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  George Spellwin's ELITE FITNESS Discussion Boards
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Author Topic:   receptor question
Joseph_stalin
Pro Bodybuilder
(Total posts: 330)
posted March 25, 2000 09:53 AM     Click Here to See the Profile for Joseph_stalin   Click Here to Email Joseph_stalin     Edit/Delete Message

i understand that steroids work by binding with the receptors in the skeletal muscles and giving them a command to produce a more positive nitrogen balance and increased protein synthesis.

but why does 700 mg a week of anadrol produce a more positive nitrogen balance than 700 mg a week of deca.

is it because the receptor has a scale. from what i heard the receptor only has 2 positions, on and off. but are there different degrees of on?
pretend there is a scale of 1-5. 1 being light protein synthesis and nitrogen retention. 5 being high protein synthesis and nitrogen retention.

does anadrol hit 4 on the scale, while deca hits 2? or does the receptor only have 2 positions, on and off.

but if the receptor only has 2 positions, on and off, then 700 mg oxymetholone shouldn't be more effective than 700 mg deca. so does oxymetholone work better because it finds more receptors than deca?

anyway, which is it for those who know. anadrol is more effective because

1. 1 mg of oxymetholone will find and bind with more receptors than 1 mg of deca.

2. 1 mg of oxymetholone will produce a more intense "on" with the receptor than deca will. ie, it will convince the same receptor to produce a higher nitrogen balance than deca.

or is it something else.

because i don't know. does anyone know. from what i heard, there are only 2 positions on skeletal muscle receptors, on and off. is there a degree of on and off? ie, does oxymetholone make the receptor more on than winstrol or deca do. or does it find and activate more receptors than deca and winstrol do.

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KANE
Pro Bodybuilder
(Total posts: 138)
posted March 25, 2000 10:08 AM     Click Here to See the Profile for KANE     Edit/Delete Message
YOU HURT MY HEAD, BUT GOOD QUESTION

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KANE

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Jonrocks
Pro Bodybuilder
(Total posts: 145)
posted March 25, 2000 10:32 AM     Click Here to See the Profile for Jonrocks   Click Here to Email Jonrocks     Edit/Delete Message
Comeone Macro, where is your answer, I am want to know about AR's.

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A-mass
Pro Bodybuilder
(Total posts: 325)
posted March 25, 2000 11:02 AM     Click Here to See the Profile for A-mass     Edit/Delete Message
I've been trying to find info on this myself. And I can answer part of the question. AS DO have different binding capabilities. Meaning that small amounts of certain AS will be able to bind with AR's as opposed to others where nearly all of the AS will bind with the AR's.

HOWEVER, I also have read that anadrol has one of the worst binding capabilities of all AS, so this doesn't explain your question.

One explanation is also that a-bombs' huge strength and size increase is a lot of water retention, too.

I'll turn it over to the experts now... and I'll add a question: Why do some AS, like a-bombs take noticeable effect nearly immediately, while others, like EQ, Deca, and some long-acting test esters, etc., take a couple or three weeks to see noticeable effect?

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the alpha male


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Tueros
Amateur Bodybuilder
(Total posts: 18)
posted March 25, 2000 02:06 PM     Click Here to See the Profile for Tueros   Click Here to Email Tueros     Edit/Delete Message
Great question. I have been wondering the same thing.

A-mass, at least a partial answer to your question can be found by reading about the different esters in the article "All tests are created Equal" right here on elite fitness.

I know that different steroids will have different affinities for binding to the AR and if it's an on or off signal then one would think that steroids with greater binding affinities would produce the best results, so Anadrol would be a bit of an anomaly there. Thus I don't think binding affinities alone can be the answer. But I would also think that all molecules that bind to the AR would send the same cellular message but I could be wrong. Someone out there must know.

Let's not forget also that there are non-AR mediated mechanisms of growth and that some steroids are thought to act in this way.

Come on all you gurus and closet cellular biologists, help us out here!

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Komo
Amateur Bodybuilder
(Total posts: 11)
posted March 25, 2000 04:46 PM     Click Here to See the Profile for Komo     Edit/Delete Message
As a closet cellular biologist I think that it has to do with wich receptors beside the testosterone receptor the AS-molecule binds to.
Deca binds both to testosterone- and progesterone receptors, and is an agonist to both of them, thus creating a biological response. Winstrol also binds to Testosterone- and Progesterone receptors, but is an antagonist to the Progesterone, thus inhibiting the biological responce of the receptor.
The Testosterone receptor and the Progesterone receptor may only differ from eachother in a couple of aminoacids, but that`s enough to attract different AS.
A lot of different biologocal transmittors are made of the sterol-skeleton and their receptors could possibly respond differently to different AS.

This is my theory, hope it helps (and is atleast near the truth)!

Keep growin

/Komo

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Komo
Amateur Bodybuilder
(Total posts: 11)
posted March 25, 2000 04:56 PM     Click Here to See the Profile for Komo     Edit/Delete Message
+ Receptor affinities of course.

/Komo

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bignate73
Pro Bodybuilder
(Total posts: 213)
posted March 25, 2000 05:51 PM     Click Here to See the Profile for bignate73   Click Here to Email bignate73     Edit/Delete Message UIN: 65081685
the way i understand it is simply like this:
think of a steroid molecule shaped like a square now think of a specific receptor looking like the outline of a square. if those 2 do not match up identically then nothing will happen. also you have to take into consideration that there are not an evenly distributed # of receptors for a particular compound in every person. thats why they say people may react differently to certain dosages. some people may have "tolerance" or "sensitivity" to a particular compound. just the way i learned it at least. so basically unless you have an equal # of receptors for anavar and deca you wont be able to make a fair assesment as to why one is more potent over another. my 2 pennies on it.

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lift eat grow!!!

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Chris0096
Amateur Bodybuilder
(Total posts: 4)
posted March 25, 2000 06:25 PM     Click Here to See the Profile for Chris0096   Click Here to Email Chris0096     Edit/Delete Message
I'm a biology major and from what I've learned there various factors affecting a steriod's effectiveness. Steriods vary in their degree of affinity for receptors. Not only do steriods wtih high affinity find receptors quicker but they stay bound longer. The longer a steriod is bound, the more protein synthesized. After a steriod detaches from a receptor it can go and bind to another one, or be converted to a weaker or completely inactivated metabolite (enzymes in the cell are responsible for converting steriods in metabolites). Steriods may also vary enough molecularly so that they can bind to different types of receptors. An anti-catabolic steriods is an antagonist for cortisol receptors and when it binds to cortisol receptors, circulating cortisol can not exhibit it's catabolic effects. Basically steriods may differ in:

1)receptor affinity
2)it's tendency to be converted to weaker metabolites by cellular enzymes
3)the type of receptors it can bind to

All these factors contribute to a steriod's effectiveness. Some factors are more influential to protein syntesis than others

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Buffalo_Bill
Amateur Bodybuilder
(Total posts: 24)
posted March 25, 2000 06:53 PM     Click Here to See the Profile for Buffalo_Bill   Click Here to Email Buffalo_Bill     Edit/Delete Message
This is a very interesting post
i would say something
and.....
Like the reseptores stop working after 1 and a half month therefor you dont have to use them more than that and if u do you will only damagde them
Like when a reseptor is activated form roids
they are !!!!
For any reason dosage depends on every person
therefor you have to map you reseptors
if you come to that for u you rmaximum level is 300 mg of deca you only use that at your ^^top^^ in your cycle
400 mg whouldnt do anything better it will only give you side-effects !!!

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Joseph_stalin
Pro Bodybuilder
(Total posts: 330)
posted March 25, 2000 08:08 PM     Click Here to See the Profile for Joseph_stalin   Click Here to Email Joseph_stalin     Edit/Delete Message

i know. it can't be binding capacity because deca has a great binding capacity but will only build 10 lbs. of muscle in 8 weeks. anadrol has a terrible binding capacity but will build 10 lbs in 10 days.

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the truth
Pro Bodybuilder
(Total posts: 251)
posted March 26, 2000 03:14 AM     Click Here to See the Profile for the truth     Edit/Delete Message
I'm not so sure, Joseph. It's difficult to compare a 17 a/a like Anadrol to Deca. I think if we were to examine them and compare their results on a milligram per milligram basis, the use of Deca might result in greater and more permanent muscle gains. Think about it: 3 Anadrol /day is not an uncommon dose (1050 mg); I personally don't know anyone who uses that much Deca (nor, to use your example, do I know anyone who uses 6 AD-50/day for any real length of time. It's possible that in addition to the affinity a given steroid has for binding to androgen receptors, it also has the property of sending a stronger or weaker signal relative to other steroids, meaning that a given amount of the steroid with a greater signal capability will seek out and (possibly) bind to more receptors than an equivalent amount of the steroid with a weaker signal. I'm not necessarily talking about actual binding capability (Deca has a greater affinity for the androgen receptors than Test, yet Test gives you better results), but how efficient the steroid is on a per dose basis at finding the greatest number of androgen receptors. I'm also not taking into account such factors as the molecule's affinity for non-androgen steroid receptor sites (eg Deca's possible affinity for progesterone receptors, etc.) and how that could possibly cross-react with the effect that it has on the androgen receptors. That's a topic for another discussion, and I don't know the answer.

[This message has been edited by the truth (edited March 26, 2000).]

[This message has been edited by the truth (edited March 26, 2000).]

[This message has been edited by the truth (edited March 26, 2000).]

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macrophage69alpha
Moderator
(Total posts: 1051)
posted March 26, 2000 05:09 AM     Click Here to See the Profile for macrophage69alpha   Click Here to Email macrophage69alpha     Edit/Delete Message
the differences are mostly a result of non AR mediated growth- Anadrol does not bind nearly as well as Deca to the AR- however Deca has absolutely no non AR mediated effects aside from its abililty to bind to the progesterone receptor.

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macrophage69alpha
Moderator
(Total posts: 1051)
posted March 26, 2000 05:21 AM     Click Here to See the Profile for macrophage69alpha   Click Here to Email macrophage69alpha     Edit/Delete Message
here is a pretty cool study that looks at the difference between TEST and DHT- it show that although the both bind to the AR the expression of the AR is different- ie there are different genes expressed. this article only looks at the single factor of AR binding and the effects of different androgens binding to the AR and the different expressions that come about. there are other NON AR mediated events that account for much of the anabolism associated with anadrol and dbol. enjoy it pretty good reading- at least I found it to be.

T and DHT mediate their effects by altering gene expression in target tissues via a single receptor, the AR. Despite the binding of T and DHT to a single receptor, the effect of these hormones on a single gene may be quite distinct. For example, differential regulatory effects of T and DHT on expression of several genes including Far-17a (84), and the cytokines interleukin-4 (IL-4), IL-5 and g-interferon (gIFN) has been reported (85). The observation that both T and DHT can differentially regulate the expression of the androgen responsive genes has led to the controversial idea that more than one AR may exist. This hypothesis is supported by the following observations (reviewed in (86)) : (1) (3H)T, when injected into rats, concentrates in the hypothalamic nuclei and 100x unlabeled DHT does not inhibit this localization; (2) hypothalamic localization is not observed after injection of (3H)DHT; and (3) the ability of T, but not DHT to induce neuronal proliferation or male sexual behavior in castrated male rats. These data are consistent with two different possibilities. One possibility is that two different androgen receptors indeed exist. On the other hand, these data may be due to different metabolic interactions of the androgens on a single androgen receptor. As discussed above, T dissociates from the AR 3 times faster than DHT and is less effective in stabilizing the AR (74). This difference in the dissociation rate has been directly related to the androgens' ability to stimulate transcription of an androgen responsive gene (87). These observations could account for the differential effects of these androgens mediated by one receptor.

Perhaps the strongest evidence for the presence of one androgen receptor is derived from the observation that genotypic XY mice and rats with testicular feminization syndrome (Tfm) do not have a fully functional AR (87-90) and even though they express both T and DHT they develop into phenotypic females. This experiment of nature demonstrates that loss of one AR can result in loss of action of both androgens.

The presence of two androgens acting on one receptor may serve several possible functions. Cells which contain steroid 5a-reductase can convert T into DHT. Thus, the overall effect of this system may be to amplify the action of T via conversion to DHT within these cells, thus providing a mechanism of local regulation.


Peace

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MP

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macrophage69alpha
Moderator
(Total posts: 1051)
posted March 26, 2000 05:31 AM     Click Here to See the Profile for macrophage69alpha   Click Here to Email macrophage69alpha     Edit/Delete Message
Oh by the way SEX HORMONE BINDING GLOBULIN is important in determining how effective androgens/anabolics are. Methandriol or DRIVE - a weak estrogen supposedly reduces the amount of SHBG or it bind to it allowing an increase of free TEST levels- steroids that are not bound by SHBG are free to activate the AR or to induce Non AR mediated effects.
OKAY- that is it for tonight

PEACE

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MP

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macrophage69alpha
Moderator
(Total posts: 1051)
posted March 26, 2000 01:52 PM     Click Here to See the Profile for macrophage69alpha   Click Here to Email macrophage69alpha     Edit/Delete Message
bump

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MP

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macrophage69alpha
Moderator
(Total posts: 1051)
posted March 26, 2000 10:38 PM     Click Here to See the Profile for macrophage69alpha   Click Here to Email macrophage69alpha     Edit/Delete Message
bump

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MP

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macrophage69alpha
Moderator
(Total posts: 1051)
posted March 28, 2000 07:48 PM     Click Here to See the Profile for macrophage69alpha   Click Here to Email macrophage69alpha     Edit/Delete Message
bump

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MP

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THESAINT
Pro Bodybuilder
(Total posts: 219)
posted March 28, 2000 09:05 PM     Click Here to See the Profile for THESAINT   Click Here to Email THESAINT     Edit/Delete Message
THERE'S A GOOD ARTICLE IN ARCHIVED TOPICS
SEARCH:RECEPTORS, ENTITLED"Re:Receptors
actually UPREGULATE with the use of heavy
androgens.

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Juicer56
Amateur Bodybuilder
(Total posts: 31)
posted March 28, 2000 10:51 PM     Click Here to See the Profile for Juicer56     Edit/Delete Message
just one thing to think about, if you taking 700mg/week of anadrol which is fast acting your getting a 100mg per day, in contrast to deca which also at 700mg/week has a 2week life so your only getting about half as much mg's/day

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