Here is a bunch of info from a person called datbtrue - he knows a lot about peptides. The short of it is that you should do multiple pins of small doses into the muscle you want to receive the largest effect of the IGF. You should do this well after you are done exercising if you want the most gain. The best time would be to only pin on your off days, but if you take no off days, then pin at the opposite time of your workout. If you work out in the morning, pin just before bed. If you work out in the evening, pin first thing in the morning. I am not sure about dosing, though.
Here is all the info that explains WHY to do this:
Attempts to Localize IGF-1 in Muscle
The ternary complex is composed of IGF-I or IGF-II, IGF-binding protein-3, and the acid-labile subunit. IGF-1 alone or unlike binary complexes of IGFBP-3 and IGF-I can leave/or go into the circulation across the endothelium (surface of blood vessels) because they are small enough.
However ternary complexes because of their size are restricted to the circulation. They act as a relatively stable reservoir of circulating IGFs. Under certain circumstances IGFs are liberated from the ternary complex to exert their biological actions in tissues.
BUT if you remember I wanted to administer the premade ternary complex into muscle tissue. There it would not be trapped in circulation but trapped locally in muscle tissue. Now IGF-1 has a stronger attraction (affinity) for its receptor. If it is hanging around via the ternary complex i will disassociate and bind to a receptor when one is available.
If you recall we talked about how a drug company makes the ternary complex and how it is more effect for certain illnesses then exogenous IGF-1.
The problem is I could not get anyone to make and offer it. I even went so far as say make the IGF-1 bound to the binding protein and the GHRPs via GH will make plenty of acid-labile subunit which will bind immediately on injection.
But it never happened.
Second Best
So IGF-1 LR3 is a modification of native IGF-1. When you make the modification it loses most of its attraction to the binding proteins but it also has a reduced attraction to its own receptor. Think "weaker magnet".
We also know that upon injection it will circulated systemically. This means it won't stay local and what it will do is float around and bind where there are the highest concentration of receptors. This is the intestines.
If you recall this was a very good thing for me. It saved my life. A lot of the IGF-1 LR3 that I administered many years ago bound to receptors in my intestines and regrew the lining and greatly repaired it ability to absorb. That was great for me but not so great if you want it to be taken up in muscle. I healed but the IGF-1 LR3 had no effect on increasing my muscle weight or mass.
So if people are administering IGF-1 LR3 it will circulate and bind everywhere but the concentration won't be high when some of it is taken up in muscle.
How Much IGF-1 is needed?
IGF-1 is made in the liver and circulates and it is made in local tissue. From the liver the amount is larger and measurable. From the muscle (or local tissue such as brain & bone) the amount that is made is super-tiny. It is not measurable w/o an expensive experiment. But that little bit is very powerful. Experiments have demonstrated that mice can grow to full length w/ that tiny local made IGF-1 in muscle and bone, but if that is shutoff the liver-made circulating IGF-1 is never enough to make them grow to full size.
So the trick is to either increase local expression of IGF-1 in muscle. That is done w/ the GHRHs and GHRPs and GH and testosterone ...but ironically IGF-1 LR3 given at the wrong time hinders this local expression.
Now if you want to use IGF-1 exogenously you need to try to make it stay local and you don't need a lot. But you want wider coverage because you are doing all of this from outside looking in.
Micro-dosing IGF-1
So this protocol is an attempt to do what was originally hoped for... that is to make some of the IGF-1 bind to available receptors locally BEFORE traveling into the blood stream. Anything more then a small amount is a waste because only the cells it will come in contact w/ and neighboring cells who can "pass on" the IGF-1 will be effected. The method requires you the administrator to seed a wider area w/ tiny amounts of IGF-1 LR3 which will have the result of more cells positively benefiting.
The reason this is done twice a day is to hit more cells. It may seem like a lot of work but people who have used this approach to heal a local injury have found it effective.
When to Inject
Post Work Out was the wrong time to take IGF-1. The reason is simple. Resistance exercise is THE event that causes the body to make MGF. That is all that is meant when you see the language "MGF is a splice variant of IGF... there is a frame shift in the gene transcription...)
Inside a muscle cell after resistance exercise the body makes a variation of IGF-1 and does not make IGF-1. The variant it makes is called MGF. MGF stays in the cell and moves to the nucleus where it acts to proliferate.
IGF-1 is usually a differentiator. This means it takes all those proliferated "cells" and defines them. Tells them go be a "muscle cell". However IF MGF is busy proliferating and IGF-1 is introduced, MGF stops and IGF-1 then defines those newly created cells... but the creation has stopped. Specific evidence for this behavior is IGF-1 doing that to Fibroblast Growth Factors proliferating action.
So post-exercise, why do you want to stop your native MGF from proliferating? Let it work! Support it by using GH or GHRH/GHRPs or testosterone. If you are an older bodybuilder THIS is where you have a muscle building failure naturally. Aging people have a harder time engaging MGF after exercise. Thats why the GH, GHRH/GHRPs and testosterone have genuine value to them.
So post exercise MGF is proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> proliferating-> THEN you introduce IGF-1 which will define the newly proliferated "cells".
The PWO protocol which everyone seems to do(i.e. the Grunt protocol or even the Lakemount protocol) results in MGF breifly proliferating-> THEN IGF-1 stops it and defines those few new cells. A better way to use IGF-1 would be away from the end of the exercise event.
Testosterone blunts IGF-1 inhibition of GH. Here is a graph that demonstrates this from Testosterone Supplementation in Older Men Restrains Insulin-Like Growth Factor***8217;s Dose-Dependent Feedback Inhibition of Pulsatile Growth Hormone Secretion, Johannes D. Veldhuis, Daniel M. Keenan, Joy N. Bailey, Adenborduin Adeniji, John M. Miles, Remberto Paulo, Mihaela Cosma and Cacia Soares-Welch,The Journal of Clinical Endocrinology & Metabolism Vol. 94, No. 1 246-254, 2009
