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Des (1-3) Igf-1

Alright- I kinda inferred the answer to my question, in a way.

LR3 half life is SHORTER then igf-1 simply because none of it gets bound or absorbed. It circulates until it activates. compared to igf-1 which...will activate JUST as fast, but some will be bound.

assuming = doses of each,
you will activate more receptors with LR3 simply because binding proteins don't interfere, using = doses

That being said; compared to LR3, the des variant would simply have a stronger binding affinity (If I remember correctly, this is the case)????

So the only limiting factor here is the response the body can produce in response to site activation? (but I thought it was a off or on switch, not a "dimming" light with different degrees of activation)

I'm just thinking through things here- would almost seem to me that if there is only one degree of activation on our body, it simply becomes a matter of activating X number of sites, which would make the des version just a more expensive option, and no better...

Thoughts?
 
xtraflossy said:
Alright- I kinda inferred the answer to my question, in a way.

LR3 half life is SHORTER then igf-1 simply because none of it gets bound or absorbed. It circulates until it activates. compared to igf-1 which...will activate JUST as fast, but some will be bound.

assuming = doses of each,
you will activate more receptors with LR3 simply because binding proteins don't interfere, using = doses

That being said; compared to LR3, the des variant would simply have a stronger binding affinity (If I remember correctly, this is the case)????

So the only limiting factor here is the response the body can produce in response to site activation? (but I thought it was a off or on switch, not a "dimming" light with different degrees of activation)

I'm just thinking through things here- would almost seem to me that if there is only one degree of activation on our body, it simply becomes a matter of activating X number of sites, which would make the des version just a more expensive option, and no better...

Thoughts?
Click to expand...

Ah well this is where things get very complicated.

hIGF-1 will not activate "as fast" as LR3 because it is bound to, say, IGFBP3, which "stores" IGF-1 until receptors are "hungry enough" to warrant freeing the IGF-1 molecule from the IGFBP and then activating the receptor. When is "hungry enough"? That is the all-important question. Whereas LR3 will activate no matter if the receptor is all alone on the cell surface or part of a just-worked muscle, very hungry for it.

That's why we inject the LR3 directly in the muscle just worked, the receptors are mightily upregulated, and you just hope that more of your LR3 goes to this specific muscle than other places. Which it would anyway if you went IV with it, since that muscle temporarily has a lot more receptors, comparatively. Still, putting it IN THERE simply CANNOT HURT. How much benefit is obtained by doing this? It cannot be easily quantified, but "some" would be appropriate.

When you state equal doses, do you mean in terms of molecule numbers or by weight? LR3 is heavier than hIGF-1, meaning fewer molecules. LR3 is known to be about 10x more potent than hIGF-1 at activating receptors, SPECIFICALLY BECAUSE the binding proteins need "hungry enough" receptors.

The body offers a number of responses to the various forms of IGF-1 activating surface receptors. On a myotube, shuttling of aminos and carbs seems to be the main effect. On a myoblast, differentiation and fusion, thus increasing the neighboring myotube's myonuclear number, is another effect. If a sufficient concentration of myoblasts exists and a sufficient number of them get to the "fusion" part at a close enough time, a new myobtube is formed, and that is possibly the holy grail of bodybuilding: a new muscle cell. But no matter if you think of it as an on/off switch or different degrees of activation on a cell basis, on an organ basis, it is very much a dark/bright continuous spectrum.

Now does LR3 exert every single one of the actions of hIGF-1 with equal efficacy? Unknown. Whereas DES IGF-1 is naturally-occuring, making it a potentially better option.

It's up in the air, really, and only people who have experience using LR3 and then DES will be able to testify. As you know, there is no human research on LR3 (except by us) and the same is true of DES.
 
Grunt76 said:
Ah well this is where things get very complicated.

hIGF-1 will not activate "as fast" as LR3 because it is bound to, say, IGFBP3, which "stores" IGF-1 until receptors are "hungry enough" to warrant freeing the IGF-1 molecule from the IGFBP and then activating the receptor. When is "hungry enough"? That is the all-important question. Whereas LR3 will activate no matter if the receptor is all alone on the cell surface or part of a just-worked muscle, very hungry for it.

That's why we inject the LR3 directly in the muscle just worked, the receptors are mightily upregulated, and you just hope that more of your LR3 goes to this specific muscle than other places. Which it would anyway if you went IV with it, since that muscle temporarily has a lot more receptors, comparatively. Still, putting it IN THERE simply CANNOT HURT. How much benefit is obtained by doing this? It cannot be easily quantified, but "some" would be appropriate.

When you state equal doses, do you mean in terms of molecule numbers or by weight? LR3 is heavier than hIGF-1, meaning fewer molecules. LR3 is known to be about 10x more potent than hIGF-1 at activating receptors, SPECIFICALLY BECAUSE the binding proteins need "hungry enough" receptors.

The body offers a number of responses to the various forms of IGF-1 activating surface receptors. On a myotube, shuttling of aminos and carbs seems to be the main effect. On a myoblast, differentiation and fusion, thus increasing the neighboring myotube's myonuclear number, is another effect. If a sufficient concentration of myoblasts exists and a sufficient number of them get to the "fusion" part at a close enough time, a new myobtube is formed, and that is possibly the holy grail of bodybuilding: a new muscle cell. But no matter if you think of it as an on/off switch or different degrees of activation on a cell basis, on an organ basis, it is very much a dark/bright continuous spectrum.

Now does LR3 exert every single one of the actions of hIGF-1 with equal efficacy? Unknown. Whereas DES IGF-1 is naturally-occuring, making it a potentially better option.

It's up in the air, really, and only people who have experience using LR3 and then DES will be able to testify. As you know, there is no human research on LR3 (except by us) and the same is true of DES.
Click to expand...


So it would seem binding affinity has no correlation then- which would imply that the receptor is either activated or it is not.

Wouldn't that imply that it wouldn't matter weather our recepters were activated by a hit from LR3 or des- the effect would be the same?
(which would mean spending more on the des would offer no benefit over LR3)

I beleive (and this isn't something new I thought of, but more a general statement) would be that the holy grail would be understanding by which mechanics the myoblast reaches or decides to fuse to a new cell over another action.


I would look into research done on bacteria and the chemical messages they give off to identify themselves to other same bacteria- (I've seen something on this recently-I think it was a simple amino acid) and the messages other bacterium give off to "intercept" this signal".. and since bacteria act simular in function to the body (single cells acting in concert..) ...I just think the operating level is simular between single cells and sourouning cells..
lol- I'm going off the deep end here most likely:rofl:
 
Bumpity
 
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