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does anyone have any Articles on Receptors becoming "full"

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TexasLifter89

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For example, when someone is running a base of lets say 1-ad or something and they want to add epistane/SD/etc... I have heard they would need to dose the 2nd higher because receptors are full from the 1-ad. Does anyone have any articles proving or disproving this that I can read?

Thanks.
 
this is pure bullsh!t....steroids compete at receptor sites this is true...but their is no reason to dose compounds higher to overcome the competition....but, no article sorry....i dont think your gonna find one...this is pure broscience....
 
From what I have seen and heard, I do think that receptors can get a "tolerence to a substance. You hear "always run test a a low dose because you will need to increase the dose next time to see the same effect" I think this holds some truth unless there is alot of time between cycles. This is just my opinion with no proof.
 
I too have no article to reference, but there are comments all over the board regarding Class I and Class II steriod....each hitting a different receptor. Withthatsaid, look into stacking a Class I steriod with a Class II steroid so there is no competition for receptor. I'm assuming the above statement is true as I believe the board members....again no real reference.

Maybe others can tell you which class each steriod is.
 
I too have no article to reference, but there are comments all over the board regarding Class I and Class II steriod....each hitting a different receptor. Withthatsaid, look into stacking a Class I steriod with a Class II steroid so there is no competition for receptor. I'm assuming the above statement is true as I believe the board members....again no real reference.

Maybe others can tell you which class each steriod is.

This class theory has been proven to be false. All AAS act through the androgen receptor but have variable off-target effects (such as inibition of aromatase etc). Receptors can become "saturated" by a given concentration of steroid and this theoretically happens at a fairly low dose. Much of the benefit of stacking steorids has to do with differences in off-target effects.
 
This class theory has been proven to be false. All AAS act through the androgen receptor but have variable off-target effects (such as inibition of aromatase etc). Receptors can become "saturated" by a given concentration of steroid and this theoretically happens at a fairly low dose. Much of the benefit of stacking steorids has to do with differences in off-target effects.

so is there anyways to control saturation? Is it true about having to dose the 2nd compound higher to see its benefits?
 
so is there anyways to control saturation? Is it true about having to dose the 2nd compound higher to see its benefits?

No and no. Saturation is more of a theoretical concept because you also have SHBG and albumin that act to remove AAS from the free state.
 
for sure. I am just really interested to learn more about this idea of saturation and all the different variables that come into play with dosing protocols and multiple designer/aas stacks.
 
Just google androgen receptor translocation. and read up.

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