Deca's Effect on HPTA; Androgen Receptor Upregulation; Lactic Acid & IGF-1/GH/Prostaglandins

by Author L. Rea

Publication Date: March 24, 2003

Nothing in this article is intended to take the place of advice from a licensed health professional. Consult a physician before taking any medication.

Q: Mr. Rea , you mention in your book CME that lactic acid increase during working out increases IGF-1 and GH in the body , but also lactic acid truncates the last 3 amino acids off the IGF-1 and creates Des(I-3) IGF-1 which you say is 10 times anabolic than IGF-1 .

You also mention that lactic acid build is a very effective PROSTAGLANDIN release stimulator, so from this, it seems lactic acid is really helpful. But then why all these supplements to reduce lactic acid during training etc etc in the bodybuilding industry ?

A: Lactic acid is a highly versatile substance when we speak of its effects in relation to bodybuilding progress…or not. It has the metabolic duties of triggering GH release through bio-feedback, truncates intracellular IGF-1 thus altering its structure to become the far more anabolic specific chemical Des (1-3) IGF-1, and of course shuts down the ATP synthesis pathways necessary to muscular contraction (the last rep is a SOB due to a lack of local/working muscle fiber ATP and the lovely burning sensation partially due to lactic acid build-up.) What we need to focus upon is the issue of ratios anytime we discuss a chemicals value or the lack there of. In this case lactic acid elevation in itself is paramount to the hormonal cascade that allows us to recover and build upon our musculature. This should seem obvious when one considers the alteration of IGF-1 to a more anabolic hormone-like substance. But that is only a part of the anabolic equation. Lactic acid also increases PGF-2a and other members of the anabolic cascade. However problems can occur when lactic acid concentrations are elevated beyond that of the anabolic substances (in activity) that we all love and cherish and the inability to perform those final reps that act as the stimulus for repair and growth is certainly detrimental to progress. So the goal becomes to allow adequate lactic acid build-up that allows the anabolic cascade to occur without reaching a point of interfering with training capacities.

Many companies have attempted to capitalize on the lactic acid issue by making it a negative one-action physiological chemical. Consumers are taught that running farther and 5 more reps is a good thing without question. The truth is that we seek that perfect balance between damage and repair that allows for our best progress in whatever athletic goal we may have. This means that damage is necessary to trigger the repair and growth pathways and that lactic acid in the correct ratio to other body chemistry plays its role in both.

Q: You have mentioned heavy resistance training results in upregulation of the androgen regulators of the muscle. And quoted this study:

J. Streng Cond. Res. 14(1): 102-113, 2000
Hormonal responses to high and moderate intensity strength training exercise. Eur.J. Appl Physiol. 82:121-128, 2000

Why do we have to increase dosages used if androgen receptor count is increased due to training? Obviously AS receptor do not up-regulate to a noticeable degree then? Is this the reason for the required higher doses each subsequent cycle for growth ?

A: You do my heart good, Lad. Your questions on this are bright and insightful. More importantly, you are thinking! Androgen receptors up-regulate as an adaptive response to various stimuli including work-load requirements that exceed 75% SRM. This is commonly accepted as a need for the organism to employ a greater number of type-IIb muscle fibers in an attempt to exceed the number required to carry the load minimal duress so to speak. In short it is another example of the body taking the easiest road to accomplish a task. The increase in androgen receptors results in a greater number of AAS pairing and subsequent transcriptions (anabolic messages in this case). As a result the long-term effect is an increase in type-II fibers at the expense of type-I thus allowing an adaptation that enables the working muscle to more easily accomplish its tasks and avoid injury as a result. (Which is another growth limiting factor we will no doubt discuss another time)

The concern relating to an increase in androgen receptors not resulting in an increase in anabolic reaction due to DNA/mRNA transcription rates is just that: An issue of rate or speed. The coupling of an AAS molecule and androgen receptor is not permanent. Each AAS variation has a binding time or the time in which it can remain lodged in its receptor delivering its message. When only a few androgen receptors are occupied by an AAS molecule, the DNA/mRNA transcription easily keeps up with time to spare. As the number of androgen receptors increases so does the odds of AAS/receptor pairing. This means that due to more receptors delivering their AAS message the time to spare is lost. But, due to the finite period of transcription being filled there is an increase in anabolism.

The primary reason AAS administration dosages are necessary to increase is due to Action/Reaction Factors. Initially there is a balance between anabolic and catabolic chemistry naturally present and active in the body…when we first administer a given amount of AAS. As example is the endogenous/natural testosterone level combined with the administered exogenous dosage to consider. As the HPTA down-regulates and shuts down the manufacture and release of endogenous testosterone, our example athlete loses the equivalent of a 200mg dosage of testosterone enanthate weekly. If the athlete were administering 600mg weekly of that testosterone the loss from the HPTA reaction is about 33%. So we already need to increase the administration dosage by 200mg weekly to maintain the initial anabolic environment. When the additional Action/Reaction Factors of binding proteins, cortisol, aromatization and others are accounted for the result is another increase in administered dosage being required.

Please realize that dosage = results is not a numerical progression. In many cases the amount of AAS administered is simply a matter of increasing the amount of circulatory androgens to a point that supports new tissue as well as old. The goal is continual progress not a quest to learn new mathematical errors at the expense of health.

Q: In your first year sample cycles section for the male (In Chemical Muscle Enhancement), the cycle outlined for weeks 1-4 is 200 mg deca per week. now that much deca per week is less anabolic than what the natural test (HPTA) can produce (test being stronger than nandrolone mg to mg) . and because of the ester attached to nandrolone , 4 weeks long is hardly enough for blood levels to reach a constant level .

Also , how is deca easy on the HTPA , you  go ahead and say post cycle meds are not necessary as deca is easy on the HTPA which we from multiple examples know is so not true , cases of testicular shrinkage , limp dick etc are so much reported normally on a deca only cycle sir . Can you please explain your logic behind this ??

You also mention cytomel increased cellular androgen receptor clearing (pg 181 and 182 in the book). How true is this sir ??

Looking forward to your answers to these questions sir , thanks .

A: Nandrolone is actually more anabolic but less androgenic than testosterone and as such allows an increase in muscle protein synthesis in excess of that seen with testosterone. So the next question should obviously be "why then does testosterone deliver more weight gain then nandrolone?" Since nandrolone is about 80% less affected by aromatase when compared to testosterone, it should seem obvious that the lack of GLUT-4 (increased muscle glycogen synthesis) activity will also result in a decrease in intracellular content but not cellular wall protein synthesis. Since we are speaking of post-cycle retention as well here we would be in error if we included the on-cycle increase in the body’s water table from estrogen/aldosterone resulting from the higher aromatizing testosterone in our comparison.

When we employ brief cycles of 4 weeks, a 200mg dosage of nandrolone decanoate would have an additive effect to the endogenous (naturally produced in the body) testosterone for the first 3 weeks. For a novice this accounts for about twice the normal rate of anabolism possible if diet is correct (anabolism is not potentiated unless the macronutrient environment is as well). Many do not realize that the body actually produces about 150mg of testosterone weekly. It circulates about 50mg of testosterone weekly, but it produces about 150mg. Much testosterone is lost to enzymic conversion to 4-androstenediols and various intermediates of DHT. So in essence we are creating a close hormone environment comparison to that realized at about week 6 of a 200mg each testosterone cypionate and nandrolone decanoate protocol.

The issue of nandrolone having such profound progesterone effects is a bit overplayed for some reason that I cannot grasp. For periods of only 4 weeks and at dosages of up to 400mg weekly, the actual progestin effect is not really of concern. Though it should be noted that the HPTA will not supply adequate testosterone (and subsequently DHT) to support a healthy libido beyond that point. And the estrogenic value is far less for nor-estrogens as a whole. As example is the effect upon HPTA function. LH and FSH are the determining factors for HPTA function itself. For this reason we can determine the degree of HPTA function inhibition that occurs as a result of the administration of different AAS. Novices that had normal LH/FSH levels prior to nandrolone administration showed an average decrease in LH/FSH of only about 33% at day 21 and 39% at day 28. Additionally at day 42 (2 weeks after discontinuance) LH/FSH level were only suppress an average of 21% thus showing a positive rebound effect. In comparison testosterone administration for the same period results in an addition decrease in LH/FSH of about 12% (bodyfat levels can have a profound effect upon this).

Normal

Male FSH reference range: 1.4-18.1 mIU/ml

Male LH reference range: 1.59.3 mIU/ml