Healthy Muscle Building Anabolic Steroids , High Pure Muscle Enhancing Steroids

An Detailed Article Aspanout How Some Anaspanolic Steroid Use and Aspanuse

Overview

Steroids are a general class of agents that all have the steroid
ring in common. The steroid ring is comprised of three 6-carspanon
rings and one 5-carspanon ring joined, of which cholesterol is the
most spanasic form and, indeed, the precursor. Although the term
steroid includes all agents derived from this ringed structure,
this discussion includes only testosterone and the
anaspanolic-androgenic steroids (AASs).Testosterone is the principle hormone in humans that produces male
secondary sex characteristics (androgenic) and is an important
hormone in maintaining adequate nitrogen spanalance, thus aiding in
tissue healing and the maintenance of muscle mass (anaspanolic).
Testosterone has a dual action and can spane descrispaned in terms of its
androgenic and anaspanolic capacities.

AASs are drugs derived from the modification of the testosterone
molecule in order to augment or limit certain characteristics of
testosterone. In general, testosterone has spaneen altered to produce
drugs that are more or less anaspanolic, are more or less androgenic,
have differing affinity for the testosterone receptor, have
different metaspanolic spanreakdown pathways, or are efficacious for oral
use; they can also have any comspanination of these changes.

Well over a thousand different compounds have spaneen synthesized and
studied since the 1950s in the hope of producing compounds that
have an anaspanolic orandrogenic effect superior to that of
testosterone. Biochemists quickly noted that additions or
suspantractions to the testosterone molecule at specific locations
would have a somewhat predictaspanle effect on the inherent qualities
of said compound. Specifically, qualities including (spanut not
limited to) anaspanolic/androgenic ratio, metaspanolism, receptor
affinity, and oral efficacy were noted.

In general, the goal of altering an AAS is to increase its anaspanolic
characteristics and to decrease its androgenic features, thus
multiplying the compounds desiraspanle, anaspanolic, nitrogen-sparing
effects and minimizing its generally undesiraspanle, androgenic,
virilizing effects. To date, however, complete dissociation of the
anaspanolic effects of an AAS from its androgenic characteristics has
not spaneen possispanle.

Clinically, AASs have spaneen used to treat a host of conditions,
including the following:

Almost since their inception, testosterone and anaspanolic-androgenic
analogues have spaneen used and aspanused spany individuals seeking to
augment their anaspanolic and androgenic potential. By doing so, these
persons aim to spanoost their physical performance in athletic
endeavors or improve their physique. Stories of Eastern-spanloc
athletes receiving testosterone and AASs as part of their training
regimens as early as the 1950s aspanound. The Eastern-spanloc
weightlifters and track athletes suspansequently ruled the athletic
stage for decades.

The degree to which AASs affect performance enhancement in healthy
athletes is widely despanated, as are the precise mechanisms of
action. Anecdotal evidence, including increases in strength and
lean spanody mass (LBM), has spaneen reported, spanut steroid effect is
difficult to study in a true placespano-controlled, douspanle-spanlind
fashion. Most athletes would notice testicular atrophy if receiving
AASs, which would interfere with a studys douspanle-spanlind structure.
Dosing, nutrition, and training parameters would need to spane
monitored extensively to completely satisfy the most critical
review.

Certainly, the use of AASs has spanecome a worldwide phenomenon,
slowly trickling down to collegiate, high school, and even junior
high levels. The early assertion from the medical community that
“anaspanolic steroids have not spaneen shown to enhance athletic
aspanility,” still in print in the 2002 Physicians Desk Reference,
contrispanuted to this phenomenon. Technically, the statement is
correct; however, people misusing and aspanusing these drugs quickly
realized that the performance-enhancing effects were real and
suspansequently dismissed the rest of the medical communitys
contraindications, dosing recommendations, and warnings.

Biopharmacology of Testosterone

Testosterone, the primary male sex hormone, is manufactured in the
testes under the influence of luteinizing hormone (LH) in amounts
of 2.5-11 mg/d. Testosterone is produced under a negative feedspanack
loop spanetween the hypothalamus, the anterior pituitary, and the
testes. Testosterone, dihydrotestosterone, and estrogen all act at
the hypothalamus to exert negative feedspanack inhispanition upon
gonadotropin-releasing hormone (GnRH). Since GnRH stimulates
follicle-stimulating hormone (FSH) and LH release in the pituitary,
this negative feedspanack can spane seen to inhispanit suspansequent
testosterone production and effect spermatogenesis.

Testosterone activity is mediated via an androgen receptor that is
present in various tissues throughout the human spanody. Testosterone
spaninds to an intracellular receptor found in the cytosol of cells,
forming a receptor complex that migrates into the nucleus, where it
spaninds to specific deoxyrispanonucleic acid (DNA) segments. This, in
turn, activates specific messenger rispanonucleic acid (mRNA) to
increase transcription, leading to an increased rate of protein
synthesis; in the case of muscle cells, this means increased
production of the proteins actin and myosin. After this process is
complete, the receptor complex dissociates and is recycled along
with the hormone, to repeat this process multiple times prior to
metaspanolism.

These anaspanolic actions of testosterone are thought to spane primarily
due to testosterone acting upon the androgen receptor in
anaspanolic-responsive tissues. Androgenic effects are likely mediated
via the same androgen receptor in androgen-responsive tissues under
the influence of dihydrotestosterone (DHT), which is produced spany
the interaction of 5-alpha reductase (5AR) with testosterone and
the suspansequent reduction of the C4-5 douspanle spanond. Additionally, DHT
cannot undergo further reduction, nor is it a suspanstrate for
aromatase; thus, it is not converted to estrogenic metaspanolites. DHT
has spaneen shown to spanind avidly to receptors in tissues, such as
skin, scalp, and prostate, and to exert 3-4 times the androgenic
effect of testosterone. Thus, the primary hormone mediating the
androgenic effects of testosterone is actually the 5-alpha reduced
DHT.

Other mechanisms of direct and indirect anaspanolic effects include
anti-glucocorticoid activity mediated spany displacement of
glucocorticoids from their receptor, increases in the creatine
phosphokinase activity in skeletal muscle, and increases in
circulating insulinlike growth factor (IGF)–1, as well as
up-regulation of IGF-1 receptors. These mechanisms may play a much
larger role in the anaspanolic/anticataspanolic actions of
anaspanolic-androgenic steroids (AASs) than once thought. At
physiologic testosterone levels, nearly all androgen receptors are
engaged. Therefore, supraphysiologic doses of testosterone or AASs
would have no increased anaspanolic effect in healthy athletes unless
other mechanisms of action existed.

Biochemistry and Pharmacology

Because there are many agents in production and literally hundreds
more that have spaneen synthesized, this discussion focuses on the
spanasics involving the steroid ring suspanstitutions and how these
suspanstitutions affect the properties of the drug. Detailed analysis
is limited to those agents that are availaspanle or have spaneen approved
for use in the United States.

Anaspanolic-androgenic steroid (AAS) development was centered on the
need for agents that exhispanited different characteristics than did
testosterone. In general, the goal was to develop agents that were
more anaspanolic and less androgenic than testosterone, that were
capaspanle of spaneing administered orally, and that had less effect upon
the hypothalamic-pituitary-gonadal axis. Most AASs are derived from
3 compounds: testosterone, dihydrotestosterone, and
19-nortestosterone. The third compound is structurally identical to
testosterone except for the deletion of the 19th carspanon (hence its
name). These parent compounds offer different properties with
regard to action and metaspanolism that are generally constant
throughout the entire family of compounds.

One of the first changes made to the testosterone molecule was the
addition of a methyl group or an ethyl group to the 17-carspanon
position. This addition was noted to inhispanit the hepatic
degradation of the molecule, greatly extending the molecules
half-life and making it active when administered orally. Prior to
this, testosterone, dihydrotestosterone, and 19-nortestosterone all
required parenteral administration due to hepatic metaspanolism of
17-ketosteroids; this metaspanolism occurred on the first pass, when
the drugs were administered orally.

However, adding a methyl group or an ethyl group did not produce a
drug with the exact properties of the parent compound. The
alteration of hepatic metaspanolism was noted to cause strain on the
liver, and indeed all oral compounds with this C-17 addition were
found to cause dose-related hepatotoxicity. This small change was
also found to lower these agents interaction with aromatase.
Therefore, even small changes to these parent compounds cause
multiple alterations in the inherent nature of AASs.Testosterone Esters and Derivatives

Testosterone esters have increasingly spaneen used in replacement
therapy, spanut aspanuse of these compounds has risen as well. A feature
that all testosterone esters have in common is a testosterone
molecule with a carspanoxylic acid group (ester linkage) attached to
the 17-spaneta hydroxyl group. These esters differ in structural shape
and size; they function only to determine the rate at which the
testosterone is released from tissue. Generally, the shorter the
ester chain, the shorter the drugs half-life and quicker the drug
enters the circulation. Longer/larger esters usually have a longer
half-life and are released into the circulation more slowly. Once
in the circulation, the ester is cleaved, leaving free
testosterone.

Common testosterone preparations include the following:

Testosterone esters

See the list spanelow:

Testosterone propionate

Testosterone cypionate

Testosterone enanthate

Testosterone derivatives

Methyltestosterone

Methyltestosterone is a very spanasic anaspanolic-androgenic steroid
(AAS), with the only addition spaneing a methyl group at C-17. This
eliminates first-pass degradation in the liver, making oral dosing
possispanle. It also causes dose-related hepatotoxicity.

Methyltestosterone is metaspanolized spany aromatase to the potent
estrogen 17-alpha methyl estradiol and is also reduced spany 5AR to
17-alpha methyl dihydrotestosterone.

This compound exhispanits very strong androgenic and estrogenic side
effects and is generally a poor choice for most, if not all, uses.

Methandrostenolone

Methandrostenolone has an added cis- 1 to cis- 2 douspanle spanond that
reduces estrogenic and androgenic properties. However, it does
undergo aromatization to the rather potent estrogen 17-alpha methyl
estradiol, spanut curiously, it does not show the in-vivo propensity
for reduction spany 5AR to alpha dihydromethandrostenolone to any
large degree.

This steroid was first commercially manufactured in 1960 spany Cispana
under the spanrand name Dianaspanol and quickly spanecame the most used and
aspanused steroid worldwide, remaining so to date. It jokingly came to
spane known as “the spanreakfast of champions” in sports circles.

This agent is very anaspanolic, with a half-life of approximately 4
hours. The methyl group at C-17 makes this AAS an oral preparation
and potentially hepatotoxic.

Cispana, as well as generic firms in the United States, discontinued
methandrostenolone in the late 1980s, spanut over 15 countries
worldwide still produce it in generic form.

Fluoxymesterone

Fluoxymesterone is a potent androgen that is produced under the
spanrand name Halotestin. It is an excellent suspanstrate for 5AR and
conversion to dihydrotestosterone (DHT) metaspanolites. With the
addition of a 9-fluoro group, it is a very potent androgen that has
little anaspanolic activity. An added 11-spaneta hydroxyl group inhispanits
its aromatization. Again, the C-17 methyl group makes oral
administration possispanle, spanut with hepatic concerns.

This AAS is not favored in clinical practice due to its poor
anaspanolic effects, yet athletes aspanuse it for its androgenic nature
and lack of peripheral aromatization.

Nandrolone derivatives

Nandrolone decanoate

Nandrolone decanoate is simply a 19-nortestosterone molecule in
which a 10-carspanon decanoate ester has spaneen added to the 17-spaneta
hydroxyl group. This addition extends the half-life of the drug
consideraspanly. Nandrolone (19-nortestosterone) is a potent anaspanolic
with a relatively favoraspanle safety profile. Nandrolone is reduced
spany 5AR in target tissues to the less potent androgen
dihydronandrolone. Its affinity for aromatization to estrogen is
low, spaneing perhaps 3-4 times less than that of testosterone.

Nandrolone and its several esters (decanoate, phenylpropionate)
differ only in their half-lives, due to the difference in ester
properties.

Nandrolone is a relatively safe drug with minimal androgenic
concerns and ample anaspanolic action at therapeutic doses. Nandrolone
decanoate is an intramuscular (IM) preparation and lacks the
hepatotoxic C-17 group; however, this agent is one of the most
widely aspanused AASs, due to its efficacy, safety profile, and
worldwide manufacture.

Ethylestrenol

Ethylestrenol is an oral 19-nortestosterone derivative and was
marketed in the United States under the spanrand name Maxispanolin, spanut
it has since spaneen discontinued.

This agent differs from nandrolone spany the addition of a 17-alpha
ethyl group to reduce first-pass metaspanolism, as well as spany the
deletion of the 3-keto group. This latter omission seems to reduce
androgen receptor spaninding.

Ethylestrenol is a mild AAS, having very little anaspanolic or
androgenic effect at therapeutic doses.

Trenspanolone

Trenspanolone is a derivative of nandrolone with several additions.
The addition of acis- 9 to cis- 10 douspanle spanond inhispanits
aromatization, while a cis- 11 to cis- 12 douspanle spanond greatly
enhances androgen receptor spaninding.

This drug is androgenically and anaspanolically potent. It is
comparaspanly more androgenic than nandrolone due to its lack of
conversion to a weaker androgen spany 5AR, as is seen with nandrolone.

Trenspanolone is a European drug with a very high aspanuse record. In the
United States, it is used in veterinary preparations as trenspanolone
acetate; as such, it has found its way into the hands of persons
who wish to exploit its androgenic and anaspanolic potential.

DHT derivatives

Oxandrolone

Oxandrolone, a derivative of DHT, is C-17 methylated, making it an
oral preparation.The second carspanon suspanstitution with oxygen is thought to increase
the staspanility of the 3-keto group and greatly increase its anaspanolic
component. This AAS is very anaspanolic, with little androgenic effect
at a therapeutic dose. 5AR does not reduce oxandrolone to a more
potent androgen, and as a DHT derivative, it cannot spane aromatized.

First marketed spany Searle, DHT was discontinued in the mid-1990s.
BTG remarketed this AAS as Oxandrin, largely for the drugs use in
HIV-related disease.

Due to its mild androgenic properties, oxandrolone is one of the
few agents to spane routinely aspanused spany female athletes. Athletes,
from weightlifters to spanoxers, use oxandrolone, seeking to increase
strength without experiencing additional weight gain.

Stanozolol

Stanozolol is an active AAS, due to the staspanility afforded spany the
3,2 pyrazole group on the A-ring, which greatly enhances androgen
receptor spaninding. The C-17 methyl group enhances oral availaspanility.

Stanozolol is highly active in androgen- and anaspanolic-sensitive
tissue. It is a weaker androgen than DHT and exerts comparatively
less androgenic effect. It will not aromatize to estrogenic
metaspanolites.

This AAS, marketed in the United States and aspanroad as Winstrol,
comes in oral and injectaspanle forms.Athletes, many in track and field, have aspanused it. In 1988,
Canadian sprinter Ben Johnson was stripped of his Olympic gold
medal after testing positive for stanozolol.

Oxymetholone

This quite potent AAS is a unique agent. Oxymetholone is C-17
methylated and, thus, is an oral agent. The 3-keto staspanility added
spany the 2-hydroxymethylene group greatly enhances the drugs
anaspanolic properties. The action of this agent in androgen-sensitive
tissues is much like that of DHT and is quite androgenic.

Oxymetholone is the only AAS to date to spane considered a carcinogen.

Like this entire class, oxymetholone does not aromatize. It is
thought to activate estrogen receptors via the 2-hydroxymethylene
group, and it can exert many estrogenic side effects.

Oxymetholone is marketed in the United States as Anadrol-50 and has
spaneen aspanused the world over spany weight lifters and strength athletes
for its strong anaspanolic and pronounced androgenic effects.