Study showing winstrols activity independent of A/R binding/DNA interaction...

[wildcat]

Then we have steroids that are potent combination steroids all by themselves(meaning they display influences on growth through both class-I and II activity,and thus are very effective as'stand-alone'anabolic agents as well as forming the 'base' of most steroid stacks)....Two compounds possess this unique characteristic-Trenbelone and Testosterone.Either of these two steroids should form the base of most users stacks,as the cover both A/R and non-A/R mediated mechanisms,and adding to them with either a class-I or II will only potentiate that particular mechanism towards muscular hypertrophy...

Now that we're aware of which compounds work through which mechanism,how do we combine them effectively to maximize each one's potential?As explained above,Testosterone and trenbelone should form the base of any serious steroid stack,but great effects can be had by combining single mechanism steroids from opposing classes....Examples of this type of synergistic combining could be(but are not limited to)

*CUTTING*
Winstrol & Equipoise
Winstrol & Primobolan
Fluoxymesterone & Equipoise or Primobolan

*BULKING*
Deca & Dianabol
Anadrol & Equipoise or Primobolan
Winstrol & deca

And of course,using test or tren as the base compound for either cutting or bulking will only make results that much more explosive.If using test for cutting,an anti-aromitase should be incorporated

Does this mean that stacking a TEST with Tren would be stupid?
For instance, would a stack of SUS, TREN and Winny be a waste of either the Tren or Test because they accomplish the same thing?

 

[HUCKLEBERRY FINNaplex]

No,because the tren binds much more aggressively to the androgen receptor than test,so it will work very nicely with test and winny.That's a tremendous trio for strength/size/hardness...

 

[Andy13]

Does this mean that stacking a TEST with Tren would be stupid?
For instance, would a stack of SUS, TREN and Winny be a waste of either the Tren or Test because they accomplish the same thing?

Tren has a much higher affinity for the AR than does test. Using an excess of both can result in more aromatization of test.

Huck and I disagree slightly on the topic of type I and type II steroids. I feel that >90% of lean muscle gains occur through the AR. There is a real lack of evidence that supports non-Ar anabolism. The key word there is anabolism since many effects from steroids occur via non-AR, however (again, IMO) they have little or no impact on actual anabolism. It would be nice to see some evidence that supports this. I realize that some AAS elevate growth factor levels more than others, but like I said, it would be nice to see some evidence that supports that this does not happen downstream of the AR activation.

click-cl-click-clickcl-ck-click-click

Did you hear that? That's everyone taking the safety off their flame throwers!!!



Andy

 

[HUCKLEBERRY FINNaplex]

Nope, Andy,this is discussion at it's finest,and I,above all,respect your opinion,and am open-minded enough to consider anything...

 

[wildcat]

Tren has a much higher affinity for the AR than does test. Using an excess of both can result in more aromatization of test.

Huck and I disagree slightly on the topic of type I and type II steroids. I feel that >90% of lean muscle gains occur through the AR. There is a real lack of evidence that supports non-Ar anabolism. The key word there is anabolism since many effects from steroids occur via non-AR, however (again, IMO) they have little or no impact on actual anabolism. It would be nice to see some evidence that supports this. I realize that some AAS elevate growth factor levels more than others, but like I said, it would be nice to see some evidence that supports that this does not happen downstream of the AR activation.

click-cl-click-clickcl-ck-click-click

Did you hear that? That's everyone taking the safety off their flame throwers!!!



Andy

So Andy---- what do your mass building stacks typically look like?

wc.

 

[Stew Meat]

One extremely benefical non-AR mediated effect of testosterone is that it not only raises IGF-1 levels, but can also increase IGF-1 receptor concentration.



-Stew

 

[Andy13]

STEW- LET ME PICK YOUR BRAIN!!

Stew- at what dose does this become significant? Does the amount of increased IGF-1 come close to what you would consider an effective exergeneous IGf-1 dosage? Is the receptor increase a result of the AAS or rather the increased amount of IGF-1? In other words, if somone took exergeneous IGF-1, would they expirience the same receptor increase? Are you positive that the increase in IGF-1 is not somewhere downstream of AR activation?

I know that estrogens raise IGF-1 levels as well... What about receptor concentration?

Also, do you feel that androgens can directly inititate tanscription of certain genes without first binding the AR(not necesarily the same sequence transcribed by the AR/steroid complex)?

The reason why 1000mg of test/week is significantly better than 500mg/week is obvioulsy because of increased AR activation... However if androgens can initiate transcription of DNA independent of the AR, that might explain the only slight benefit from going from 1000mg/week to 2000mg/week.

Thanks, Stew

Andy

 

[mipada]

All I can say is "That's one hell of a conversation" This is why I love this board and even after being out of the net for almost a year, I come right back to this board. Keep the info comming bro's...

 

[Stew Meat]

Re: STEW- LET ME PICK YOUR BRAIN!!

Originally posted by Andy13
Stew- at what dose does this become significant? Does the amount of increased IGF-1 come close to what you would consider an effective exergeneous IGf-1 dosage? Is the receptor increase a result of the AAS or rather the increased amount of IGF-1? In other words, if somone took exergeneous IGF-1, would they expirience the same receptor increase? Are you positive that the increase in IGF-1 is not somewhere downstream of AR activation?

I don't know what the dose at which it becomes signifigant, but the IGF-1 expression is dose dependant. Testosterone raises IGF-1 receptor concentrations directly, independent of IGF-1's activity; high IGF-1 levels will also increase IGF-1 receptor concentration. However, high levels of IGF-1 will not raise the androgen receptor concentrations. The IGF-1 increase is not understood to be related to AR function... an entirely non-AR mediated anabolic effect of testosterone. It is not known whether other androgens will have the same effect as testosterone in raising IGF-1 levels and IGF-1 receptor concentrations.

The above muscle cell IGF-1/AR expresssion experiment was done on partially aborded fetuses, btw...

The same study outlined the following: In men, Heavy resistance training leads to hypertropy which leads to increased testosterone levels. Hypertrophy can also increase IGF-1 levels slightly. But in Women, hypertrophy does NOT lead to increased testosterone levels but leads to an even higher IGF-1 concentration than with men (and control group).

I know that estrogens raise IGF-1 levels as well... What about receptor concentration?

I haven't studied estrogen to any large extent so I don't know the direct method of involvemen with it and IGF-1.

Also, do you feel that androgens can directly inititate tanscription of certain genes without first binding the AR(not necesarily the same sequence transcribed by the AR/steroid complex)?

Definately... hence the IGF-1 receptor increase.

The reason why 1000mg of test/week is significantly better than 500mg/week is obvioulsy because of increased AR activation... However if androgens can initiate transcription of DNA independent of the AR, that might explain the only slight benefit from going from 1000mg/week to 2000mg/week.

I agree... However, you also have to keep in mind that receptor concentration is also going to be increasing slightly...


Everything I said is backed by research. I know of no more non-AR muscular enhancing benefits of steroids.






-Stew

 

[Unity66]

like testosterone, trenbolone exhibits both class-I and class-II properties within the body; yet trenbolone binds much more aggressively to the AR than does test......

taken without permission from Mr. H's website is the following:

"Not only does TA improve nitrogen retention, but it also raises many hormone levels. In a study performed by the Department of Animal Sciences, rats were injected with Trenbolone Acetate daily for two weeks and then were tested for an increase in growth hormone (GH), insulin-like growth factor (IGF-1) and fibroblast growth factor (FGF). Not only did treated rats grow more rapidly, deposit less bodyfat and retain more protein, but satellite cells cultured from the Trenbolone-treated rats exhibited greater sensitivity to FGF and IGF-1 than cells cultured from control rats. This increased sensitivity was also accompanied by increased levels of GH, IGF-1 and FGF in the bodies of the rats. With an elevated cocktail of these growth promoting hormones flowing in an animals body, it cannot help but grow. Not only are the cells more sensitive to these hormones, there are more hormones available to utilize. It would be safe to say that similar kinds of hormonal increases and sensitivities would also be found in humans that used Trenbolone Acetate. A large increase in these hormone levels would not only help with growth, but would skyrocket the effectiveness of this drug due to the cocktail of the anabolic hormones present in the body."

im dieting now and making excellent progress using an AS stack typically associated with bulking--test/tren/dbol.........add T-3 (pyramid), clen, liquidex with cardio and a good diet/training regimine and

Unity66