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.
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: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.
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
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
ER alpha and beta receptors are virtually absent in skeletal muscle
There is no gender difference between the densities of ER receptors between men or women.
Manipulating estrogen levels has been proven to produce no effect on skeletal muscle hypertrophy in humans and animals.
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:
http://www.ncbi.nlm.nih.gov/pubmed/10902781Contrary 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.
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).
Anastrozole has demonstrated an ability to elevate testosterone up to 100% and decrease estrogen by ~50% in elderly men (1mg/day).
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.
In an article analyzing women athletes and estrogen:
http://www.ncbi.nlm.nih.gov/pmc/arti...2/?tool=pubmedIn 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.
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.
Thread: Estrogen and Muscle Mass