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Binding Affinity: Different anabolic androgenic steroids chemical structures or deviations either
increase or decrease the molecule's attraction to its respective receptor-sites. The
greater the affinity the specific AAS possess the greater the chance of a higher rate of
molecule / receptor-site mergence.
Binding Time: Each variant of AAS has a common binding time unique to its
structure. This means that the molecule binds to its respective receptor-sties, both
androgenic and corticoid, for a given period of time. The longer the binding time, the
greater the period of activity. This also affects a drugs anabolic/catabolic ratio.
Percentage Bound/Unbound: All sex steroids and hormones exist in the body
in either a bound or unbound state. Kind of like "The Taming of O", but on a much
larger scale. Bound refers to the inactive portion of a given level (amount) of an AAS
or natural hormone. Unbound refers to the free or active portion. In both cases, we
are referring to the circulatory or blood plasma levels.
Only the free unbound AAS molecules can merge with a receptor-site and
therefore be termed as active. The bondage team that binds hormones are blood
proteins called Sex-Hormone-Binding-Globulin (SHGB) and Albumin. Different
alterations in chemical structures, either man-made or naturally occurring, are either
more or less resistant to binding. This means alterations in an AAS chemical structure
could allow it to exist in a greater percentage of unbound/active state. So less could
do more.
Testosterone circulates in a bound state at a rate (or percentage) of 98-99% and
an unbound state at a rate of 1 -2%. For the curious, 65% is bound by sex hormone binding globulin , and 33% is
bound by Albumin, plus or minus 1%.
So the higher the percentage of an AAS circulating in the blood stream in the
unbound/active state, the greater the number of potential bindings /mergence with
receptor-sites.
Active-Life/Half-Life: All drugs have an active-life and a half-life. Knowing a
drug's average effective active-life and half-life is important information. An active-
life is the entire period of time a parent drug remains active once administered.
A drug's half-life is one half of its active-life and the period of time required for
half of its administered dosage to disperse and metabolize.
Of course there are other pathways and mechanisms by which AAS induce
the growth process.
• When 17-alfa-alkylated steroids are detoxified/deactivated by the liver there is a significant increase in hepatic IGF-1 production and secretion.
• AAS increase CP (Creatine Phosphate) synthesis.
• AAS increase circulatory amino acid (s) levels by redirecting amino acids away
• from liver oxidation / destruction.
• AAS susceptible to estrogenic conversion suppress cortisol levels and activity by
stimulating gh - growth hormone (somatropin) - /IGF-1 production.
• AAS inhibit the synthesis of fat by blocking the enzyme lipoprotein lipase which
in turn spares calories that can be utilized for the growth process of muscle
tissue.
• Some AAS increase muscle cell PGE-1 and PGF-2 receptor-site
count/concentrations.
• By stimulating an increase in nitric oxide synthesis, AAS increase vascular
endothelial growth factor (VEGF) which is responsible for capillary formation.
Nitric oxide also positively effects erectile function. (Think about it)
There are several other mechanisms by which AAS induce or mediate the
growth process but for now we will simply accept that a foundation for greater
knowledge has been laid down
increase or decrease the molecule's attraction to its respective receptor-sites. The
greater the affinity the specific AAS possess the greater the chance of a higher rate of
molecule / receptor-site mergence.
Binding Time: Each variant of AAS has a common binding time unique to its
structure. This means that the molecule binds to its respective receptor-sties, both
androgenic and corticoid, for a given period of time. The longer the binding time, the
greater the period of activity. This also affects a drugs anabolic/catabolic ratio.
Percentage Bound/Unbound: All sex steroids and hormones exist in the body
in either a bound or unbound state. Kind of like "The Taming of O", but on a much
larger scale. Bound refers to the inactive portion of a given level (amount) of an AAS
or natural hormone. Unbound refers to the free or active portion. In both cases, we
are referring to the circulatory or blood plasma levels.
Only the free unbound AAS molecules can merge with a receptor-site and
therefore be termed as active. The bondage team that binds hormones are blood
proteins called Sex-Hormone-Binding-Globulin (SHGB) and Albumin. Different
alterations in chemical structures, either man-made or naturally occurring, are either
more or less resistant to binding. This means alterations in an AAS chemical structure
could allow it to exist in a greater percentage of unbound/active state. So less could
do more.
Testosterone circulates in a bound state at a rate (or percentage) of 98-99% and
an unbound state at a rate of 1 -2%. For the curious, 65% is bound by sex hormone binding globulin , and 33% is
bound by Albumin, plus or minus 1%.
So the higher the percentage of an AAS circulating in the blood stream in the
unbound/active state, the greater the number of potential bindings /mergence with
receptor-sites.
Active-Life/Half-Life: All drugs have an active-life and a half-life. Knowing a
drug's average effective active-life and half-life is important information. An active-
life is the entire period of time a parent drug remains active once administered.
A drug's half-life is one half of its active-life and the period of time required for
half of its administered dosage to disperse and metabolize.
Of course there are other pathways and mechanisms by which AAS induce
the growth process.
• When 17-alfa-alkylated steroids are detoxified/deactivated by the liver there is a significant increase in hepatic IGF-1 production and secretion.
• AAS increase CP (Creatine Phosphate) synthesis.
• AAS increase circulatory amino acid (s) levels by redirecting amino acids away
• from liver oxidation / destruction.
• AAS susceptible to estrogenic conversion suppress cortisol levels and activity by
stimulating gh - growth hormone (somatropin) - /IGF-1 production.
• AAS inhibit the synthesis of fat by blocking the enzyme lipoprotein lipase which
in turn spares calories that can be utilized for the growth process of muscle
tissue.
• Some AAS increase muscle cell PGE-1 and PGF-2 receptor-site
count/concentrations.
• By stimulating an increase in nitric oxide synthesis, AAS increase vascular
endothelial growth factor (VEGF) which is responsible for capillary formation.
Nitric oxide also positively effects erectile function. (Think about it)
There are several other mechanisms by which AAS induce or mediate the
growth process but for now we will simply accept that a foundation for greater
knowledge has been laid down
