Study Shows That Arimidex Boosts Testosterone

liftsiron

Community Veteran, Longtime Vet
posted by df2003 on musclesci


Study Shows That Arimidex Boosts Testosterone

Estrogen suppression in males: metabolic effects.
J Clin Endocrinol Metab 2000 Jul;85(7):2370-7 (ISSN: 0021-972X)
Mauras N; O'Brien KO; Klein KO; Hayes V nmauras@nemours.org.

We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production. It is not clear,,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole). First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2
concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. 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. However, E2 concentrations decreased 48% (P = 0.006), with
no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and
rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein
synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound
growth retardation without the confounding negative effects of gonadal androgen suppression.
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i didnt see a date on this study but it looks like PART of one that came out few years ago. they also used clo, if this is the same one. bottom line is that this study shoots a hole in theory that higher estrogen levels are required to acheive maxiumum gains from andros. in th estudy i read they proved that E actually inhibited T from binding with receptors.

now how much stock can we put in a report like this? who knows as there are reports that claim this one to be false. also they used 16 year old boys for part of it.

but none the less a good post to stir the grey matter.
 
pullinbig said:
i didnt see a date on this study but it looks like PART of one that came out few years ago. they also used clo, if this is the same one. bottom line is that this study shoots a hole in theory that higher estrogen levels are required to acheive maxiumum gains from andros. in th estudy i read they proved that E actually inhibited T from binding with receptors.

now how much stock can we put in a report like this? who knows as there are reports that claim this one to be false. also they used 16 year old boys for part of it.

but none the less a good post to stir the grey matter.


I find studies like this interesting, but I don't get shocked if I happen accross a study that shows contrary results. So many X factors are involved when athletes are self experimenting with aas, AI's and what ever else.
 
Sure, reducing systemic E will upregulate HPTA and therefore increase T synthesis, but I'm still sold on the anabolic effects of estrogen:

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=12676172

Int J Biochem Cell Biol. 2003 Jun;35(6):855-66. Related Articles, Links


Skeletal muscle RAS and exercise performance.

Jones A, Woods DR.

Department of Cardiovascular Genetics, 3rd Floor, Rayne Institute, University College London, 5 University Street, London WC1E 6JJ, UK.

A local renin-angiotensin system (RAS) may be suggested by evidence of gene expression of RAS components within the tissue as well as physiological responsiveness of this gene expression. This review will focus on the evidence supporting the existence of the constituent elements of a physiologically functional paracrine muscle RAS. The effect of local skeletal muscle RAS on human exercise performance will be explored via its relation with pharmacological intervention and genetic studies.The most likely configuration of the muscle RAS is a combination of in situ synthesis and uptake from the circulation of RAS components. A reduction in angiotensin-converting enzyme (ACE) activity reverses the decline in physical performance due to peripheral muscle factors in those with congestive heart failure and may halt or slow decline in muscle strength in elderly women. Genetic studies suggest that increased ACE and angiotensin II (Ang II) mediate greater strength gains perhaps via muscle hypertrophy whereas lower ACE levels and reduced bradykinin (BK) degradation mediate enhanced endurance performance perhaps via changes in substrate availability, muscle fibre type and efficiency.
 
" Sure, reducing systemic E will upregulate HPTA and therefore increase T synthesis, but I'm still sold on the anabolic effects of estrogen:"


I agree, an ideal balance between test and estrogen leads to greater gains. I'm fimiliar with the study posted on ACE inhibition. I can state from experience that while I was being treated for CHF with an ACE I, I lost muscle mass and tone, strength and endurence. When I was switched to the bata-blocker coreg, I gained back much of what I had lost. Of course we each have our individual X factors, so what I noticed may not be as evident in another.
 
even the article einstein posted is full of 'seems to", "may be suggested by" and "mays"

wonder why these guys wont come out and say "deffiately", "with out a doubt" or some other deffinative statement. i mean who pays these folks? cmon guys tell us the truth.

bottom line is this. educate yourselves then start trying this stuff out on your self and see what holds true for and what dont.
 
so would ya'll say that if you run .5g of amidex ed and 15mg of nova ed during a cycle that it will limit your gains?
 
jarbulldog said:
so would ya'll say that if you run .5g of amidex ed and 15mg of nova ed during a cycle that it will limit your gains?

I think you mean .5mg right? I think it all depends on the person. I am trying .25mgED this time to help with bloat as well as gyno, but before I have used .25 E4D and it worked for gyno really well.
 
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