Site enhancement theory...
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bold for the short answer part of this.
Unedited and again, like Plang mentioned, just theory. But, let me know your thoughts on it.
I've mentioned this somewhat before. But, the more I think about it and it sinks in, the more I believe it makes sense. It's clear that mgf is most effective when produced within the muscle cells themselves- it's the only place mgf can "act as" mgf and do it's thing! Mgf is produced during a workout- especially when concentrating on the eccentric portion of the movement. This is one of the ways we grow and recover from training. It's basically a response to micro-trauma within the muscle.
As bodybuilders, we tend to think that everything has to be injected to be most effective. But, how much mgf is getting "inside" the actual muscle cells to be effective when site-injected? At best, I imagine a minimal amount is going to work as needed. The rest is hanging around systemically. He who was recently banned speculated that proliferation could be triggered by injecting peg-mgf into the muscle worked directly after a workout and that it would last as long as the peg-mgf was in your system. Really? Because only a small amount is getting into the muscle (in the form of "bleed through") and that, once used for proliferation, isn't likely to continue to work indefinitely. What
is long lasting in that scenario is the "rest" of the peg-mgf which is floating around systemically.
My point to the prior paragraph is that there is only "so much" we can do to induce proliferation (activation of satellite cells) via injection with mgf or peg-mgf and that having a longer-acting mgf like peg-mgf will not necessarilly lead to greater results in this area. All the successful studies on mgf were done with viral techniques where the muscles were programmed (by introduction of a virus) to produce mgf. This is where we see the 20% muscle weight gains etc. not by injection. Unfortunately, we gym rats don't have access (that I know of) to that kind of technology!
But, there are alternatives. Years back Pat Arnold talked about an alternative site-enhancement technique using a solution containing lambda carrageenan- a seaweed extract usually injected into meat products to provide a thicker, heavier product. Basically scientists injected a solution of various % of lambda carrageenan in a controlled way to produce specific muscle damage in leg muscles and tendons in mice. At some percentages the muscle damage was too great, at others it didn't produce a noticeable effect. But, at certain percentages the right amount of muscle damage was caused triggering a steady release of mgf in an effort to repair the damage.
I was able to get ahold of some lambda carrageenan powder and I did my own little experiment. To be honest, so many injections were needed and such a high volume of product that I got tired of messing with it before I saw any real measurable results. But, years later when I gave syntherol a try, the constant dull-ache from the injections reminded my of my brief experiment with the carrageenan. See, there's nothing inherent in carrageenan that causes mgf expression. It's just an irritant- but, a controllable one. You can obviously get the same kind of inflamation from a shot of test prop or some other injectable like syntherol.
What stands out to me about the scientific study on mice is that even the lower doses of carrageenan had some effect and elicited some mgf expression, but it wasn't enough to have substantial results. That tells me that mgf expression is somewhat determined by the amount of irritation caused. As long as there isn't too much to "come back from" where the muscle is seriously compromised, there should be mgf expression. It's my theory that this is a
part of what makes syntherol site-enhancement effective. The other parts are increased blood flow/nutrient uptake and stretching of the muscle fascia.
With everyone looking for the longest acting igf-1 drug available it appears the thinking is "whatever lasts the longest is most effective!" But, that's not true in this case. While drugs like peg-mgf and igf1-lr3 will give you the best insulin like effects (when compared to their shorter-acting counterparts) we don't necessarily want to affect our system for long periods of time with igf-1! For one thing it's dangerous. Many of the receptors are in the intestines and vital organs. If there is a cancer or growth present, said igf-1 will cause that to grow at an increased rate. Plus, as it concerns site-enhancement/hyperplasia, igf-1's job is to cause "differentiation"- the part of the process that tells newly activated satellite cells to become muscle! If an igf-1 is constantly present in the system, then the actual activation of those satellite cells is inhibited!
What we want is to do is 1) Induce proliferation (activation) of satellite cells and keep that going as long and as often as possible. 2) Induce differentiation to help form new muscle tissue briefly but often.
My basic theory is to add a schedule of using DES (1-3) igf-1 to a "normal" syntherol protocol. Using the syntherol, in conjunction with hard training and a good anabolic environment, will (in theory) cause mgf to be produced within the temporarily damaged muscle. 1/2 hr to 1 hr after said muscle is trained, a dose of DES (1-3) Igf-1 is injected into the specific muscle to induce differentiation. With the DES being out of your system within a half hour or so, this should allow the muscle to go back to producing more mgf and inducing more proliferation/activation of more satellite cells.
So, let's say you are injecting your bis and tris with syntherol. They are sore and swollen, but you are still doing your regular training. You can hit each on arm day, bis on back day, and tris on chest/shoulder day etc. However you work it, I think the theory makes some sense. Let me know what you think.