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Best efficient way to induce hyperplasia???

Ramacher, that's not an article, you've given a thread to another BB'ing board, just like this board discussing the same topic.

While "Pinnicle" shows you his big legs claiming one thing, I'll show you scientific studies proving another. :cool:

There is someone in that thread questionig if the legs are even his....regardless he offers nothing by opinion and when he talks about studies he posts none....likes to chang the subject...seems like an Internet bs artist to me
 
I'm no expert when it comes to science, but isn't the whole point of modifying the IGF chain (replacing glut with arg at position 3 yada yada yada) simply to make it more active in the body? Or is this changing how the IGF molecule actually acts when it binds to a receptor? Because in that thread mr. pinnacle actively acknowledges that IGF causes muscle growth, yet says the LR3 version does not. :confused:
 
Because in that thread mr. pinnacle actively acknowledges that IGF causes muscle growth, yet says the LR3 version does not. :confused:

Yes, Mr. Pinnicle has ran his own tests on himself and claims the LR3 version doesn't work. Besides a grade/receptor type (supposed to change effectiveness slightly), it's basically the half life between the two. The LR3 remains active for days, whereas the reg. is gone in minutes.

Other than that, in LR3, there's one substitution and one extention. Specifically, LR3 (Long Recumbent 3), substitutes the Arg for the Glu in position 3 (thus the R3), and adds a 13 amino acid extension (peptide) at the N-terminus (thus the Long).
 
I'm no expert when it comes to science, but isn't the whole point of modifying the IGF chain (replacing glut with arg at position 3 yada yada yada) simply to make it more active in the body? Or is this changing how the IGF molecule actually acts when it binds to a receptor? Because in that thread mr. pinnacle actively acknowledges that IGF causes muscle growth, yet says the LR3 version does not. :confused:

Good point! How is this possible? If it stays in system longer, how could it NOT build muscle as well?



PO
 
Good point! How is this possible? If it stays in system longer, how could it NOT build muscle as well?



PO

It has its drawbacks..Most of the lr3 we pin goes sytemic immediatley as the peptide is too small to remain local...hence the hypothesis that it would be more effective microdosing in multiple areas over the entire muscle(s). Not to mention that the majority of IGF receptors in the body are present in the intestines. Abuse of GH or IGF leads to what we know as "GH Gut", because of the hyperplasia/hypertrophy in the smooth muscle of the intestines....
The goal with Igf is to train as hard as possible to create as much "tears" as possible, so that the muscles worked "call out" for the IGF to assist in healing....there will be more receptors in the area available in that scenario...
 
GH does amazing things in the long term if your getting brand name gh at least all the ramazing esults that I can speak of are from brand gh.
 
It has its drawbacks..Most of the lr3 we pin goes sytemic immediatley as the peptide is too small to remain local...hence the hypothesis that it would be more effective microdosing in multiple areas over the entire muscle(s). Not to mention that the majority of IGF receptors in the body are present in the intestines. Abuse of GH or IGF leads to what we know as "GH Gut", because of the hyperplasia/hypertrophy in the smooth muscle of the intestines....
The goal with Igf is to train as hard as possible to create as much "tears" as possible, so that the muscles worked "call out" for the IGF to assist in healing....there will be more receptors in the area available in that scenario...


Ah, gottcha! Makes sense!



PO
 
Good point! How is this possible? If it stays in system longer, how could it NOT build muscle as well?



PO

IGF-1 LR3 has a shorter life then IGF-1 bound to one of the IGF Binding proteins or better yet the terniary complex.

It has a longer half-life then native IGF-1 but most of the time IGF-1 finds itself bound to a Binding Protein.

Just to be accurate.

In addition the binding affinity and binding strength of the IGF-1 analogs to its receptor are lower then IGF-1.

None of that speaks to what the thread is about... just trying to be accurate.
 
IGF-1 LR3 has a shorter life then IGF-1 bound to one of the IGF Binding proteins or better yet the terniary complex.

It has a longer half-life then native IGF-1 but most of the time IGF-1 finds itself bound to a Binding Protein.

Just to be accurate.

In addition the binding affinity and binding strength of the IGF-1 analogs to its receptor are lower then IGF-1.

None of that speaks to what the thread is about... just trying to be accurate.

Could it be?? Could it be?? DAT!!!! Yes! It is!!! Welcome back buddy :)
 

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