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How estrogen effects muscle growth.

pharma1

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Came across a great article I wanted to share on managing estrogen and how dynamic it actually is.

Short summary: Use enough anti-e to keep side effects at bay. But don't over do it! Estrogen plays rolls in IGF-1 production, glucose metabolism, and muscle growth.




Stronger doesn't always equate to better

Can estrogen work to augment muscle growth? Is this hormone always unwanted when we are taking anabolic steroids? Anecdotal reports from athletes suggest that the use of estrogen maintenance drugs such as tamoxifen (anti-estrogen) or aminoglutethimide (anti-aromatase) may slightly hinder muscle mass gains during steroid therapy. An explanation or even clarification for this observation has not been easy to come by. Here I would like to take a look at the comparative effectiveness of certain aromatizable and non-aromatizable drugs, as well as the possible mechanism in which estrogen can play a beneficial role to the athlete.

The Androgen Receptor
All anabolic/androgenic steroids promote muscle growth primarily via the cellular androgen receptor (abbreviated as AR in this article). The steroid attaches to and activates the androgen receptor, which ultimately gives the cell an order to increase protein synthesis. This process is well understood. But it has been suggested that other mechanisms may foster muscle growth during steroid therapy as well, which lie outside of the androgen receptor. One way this is evidenced is by the fact that steroids displaying a high affinity for the AR in muscle tissue do not always promote an equally high level of muscle growth. In other words, anabolic potency does not always correspond perfectly to receptor affinity. Clearly there are some disparities that lead into question whether or not the androgen receptor is the only thing at work concerning growth.

Testosterone, Nandrolone and Methenolone
Testosterone is without question one of the most effective steroids for building muscle mass available to athletes. However it does not have the highest affinity for the androgen receptor compared to some other steroids. For example, it has been shown that by eliminating the 19-methyl group (nandrolone) the affinity of the steroid for the androgen receptor is greatly enhanced. Nandrolone thus displays approximately 2-3 times greater affinity for the androgen receptor compared to testosterone, yet its ability to promote muscle growth seems to be considerably lower than testosterone at an equal dosage. One discussed possibility for this occurrence is the reduced androgenic potency of nandrolone. While testosterone converts to the more active steroid dihydrotestosterone (3-4 times greater AR affinity) upon interaction with the 5-alpha reductase enzyme in various androgenic target tissues such as the skin, scalp, prostate, CNS and liver, nandrolone drops to a third of its original potency by converting to the weak steroid dihydronandrolone. However this action is very site specific, and in muscle tissue nandrolone dominates as the active form of the steroid. Therefore this explanation may not suffice.

Nandrolone also differs from testosterone in its ability to be converted by the aromatase enzyme to estradiol (an active estrogen). In comparison, nandrolone aromatizes at approximately 20% of the rate testosterone does, and as such is not known as a very estrogenic steroid. It is likewise favored when reduced estrogenic side effects such as water retention, fat deposition and gynecomastia are desired. However athletes know that there is a trade off with the reduced tendency for nandrolone to promote side effects, in that it is a less anabolic steroid. With its known high affinity for the AR in muscle tissue, could this suggest that estrogen may also be a key mediator of muscle growth?

When we look at Primobolan??? (methenolone) we see a similar trend. Methenolone is at least as good a binder of the androgen receptor as testosterone. By some accounts it is on par with nandrolone. However it is known to be much weaker than both steroids at promoting muscle growth. We know that methenolone does not interact with 5-alpha reductase, and as such its affinity for the AR does not increase or decrease in androgen target tissues. This would logically seem like a more favorable trait for anabolism over the weakening we see with nandrolone. However methenolone is a markedly weaker anabolic, and requires relatively high doses to promote growth. This also brings into question the role of 5-alpha reductase in promoting an anabolic state. Perhaps the fact that Primobolan??? is a non-aromatizable steroid is more relevant.

Estrogen and GH/IGF-1
>To date the most common explanation for why anti-estrogens may be slightly counterproductive to growth in the sports literature has been the suggestion that estrogen plays a role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known as somatomedin is of course an anabolic product released primarily in the liver via GH stimulus. IGF-1 is responsible for the growth promoting effects (increased nitrogen retention, cell proliferation) we associate with growth hormone therapy. We do know that women have higher levels of growth hormone than men, and also that GH secretion varies over the course of the menstrual cycle in direct correlation with estrogen levels. Estrogen is likewise often looked at as a key trigger in the release of GH in women under normal physiological situations.

It is also suggested that the aromatization of androgens to estrogens in men plays an important role in the release and production of GH and IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing the effects of testosterone replacement therapy on GH and IGF-1 levels with and without the addition of tamoxifen. When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels. Yet another study shows that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably due to its strong anti-estrogenic/gonadotropin suppressing action. All of these studies seem to support a direct, estrogen-dependant mechanism for GH and/or IGF-1 release in men. It is difficult to say at this point just how important estrogen is to IGF-1 production as it relates to the promotion of anabolism in the steroid using athlete, however it remains an interesting subject to investigate.

Glucose Utilization and Estrogen
Estrogen may play an even more vital role in promoting an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering the level of available glucose 6-phosphate dehydrogenase. G6PD is an important enzyme in the support anabolism, as it is directly tied to the use of glucose for muscle growth and recuperation. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role in what is known as the pentose phosphate pathway, and as such this rise is believed to enhance the PPP related process in which nucleic acids and lipids are synthesized in cells; fostering the repair of muscle tissue.

A 1980 study at the University of Maryland has shown that levels of glucose 6-phosphate dehydrogenase rise after administration of testosterone propionate, and further that the aromatization of testosterone to estradiol is directly responsible for this increase.[x] In this study neither dihydrotestosterone nor fluoxymesterone could mimic the affect of testosterone propionate on levels of G6PD, an affect that was also blocked by the addition of the potent anti-aromatase 4-hydroxyandrostenedione to testosterone. 17-beta estradiol administration caused a similar increase in G6PD, which was not noticed when its inactive estrogen isomer 17-alpha estradiol (unable to bind the estrogen receptor) was given. An anti-androgen could also not block the positive action of testosterone. This study provides one of the first palatable explanations for a direct and positive effect of estrogen on muscle tissue.

What does this all mean?
It is a long held belief among athletes that estrogen maintenance drugs can slightly hinder muscle gains during steroid therapy with a strong aromatizable steroid such as testosterone. Whether or not we have plausibly explained this remains to be seen, however the above evidence certainly does provide strong support for a direct and positive affect of estrogen on growth. Does this mean we should abandon estrogen maintenance drugs? I don???t think that should be the case. It is important to remember that estrogen can deliver many unwanted effects such as increased water retention, fat deposition and the development of female breast tissue when it becomes too active in the male body. Clearly if we plan a high-dose cycle with an aromatizable steroid, anti-estrogens will be an important inclusion. However we cannot ignore the suggestion of using estrogen maintenance drugs only when they are necessary to combat visible side effects during mild to moderately dosed cycles, especially if bulk is the ultimate goal of the athlete.


by William Llewellyn
 

BIGMURPH

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Excellent post written by a man I have alot of respect for

Estrogen is so important in growing muscle mass during a cycle it is a powerful anabolic hormone.
I usually run my estrogen just below 60 when on cycle just to take advantage of the estrogen.

I always say don't use an AI unless it's necessary ive even run cycles just using nolvadex for protection no AI with limited testosterone you might not even need nolvadex and the e2 will help you grow as long as the testosterone to estrogen is the right ratio the synergy is amazing.
 

b_cornelius

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I learned just how important estrogen is for endogenous GH. It's right at the top for importance. Crush your estrogen, crush your natural GH.

This is important for cutting as well, especially if you are relying on endogenous GH. Estrogen isn't really that bad for cutting once you compare the effects of everything. Your GH levels are certainly more important to cutting than estrogen, so in most cases, don't crush your estrogen levels too low.
 

Unstopppable1

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I totally agree! I hardly ever use AIs anymore. I used to overuse them like crazy, now that I let me estro run higher it's made a dramatic difference in my lean muscle accrual.
 

johnjuanb1

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This is why I take female birth control pills, the ones higher in estrogen, not the tricyclic ones. They stack perfect will dbol for insane gains! They also keep me from getting pregnant and my hair has never been shinier.

P.S. I’m just fukking with you!!! 🤣
I could have adding this on another post to string it along but I know one of you mother fukkers would try it before you saw the follow up post. 😆
In all seriousness, there is a reason cattle implants have estrogen added to the tren and test prop. It’s because the synergy creates cattle with more mass.
 

BIGMURPH

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This is why I take female birth control pills, the ones higher in estrogen,
Really you supplement with estrogen?
How much does this really help brother its the first time I have ever seen this method its interesting if you're really looking for an e2 boost

WTF JJ

I actually thought that you were serious lol
 

johnjuanb1

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Really you supplement with estrogen?
How much does this really help brother its the first time I have ever seen this method its interesting if you're really looking for an e2 boost

WTF JJ

I actually thought that you were serious lol
Hahaha funny. BigMurph, I usually only read the beginning of a long post so I figured I’d get some guys on that. Hahaha 😝
 

Matsuo Munefusa

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There’s plenty guys supplementing with e2 cream actually. You might be surprised. Low estrogen is fucking hell.

Personally I’d rather run test a little higher and get all the e2 I need that way but as I get older I may consider especially if I have low dose primo thrown in which can tank estro.
 

BIGMURPH

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There’s plenty guys supplementing with e2 cream actually. You might be surprised. Low estrogen is fucking hell.
That really does interest me I didn't know about e2 supplementation I've tried DHEA it definitely raises e2 and igf1 I did blood work but I have never seen or heard of anyone actually using e2.
Low e2 is hell
 

Matsuo Munefusa

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That really does interest me I didn't know about e2 supplementation I've tried DHEA it definitely raises e2 and igf1 I did blood work but I have never seen or heard of anyone actually using e2.
Low e2 is hell
You should read reddit. There is a MUCH larger user base to reddit so trends and also subversive behavior is easier to study (Not saying taking e2 as a straight man is subversive). Forums are pretty outdated/antiquated so they tend to be vacuums for new trends.
 

BIGMURPH

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You should read reddit. There is a MUCH larger user base to reddit so trends and also subversive behavior is easier to study (Not saying taking e2 as a straight man is subversive). Forums are pretty outdated/antiquated so they tend to be vacuums for new trends.
Very true I actually haven't ever really been on reddit I checked it out before but I guess I will do some research on reddit.
I always thought of reddit being a bunch of 16yr olds I know that decca test is over there he is a good guy.
Thanks brother
 

Matsuo Munefusa

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Very true I actually haven't ever really been on reddit I checked it out before but I guess I will do some research on reddit.
I always thought of reddit being a bunch of 16yr olds I know that decca test is over there he is a good guy.
Thanks brother
Reddit has “grown up” in a lot of ways the last few years. Worth taking a dive if you have a bit of spare time (and we all do here otherwise we wouldn’t be on here). Side note, but I absolutely love it when guys mention on forums they don’t have enough time. It’s like then why da fuck you talking to us!?!? lol
 

buck

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This is why I take female birth control pills, the ones higher in estrogen, not the tricyclic ones. They stack perfect will dbol for insane gains! They also keep me from getting pregnant and my hair has never been shinier.

P.S. I’m just fukking with you!!! 🤣
I could have adding this on another post to string it along but I know one of you mother fukkers would try it before you saw the follow up post. 😆
In all seriousness, there is a reason cattle implants have estrogen added to the tren and test prop. It’s because the synergy creates cattle with more mass.
Not to be argumentative. But farmers also want to fatten their cattle up and get more marbling as they get paid by the pound and a fatter com can bring more profit. Just loot at Kobe or Wagyu beef and the price of it.
 

BIGMURPH

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Reddit has “grown up” in a lot of ways the last few years. Worth taking a dive if you have a bit of spare time (and we all do here otherwise we wouldn’t be on here). Side note, but I absolutely love it when guys mention on forums they don’t have enough time. It’s like then why da fuck you talking to us!?!? lol
Lol you're a trip brother
I will take a trip over there and check it out though im curious
 

johnjuanb1

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Not to be argumentative. But farmers also want to fatten their cattle up and get more marbling as they get paid by the pound and a fatter com can bring more profit. Just loot at Kobe or Wagyu beef and the price of it.
True. They want mass/bulk weight.
 

Type-IIx

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Good find! In terms of research, Tren+E2 pellets (rather than Tren alone) in cattle yields far greater quantity and quality of meat (due mostly to elevated IGF-I), for what it's worth.
 

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