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akn
05-09-2014, 04:59 PM
Testosterone is the primary substrate used in the male
body for the synthesis of estrogen (estradiol), the principal
female sex hormone. Although the presence of estrogen
may seem quite unusual in men, it is structurally very
similar to testosterone. With a slight alteration by the
enzyme aromatase, estrogen is produced in the male
body. Aromatase activity occurs in various regions of the
male body, including adipose,22 liver,23 gonadal,24 central
nervous system,25 and skeletal muscle26 tissues. In the
context of the average healthy male, the amount of
estrogen produced is generally not very significant to
one's body disposition, and may even be beneficial in
terms of cholesterol values (See Side Effects:
Cardiovascular Disease). However, in larger amounts it
does have potential to cause many unwanted effects
including water retention, female breast tissue
development (gynecomastia), and body fat accumulation.
For these reasons, many focus on minimizing the build-up
or activity of estrogen in the body with aromatase
inhibitors such as Arimidex and Cytadren, or antiestrogens
such as Clomid or Nolvadex, particularly at
times when gynecomastia is a worry or the athlete is
attempting to increase muscle definition.
We must, however, not be led into thinking that estrogen
serves no benefit. It is actually a desirable hormone in
many regards. Athletes have known for years that
estrogenic steroids are the best mass builders, but it is
only recently that we are finally coming to understand the
underlying mechanisms why. It appears that reasons go
beyond the simple size, weight, and strength increases
that one would attribute to estrogen-related water
retention, with this hormone actually having a direct
effect on the process of anabolism. This is manifest
through increases in glucose utilization, growth hormone
secretion, and androgen receptor proliferation.

Glucose Utilization and Estrogen

Estrogen may playa very important role in the promotion
of an anabolic state by affecting glucose utilization in
muscle tissue. This occurs via an altering of the level of
available glucose 6-phosphate dehydrogenase, an
enzyme directly tied to the use of glucose for muscle
tissue growth and recuperation.27 28 More specifically,
G6PD is a vital part of the pentose phosphate pathway,
which is integral in determining the rate nucleic acids and
lipids are to be synthesized in cells for tissue repair. During
the period of regeneration after skeletal muscle damage,
levels of G6PD are shown to rise dramatically, which is believed to represent a mechanism for the body to
enhance recovery when needed. Surprisingly, we find that
estrogen is directly tied to the level of G6PD that is to be
made available to cells in this recovery window.
The link between estrogen and G6PD was established in a
study demonstrating levels of this dehydrogenase
enzyme to rise after administration of testosterone
propionate. The investigation further showed that the
aromatization of testosterone to estradiol was directly
responsible for this increase, and not the androgenic
action of this steroid.29 The non-aromatizable steroids
dihydrotestosterone and fluoxymesterone were tested
alongside testosterone propionate, but failed to duplicate
the effect of testosterone. Fu rthermore, the positive effect
of testosterone propionate was blocked when the
aromatase inhibitor 4-hydroxyandrostenedione
(formestane) was added, while 17-beta estradiol
administration alone caused a similar increase in G6PD to
testosterone propionate.The inactive estrogen isomer 17alpha
estradiol, which is unable to bind the estrogen
receptor, failed to do anything. Further tests using
testosterone propionate and the anti-androgen flutamide
showed that this drug also did nothing to block the
positive action of testosterone, establishing it as an effect
independent of the androgen receptor.

Estrogen and GH/IGF-l

Estrogen may also play an important role in the
production of growth hormone and IGF-1. IGF-1 (insulinlike
growth factor) is an anabolic hormone released in the
liver and various peripheral tissues via the stimulus of
growth hormone (See Drug Profiles: Growth Hormone).
IGF-1 is responsible for the anabolic activity of growth
hormone such as increased nitrogen retention/protein
synthesis and cell hyperplasia (proliferation). One of the
first studies to bring this issue to our attention looked at
the effects of the anti-estrogen tamoxifen on IGF-1 levels,
demonstrating it to have a suppressive effect.3D A second,
perhaps more noteworthy, study took place in 1993,
which looked at the effects of testosterone replacement
therapy on GH and IGF-1 levels alone, and compared them
to the effects of testosterone combined again with
tamoxifen.31 When tamoxifen was given, GH and IGF-1
levels were notably suppressed, while both values were
elevated with the administration of testosterone
enanthate alone. Another study has shown 300 mg of
testosterone enanthate weekly to cause a slight IGF-1
increase in normal men. Here the 300 mg of testosterone ester caused an elevation of estradiol levels, which would
be expected at such a dose. This was compared to the
effect of the same dosage of nandrolone decanoate;
however, this steroid failed to produce the same increase.
This result is quite interesting, especially when we note
that estrogen levels were actually lowered32 when this
steroid was given. Yet another demonstrated that GH and
IGF-l secretion is increased with testosterone
administration on males with delayed puberty, while
dihydrotestosterone (non-aromatizable) seems to
suppress GH and IGF-l secretion.33

Estrogen and the Androgen Receptor

It has also been demonstrated that estrogen can increase
the concentration of androgen receptors in certain
tissues. This was shown in studies with rats, which looked
at the effects of estrogen on cellular androgen receptors
in animals that underwent orchiectomy (removal of
testes, often done to diminish endogenous androgen
production). According to the study, administration of
estrogen resulted in a striking 4800/0 increase in
methyltrienolone (a potent oral androgen often used to
reference receptor binding in studies) binding in the
levator ani muscle.34 The suggested explanation is that
estrogen must either be directly stimulating androgen
receptor production, or perhaps diminishing the rate of
receptor breakdown. Although the growth of the levator
ani muscle is commonly used as a reference for the
anabolic activity of steroid compounds, it is admittedly a
sex organ muscle, and different from skeletal muscle
tissue in that it possesses a much higher concentration of
androgen receptors. This study, however, did look at the
effect of estrogen in fast-twitch skeletal muscle tissues
(tibialis anterior and extensor digitorum longus) as well,
but did not note the same increase as the levator ani.
Although discouraging at first glance, the fact that
estrogen can increase androgen receptor binding in any
tissue remains an extremely significant finding, especially
in light of the fact that we now know androgens to have
some positive effects on muscle growth that are mediated
outside of muscle tissue.

Estrogen and Fatigue

"Steroid Fatigue" is a common catchphrase these days,
and refers to another important function of estrogen in
both the male and female body, namely its ability to
promote wakefulness and a mentally alert state. Given the
common availability of potent third-generation
aromatase inhibitors, bodybuilders today are (at times)
noticing more extreme estrogen suppression than they
had in the past. Often associated with this suppression is
fatigue. Under such conditions, the athlete, though on a productive cycle of drugs, may not be able to maximize
his or her gains due to an inability to train at full vigor.This
effect is sometimes also dubbed "steroid lethargy." The
reason is that estrogen plays an important supporting
role in the activity of serotonin. Serotonin is one of the
body's principle neurotransmitters, vital to mental
alertness and the sleep/wake cycle.35 36 Interference with
this neurotransmitter is also associated with chronic
fatigue syndrome,37 38 so we can see how vital it is to
fatigue specifically. Estrogen suppression in menopause
has also been associated with fatigue,39 as has the clinical
use of newer (more potent) aromatase inhibitors like
anastrozole,4o letrozole,41 exemestane,42 and fadrozole43
in some patients. These things may be important to
consider when planning your next cycle. Although not
everyone notices this problem when estrogen is low, for
those that do, a little testosterone or estrogen ca n go a
long way in correcting this. It is also of note that the use of
strictly non-aromatizable steroids sometimes causes this
effect as well, likely due to the suppression of natural
testosterone production (cutting off the main substrate
used by the male body to make estrogen).

Anti-Estrogens and the Athlete

So what does this all mean to the bodybuilder looking to
gain optimal size? Basically I think it calls for a cautious
approach to the use of estrogen maintenance drugs if
mass is the key objective (things change, of course, if we
are talking about cutting). Obviously, anti-estrogens
should be used if there is a clear need for them due to the
onset of estrogenic side effects, or at the very least, the
drugs being administered should be substituted for nonestrogenic
compounds. Gynecomastia is certainly an
unwanted problem for the steroid user, as are noticeable
fat mass gains. But if these problems have not presented
themselves, the added estrogen due to a cycle of
testosterone or Dianabol, for example, might indeed be
aiding in the buildup of muscle mass, or keeping you
energetic. An individual confident they will notice, or are
not prone to getting, estrogenic side effects, may
therefore want to hold off using estrogen maintenance
drugs so as to achieve the maximum possible gains in
tissue mass.

bigdaddyo1617
05-09-2014, 06:44 PM
Keep it coming good post