So there is no downregulation of androgen receptors?

[nooby]

So why do you guys say AAS becomes less effective after 8 weeks. Can someone expound on that, or point me in the right direction so I can do some research. The reason I want to know is, I am trying to determine how long I can cycle. Due to an endocrine disorder(non AAS related) I don't have to worry about shutting down my test production.

So since I don't have to worry about that, I am looking into the idea of a longer cycle. I need to know more about why dosages need to be increased after a certain point, and the exact mechanism that causes this, so that I can determine if this would be beneficial to me. I am also wondering if switching compounds would make a difference, but since I don't know what causes the decrease in effectiveness after a certain time period, I can't answer that question.

[DanB]

from what i understand myostatin build up is a factor hence the need for a deload every so often

mabey ronnie's sticky on slingshot training/cycling could be of interest to you if your sure that you neednt worry about recovery

http://forums.steroid.com/showthread...!#.T6y5M1JvCSo

[AD]

what is your endocrine condition? what treatment are you currently on?

[nooby]

Thanks, that thread was interesting. Anyone know where I can find info on what causes myostatin levels to increase, any studies or anything like that?


Asiandude, I don't want to post any information that could identify me, to someone who knows me. But my test levels were 107 at 30 years old, prior to any AAS use. I am not on any treatment as of now, but am currently 4 weeks into a cycle.

[DanB]

Thanks, that thread was interesting. Anyone know where I can find info on what causes myostatin levels to increase, any studies or anything like that?

Asiandude, I don't want to post any information that could identify me, to someone who knows me. But my test levels were 107 at 30 years old, prior to any AAS use. I am not on any treatment as of now, but am currently 4 weeks into a cycle.

I'm on app so can't link anything, but just Google myostatin or myostatin inhibit muscle growth, myostatin build up etc there is an abundance of info

[Sgt. Hartman]

As far as length of cycle, I'd be more concerned with general health issues, high BP, high RBC and hematocrit, lipid profile, etc.

[MR10X]

Its not the steroids becoming ineffective,its your body reaching a sticking point.

[MR10X]

"The concept that AR activity is measured by “gains” is simply ridiculous. The function of the activated AR is not to produce gains per se, but to increase protein synthesis. That will only result in gains if muscle catabolism is less than the anabolism. As muscle mass becomes greater, so does catabolism. At some point under any hormonal and training stimulus, equilibrium is reached, and there are no further gains. With high dose AAS use, that point is at a far higher muscle mass than if androgen levels are at only normal values. The concept that the steroids are “not working” for the bodybuilder who is maintaining 40 lb more muscular weight than he ever could achieve naturally, and who might even still be gaining slowly (but not as fast as in his first cycle) is, at best,an example of poor reasoning..

Moderate dose steroids, even though they are sufficient to saturate the AR, don’t take one as far as high dose steroids can. The difference cannot be substantially increased percentage of occupied receptors, since almost all are occupied in either case.

What does that leave as the possibilities? More receptors, or non-receptor-mediated activity.

Is there evidence that muscles are more responsive to the same level of androgen after having been exposed to high dose androgen? That would be the case, at least temporarily, if upregulation occurred. The answer is yes, there is such evidence, anecdotally. If a brief cycle (2 weeks) of high dose AAS with short-acting acetate ester is used, there can be substantially increased androgenic activity, relative to baseline, in weeks 3 and 4 even though the exogenously-supplied androgen is long out of the system. This is what would be expected if upregulation occurred. It could not be the case if substantial downregulation occurred.

“The longer a course of treatment lasts, the more users are obliged to take drugs to compensate for the loss of potency.”

This is simply untrue. I know of no cases of steroid users who found that they began losing muscle mass while remaining on the same dose. The illogic here is confusing cessation or slowing of gains with cessation of effect. One instead should look at,. What muscular weight set-point is the body experiencing with this hormonal and exercise stimulus?

With higher dose AAS, that setpoint is higher. Once it is nearly achieved or achiever, of course gains slow or stop. And besides this, even if the body has not yet fully achieved the higher mass that may be possible with a given level of AAS, it is harder for many reasons for the body to grow after it has recently grown a fair deal. It needs time before being ready to again grow some more. This is observed whether steroids are involved or not.

The illogic of people who correlate rate of gains with AR level is amazing. I suppose they would have it that the AR downregulates after the first 6 months of natural training as well. After all, gains slow down then."

[DanB]

Excellent post above

[nooby]

Thanks for that post MR10X. That is what I suspected. Since there is no up or down-regulation of AR's, the dosage should never really change, unless you aren't taking enough to completely attach to all AR's. But once the AR's are full, taking more would not really help.

So until science figures out a way to stop the build-up of myostatin, and discovers whatever other mechanisms cause the decrease in effectiveness, then we have to take breaks. Interesting.


Also, I am wondering, if some AAS have a higher binding affinity to AR's, why would you stack with other AAS with a lower binding affinity? Wouldn't it be a waste? Since all the AR's are full from the higher binding affinity steroid?

[nooby]

Also, I am wondering, if some AAS have a higher binding affinity to AR's, why would you stack with other AAS with a lower binding affinity? Wouldn't it be a waste? Since all the AR's are full from the higher binding affinity steroid?

Anyone know the answer to this?

[Bonaparte]

Also, I am wondering, if some AAS have a higher binding affinity to AR's, why would you stack with other AAS with a lower binding affinity? Wouldn't it be a waste? Since all the AR's are full from the higher binding affinity steroid?

It would be nearly impossible to occupy all the ARs in your body.

[MR10X]

It would be nearly impossible to occupy all the ARs in your body.

So we have AR's in our body with no androgen in them?

[Bonaparte]

So we have AR's in our body with no androgen in them?

Of course.
You wouldn't live too long if every AR in your body were constantly being occupied/activated (because you'd be running some insane doses).

[kelkel]

Well written Mr10!

[AD]

to mr10x, may i know the source of your paragraph? is it a medical paper or is it someone's personal opinion?

[jimmyinkedup]

to mr10x, may i know the source of your paragraph? is it a medical paper or is it someone's personal opinion?

I cant say word for word who wrote his post but I can say Bill Roberts actually wrote it .
Also he (bill roberts) plagiarized a lot of it from a book written by Dr Albert Brinkman- pretty famous endo from the netherlands.

[AD]

I cant say word for word who wrote his post but I can say Bill Roberts actually wrote it .
Also he (bill roberts) plagiarized a lot of it from a book written by Dr Albert Brinkman- pretty famous endo from the netherlands.

in other words, gospel truth? or hearsay? or somewhere in between with a bit of both?

[kelkel]

Lovely.