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Just came across this text and it got me very interested in this topic. One thing I clearly know from my experience is that I made better gains on cycle when I didn't use high doses of AI's and let my E2 rise to supraph. levels
Basically everything I want to ask is written in the article.
What do you guys think about it? Especially interested in hearing the vets' opinions.
thanks!
Basically everything I want to ask is written in the article.
What do you guys think about it? Especially interested in hearing the vets' opinions.
thanks!
Read about how estrogen can be anabolic, if testosterone is crucial for muscle growth, if DHEA is good for fat loss and more...
By: Big Cat Apr 14, 2004
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Estrogen As An Anabolic? More Important Than You Think.
This illustrious issue has been hotly debated in the past. Does estrogen have an anabolic contribution to make? That it does is not so much an issue any more, several studies have demonstrated that indeed growth is promoted with strong androgens, more so in the presence of estrogen. This is also the reason many cattle implants today contain a form of estrogen as well, next to a potent androgen.
The debate today mainly centers around whether or not supraphysiological doses of estrogen can benefit growth more than a permissive, physiological dose of estrogen. Extensive experience as well as a lot of indirect evidence has taught me that this is definitely the case.
Of course, if I could have proven it conclusively before, it wouldn't have been much of a debate. Now, however, evidence clearly demonstrates that estrogen is anabolic in a dose responsive way. Even more important it clearly shows how levels of estrogen can help determine whether you are more likely to become a strength athlete or an endurance athlete.
In the past estrogen has been shown to increase local IGF-1, probably through a decrease in systemic liver-derived IGF-1 and a subsequent increase in circulating growth hormone. It has been shown to activate the mitogen activated protein kinase cascade (1), one of the ways in which IGF-1 and insulin exert anabolic effects, and it has been shown to increase cyclo-oxygenase activity (2) which would result in an enhanced immune-response and increased manufacture of prostaglandins.
Several prostaglandins have been implicated in enhancing both muscle anabolism and fat loss, by sensitizing tissues to the effects of testosterone and IGF-1. However none of these effects have been shown to occur specifically in skeletal muscle tissue, and for none of them it has been determined whether or not the effects are enhanced with increased doses of estrogen or not.
Estrogen works through so many ways that are anabolic or potentially anabolic, and a few of those are bound to increase in supraphysiological doses, but nonetheless, previously this was all conjecture.
One system we do know however that is dose responsive to estrogen, is the renin-angiotensin system. Estrogen increases the activity of this system, renin converts angiotensinogen to Angiotensin I, and then Angiotensin converting enzyme (ACE) converts it to Angiotensin II (AngII). Angiotensin II in turn stimulates aldosterone release. AngII and aldosterone are the main hormonal factors implicated in elevated blood pressure and water retention.
As any seasoned steroid user knows, estrogen has a very dose responsive reaction on this system. Drugs with a very rapid and high increase in estrogen or estrogenic actions, like testosterone suspension, Anadrol and Dianabol, cause massive increases in blood pressure, headaches and water retention.
Many tissues express a local Renin-angiotensin System (RAS), including skeletal muscle tissue, that exists partially through uptake of systemic RAS components and partially through de novo synthesis of its components (AngII, ACE). One study in particular linked this skeletal muscle RAS to exercise performance (3), and the results were quite remarkable to say the least.
High ACE, and consequently AngII, resulted in a poorer athletic performance, but greater muscular strength and muscular hypertrophy. Subjects with higher levels of ACE had a higher level of Type II fiber and intracellular glucose stores, whereas people with lower ACE had higher Type I fiber, higher degree of vascularization and higher levels of interstitial glucose.
This higher interstitial glucose means a lot of the glucose is excreted from intracellular stores and can be readily mobilized. All these things are supportive a greater endurance and greater athletic performance. In the former situation, performance would suffer, but strength would increase to a much greater extent.
The implication of this is quite profound, since it offers a reason for genetic phenotyping. In humans ACE expression is dependent on insertion (I) or deletion (D) of a 287 base pair sequence in intron 16. That means three phenotypes exist, I/I, I/D and D/D.
The distribution of these phenotypes among Caucasian males is 25%, 50% and 25%. That means if you fall in the former or latter category, you have a genetic tendency to become better at endurance or strength sports. I/I has the lowest RAS expression, and D/D has the highest RAS expression.It also offers a point of manipulation to reach your desired goal. Logically said manipulation would be most successful in the I/D phenotype, since promoting or reducing RAS activity could push you in either direction, while the promoting RAS in I/I or inhibiting it in D/D would most likely push you towards more of an I/D type.
Since estrogen is a dose-dependent activator of the RAS, it not only increases muscle strength and hypertrophy, it also helps determine to a large degree how much Type I or Type II fiber a certain muscle group has. Type II muscle fibers grow faster and bigger than Type II fibers and promote more explosive strength, while Type I fibers are well vascularized, grow slowly, but are more fit for longer, lower intensity tasks. By inhibiting estrogen, we may therefore be slowing our muscle gains, both short term, but especially long term.
These findings vindicate a number of theories I have defended for a long time. First and foremost that estrogen is indeed a dose-dependent anabolic steroid, especially in combination with androgens, in supra-physiological doses, such as seen with several high-estrogenic drugs. For a very long time we have known that drugs with extremely poor androgenic qualities like oxymetholone and methandrostenolone are very strong anabolics.
Many have denied the role of estrogen in this, instead sinning against ockham's razor and finding all sorts of far-fetched theories. We first dismissed the growth as being mostly water. A lot of it was, since RAS increases water retention, but obviously not all mass gained could be explained by water. Then some people attempted to explain it by claiming it was the result of more androgenic by-products.
But no by-product had sufficient androgenic effects, or was expressed to a large enough degree to explain why these drugs performed as good as less estrogenic drugs, sometimes outperforming them despite imminently lower androgenic binding. Following ockham's razor, the logical conclusion was that the higher degree of anabolism was a result of their higher degree of estrogen receptor activation, either direct (oxymetholone) or indirect via aromatization to potent estrogens (methandrostenolone).
Cattle ranchers have known this for a long time. Cattle implants contain a certain amount of estradiol, which not only improves the total amount of muscle mass, but also the quality of the meat. More Type II fibers equates more meat, and more usable quality meat since it is less vascularized.
The downsides are however that we again corroborate the fact that being good at predominantly endurance activities, rules out being extremely good at building muscle mass and vice versa. Through activation of RAS, local and systemic, estrogen would reduce aerobic capacity and Type I fiber formation in favour of Type II muscle. It would also increase blood pressure and water retention.
The same holds true the other way around, endurance activity may very well lower estrogen, since regular exercise has been shown to lower blood pressure and favour Type I muscle growth. The implications of that, would once again be huge, since it puts a negative aspect on doing cardio during bulking phases.
The take home message however is that estrogen is indeed a potent anabolic aid, especially in combination with androgens, and that this effect is very much dose-responsive and thus holds up in higher, supraphysiological doses. Together with a previously discussed item in this column, regarding increased estrogenic problems after the use of anti-estrogenic drugs, this seriously questions the importance some bodybuilders attach to anti-estrogens.
Clearly the uneducated use of anti-estrogenic drugs needs some re-examination, and bodybuilders need to see that estrogen can not only be a major contributor to growth, but not using anti-estrogens will often prevent many of the problems their use supposedly cures. So unless you are extremely prone to estrogenic side-effects, I would seriously think twice about incorporating potent anti-estrogenic drugs during the course of a steroid or prohormone cycle.
References
Wade CB, Robinson S, Shapiro RA, Dorsa DM. Estrogen receptor (ER)alpha and ERbeta exhibit unique pharmacologic properties when coupled to activation of the mitogen-activated protein kinase pathway. Endocrinology. 2001 Jun;142(6):2336-42.
Calkin AC, Sudhir K, Honisett S, Williams MR, Dawood T, Komesaroff PA. Rapid potentiation of endothelium-dependent vasodilation by estradiol in postmenopausal women is mediated via cyclooxygenase 2. J Clin Endocrinol Metab. 2002 Nov;87(11):5072-5.
Jones A, Woods R. Skeletal muscle RAS and exercise performance. Int J Biochem Cell Biol. 2003 Jun;35(6):855-66.
at least I hope so
