitized from over use of exogenous Insulin. Ever notice how fat diabetic couch potatoes get? This is because the lack of exercise allows muscle cell insulin receptor- sites to become insulin resistant and the fat cells become the main point of storage. Which of course sucks! For this reason, (and others) long protocols with exogenous Insulin could have greatly reduced long term potential.

There were some supplements employed that enhanced Insulin sensitivity and allowed for lower dosages to be more effective. This in turn helped to prevent Insulin resistance. Alfa Lipoic Acid, Chromium, Corosolic Acid, D-Pinitol, Selenium, 4- Hydroxyisoleucine, L-Phenyl Alanine, and Courdin which is a fraction from bitter melon (Momridica Charantia).

These supplements made a huge difference in results both during and post- Insulin use. Frank always included a mixture of 200 mg Lipoic Acid, 1000 mg L-Phenyl Alanine, and 50 mg of D-Pinitol twice daily with Insulin, and twice daily for 14 days after with 4-hydroxyisoleucine added at a dosage of 200mg 2xd.

Over the years, I have noted many athletes obtained the same results utilizing "up to" half of their normal exogenous Insulin dosages with this supplement schedule. They also stored less fat.

Another addition said to lower fat storage was HCA (Hydroxycitric Acid) which is supposed to decrease conversion of carbohydrates to fat by inhibiting its conversion enzyme. 1000 mg 2-4 times daily. My personal experience has been that HCA is not effective.

The essential fatty acid supplement CLA was probably the best OTC product for fat synthesis inhibition during exogenous insulin use. (We are currently patenting a fat that tells the body to not store fat and to burn fat at a higher rate. This is like super CLA x 1 0)

Misuse of Insulin and the normally required 10 g of carbs or appropriate super substrate per i.u. has been known to lead to coma, beta cell burn out, pancreatic damage, and blindness among other things such as cataracts.

Insulin significantly and quickly reduces blood sugar and can create a state of hypoglycemia. You will need to know that later. (There will be a test) This means Insulin is a major storage hormone, right?! So it was absolutely vital for Frank or any of the beasts to protect against Insulin insensitivity. GH release was inhibited by elevated blood sugar by the way. Think about it.

The examples that follow often list Humalog or Humulin-R insulin because they are fast/short acting and easier to control. Going to sleep with supraphysiological Insulin levels could have killed. So by utilizing a fast acting Insulin, the system was mostly clear within 1.5-3 or 6-8 hours respectively after injection.

Obviously a meal before sleep was a must. For Frank, or any beast, a single injection of Humulin-R that exceeds 1 i.u. per 10 lbs. of body weight would have significantly increased risks. This was simply because metabolic processes would not have been able to keep up with necessary glucose supplies in most cases.