Anabolic Steroids, Site injection

csuperman

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The topic of steroid site injections is one of the most controversial in modern BB’ing, no doubt due to the recent proliferation of Synthol within the sport; a similar, although different approach to site enhancement. While not all advocate using AAS for site enhancement, it is generally looked at by the BB’ing community as an acceptable practice. Despite there being more similarities than differences, the same cannot be said of Synthol—a black mark on the sport according to many.


You don’t have to look any farther than YouTube to find a smorgasbord of mentally handicapped individuals proudly displaying Synthol treated bodyparts that can only be described as deformities. With this type of ongoing advertisement it is not hard to see how Synthol got its bad rap, but we’ll get back to Synthol in a moment.


There is some disagreement as to the effectiveness of AAS site injections. Namely, are the gains due to an actual increase in muscle size, or to temporary inflammation? In addition, which type of steroids can be used for site injections? Must they be non-esterfied, or can esterfied steroids lead to local increases in muscle growth? These are a just a few of the questions we will cover today.


There is a bit of confusion regarding which type of steroids are effective for site enhancement. On one side, we have those who say that only non-esterfied steroids can be used for this purpose, while others claim that any type of steroid will work. With people from both sides of the fence claiming results, who is right and who is wrong? Let’s look at all sides of the argument as we search for an answer.


Those who state that esterfied steroids are worthless for site enhancement often point to the drugs’ pharmacokinetics as the main reason for their ineffectiveness. In this regard, they are correct, as esterfied steroids are incapable of initiating AR induced muscle growth at the injection site. Before an esterfied steroid can be used by a muscle, the attached ester must first be enzymatically cleaved from the steroid molecule; a process which primarily takes place in the liver, and to a lesser degree in the bloodstream. In other words, the steroid must first leave the injection site and be transported to the liver, at which point it is liberated of its attached ester and made bioavailable to muscle tissue, but by that point the steroid has already gone systematic (entered the bloodstream) and will affect all the muscles of the body equally.
So, I guess that answers that question. Site enhancement does not take place with esterfied gear, right? Well, that depends on whether or not AR activation is the only mechanism by which esterfied steroids might initiate muscle growth. Upon closer inspection, we find that muscle growth indeed can occur through alternate mechanisms, which have nothing to do with the steroid itself. In order to find our answer, we must delve into perhaps the most controversial subject of all—Synthol.


Invented by Chris Clark, Synthol came on the BB’ing scene about 20 years ago. For many years it was largely misunderstood and even today most remain ignorant regarding its mechanisms of action. Synthol used properly increases muscle size through 3 main pathways: inflammation, increased muscle volume due to the presence of the oil, and genuine muscle fiber growth. After the initial application, most users will witness a near immediate increase in muscle size, which is due almost solely to inflammation. When treating the biceps & triceps, for example, and depending on the starting size of one’s arms, it is common to experience an increase in size of ½ to 1 inch within the first few days alone. As repeated rounds of injections are administered, oil volume begins to build within the muscle, which further increases muscle size. With continued exposure, the muscle itself will eventually begin to increase in size. How this takes place is open to debate, but we now know that this does occur.


As the years went by and Synthol was used by more and more people, it became readily apparent than muscles of ex-Synthol users never reverted back to their original size, even when the product had been discontinued years prior. Some claimed that the oil never dissipated, but remained for many years. This would certainly explain the long-term size increase in prior users, but this was just speculation. In order to get legitimate answers, inspections would need to be conducted on the muscles of former Synthol users, in order to determine how much, if any oil remained after a given period of time. So, that is what happened.


An evaluation of the results showed that the muscles of ex-Synthol users were free of oil, with muscle fiber alone accounting for the size of the muscle. These results confirm what we know today about MCT oil (the oil used in Synthol); that MCT oil has a clearance rate of about 3 months, during which time it slowly dissipates from the injection site and is efficiently metabolized by the body.


So, how does Synthol, which is nothing more than a sterile oily solution, cause muscle growth? Likely the same way that esterfied steroids do. The creator of Synthol, as well as those who sell their own version of the same product, typically claim that it causes growth by stretching the muscle fascia—a thin sheath of fibrous connective tissue which envelops skeletal muscle. Fascia acts as a protective mechanism by lending muscular support, as well as reducing friction during contraction. However, the very characteristics which make it effective as a support structure may also hinder muscle growth. Advocates of Synthol postulate that fascia’s tough, non-pliable nature limits growth rate by unnecessarily constricting the muscle, but through the proper application of Synthol, the fascia can be stretched, thereby opening up new room for uninhibited growth.


This is not a new idea and was originally discussed in depth by John Parillo, who was a big proponent of manual facial stretching. While his program did achieve some measure of popularity and results were noted, it did not really catch on in the BB’ing community as he had hoped and for good reason. The biggest complaint lodged against this method of stretching was the unacceptably high risk of injury. Unfortunately, the intensity of stretching required to permanently expand the fascia often proved too much for the muscles to handle, occasionally leading to pulled and sometimes even torn muscles. With such reports becoming more frequent, it didn’t take too long for this practice to be abandoned by most.


With Synthol, the principle is the same, although the manner in which results are obtained is quite different. In order to adequately explain the difference between these two types of stretching, mentally picture the fascia as a balloon. There are two ways we can stretch a balloon. We can either pull and tug at the corners, which will change its dimensions at the point of tension…or we can simply blow it up, which will cause the entire surface area of the balloon to expand. We can achieve a much greater degree of expansion by blowing up the balloon, rather than with manual stretching. It is the same with Synthol use. However, unlike a balloon, which reverts back to its original size as soon as the pressure is removed, the muscle fascia permanently stretches to accommodate the increased internal pressure. Although the oil used to suspend esterfied steroids clears more quickly than the oil used in Synthol (1-3 weeks compared to 3 months), this same effect can be duplicated to a lesser degree with longer-estered gear.


Another, although less frequently mentioned mechanism, which may be partially responsible for the muscle growth which occurs with AAS site injections, is inflammation. Inflammation can be stimulated by a variety of events, including burns, infections, or injuries, which can include or be caused by muscle tears, intramuscular injections, or even training. Therefore, when performing site injections, the trauma of the injection itself, as well as irritants in the oil (which can vary in both type of quantity) signal local cells to initiate the inflammatory response. Once activated, the cells release a variety of inflammatory mediators responsible for a cascade of complex biochemical events. Although the inflammatory process associated with training is well known to play an essential role in the muscle growth process, some of the general responses associated with the 5 cardinal signs of inflammation, such as increased blood flow via increased nitric oxide, increased blood vessel permeability, etc, may also enhance growth process.


This is purely speculation, but after repeatedly witnessing local growth take place with the prolonged administration of esterfied steroids, even when the amount of oil utilized was not sufficient to stretch the fascia, one must wonder just where the growth is coming from. Could it be that repeated bouts of injection–induced inflammation, which results in chronic muscle swelling, is in itself enough to mildly stretch the fascia and initiate growth? This may be the case, as even small oil volumes have been known to cause long-term growth when inflammation is present, but when inflammation is absent, as can occur with some non-irritating oils, growth does not take place.


There have been quite a few BB’rs who have had varying degrees of success using esterfied steroids for site enhancement, although the most extreme results do involve injecting large volumes of oil with longer-estered gear. The slower clearance rate of the longer-esters allows for a larger build-up of oil in the muscle and greater stretching of the fascia. When compounded with moderate inflammation, growth seems to be even more pronounced.


So, where does this leave us with non-esterfied AAS? Unlike esterfied gear, non-esterfied steroids clear the injection site quickly, being fully metabolized within roughly 24-48 hours. This significantly reduces the amount of oil build-up, making it unlikely for fascia stretching to occur through this mechanism. However, the absence of an ester allows the steroid to freely attach to the AR at the site of injection, potentially causing a greater growth response through increased availability. While any additional benefit obtained is probably minor, even small differences, over time, can translate into visually noticeable improvements in muscle size.


As with many things in bodybuilding, things are not always as they appear. While esterfied AAS have often been labeled as worthless among the inexperienced, those who have used them to generate substantial and long-standing gains in muscle size know better. Unfortunately, one can’t use minimal quantities of injectables AAS and expect to experience dramatic improvements in local growth. If we accept the fascial stretching theory as valid (this theory has not yet been validated in the medical community or in any respected clinical setting), we can logically conclude that small amounts of oil simply won’t elicit a great enough stretch on the muscle fascia to cause substantial growth.


With esterfied and non-esterfied AAS working through two completely separate pathways, the combination of the 2 tends to produce the greatest gains in muscle size. For those individuals seeking maximum growth, a combination of Synthol and non-esterfied AAS, such as trenbolone and testosterone base, can prove even more effective. Remember, using Synthol is no different than using esterfied AAS to increase muscle size, with the only difference being that Synthol contains a longer lasting oil and is normally injected in large quantities; a practice I am often in disagreement with. The morons we see on YouTube with grossly deformed, oil-logged arms do not represent the typical, intelligent user. Ridiculous amounts of oil, along with improper application technique, are the primary reasons for their grotesque appearance. As long as Synthol is used properly (which in my opinion means using a low-moderate amount of oil and a specific method of application) it will allow the BB’r to maintain the natural contours of his muscles, while enhancing roundness and overall size without negatively affecting muscular detail. In other words, all you will see is tremendous arm development, with no outward signs of its use being apparent.


My opinion has changed drastically over the last few years in regards to Synthol. As with anything, abuse garners poor results, but when used as a means to balance the physique, it has its place. Of course, one should first attempt to build their weak points without the use of Synthol, but this is not always possible and that is where Synthol comes in.
 
deesterification does not happen primarily in the liver. It happens at the interface betweeen the cell membrane and the extrecellular milliue. The esterified steroid molecule is too hydrophobic to move to the blood, stay there long enough to reach the liver, and undergo the reaction. It will quickly pass into the nearest cell membrane where the lipid environment more accomodating and the passage is much more energetically favorable.
 
deesterification does not happen primarily in the liver. It happens at the interface betweeen the cell membrane and the extrecellular milliue. The esterified steroid molecule is too hydrophobic to move to the blood, stay there long enough to reach the liver, and undergo the reaction. It will quickly pass into the nearest cell membrane where the lipid environment more accomodating and the passage is much more energetically favorable.

where's this info coming from?
not doubting you, just doesnt sound physiologically correct,

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i guess i am doubting you
 
Great post. I guess I should have stayed in chem class. By the way Ray you should have been a comedian. You could have made a fortune bro.
 
I am a Ph. D. biochemist. It is correct but you can believe what you wish.

he didn't question your credentials bro, he simply asked where that info came from, proof, back up, something to chew on so to speak, another words , read?
 
he didn't question your credentials bro, he simply asked where that info came from, proof, back up, something to chew on so to speak, another words , read?

Ok maybe my answer was a little glib. This is something that comes to me from basic principles and reading over the years. Lipids and other hydrophobic compounds will partition into hydrophobic environments much more effectively than into hydrophilic environments. This is a concept used widely throughout chemistry/biochemistry and in nature. A steroid ester is composed of a steroid molecule which in itself is amphiphatic meaning it has polar and non-polar groups. In cell biology and biochemistry at college level you will learn that amhiphatics like phospholipids and steroid molecules like cholesterol form the cell membrane. Amphiphatic lipids form bilayers where other lipids and amphiphatics can cross. When an ester is made from an aliphatic acid and a steroid molecule the steroid ester is very similar in charachter to a phospholipid, it has a hydrophobic end. and a hydrophilic end. This characteristic is imparted to allow a depot to form at the injection site. The depot slowly disipates from the injection site according to a characteristic partitioning coefficient, which can be calculated. Physically, the partitioning is the movement into and out of the extracellularmatrix (ECM) and plasma. The equilibrium strongly favors the resident time of the steroid ester in the more hydrophobic environment of the lipid bilayer, the cell membrane. When the steroid ester is resident in the ECM/plasma it can be hydrolyzed into the aliphatic acid and steroid base by plasma esterase. Once hydrolyzed the steroid can join with steroid binding blobulins and enter a different partitioning environment from the globulin to the tissues as it is carried in the blood. This is essentially how it works. The dissipation time of the steroid ester out of the depot is governed by the length of the aliphatic chain moiety, The longer the chain the less time it spends in the ECM/plasma and more time it spends in the cell membrane and the longer it takes for the depot to be fully exhausted. An example is to compare testosterone propionate (short aliphatic chain) and testosterone enanthate (longer aliphatic chain). The propionate ester disipates at a much faster rate than the enanthate ester.
 
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