philipebrown

I could do with something clearing up here lads,

steroids bind to the androgen receptors yes/no?

oestrogen binds to specific oestrogen receptors yes/no?

I have been told that using anti oestrogens such as nolvadex during a cycle can hamper your gains as you are restricting the number of receptor sites the steroids can bind to as nolvadex can compete for the same sites yes/no? and that a little extra oestrogen during a cycle can be beneficial?

However i was under the impression that the two hormones bind to seperate receptor sites yes/no? and if this is the case, then using nolvadex during a cycle shouldnt harm your gains at all?

Can someone clear this up?

hackskii

Well, that has been a big debate for awhile.
I heard that estrogen can help with gains.
Estrogen will make you hold more water and this can help gains (strength) by having a leveraging effect within the muscle.
I have also heard that estrogen can shut down your HPTA making recovery harder.

So with that, I really dont know what to think anymore. Proviron makes me break out so bad and takes weeks to get rid of the zits.
I hear that proviron on cycle can free up unbound test and help gains while blocking estrogen. Hmmm
Cant take proviron as my BP will be high and will have massive acne and I never get acne.

So in my situation it is a catch 22. If there is evedence of gyno then I will drop some nolvadex and maybe proviron but other than that I am going to save it for PCT (not the proviron).

I dont think this is going to help and maybe even add to the confusion.
I am really curious to see how this thread is going to go

__________________
Power over others is weakness disguised as strength.

Scott

philipebrown

at the moment as you know i am taking non aromatising steroids with the exception of test prop as i prepare for my hols. I am also taking 10mg of Tamoxifen per day, just as a precautionary measure and to keep any water build up at bay, as it effects my skinfold measurements which i am trying to reduce. Depending on how my nuts are i might go for some HCG toward the end of the cycle followed by Clomid for PCT, which i have never tried before. If I am using Clomid and dont have much estrogen at the end of the cycle is there any point in continuing my nolvadex then too?

hackskii

I use both myself and stockpile it.
If you are really concerned then you can add that herbal one in the mix.
I have an article in the article selection that I used and worked like a champ for me. I might modify it some like add L-Lycene, echinacea, and golden seal to boost my immune system just after the cycle. I tend to get sick and all three of these will help the immune system prior to comming back online.

__________________
Power over others is weakness disguised as strength.

Scott

philipebrown

quote: Hackskii

"Well, that has been a big debate for awhile.
I heard that estrogen can help with gains.
Estrogen will make you hold more water and this can help gains (strength) by having a leveraging effect within the muscle.
I have also heard that estrogen can shut down your HPTA making recovery harder. So with that, I really dont know what to think anymore."



Looks like weve finally caught you out, you must be slipping mate, lol!

Only kidding, this one could go a long way if anyone can find any articles or evidence that supports either argument!

Predator

Insanity posted some info on Clomid at the top as a sticky if that helps!?

Predator

big pete

meds such as tren require estrogen to work there magic, therefore they need an aromatisable med to do it justice (dbol,sust etc) otherwise it just makes you "harder" with the exception of the old donger.

there are androgen/estrogen receptors. differant meds attatch themselves differantly to the receptors, thats why some meds yeild better gains than others. of course it can vary on other things too.

as hackskii says, the only way nolvadex is said to hinder gains is that it reduces water. which is almost bollox, cos its a SERM, and only blocks estrogen in the hypothalamus (which is why its also used for PCT)

hackskii

Just found this: What we discovered is that Nolvadex reduces the effect of the growth hormone—as measured by IGF-1 levels—by about 50%.

Ha ha ha philipbrown.

It came from here but it is a good long read.
http://www.t-mag.com/html/27testo.html

__________________
Power over others is weakness disguised as strength.

Scott

philipebrown

Aye, i thought it wouldnt take you long mate, lol!

If thats the case, and growth hormone helps you lose fat, then maybe i should keep off the nolva for this cycle. Dont seem to be gaining water anyway.

philipebrown

Just found this from an extract about equipoise

"However small aromatisation is desirable as estrogen too mediates anabolic activity. It can be responsible for better glucose utilization3,4 (repleting lost glycogen stores after exercise) and stimulating increased growth hormone release5. But most notably estrogen is responsible for an upgrading of the androgen receptor6 allowing hormones that act on the androgen receptor to exert a larger anabolic effect. This is why hormones that are strong androgens but also aromatize heavily, like anadrol and testosterone, can put the most mass on your frame".

So i guess estrogen is a good thing to have!

hackskii

Just found this too.

Estrogen & Muscle Gains

Hey Pat,

Will lowering my estrogen levels, while keeping my androgen levels constant, hurt or hinder my muscle gains?

Good question. The use of agents to lower estrogen levels (aromatase inhibitors), or to block estrogen action at the receptor (estrogen receptor antagonists), has become quite en vogue lately. Personally, I think they are overused and could hinder muscle mass gains.

I have discussed before the potential suppressant effects of anti-estrogen compounds on GH and IGF-1 production. But beyond that, there may be direct beneficial effects of estrogen on androgen activity in muscle that may be blocked by anti-estrogens.

One important mechanism involved in muscle growth is the formation of NADPH, which is used as the prime source of energy (reducing power) in anabolic processes. Androgens are well known to stimulate one of the key enzymes involved in the formation of NADPH, called glucose 6-phosphate dehydrogenase. Furthermore, glucose 6-phosphate dehydrogenase is also involved in the production of raw materials for nucleic acid synthesis. Nucleic acids biosynthesis is required at high rates in regenerating tissues.

One of the most widely documented effects of androgens is stimulation of glucose 6-phosphate dehydrogenase, and this is thought to be key to their anabolic activity. A recent study found however that without estrogens, androgens are not able to fully exert their stimulatory activity on this enzyme. The authors conclude that androgens and estrogens may exert synergistic effects on skeletal muscle. (Max SR ,"Androgen-estrogen synergy in rat levator ani muscle: glucose-6-phosphate dehydrogenase", Mol Cell Endocrinol 1984 Dec;38(2-3):103-7)

The same author also found another mechanism by which estrogens may increase the activity of androgens in skeletal muscle. He used rats that had their testes removed and then administered androgens to them, with and without estrogens. What he found was that estrogens caused a very substantial increase in the binding of androgens to their receptors. He hypothesized that this is due either to a greater synthesis, or a decreased degradation of, androgen receptors. (Rance NE, Max SR, "Modulation of the cytosolic androgen receptor in striated muscle by sex steroids", Endocrinology 1984 Sep;115(3):862-6)

So you see that it may be time for bodybuilders to rethink the use of anti-estrogen compounds. I think that a risk to benefit determination has to be considered, and unless someone feels that he is a high-risk case for estrogen related side effects, he probably should pass on the anti-estrogens.

__________________
Power over others is weakness disguised as strength.

Scott

hackskii

I think I am only going to use the Anti-E's for gyno or Post cycle therapy.
From what I have been reading this seems to be the best approach.

__________________
Power over others is weakness disguised as strength.

Scott

hackskii

by William Llewellyn

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[i]. 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[ii]. 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[iii]. 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 C) 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[iv]. 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[v]. 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[vi]. 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[vii]. 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[viii] [ix]. 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.

Bibliography

[i] Comparison of the receptor binding properties of Nandrolone and Testosterone under in vitro and in vivo conditions. J Steroid Biochem 22(6) 831-36 1985

[ii] Relative binding affinities of testosterone, 19-nortestosterone and their 5-alpha reduced derivatives to the androgen receptor and to other androgen-binding proteins… J Steroid Biochem 17 653-60 1982

[iii] Relative Binding affinity of anabolic-androgenic steroids… Endocrinology 114(6) 2100-06 1984

[iv] Pulsatile growth hormone release in normal women during the menstrual cycle. Clin Endocrinol 36: 591-96 1992

[v] Activation of the somatotropic axis by testosterone in adult males: Evidence for the role of aromatization. J Clin. Endocrinol Metab 76:1407-12 1993

[vi] Testosterone administration increases insulin-like growth factor-I levels in normal men. J Clin Endocrinol Metab 77(3):776-9 1993

[vii] Androgen-stimulated pubertal growth:the effects of testosterone and dihydrotestosterone on growth hormone and insulin-like growth factor-I in the treatment of short stature and delayed puberty. J Clin Endocrinol Metab 76(4)996-1001 1993

[viii] Pentose Cycle Activity in Muscle from Fetal, Neonatal and Infant Rhesus Monkeys. Arch Biochem Biophys 117:275-81 1966

[ix] The pentose phosphate pathway in regenerating skeletal muscle. Biochem J 170: 17 1978

[x] Aromatization of androgens to estrogens mediates increased activity of glucose 6-phosphate dehydrogenase in rat levator ani muscle. Endocrinol 106(2):440-43 1980

__________________
Power over others is weakness disguised as strength.

Scott