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trenbolone VS anadrol

Lao Tzu

New member
both have short half lives, and both are more anabolic/androgenic than regular testosterone.

so why are the gains off of trenbolone supposedly permanent while the gains from anadrol are temporary?

it can't be because anadrol is more anabolic/androgenic than test, if that were the reason tren would be considered a drug that only gave temporary gains too. but it isn't, it is considered the opposite. tren gives permanent gains (in the underground literature i have read).

it can't be the half life either. injectible anadrol probably has the same half life (just about i guess) as trenbolone acetate.

so is it the mechanism of action that makes the gains from one permanent & the gains from another temporary or what.
 
this is a valid question. why is one considered to be terrible for keeping gains and another great. they both are stronger than natural test & both have short half lives. what does tren do that anadrol doesn't. is it due to anadrol's effect on red blood cells or what.
 
I think, thats means I'm not sure, but I believe its their mechanisms. Tren binds to the androgen receptor whereas anadrol dosen't, it's mechanism is different. I may be confusing it with dbol. BUMP for more info.....

WRJ
 
Trenbolone has a much greater affinity to androgen receptor, in a matter of fact, it's as strong as DHT, while Anadrol has one of the weakest, that's why the tabs are 50mg( a lot for the tab!)
 
Drol works through non-ar mediated mechanisms while tren has a very strong affinity for the AR, thats the difference.
 
Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin.

Endocrinology 1984 Jun;114(6):2100-6 (ISSN: 0013-7227)

Saartok T; Dahlberg E; Gustafsson JA [Find other articles with these Authors]

It is unclear whether anabolic steroids act on skeletal muscle via the androgen receptor (AR) in this tissue, or whether there is a separate anabolic receptor. When several anabolic steroids were tested as competitors for the binding of [3H]methyltrienolone (MT; 17 beta-hydroxy-17 alpha-methyl-4,9,11-estratrien-3-one) to the AR in rat and rabbit skeletal muscle and rat prostate, respectively, MT itself was the most efficient competitor. 1 alpha-Methyl-5 alpha-dihydrotestosterone (1 alpha-methyl-DHT; mesterolone) bound most avidly to sex hormone-binding globulin (SHBG) [relative binding affinity (RBA) about 4 times that of DHT]. Some anabolic-androgenic steroids bound strongly to the AR in skeletal muscle and prostate [ RBAs relative to that of MT: MT greater than 19-nortestosterone ( NorT ; nandrolone) greater than methenolone (17 beta-hydroxy-1-methyl-5 alpha-androst-1-en-3-one) greater than testosterone (T) greater than 1 alpha-methyl-DHT]. In other cases, AR binding was weak (RBA values less than 0.05): stanozolol (17 alpha-methyl-5 alpha- androstano [3,2-c]pyrazol-17 beta-ol), methanedienone (17 beta-hydroxy-17 alpha-methyl-1,4-androstadien-3-one), and fluoxymesterolone (9 alpha-fluoro-11 beta-hydroxy-17 alpha-methyl-T). Other compounds had RBAs(relative binding affinity) too low to be determined (e.g. oxymetholone (17 beta-hydroxy-2-hydroxymethylene-17 alpha-methyl-5 alpha-androstan-3-one) and ethylestrenol (17 alpha-ethyl-4- estren -17 beta-ol). The competition pattern was similar in muscle and prostate, except for a higher RBA of DHT in the prostate. The low RBA of DHT in muscle was probably due to the previously reported rapid reduction of its 3-keto function to metabolites, which did not bind to the AR [5 alpha-androstane-3 alpha, 17 beta-diol and its 3 beta-isomer (3 alpha- and 3 beta-adiol, respectively)]. Some anabolic-androgenic steroids (only a few synthetic) bound to SHBG (1 alpha-methyl-DHT much greater than DHT greater than T greater than 3 beta-adiol greater than 3 alpha-adiol = 17 alpha-methyl-T greater than methenolone greater than methanedienone greater than stanozolol). The ratio of the RBA in rat muscle to that in the prostate (an estimate of the myotrophic potency of the compounds) was close to unity, varying only between about 0.4 and 1.7 in most cases.(ABSTRACT TRUNCATED AT 400 WORDS).
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"Too low, to be determined" - that's low!

The only explanation for great water retention, that I can see, would be cross binding to progesteron receptor. And it has to be really strong.
While Trenbolone's affinity to PR is as strong as progesteron itself, still, most likely, it's strong binding to AR prevent water retention, and actually, provides "dry" appearence(the way Drostanolone(Masteron) does)
 
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