Some info for the inquiring mind, this is an excerpt…if you have a short attention span don’t waste your time…
The goal of any growth inducing protocol was to gain as much lean mass as possible. To do this with a plan meant to gain, not merely maintain or regain losses from prior cycles.
The body has Action/Reaction periods and factors. Basically the body begins to adapt significantly to most attempts at altering homeostasis after 2-3 weeks. This sucked since the best results from a cycle usually came during days #10-30. But we also profited from this information and used it to Frank’s advantage by utilizing brief phases and cycles of 21-30 days, (this is the point where cycles provided serious results) then got out before side effects out weighed benefits.
“To be successful it is necessary to create maximum growth thresholds and stop before the body is able to achieve its own counter measure thresholds.”
Let me explain. My experience has been that a cycle of 8 weeks providing a continuous plasma level weekly of 400-800 mg testosterone begins to fail to provide results about week #6 in most cases. This is because the level of endogenous catabolic hormones becomes elevated as a reaction to the exogenous testosterone administration and cellular signaling proteins begin to become overwhelmed, which is due to the action of increase androgens. So anabolism and catabolism are again about equal. Remember to create a growth environment one or both sides of the anabolic/catabolic ratio must be altered in favor of either more tissue building or less tissue wasting.
At the 6 weeks point an athlete’s body produces and maintains somewhat higher cortisol levels than normal. An increase in the administered dosage would again overwhelm the cortisol and increase signaling protein activity, but eventually it will catch up… .again. Worse yet, when the athlete goes off cycle, the elevated levels of catabolic hormones overwhelm the declining anabolic chemistry (and activity) and most of the cycle gains are lost.
“Yes, Frank. I realize that you lost a great deal of lean tissue mass after AAS discontinuance in the past. But what if an athlete, yes you Frank, utilized a brief protocol that allowed maximum growth and got out before endogenous catabolic and anabolic chemistry altered significantly? Yes, you are right. The athlete would retain much more of the protocol gains post cycle, and “Look honey, I don’t have raisins” could be declared to your significant other.”
“Now, what if we created following or layered protocols that either reduced the catabolic side of the ratio or used other metabolic possibilities to again increase anabolism? Yes, again you are right. The beast would be in a near continuous growth phase instead of fighting to regain.”
“Now, what if we inhibited the negative feed-back loops responsible for post-cycle loss of lean mass tissue? I will explain this too, my lad. All in good time. The days of the genetically gifted only are over. The hard-core average genetic athlete is and will have their days of domination. Mediocrity sucks, Frank.”
DRUG’S “MOST EFFECTIVE PERIODS”
Now that we have discussed theoretical half- and active- lives of drugs and plasma levels/plasma thresholds, let’s look at “most effective periods”. I realize this may seem like a great deal of information to deal with. But to construct any protocol that would provide maximum results all action/reaction factors had to be considered. Frank was not a steroid gun-slinger, but he did become a beast.
We know the half- and active- lives of injectable AAS are determined by the chain length of their ester. We have discussed the method by which the enzyme esterase acts upon an injection site dosage to induce migration of the freed AAS into the vascular system. We have also seen how different stacks and athletes have realized alterations in active- and half- lives. Now we need to understand drug “Most Effective Periods” or ranges.
Any drug introduced into the body by any method will have a range or period of time that it is “most effective.” This is the part of a drug’s active- life that provides the greatest results. It would appear a drug would have the same effect during its complete active-life. Sadly, it is not that simple.
After an injection of a drug is given, it takes a period of time for the enzyme esterase to act upon the drugs ester and subsequent release into the vascular system. The longer the AAS (or any drug) ester chain, the longer its active-life. This also means the longer it will take before migration.
Once the drug has migrated into the vascular system it may, depending on its structure, take a period or time to become effective. Believe it or not, this is not as difficult to predict as it would seem. I will give a few charts and graphs to help in a minute, but generally speaking a drugs most effective period is about equal to its half-life.
No, not the first half of its active-life, but usually the center portion of its active-life. As example, if a drug has an active-life of 16 days, it will have a “most effective period” of about 8 days. (Huh?)
MAX ANDROGEN PHASES
Now that we have a few fundamentals let’s begin putting to rest all of the “what and huh?” moments I have created. But first, let’s look at the below graphs …
Look at graph A. (next page) This is a drug “most effective period” for an ester with an active- life of 14-16 days. The drug begins activity on day #1 but does not begin its true effect potential until about day #4. This drug would remain in its “most effective period” from about day #4 until or through about day #1 2, which is 8 days. Deca Durabolin, Testosterone Cypionate and Primobolan Depot are examples of the graph. (The drug remains “active” until day #16)
Now look at graph B. (next page) This is a drug with an active- life of about 3 days or 72 hours. The most effective period would be from about hour 18 to hour 54. Remember; the drug is still active before and after the most effective period. That is why it is called an active-life. Durabolin and Testosterone Propionate are examples of this graph. Bet you already knew graph C would be for an ester such as testosterone enanthate. Pretty simple, huh?
PTOR and Homeostasis
The body normally maintains weight and size of all cellular structures through homeostasis (assuming that our discussion focus is our protein synthesis rate/PTOR). The body maintains homeostasis or balance by both building and destroying an equal amount of protein based tissue daily. In fact, most research states that the body both gains and loses protein bases tissue at a rate of bodyweight multiplied by 1 .818 expressed in grams daily. So a 200 LB bodybuilder gains and loses 363.3 grams of protein bases tissue daily; 200 LBS x 1.818 = 363.3 grams. So a 200 LB bodybuilder has a PTOR of 363.3 grams.
Homeostasis is controlled by hormones and hormone-like substances. Some are anabolic and create a state of protein synthesis and growth, while others are catabolic and create a state of protein destruction or waste. When chemical/hormone levels are balanced, or equal in Action/Reaction, there is a state of balance and no change we call homeostasis. If you do not get this yet, do not worry. It is explained and referred to multiple times throughout this book. This is due to the fact that without understanding of this fact, maximum progress is dwarfed. Understanding all details of Frank’s story is paramount.
To increase protein based tissue mass (Like uh, muscle) we must alter the ratio of "protein synthesis/protein wasting in favour of net total protein mass increase. This means triggering either anabolism (protein synthesis) in excess of catabolism (protein wasting) or decreasing protein wasting. Any substance that decreases the catabolic side of this ratio is considered anti-catabolic or protein sparing.
If we could increase the anabolic side of this ratio 100% without altering the catabolic side, our 200 LB bodybuilder would realize a daily net increase in protein based tissue of 363.3 grams. If we decreased the catabolic side of the ratio 100% the result would be the same. Many chemical muscle enhancement substances possess both anabolic and anti-catabolic qualities in carious ratios.
The goal of Frank’s Max Androgen Phases was to stimulate protein synthesis on multiple levels through multiple metabolic pathways. By stimulating the muscle cell androgen receptor-sites, we triggered cellular protein synthesis signals. By inhibiting cortisol receptor-sites, we decreased catabolism.
Also, by inducing a very high androgenic environment we allowed the musculature to significantly increase weight (strength) and work-load capacity. This was quite synergistic: We were able to train muscle more intensely. By increasing protein synthesis and decreasing protein wasting we were able to quickly repair the damage induced. With adequate macronutrient intake, we allowed for super over compensation or adaptation. The result was more muscle mass to carry greater work?loads. This was an adaptive process due to Action/Reaction Factors.
Unfortunately, the body realized we had altered homeostasis and the PTOR all to quickly. The body began to react to our anabolic/androgenic steroid (AAS) induced alteration after two to three weeks and began its own catabolic counter measures as a means of re-establishing homeostasis. To do this the body stepped-up production of cortisol a bit and estrogen as well. Since estrogen triggers a negative feed-back loop that induces H PTA (Hypothalamus/Pituitary/Testes/Axis) inhibition, the result was little or no endogenous testosterone synthesis.
Cortisol is a catabolic hormone that triggers cortisol receptor-sites. This results in protein wasting. If an AAS protocol ran too long, circulatory cortisol levels became elevated to a point where they equaled circulatory androgen activity even from exogenous sources. The result was homeostasis again. When the AAS protocol was discontinued and circulatory androgen levels decreased, the elevated cortisol levels overwhelmed the anabolic/catabolic ratio in favor of protein wasting. The result was
the loss of most, if not all, lean mass tissue gains induced by the AAS protocol. Which sucked! We had to exit before this could happen.
*l have (and will again) explained the effects of elevated estrogen levels post-cycle or after AAS discontinuance.
To further aggravate this post-cycle catabolic situation from long AAS protocols, the HPTA was suppressed and natural or endogenous androgen production was on girl-status. This allowed still existing elevated cortisol and estrogen levels to remain unchecked. (Which should cause testes challenged readers to say “yikes” in a high pitched voice) But this was all so unnecessary and no male needs “raisin syndrome”.
But on the plus side, shaving would be much easier as would singing those old girl-band song of the past. Again, we had to exit the AAS protocol before this can occur.
First things first: The Max Androgen Phases constructed for Frank were intended as a means of altering the anabolic/catabolic ratio in favor of net protein mass increase on a very significant level. (I do like that word “significant”) To do this Frank needed a plan that took into account Action/Reaction Factors so that he could keep much more AAS induced muscle mass gains post-cycle to build further upon as we progressed.
"Okay, we know the body adapts by reaction to AAS beginning after 2-3 weeks. We know that some AAS aromatize to estrogen which needs to be checked and eliminated before we allow you to exit your AAS protocol, Frank. But we also know estrogen levels can actually enhance AAS results by several pathways including increased GH/IGF-1 production and increased muscle glycogen synthesis. We also know any androgenic induced muscle mass gains not solidified into high quality lean muscle tissue by a high anabolic environment will be lost quickly post-cycle. There is only one more main factor to consider. “Support networks”. Think, Frank. Think!
*Just remember the term “support networks” for now. It will be explained later…a lot.
The Right Time Frames
We saw the greatest results from any chemically induced alteration in homeostasis and the PTOR rate when we had a plan. First, we got in, grew hard, and got out before Frank’s body could mount adequate counter measures. This meant a
time frame of 21-30 days. So no Max Androgen Phase (or any other protocol) could have had a high activity level beyond 30 days.
We had to create a quick and elevated androgenic environment to quickly increase mass and strength. No time was wasted that would have allowed the body to catch up with its anti-muscle counter measures. We called this the “androgenic dominance period”. We also had to allow a high anabolic moderate - low androgenic elevated environment to solidify Frank’s mass gains into quality muscle. We called this the “anabolic dominance period”.
Most athletes have realized the greatest results and post-cycle lean mass retention when these two periods were about equal with an equal androgenic - to - anabolic transition period in between. Additionally, we had to create a long “most effective period” without significant inducing HPTA inhibition. Easy !
Estrogen Control, NOT Elimination
Estrogen control was paramount for health and long-term result potential. But estrogen can increase IGF-1 production too, which was good. Estrogen also increases androgen receptor-site sensitivity. So we wanted estrogen to run rampid for the first two weeks of Frank’s Max Androgen Phases without allowing it to cause gyno and female pattern fat deposits. Simple: We used an estrogen antagonist to block receptor-sites but allowed plasma estrogen levels to remain high.
Using Clomid as an example, it has been my experience that a novice AAS user required (if any) only 50 mg/d (50 mg per day). And an intermediate AAS user required 20-30 mg/d. An advanced AAS user commonly required 30-50 mg/d. A very advanced AAS user sometimes required 40-60 mg/d, and in most cases, some additional help from an aromatase inhibitor.
The key was to watch for signs of gyno and female pattern fat deposits, while keeping a close eye on blood pressure. This was always of the utmost concern during the building of the perfect beast. High blood pressure can introduce a variety of long term and life threatening negative side effects.
*Nolvadex decreases GH/IGF-1 synthesis and is therefore a poor choice as an estrogen antagonist.
Things we have learned from experience…
Estrogen levels were kept near normal or below before we exited the AAS protocols. So we added an estrogen esterase inhibitor at about day #15 of a Max Androgen Phase to clear the system of excess estrogen before we exited. I have not noted many novice AAS/Max Androgen Phase users whom needed this precaution. But this was in relevance to dosages administered.
Some intermediate AAS users opted for Arimidex 0.5-1.0 mg/d, or Proviron 50- 100 mg/d. Most advanced AAS users successfully utilized Arimidex 1.0-2.0 mg/d or Aromasin 50mg/d. This was, of course, unnecessary when a Cortisol/Estrogen Suppression Phase was layered in at the half-way point or beginning day #15 of a Max Androgen Phase.
I have and will repeat this fact again and again: Any effective plasma threshold exceeded before it failed to provide results was a growth period lost. This was true of any chemical muscle enhancer. This is in fact why so many athletes reached only 50- 70 % of their potential. Receptor-site insensitivity (not AAS receptor sites) and the body learning new tricks to force homeostasis was the number one reason why we had often seen 220 LB 6 foot off-season bodybuilders using crazy dosages with poor results.
Of course there are ways to beat this too that I created for Frank, but we will discuss that later. First let’s look at what the basic threshold for results were when long term potential and permanent gains were to be realized.
Since this section is about Frank’s AAS protocols, let’s focus upon them for now. Growth thresholds were established by plasma level in this discussion. Although there were several thresholds for each level of experience and drug, there were predictable ranges of dosages expressed in daily plasma levels we used as a basis.
First let me say again that it has been my experience that no athlete should have ever utilize AAS or other muscle chemistry until they have trained hard-core for at least 2-3 years as a natural.
If this was Frank, and he was a natural or somewhere in between, I would have utilized the following rough guide-lines. Natural training is a growth threshold also. I have trained some 250 LB, 8% body fat naturals, too.
Never waste a growth threshold. You need to do the physical work required first and foremost, you weenie.