Estrogen and Muscle Mass

[neuron]

Estrogen and Muscle Mass

Due to the heavy incorporation of aromatase inhibitors in the supplement market, the issue of "how much" estrogen is needed to support hypertrophy should to be addressed. In the 2007 Gasapri Novedex XT study, testosterone elevations were observed to increase up to 625%, with corresponding, but nonsignificant, increases in estrogen. Interestingly enough, body composition measurements like total body mass or fat-free mass, hardly changed, although mean fat mass decreased by 3.5% (1). Since current prevailing wisdom suggests that AI's are incapable of producing skeletal muscle hypertrophy because they "crush" estrogen, then why didn't Novedex XT produce greater gains in lean mass? One explanation is that ATD, and/or its metabolites, cross reacted with the assay used to measure testosterone levels, greatly exaggerating its effect on testosterone levels (2). Similar to the study posted below, the Gaspari study measured hormone levels with enzyme linked immunoabsorbent assays.

Immunological interference of the synthetic aromatase inhibitor 1,4,6-androstatriene-3,17-dione (ATD) and its metabolite(s) in the radioimmunoassay for testosterone.
Donaldson MD, Forest MG.

Radioimmunoassay (RIA) for testosterone (T) in unchromatographed plasma extracts from ATD-treated rats gave spuriously high values for T. Cross-reaction and chromatographic studies subsequently showed that ATD and, to a much greater extent, its metabolite(s) were responsible for this overestimation. Celite column chromatography proved to be an effective way of separating T from ATD and its product(s) of metabolism.

However, there is a plethora of evidence in the literature that aromatase inhibitors like anastrozole have little impact on lean mass or body composition. One possible explanation for the discrepancy with the Gaspari study and other AI studies with respect to Novedex XT's effect on fat loss is the population targeted. The majority of studies examining the effects of aromatase inhibitors were utilizing hypogonadal populations, or simply an extract from the population at large. The Gaspari study, on the other hand, targeted physically active, "resistance trained," adult men. It is likely that the results of the Gaspari study could be replicated with other aromatase inhibitors like anastrozole. The next logical question is:

1) is the lack of impact on skeletal muscle the result of diminished estrogen or
2) simply that the amount of testosterone, even up to a 100% increase, is simply not enough to support anabolism?

The literature makes a pretty strong case that estrogen is only a very minor player in skeletal muscle mechanics, although rat studies tend to demonstrate varied results. It should also be noted that some AI's decrease IGF-1 (like anastrozole), although its relevancy in the context of skeletal muscle hypertrophy is unknown. Some AI's like exemestane and formestane show little effect on IGF-1 production, although studies using eugonadal adult men are lacking.

Ultimately, the idea that estrogen is a requisite for skeletal muscle hypertrophy is not evident in scientific journals - quite the contrary, actually. Here is a quick literature review:

Aromatase enzyme expression is incredibly low skeletal muscle
http://www.ncbi.nlm.nih.gov/pubmed/17018772

Daily conversion of testosterone is estrogen is ~0.3%, which takes place mostly in the brain, fat, and bones, with very little conversion taking place in skeletal muscle
http://www.ncbi.nlm.nih.gov/pubmed/15083377

ER alpha and beta receptors are virtually absent in skeletal muscle
http://www.ncbi.nlm.nih.gov/pubmed/11036937
http://www.ncbi.nlm.nih.gov/pubmed/17132854
http://www.ncbi.nlm.nih.gov/pubmed/17615392

There is no gender difference between the densities of ER receptors between men or women.
http://www.ncbi.nlm.nih.gov/pubmed/12618573

Manipulating estrogen levels has been proven to produce no effect on skeletal muscle hypertrophy in humans and animals.
http://www.ncbi.nlm.nih.gov/pubmed/8976803
http://www.ncbi.nlm.nih.gov/pubmed/12161047
http://www.ncbi.nlm.nih.gov/pubmed/15160484
http://www.ncbi.nlm.nih.gov/pubmed/16260975
http://www.ncbi.nlm.nih.gov/pubmed/15917154
http://www.ncbi.nlm.nih.gov/pubmed/12065171

In a study examining the effects of anastrozole on younger males (15-22 yr) in a 10 day trial (0.5 or 1 mg), mean testosterone rose by 58% and mean estrogen decreased by 47%. The authors concluded:

Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations.

http://www.ncbi.nlm.nih.gov/pubmed/10902781


How much testosterone is necessary for skeletal muscle hypertrophy?

Aromatase inhibitors like exemestane have demonstrated an ability to elevate testosterone up to 60% and decrease estrogen up to 62% in healthy adult males (50mg/day).
http://www.ncbi.nlm.nih.gov/pubmed/14671195

Anastrozole has demonstrated an ability to elevate testosterone up to 100% and decrease estrogen by ~50% in elderly men (1mg/day).
http://www.ncbi.nlm.nih.gov/pubmed/15856361

In a study comparing the effects of exogenous testosterone in elderly men versus younger adult men, the lowest concentration of injectable testosterone found to produce statistically significant increases in muscle mass was 125mg/wk which caused a 100% elevation in testosterone from baseline. Those individuals receiving 600mg of testosterone/week had elevations in plasma testosterone of ~800%, and also had the greatest amount of muscle mass increases.
http://www.ncbi.nlm.nih.gov/pubmed/15562020
http://jcem.endojournals.org/content...512400002.jpeg

In an article analyzing women athletes and estrogen:

In summary, there is no convincing evidence that oestrogen blockers cause any consistent, biologically significant increase in blood testosterone concentrations in women. In the absence of direct testing of ergogenic or myotrophic properties, using blood testosterone as a surrogate marker suggests that drug-induced performance enhancement is most unlikely from oestrogen blockade. Nor is there any reason to believe that oestrogens have any other ergogenic effect whether directly on muscle, haemoglobin or indirectly via motivational effects in healthy pre-menopausal women.

http://www.ncbi.nlm.nih.gov/pmc/arti...2/?tool=pubmed

(1) http://www.ncbi.nlm.nih.gov/pubmed/17460335
(2) http://www.ncbi.nlm.nih.gov/pubmed/7210060



Feel free to add your thoughts, anecdotes, theories. Until some well elucidated research is carried out in this area, there really is no right/wrong answer.

[Adjusting]

Do exogenous hormones have a greater affinity for androgen receptors? Perhaps that could be one reason why endogenously raised levels of testosterone don't build muscle.

[michael3435]

Do exogenous hormones have a greater affinity for androgen receptors? Perhaps that could be one reason why endogenously raised levels of testosterone don't build muscle.

part of the answer may lie in SHBG. exogenous testosterone administration actually decreases SHBG by a ALOT. i think its around 80 percent. i dont know about the binding affinity for different steroids to SHBG but the affinity to the AR depends strongly on the compound.

[THEHUGE]

Androgen-estrogen synergy in rat levator ani muscle: glucose-6-phosphate dehydrogenase



Stephen R. Maxa

Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201 U.S.A.


Abstract
The effects of castration and hormone administration on the activity of glucose-6-phosphate dehydrogenase in the rat levator ani muscle were studied. Castration caused a decrease in enzyme activity and in wet weight of the levator ani muscle. Chronic administration of testosterone propionate increased glucose-6-phosphate dehydrogenase activity in the levator ani muscle of castrated rats; the magnitude of the recovery of enzyme activity was related to the length of time of exposure to testosterone propionate after castration as well as to the length of time the animals were castrated. The longer the period of castration before exposure to testosterone propionate, the greater the effect. This result may be related to previously reported castration-mediated increases in androgen receptor binding in muscle. Dihydro-testosterone was less effective than testosterone propionate in enhancing glucose-6-phosphate dehydrogenase activity in the levator ani muscle from castrated rats; estradiol-17β alone was ineffective. Combined treatment with estradiol-17β and dihydrotestosterone, however, was as effective as testosterone alone. Thus, androgens and estrogens may exert synergistic effects on levator ani muscle.

[THEHUGE]

Tamoxifen and oestrogen both protect the rat muscle against physiological damage


R.W. Koot1, G.J. Amelink1, 2, M.A. Blankenstein3 and P.R. Bär, 1, 2

1Department of Neurology, Research Laboratory, University of Utrecht, Utrecht, The Netherlands

2Janus Jongbloed Research Centre, University of Utrecht, Utrecht, The Netherlands

3Department of Endocrinology, University of Utrecht, Utrecht, The Netherlands




Abstract
Tamoxifen (TX), an oestrogen antagonist, was used to characterize the protective effect of oestradiol (E2) on exercise-related creatine kinase (CK) release from skeletal muscle of the rat. Subcutaneous administration of TX for 3 weeks in female rats had a profound antioestrogen effect as evidenced by a reduced weight of the uterus. The CK release after electrical stimulation of the isolated soleus muscle, previously shown to be E2-dependent, was markedly reduced (30–50%) after treatment with TX; this observation points to an E2-like protective action of TX instead of E2-antagonism. This effect was dose-dependent (0.25–1.00 mg/kg) and was not seen when TX was given shortly (24 h) before the experiments. In ovariectomized females, that show more CK leakage due to the lack of circulating E2, both E2- and TX-treatment resulted in a 60% reduction of the CK leakage. Muscles from male rats, treated with TX, showed a similar response: after contractions the CK release was significantly lower. We conclude that TX, like E2, reduces contraction-induced muscle damage in the rat and, thus, has E2-agonistic properties on skeletal rat muscle.

[neuron]

Do exogenous hormones have a greater affinity for androgen receptors? Perhaps that could be one reason why endogenously raised levels of testosterone don't build muscle.

Different analogues of testosterone have different levels of anabolism or androgenism based on stereochemistry, conformation, exc.

part of the answer may lie in SHBG. exogenous testosterone administration actually decreases SHBG by a ALOT. i think its around 80 percent. i dont know about the binding affinity for different steroids to SHBG but the affinity to the AR depends strongly on the compound.

That probably plays a large role.

The literature makes a pretty strong case that estrogen is only a very minor player in skeletal muscle mechanics, although rat studies tend to demonstrate varied results.

synergy in rat levator

protect the rat muscle

Estrogen is also anabolic (via the ERalphaR) in the rat, although this does not appear to be conserved among humans.

Manipulating estrogen levels has been proven to produce no effect on skeletal muscle hypertrophy in humans and animals.
http://www.ncbi.nlm.nih.gov/pubmed/8976803
http://www.ncbi.nlm.nih.gov/pubmed/12161047
http://www.ncbi.nlm.nih.gov/pubmed/15160484
http://www.ncbi.nlm.nih.gov/pubmed/16260975
http://www.ncbi.nlm.nih.gov/pubmed/15917154
http://www.ncbi.nlm.nih.gov/pubmed/12065171

[THEHUGE]

Also aromatization of testosterone to estrogen is likely the proximate sex-steroid stimulus amplifying secretory activity of the hypothalamo-pituitary/GH-IGF-1 axis.

[neuron]

Also aromatization of testosterone to estrogen is likely the proximate sex-steroid stimulus amplifying secretory activity of the hypothalamo-pituitary/GH-IGF-1 axis.

Some AI's do effect IGF1 production, although both the Novedex XT study and the 6-OXO study showed elevated testosterone with elevated estrogen and neither study demonstrated gain in fat free mass. In the 6-OXO study, testosterone rose ~60% with a significant elevation in estrogen. The idea that 'estrogen,' or lack thereof, is the reason for the lack of skeletal muscle hypertrophy with AI's is unfounded and unlikely. In rats, ATD is a competitive antagonist with testosterone in thalamic nuclei. It is conceivable that this antagonism is also taking place in the periphery (muscle tissue), which may partially explain its absence in effecting myotrophy.

[THEHUGE]

Some AI's do effect IGF1 production, although both the Novedex XT study and the 6-OXO study showed elevated testosterone with elevated estrogen and neither study demonstrated gain in fat free mass. In the 6-OXO study, testosterone rose ~60% with a significant elevation in estrogen. The idea that 'estrogen,' or lack thereof, is the reason for the lack of skeletal muscle hypertrophy with AI's is unfounded and unlikely. In rats, ATD is a competitive antagonist with testosterone in thalamic nuclei. It is conceivable that this antagonism is also taking place in the periphery (muscle tissue), which may partially explain its absence in effecting myotrophy.

As you pointed out in the first post ATD and/or its metabolites, cross reacts with the assay used to measure testosterone levels, greatly exaggerating its effect on testosterone levels unless you use a celite column chromatography . Some of its metabolites could cross react with estradiol/estrone/estriol as well.
Its possible peripheral ARs antagonism could definitely play a role as well.
The same could be said for 6-oxo and its metabolites as the researchers themselves hypothesized.
https://beardocs.baylor.edu/bitstrea...le_masters.pdf
They even hypothesized that 6-oxo could compete with testosterone at the androgen receptor for binding.
The lack of a statistically significant (if any) increase in LH is perplexing,to say the least.

[papagunz]

part of the answer may lie in SHBG. exogenous testosterone administration actually decreases SHBG by a ALOT. i think its around 80 percent.

Is it possible that exogenous test just binds to the bulk of SHBG rendering it ineffective rather than actually decreasing it?

[michael3435]

Is it possible that exogenous test just binds to the bulk of SHBG rendering it ineffective rather than actually decreasing it?

im not even sure if some compounds would bind to SHBG to be honest. test would, but for other compounds, it might depend on the AR affinity or other parts of its structure im not sure. let me post the study below, from the abstract it appears it decreases SHBG in total.

i was thinking that many feedback mechanisms for SHBG are at a level at or lower than the testes. as you get shutdown from exogenous test and the testes atrophy, that may upregulate many mechanisms that make exogenous testosterone so effective. with an AI, the effect would be the opposite.

Response of serum testosterone and its precursor steroids, SHBG and CBG to anabolic steroid and testosterone self-administration in man.

Ruokonen A, Alén M, Bolton N, Vihko R.
Abstract

The influence of high doses of testosterone and anabolic steroids on testicular endocrine function and on circulating steroid binding proteins, sex hormone binding globulin (SHBG) and cortisol binding globulin (CBG), were investigated in power athletes for 26 weeks of steroid self-administration and for the following 16 weeks after drug withdrawal. Serum testosterone and androstenedione concentrations increased (P less than 0.05) but pregnenolone, 17-hydroxypregnenolone, dehydroepiandrosterone, 5-androstene-3 beta, 17 beta-diol, progesterone and 17-hydroxyprogesterone concentrations strongly decreased (P less than 0.001) during steroid administration. Serum pregnenolone, 17-hydroxypregnenolone and dehydroepiandrosterone sulphate concentrations followed the changes of the corresponding unconjugated steroids but 5-androstene-3 beta, 17 beta-diol and testosterone sulphate concentrations remained unchanged during the follow-up time. 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. The depressed circulating levels of dehydroepiandrosterone and its sulphate may indicate that the androgenic-anabolic steroids also suppress adrenal androgen production.

[Harpagan]

"Animal study: ATD doesn’t help steroids users"

More muscle and bigger balls. That’s the promise that the American producers of designer supplements containing the androgenic steroid ATD hold up to bodybuilders. But according to a Swedish animal study, the results of which were published recently in Behavioural Brain Research, it’s an empty promise.

Whole article with details and graphics: http://www.ergo-log.com/atd.html

[gonzo77]

So I'm getting ready to start testosterone injection tomorrow. I have enough for 10 wks do I need to worry about my estrogen levels? Should I take some kind of estrogen blocker? Thanks forcall the help.

[neuron]

Ultimately, the idea that estrogen is a requisite for skeletal muscle hypertrophy is not evident in scientific journals - quite the contrary, actually.

This is the most important excerpt of this article.

[gonzo77]

This is the most important excerpt of this article.

Higher estrogen levels can cause more chest and belly fat?

[7percent]

This is the most important excerpt of this article.

Does that mean lowering estrogen is useless in order to increase test? Higher test, lower estro = / = more muscle mass?

[PinchTheBear]

Does that mean lowering estrogen is useless in order to increase test? Higher test, lower estro = / = more muscle mass?

Not exactly, but a transient shift in the ratio is not likely useful. Fat burning is a whole other topic as well with respect to T/E.

[Sldge]

This is the most important excerpt of this article.

I think there were a couple studies showing that low estrogen resulted in a lower conversion of GH to IGF1.

[neuron]

I think there were a couple studies showing that low estrogen resulted in a lower conversion of GH to IGF1.

From the OP, you can see that I've linked to studies showing the manipulation of the estrogen variable in every way conceivable: men, women, animal, en vitro. Estrogen is definitely not a necessary prerequisit for muscle building - and, in fact, its presence (or absence) is not even noticed locally within muscle tissue (generalized lack of estrogen receptors). In one of the best models for studying this relationship (post-menopausal women), increasing or decreasing estrogen does not impact muscle growth; only testosterone. This would discount a lot of the merit for implicating IGF-1's absence (due to decreased estrogen) for the lack of myotrophy on AI's. The more likely explanation is that the testosterone threshold for inducing myotrophy is not breached through endogenous manipulation.

[Bane]

I think there were a couple studies showing that low estrogen resulted in a lower conversion of GH to IGF1.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1289262/

However there may be a benefit in reducing fat mass?

http://jcem.endojournals.org/cgi/content/full/90/6/3592

Edit:Good read
http://books.google.com/books?id=AsI...page&q&f=false

Great thread btw.

[neuron]

Does that mean lowering estrogen is useless in order to increase test? Higher test, lower estro = / = more muscle mass?

The purpose of this article is to highlight the fact that estrogen is not especially necessary in inducing muscle mass; despite what supplement companies tend to say.

"Oh noez you don't want estrogen to go too low or u won't get the jacked fibraz"

Some AI's do decrease IGF-1, as sldge pointed out, and as I pointed out in the OP, but this decrement is likely not the cause for the lack of myotrophy seen with AI's. The more likely explanation is that AI's simply do not elevate testosterone "enough" to cause increases in muscle mass. As I pointed out in the OP, one of the (very few) studies which examined exogenous testosterone versus muscle mass, decribed the minimum increase in testosterone necessary to produce muscle mass increased testosterone like 800%. Most "test boosters" increase test like 30-60 %.

[FoolontheHill]

why is neuron not the president of these forums? consistently thought provoking and well-thought out posts, old friend.

[asteve5]

The purpose of this article is to highlight the fact that estrogen is not especially one of the (very few) studies which examined exogenous testosterone versus muscle mass, decribed the minimum increase in testosterone necessary to produce muscle mass increased testosterone like 800%. Most "test boosters" increase test like 30-60 %.

is this number for total test or bio-available test?

[THEHUGE]

The purpose of this article is to highlight the fact that estrogen is not especially necessary in inducing muscle mass; despite what supplement companies tend to say.

"Oh noez you don't want estrogen to go too low or u won't get the jacked fibraz"

Some AI's do decrease IGF-1, as sldge pointed out, and as I pointed out in the OP, but this decrement is likely not the cause for the lack of myotrophy seen with AI's. The more likely explanation is that AI's simply do not elevate testosterone "enough" to cause increases in muscle mass. As I pointed out in the OP, one of the (very few) studies which examined exogenous testosterone versus muscle mass, decribed the minimum increase in testosterone necessary to produce muscle mass increased testosterone like 800%. Most "test boosters" increase test like 30-60 %.

Pulling numbers out of your ass or do you have anything to substantiate your bold 800% and 30%, brah?

Older men are as responsive as young men to the anabolic effects of graded doses of testosterone on the skeletal muscle.
Bhasin S, Woodhouse L, Casaburi R, Singh AB, Mac RP, Lee M, Yarasheski KE, Sinha-Hikim I, Dzekov C, Dzekov J, Magliano L, Storer TW.

Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, University of California, Los Angeles, CA 90059, USA. sbhasin@ucla.edu

Abstract
Although testosterone levels and muscle mass decline with age, many older men have serum testosterone level in the normal range, leading to speculation about whether older men are less sensitive to testosterone. We determined the responsiveness of androgen-dependent outcomes to graded testosterone doses in older men and compared it to that in young men. The participants in this randomized, double-blind trial were 60 ambulatory, healthy, older men, 60-75 yr of age, who had normal serum testosterone levels. Their responses to graded doses of testosterone were compared with previous data in 61 men, 19-35 yr old. The participants received a long-acting GnRH agonist to suppress endogenous testosterone production and 25, 50, 125, 300, or 600 mg testosterone enanthate weekly for 20 wk. Fat-free mass, fat mass, muscle strength, sexual function, mood, visuospatial cognition, hormone levels, and safety measures were evaluated before, during, and after treatment. Of 60 older men who were randomized, 52 completed the study. After adjusting for testosterone dose, changes in serum total testosterone (change, -6.8, -1.9, +16.1, +49.5, and +101.9 nmol/liter at 25, 50, 125, 300, and 600 mg/wk, respectively) and hemoglobin (change, -3.6, +9.9, +20.9, +12.6, and +29.4 g/liter at 25, 50, 125, 300, and 600 mg/wk, respectively) levels were dose-related in older men and significantly greater in older men than young men (each P < 0.0001). The changes in FFM (-0.3, +1.7, +4.2, +5.6, and +7.3 kg, respectively, in five ascending dose groups) and muscle strength in older men were correlated with testosterone dose and concentrations and were not significantly different in young and older men. Changes in fat mass correlated inversely with testosterone dose (r = -0.54; P < 0.001) and were significantly different in young vs. older men (P < 0.0001); young men receiving 25- and 50-mg doses gained more fat mass than older men (P < 0.0001). Mood and visuospatial cognition did not change significantly in either group. Frequency of hematocrit greater than 54%, leg edema, and prostate events were numerically higher in older men than in young men. Older men are as responsive as young men to testosterone's anabolic effects; however, older men have lower testosterone clearance rates, higher increments in hemoglobin, and a higher frequency of adverse effects. Although substantial gains in muscle mass and strength can be realized in older men with supraphysiological testosterone doses, these high doses are associated with a high frequency of adverse effects. The best trade-off was achieved with a testosterone dose (125 mg) that was associated with high normal testosterone levels, low frequency of adverse events, and significant gains in fat-free mass and muscle strength.

[w_llewellyn]

It is a little late, but one thing I do want to caution on is relying solely on the study conclusions with regard to muscle mass changes, especially with exercise. This is a very tough variable to lock down, especially when both sides of the intervention are also trying to gain muscle mass via exercise. True homogeneity is not really possible; individual variability in response can easily blur these results.

In the case of the 6-oxo study, I don't believe for a minute a doubling of testosterone has no anabolic value on the participants. I think it much more likely that the change was a strong benefit to some, but because there weren't enough people and both groups exercised it just didn't reach a statistically significant conclusion. I'd bet looking at the individuals numbers would yield more compelling results; you just can conclude anything with certainty on them.

Estrogen is not a prerequisite for gains, as Neuron pointed out. People can increase mass even with very low levels. This all started for me, however, when noticing something consistent: stronger gains on more estrogenic drugs (testosterone, methandrostenolone, oxymetholone). These almost always seem to outperform their non-estrogenic derivatives. Also, strong AI's do seem to interfere with their gains (except oxy), to some extent, but again, anecdotally. There is no study directly comparing gains with AI to gains without, to my knowledge.

If the anabolic effect of estrogen in AAS using or eugonadal men ever bear out in clinical studies, I don't know. I only proposed mechanisms affected by estrogen that seem to make sense. It has been a while since I've had my head in these studies. It is indeed a fascinating subject. I recall some potential advantages with women next to men regarding muscle damage and repair also. That may be worth looking at.

Very interesting stuff though. Recognition to Neuron for digging all these studies up and proposing some interesting ideas.

[w_llewellyn]

Of course I couldn't completely discount the possibility of some androgen receptor antagonism with 6-oxo as was proposed, but am inclined to think this very unlikely. Interaction with the AR is largely dependent on a functional 17b-hydroxyl group. I would think it relatively inactive here, like androstenedione.

I haven't looked at the study closely, but suspect the individual numbers would tell more.

[nunes]

short and simple ,imo , you need at least 50mg test (talking on propionate ester)ed to see something on muscle growth, the estrogen levels if kept on a normal value will not make a big diference.
I don't think any ai will raise testosterone to that levels