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Tren Receptor Downgrade/Saturation Question

gabrial

New member
So lets say someone is running test for like 2 months. Those receptors are obviously going to be shot. Now if they switch to the tren at the end of those two months will gains persist, due to the activation of a new receptor?
 
What makes you say they will be shot? cells have receptors of many kinds, outside and inside the cell. For AAS the receptor that concerns us most is the androgen receptor. This is the primary binding site for all AAS not just test. Now, in addition to that, many AAS exhibit other bindings which is what makes them unique.
 
There is no new receptor activation. THere is only one direct receptor responisble for the anabolic induced effects of AAS. The androgen receptor. All AAS exert thier anabolic effects through this receptor. Various AAS may act upon other receptors to enhance anabolic effects, such as agonizing glucocorticoid receptors and increasing the gene expression for various growth factors, but all AAS bind to the androgen receptor to exert a direct anabolic effect. Thus changing drugs will no change the repeptor bound. Running any kind of AS for two months will not amke a receptor "shot". Androgen receptors have a short half life (a few hours) and as such are constantly being regenerated.
 
the problem does not lie with "shuting down" receptors, but rather with SHBG (sex hormone binding globulin), once you introduce andogeneous testosterone into your body it exists in a free state, during that time you grow, however to compensate your body ups the levels of SHBG which binds free testosterone thats when the growth slows and evantually comes to a halt
 
Guys guys guys, speak English to me. I do appreciate these replies. But sum it up in gym talk. Will the tren keep me gaining after taking sust at a dose 1000mgs for 2 months or so and 50mgs of dbol ed. Obviously you need to compensate with higher and higher amounts, and eventually no that doesnt matter any more growth will halt. But im wanting to know time periods here. Ive been doing the tren 75mgs ed with 100mg of dbol .50 of armidex ed (No liver knocks). Should i just start the gains keepers formula or keep going like i want to? Will i still gain
 
Beezers said:
There is no new receptor activation. THere is only one direct receptor responisble for the anabolic induced effects of AAS. The androgen receptor. All AAS exert thier anabolic effects through this receptor. Various AAS may act upon other receptors to enhance anabolic effects, such as agonizing glucocorticoid receptors and increasing the gene expression for various growth factors, but all AAS bind to the androgen receptor to exert a direct anabolic effect. Thus changing drugs will no change the repeptor bound. Running any kind of AS for two months will not amke a receptor "shot". Androgen receptors have a short half life (a few hours) and as such are constantly being regenerated.
Now this man should be a MOD...great reply
 
the problem does not lie with "shuting down" receptors, but rather with SHBG (sex hormone binding globulin), once you introduce andogeneous testosterone into your body it exists in a free state, during that time you grow, however to compensate your body ups the levels of SHBG which binds free testosterone thats when the growth slows and evantually comes to a halt

Actually, androgen administration lowers SHBG:

" During drug administration SHBG concentrations decreased by about 80 to 90% and remained low even for the 16 weeks following steroid withdrawal. Steroid administration had no influence on serum CBG concentrations. In conclusion, self-administration of testosterone and anabolic steroids soon led to impairment of testicular endocrine function which was characterized by low concentrations of testosterone precursors, high ratios of testosterone to its precursor steroids and low SHBG concentrations. Decreased concentrations of SHBG and testicular steroids were still partly evident during the 16 weeks after drug withdrawal." (1)

Additionally, testosterone administration upregulates androgen receptors in muscle satellite cells. This is thought to be at least one reason why supraphysiological doses of test can continue to increase muscle growth:

The purpose of this study was to determine whether androgen receptors (AR) are present in cultured skeletal muscle satellite cells and myotubes and examine the effects of testosterone on satellite cell proliferation and differentiation. Immunoblot analysis using polyclonal AR antibodies (PG-21) revealed an immunoreactive AR protein of approximately 107 kDa in porcine satellite cells and myotubes. Immunocytochemical AR staining was confined to the nuclei of satellite cells, myotubes, and muscle-derived fibroblasts. Administration of 10(-7) M testosterone to satellite cells, myotubes, and muscle-derived fibroblasts increased immunoreactive AR. In satellite cells and myotubes, AR increased incrementally after 6, 12, and 24 h of exposure to testosterone. (2)

(1) J Steroid Biochem 1985 Jul;23(1):33-8
Response of serum testosterone and its precursor steroids, SHBG and CBG to anabolic steroid and testosterone self-administration in man.
Ruokonen A, Alen M, Bolton N, Vihko R.

(2) Endocrinology 1996 Apr;137(4):1385-94
Testosterone up-regulates androgen receptors and decreases differentiation of porcine myogenic satellite cells in vitro.
Doumit ME, Cook DR, Merkel RA.
 
You guys are speaking greek to me tonight, forgive me but im fuckin tired, and im not going to read medical journal reports, that even with a clear head i would probably have trouble understanding, will someone please answer my fuckin question in laymen terms, thank you for all the input so far.
 
gabrial said:
You guys are speaking greek to me tonight, forgive me but im fuckin tired, and im not going to read medical journal reports, that even with a clear head i would probably have trouble understanding, will someone please answer my fuckin question in laymen terms, thank you for all the input so far.
Just slow down and put some energy into understanding what these gentlemen have given you so far. Make an effort to understand what you have not made an effort to understand.
 
gabrial said:
So lets say someone is running test for like 2 months. Those receptors are obviously going to be shot. Now if they switch to the tren at the end of those two months will gains persist, due to the activation of a new receptor?

If the gains stop on test, your body has prolly reached a plateau in growth since it cannot grow at full force 24/7/52 ...

switching to tren will probably do jack shit. adding tren may help. this has nothing to do with "new receptors." the biggest myth in bb is that receptors rae affected, they are upregulated in response to gear!!!! also SHBP is upregulated, so less unbound AS is in the system.

Hope that helps!
NFG
 
In a nutshell what they are saying is that anabolic steriods all connect to androgen receptors...these regenerate themselves every few hours..so there is no breakdown of the receptors. The test has *saturated the stuff that makes your muscles grow. The only way you will grow bigger is if the tren has a higher anabolic effect to your system than the test. That's why stacking AAS gives better gains than just running say, test alone.


I might be and prob am wrong in how i oversimplified this, 4yrs since my neuro-pharmacology class. Back then it was commonly accepted that AR's downgraded like Beta-receptors. Just curious on whether I have a handle on the new train of thoughts. Taking an AS like Test overtime actually up-regulate AR's. When the androgens then aromatize they increase GH, IGF-1 and satellite cells which enhances our growth factor. The IGF-1 also enhances the sensitivity of satellite cells (a form of stem cell). These satallite cells bind with damaged muscle fiber thus increasing myonuclei for repair and growth. These myonuclei in turn increase one's protein-synthesizing capacity and AR's per muscle fiber. When you lower the amount of AAS there is less activity in the satellite cells which can no longer fuse with all the excess myonuclei (the potential remains) and no new growth occurs. So BB's with more cycle’s benefit from higher doses due to their increased protein-synthesizing capacity, number of AR's and amount of myonuclei capable of receiving the stimulated satellite cells. It’s too late to think about what AAS’s ancillary affects might be.

Am I in the ballpark with my understanding of today’s thoughts on up-regulating and AR's?? Please slap me down if I’m off base, just give me the right info for later.
 
Silent Method said:

Just slow down and put some energy into understanding what these gentlemen have given you so far. Make an effort to understand what you have not made an effort to understand.
Well said silent. Gabrial, educating yourself is kind of like lifting, if it was easy, everyone would be genius. I have found that reading stuff, even if you dont understand it helps. As you progress your studies you will start to recognize words, terms etc. Take it a step farther and do some looking on the web, there are a lot of medical dictionaries around, if you hit a word that you dont understand, look it up. There are also many books on endocrinology available all over including ebay, amazon etc. spend a little money on some books and spend a little time reading them, in the long run you will be thankfull you did.
 
gabrial said:
You guys are speaking greek to me tonight, forgive me but im fuckin tired, and im not going to read medical journal reports, that even with a clear head i would probably have trouble understanding, will someone please answer my fuckin question in laymen terms, thank you for all the input so far.


The steroid of your choice that you have injected is made of a unique molecule that gives the steroid its properties. This molecule is like a key. All cells contain receptors which are like key holes. Certain molecules(keys) fit into certain receptors(key holes). In muscle cells and muscle satelite cells there are anrogen receptors. Steroids are androgens and thus the keys to fit into the androgen receptor, or the key hole. Whne the key goes into the key hole it turns the receptor on. The receptor moves to the nucleus of the cell...goes to its library(DNA) and makes copies of specific genes. That copy is then used as a blueprint to synthesize new components of the cell and a whole slew of other tasks, but for our puposes the blueprint is used to build new muscle. The androgen (test, tren, EQ, Nandrolone, ect.) binds to the androgen receptor on muscle cells and initiates the copying and synthesis of new muscle proteins. To build these new muscle proteins requires materials....In our case amino acids(protein). This is why you have to eat to grow. So all steroids anabolic in nature initaite this same process via the androgen receptor. The androgen receptors are dynamic. They are always being formed and "dying". Thus an andorgen receptor you had yesterday is no longer there. This is why changing drugs doesn't change the receptor used. They all use the androgen receptor.
 
You do realize that stanozolol has its own, unique, receptor.

To answer your question, adding tren will most likely only cut back the protien degredation, as tren is the ultimate anti-catabolic, and therefore you could potentially realize better gains, because testosterone actually increases degredation as well as synthesis.

So the synthesis will not be hindered, but the degredation will be countered. This would result in better kept gains to build on as you progress.

Now, another thing about tren is that it actually works better in the presence of estrogen. So you might even see something extra in that regard, who knows?

Of course, this is all predicated on proper caloric intake.
 
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