Enhanced protein synthesis

Enhanced protein synthesis

Enhanced growth factor activity (e.g. GH, IGF-1, etc.)

Enhanced activation of myogenic stem cells (i.e. satellite cells)

Enhanced myonuclear number (to maintain nuclear to cytoplasmic ratio)

New myofiber formation

Starting with enhanced growth factor activity, we know that testosterone increases GH and IGF-1 levels. In a study by Fryburg the effects of testosterone and stanozolol were compared for their effects on stimulating GH release.2 Testosterone enanthate (only 3 mg per kg per week) increased GH levels by 22% and IGF-1 levels by 21% whereas oral stanozolol (0.1mg per kg per day) had no effect whatsoever on GH or IGF-1 levels. This study was only 2-3 weeks long, and although stanozolol did not effect GH or IGF-1 levels, it had a similar effect on urinary nitrogen levels.

What does this difference in the effects of testosterone and stanozolol mean? It means that stanozolol may increase protein synthesis by binding to AR receptors in existing myonuclei, however, because it does not increase growth factor levels it is much less effective at activating satellite cells and therefore may not increase satellite cell activity nor myonuclear number directly when compared to testosterone esters. I will explain the importance of increasing myonuclear number in a moment, first lets look at how increases in GH and IGF-1 subsequent to testosterone use effects satellite cells.

Don't forget Satellite cells!
Satellite cells are myogenic stem cells, or pre-muscle cells, that serve to assist regeneration of adult skeletal muscle. Following proliferation (reproduction) and subsequent differentiation (to become a specific type of cell), satellite cells will fuse with one another or with the adjacent damaged muscle fiber, thereby increasing the number of myonuclei for fiber growth and repair. Proliferation of satellite cells is necessary in order to meet the needs of thousands of muscle cells all potentially requiring additional nuclei. Differentiation is necessary in order for the new nucleus to behave as a nucleus of muscle origin. The number of myonuclei directly determines the capacity of a muscle cell to manufacture proteins, including androgen receptors.

In order to better understand what is physically happening between satellite cells and muscle cells, try to picture 2 oil droplets floating on water. The two droplets represent a muscle cell and a satellite cell. Because the lipid bilayer of cells are hydrophobic just like common oil droplets, when brought into proximity to one another in an aqueous environment, they will come into contact for a moment and then fuse together to form one larger oil droplet. Now whatever was dissolved within one droplet (i.e. nuclei) will then mix with the contents of the other droplet. This is a simplified model of how satellite cells donate nuclei, and thus protein-synthesizing capacity, to existing muscle cells.

Enhanced activation of satellite cells by testosterone requires IGF-1. Those androgens that aromatize are effective at not only increasing IGF-1 levels but also the sensitivity of satellite cells to growth factors.3 This action has no direct effect on protein synthesis, but it does lead to a greater capacity for protein synthesis by increasing fusion of satellite cells to existing fibers. This increases the number of myonuclei and therefore the capacity of the cell to produce proteins. That is why large bodybuilders will benefit significantly more from high levels of androgens compared to a relatively new user.

Testosterone would be much less effective if it were not able to increase myonucleation. There is finite limit placed on the cytoplasmic/nuclear ratio, or the size of a muscle cell in relation to the number of nuclei it contains.4 Whenever a muscle grows in response to training there is a coordinated increase in the number of myonuclei and the increase in fiber cross sectional area (CSA). When satellite cells are prohibited from donating viable nuclei, overloaded muscle will not grow.5,6 Clearly, satellite cell activity is a required step, or prerequisite, in compensatory muscle hypertrophy, for without it, a muscle simply cannot significantly increase total protein content or CSA.

More myonuclei mean more receptors
So it is not only true that testosterone increases protein synthesis by activating genetic expression, it also increases the capacity of the muscle to grow in the future by leading to the accumulation of myonuclei which are required for protein synthesis. There is good reason to believe that testosterone in high enough doses may even encourage new fiber formation. To quote the authors of a recent study on the effects of steroids on muscle cells:

"Intake of anabolic steroids and strength-training induce an increase in muscle size by both hypertrophy and the formation of new muscle fibers. We propose that activation of satellite cells is a key process and is enhanced by the steroid use."7

Simply stated, supraphysiological levels of testosterone give rise to increased numbers of myonuclei and thereby an increase in the number of total androgen receptors per muscle fiber. Keep in mind that I am referring to testosterone and testosterone esters. Not the neutered designer androgens that people take to avoid side effects. This is not an argument to rapidly increase the dosages you use. It takes time for these changes to occur and the benefits of higher testosterone levels will not be immediately realized.

Maintenance of the kind of muscle mass seen in top-level bodybuilders today requires a given level of androgens in the body. That level will vary from individual to individual depending on their genetics. Nevertheless, if the androgen level drops, or if they were to "cycle off" the absolute level of lean mass will also drop. Likewise, as the level of androgens goes up, so will the level of lean mass that individual will be able to maintain. All of this happens without any evidence of AR down regulation. More accurately it demonstrates a relationship between the amount of androgens in the blood stream and the amount of lean mass that you can maintain. This does not mean that all you need is massive doses to get huge. Recruitment of satellite cells and increased myonucleation requires consistent "effective" training, massive amounts of food, and most importantly, time. Start out with reasonable doses. Then, as you get bigger you can adjust your doses upwards.

Thats a great article

So basically, a steady increase in mg per injection over multiple cycles will increase the population of receptors and thus the number of satellite or free cells. I get it, go slow, take rests between cycles, and always include test in your cycle!

Is it true that oxandrolone can replace testosterone to get this effect?

point is that would make it like testosterone, good at both AR and non-AR mechanisms.

References:

1.Kemppainen JA, Lane MV, Sar M, Wilson EM. Androgen receptor phosphorylation, turnover, nuclear transport, and transcriptional activation. Specificity for steroids and antihormones. J Biol Chem 1992 Jan 15;267(2):968-74

2.Fryburg DA., Weltman A., Jahn LA., et al: Short-term modulation of the androgen milieu alters pulsatile, but not exercise- or growth hormone releasing hormone-stimulated GH secretion in healthy men: Impact of gonadal steroid and GH secretory changes on metabolic outcomes. J Clin Endocrinol. Metab. 82(11):3710-37-19, 1997

3.Thompson SH., Boxhorn LK., Kong W., and Allen RE. Trenbolone alters the responsiveness of skeletal muscle satellite cells to fibroblast growth factor and insulin-like growth factor-I. Endocrinology. 124:2110-2117, 1989

4.Rosenblatt JD, Yong D, Parry DJ., Satellite cell activity is required for hypertrophy of overloaded adult rat muscle. Muscle Nerve 17:608-613, 1994

5.Rosenblatt JD, Parry DJ., Gamma irradiation prevents compensatory hypertrophy of overloaded extensor digitorum longus muscle. J. Appl. Physiol. 73:2538-2543, 1992

6.Phelan JN, Gonyea WJ. Effect of radiation on satellite cell activity and protein expression in overloaded mammalian skeletal muscle. Anat. Rec. 247:179-188, 1997

7.Kadi F, Eriksson A, Holmner S, Thornell LE. Effects of anabolic steroids on the muscle cells of strength-trained athletes. Med Sci Sports Exerc 1999 Nov;31(11):1528-34

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If it is not a published study then it was not open to dissection by other academic (or experts in that field).

I call bullshit on this "theory". Just because he has references does not mean that he is telling the truth (or that he has not manipulated their findings).

Oxandrolone aka Anavar is a very popular steroid which was relegalized and put back on the market in the USA for the appropriate medical use. It's new name is Oxandrin. They come in 2.5mg tabs and are sold by BTG. They were approved for catabolism or loss of lean mass associated with cancer, hepatitis and Aids. Even though it IS a 17-alpha alkylated drug it is extremely safe. It does NOT convert to estrogen. It has actually been shown to improve liver function in test groups. This drug is highly recommended for people with impared immune systems. These are the facts!

I call bullshit on this "theory". Just because he has references does not mean that he is telling the truth (or that he has not manipulated their findings).
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2Thick: Nobody runs a test (like the one you mentioned) because of the liver toxicity of Oxandrolone. I remember a study that claimed Oxadrin was more liver toxic than Anadrol.
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These two statements came from the same guy??
What peer reviewed article did "Oxadrin was more liver toxic than Anadrol" come from??

Tests on Oxandrolone's liver toxicity were done at up to 80mg/day.

The oral LD50 of oxandrolone in mice and dogs is greater than 5,000 mg/kg. So if you ate 50,000mg, about 4 lbs, all at once and you weighed 220lbs you would have a 50% chance of living. Try that with Anadrol or even Tylenol for that matter.

I think its humorous when people wont accept any information unless its backed by a double blind independent study - then qualified by a board of experts. There have been plenty of solid research studies done that have later been discounted.

quote:

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Originally posted by ulter:
These two statements came from the same guy??

What peer reviewed article did "Oxadrin was more liver toxic than Anadrol" come from??

Tests on Oxandrolone's liver toxicity were done at up to 80mg/day.

The oral LD50 of oxandrolone in mice and dogs is greater than 5,000 mg/kg. So if you ate 50,000mg, about 4 lbs, all at once and you weighed 220lbs you would have a 50% chance of living. Try that with Anadrol or even Tylenol for that matter.

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Ulter,

The reason why one article needed back up was because it was based on bio-chem and physiology. That should be easily dissected by experts in their respective fields.

The second one was from a published article (I believe). I will find that article for you. I said that I remember it so I will dig it up.

Also the dosages of Oxymethalone in human reach 600mg/day so it is not that far off the Oxandrolone dosage.

Note: For those of you reading this who may not be familiar with this term LD50, that is the Lethal Dose for 50% of those who might take a particular drug.

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The Other Board. Click

It's hopeless to argue with him....if something is written about Deca " The almighty Wonder Juice " he acts like it comes straight from the burning bush....

But, if anything remotely positive is written about Test, or Insane-O dosage....He throws the " Bullshit Flag "!!!

Hahahahahahahahahahahaha.......INCREDIBLE...!!!

quote:

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Originally posted by ulter:

Tests on Oxandrolone's liver toxicity were done at up to 80mg/day.

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This is why I mentioned that the dosage that doctors would measure for would be the medical dosage of up to 600mg/day. That is not much different from 80mg/day for Oxandrolone.

I am not a dog nor a mouse so their LD50 does not apply to me (or any other human). I am not sure why you brought it up since I do not like to refer to studies performed on mice.

I am going to throw a bullshit flag on you, set it on fire then piss on it.

Glad ta see ya still got a sense of humor....heh heh heh.......Piss on it....too fucking much!!!!

Good god man there are over 600 studies showing that oxandrolone is not as liver toxic as even Tylenol. Go to Medline and look it up. I have posted it a dozen times already so I won't do it again.

Here we go again....BUT, I got my flag ready this time....heh heh heh

INTERLUKIN

"The Grunfeld study that showed that Oxandrin caused elevated SGOT and SGPT enzymes raises questions about whether Oxandin is just as potentially toxic as any other steroid at higher doses. New data suggests that Oxandrin may have significant interaction with the 3A4 p450 enzyme system that metabolizes protease inhibitors, while this does not appear to be the case with Anadrol."

If you want to learn more, go to...

Well here is a more resent finding, much more believable to me.

In an 8-week* double-blind, randomized, placebo-controlled trial, patients with HIV-associated weight loss were placed on a regimen of supervised resistance exercise and physiologic testosterone replacement with either OXANDRIN 20 mg/day or placebo. The trial demonstrated that when OXANDRIN is added to a program of resistance exercise, it increases weight, builds lean body mass, and enhances physical strength. Gains in lean body mass nearly doubled in patients treated with OXANDRIN.

Seems we have a difference in results here.

I will put my faith in the research of the last 5 years, by researchers who have better methods of testing and much more prior research at their disposal.

P.S. you didn't have to Email me, I'd find you.

quote:

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Originally posted by ulter:
This is the same tired, 20 year old study that gets dragged out everytime I have this argument.

I will put my faith in the research of the last 5 years, by researchers who have better methods of testing and much more prior research at their disposal.

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I hate to make you look misinformed or blind to the facts but...

This new data was presented in 1998 [which is about 2-3 years ago] at the Geneva AIDS Conference by Grunfeld. It showed evidence of potential liver toxicity with doses of 40 or 80 mg per day with HIV patients.

So it was done relatively recently (2-3 years ago) at a worldwide conference (and therefore widely available for peer-review).

quote:

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Originally posted by 2Thick:
Huck,

Nobody runs a test (like the one you mentioned) because of the liver toxicity of Oxandrolone. I remember a study that claimed Oxadrin was more liver toxic than Anadrol.

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Yes 2thick Grenfelds presentation was in 1998 but he used the criteria used in the 1980 study to base his research on. And I still ask where are Grenfelds finding published? They are not in Medline�s Library. It is one thing to say it, it is another to prove it.
But do you know what has been proven? http://www.harcourthealth.com/scripts/om.dll/serve?arttype=full&article=a106517#R106517005 (last paragraph)
"The newer anabolic steroid oxandrolone also has known fibrinolytic activity,5 but unlike the majority of oral anabolic steroids it undergoes limited hepatic metabolism and is associated with a lower incidence of hepatotoxicity". (I suppose they could have used anadrol instead, since winny was to heptoxic). http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7420218&dopt=Abstract
"The effects of anabolic steroids on growth, body composition, and metabolism in boys with chronic renal failure on regular hemodialysis".
"Eight boys aged 9.5 to 17 years, on regular hemodialysis for chronic renal failure, were treated for 0.4 to 1.3 years with the anabolic steroid oxandrolone". "Hepatotoxicity, which was reversible, was seen in a ninth boy who did not complete the study". (Only one out of 9 children, again they should have used Anadrol)

These are only two studies, and their purposes were not actually to discover Oxandrolones effects on the liver per se. The most conclusive study and the one that is on file with the FDA is the study done by Ferraresi RW. Entitled "Clinical profile of Oxandrin". BTG Pharmaceuticals Drug Monograph. 1995 Look it up.
You couldn't make me look blind to the facts about Oxandrolone if you spent the rest of your natural life trying to do it.

quote:

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Originally posted by ulter:

Yes 2thick Grenfelds presentation was in 1998 but he used the criteria used in the 1980 study to base his research on. And I still ask where are Grenfelds finding published? They are not in Medline�s Library. It is one thing to say it, it is another to prove it.

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His presentation is based on new edvidence. Just because it is not on Medline does not mean it does not exist.

All I can add is that with every cycle of Anavar, the blood work has come back with the same of better liver values.... Now granted it was not 50+ mg per day. But I would be happy to be the test subject on this if you all would contribute a small portion of your weekly pay check

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LAte

Now you may continue

Great info guys..