The AR is a large protein molecule, produced from one and only one
gene in DNA. There aren't lots of different kinds of receptors, as
some authors claim. There are not, for example, ARs specific for oral
or injectable anabolics, nor for different esters of testosterone, nor for
any different kinds of AAS.

The first important question to ask is, "How many ARs do you have?
Is the number small or large? Can it be changed?" Since these are, in
effect, little machines which are either on or off, and their effect is
greater as more are activated, we want as many of them switched on
as possible.

There are far fewer ARs than most people realize. Some authors who
are opposed to AAS doses beyond 200 mg/week say that only this
amount will be accepted by the receptors in muscle, and everything
past that will "spill over" and go into receptors in the skin and
elsewhere.

Research shows that muscle tissue has, roughly, 3 nanomoles of ARs
per kg. Then your body probably has less than 300 nanomoles of
ARs, grand total, let's say.

Well, one 2.5 mg tab of oxandrolone supplies about 8000 nanomoles
of AAS. Clearly, that's far more molecules than your body has
receptors.

A little math shows that all those receptors combined could bind only
a small percentage of the molecules of AAS in one little 2.5 mg tab.
So binding to ARs cannot appreciably reduce the concentration of
AAS in the blood. Therefore, the ideas that ARs will bind most of
whatever dose some author recommends, or that "spill-over" will
occur beyond that, are entirely wrong. There just aren't that many
receptors.

Typical doses of AAS are high enough that a high percentage of the
ARs are bound to AAS, whether the dose is say 400 mg/week or
1000 mg/week. If similar percentages of ARs are active � close to
100% in each case -- then why do higher doses give more results?
It's a fact that they do, but there is not any large percentage of
unoccupied receptors at the moderate dose. Thus, there is little room
for improvement there. So at least part of the cause must be
something other than simply occupying a higher percentage of
receptors.

And why did I pick those doses, rather than comparing normal levels
with say 400 mg/week?

The fact that the ARs must form dimers to be active has an interesting
consequence. The mathematics are such that if two ARs must join
together to form an activated dimer, and both must bind a molecule of
AAS, then the square must be taken of the percentage. This means
that if say 71% of receptors are binding steroid, only 50% of the
dimers will be activated. Thus, at low levels, there is more room for
improvement than one would think. But if say 95% are occupied, then
even after squaring that, there would still only be 10% room for
improvement.

But actual improvement � increase in effect � seems to be much more
than 10%. Anabolism increases even as the dose becomes more than
sufficient to ensure virtually complete binding. Why?