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My take on IGF-1

Too bad for you really. Damn governments and their meddling.

There are SO MANY things that are great ideas, heck, I have like 28 of them right here for kick-ass products, but obtaining the raws and then having no lab keeps them all at the "idea" level... :(

Good luck with stuff.


well i am lucky in that i have a lab and i am able to synthesize bench scale quantities of alot of products i am interested in (if they are not already available commercially)

so i have several product ideas whose manufacture i have already worked out but either they are not quite economical or i don't want to release them without the necessary marketing capital to back them up
 
Too bad for you really. Damn governments and their meddling.

There are SO MANY things that are great ideas, heck, I have like 28 of them right here for kick-ass products, but obtaining the raws and then having no lab keeps them all at the "idea" level... :(

.


FYI we are equipped to do custom synthesis for products. but they really have to be DSHEA compliant or at least on the whiter side of grey for us to be interested
 
stimulation of cancer growth is something that is a concern with R3 possibly. in the latest muscular development i do a review of GH, IGF-1, and cancer. you will see there is some rationale to my concerns

definitely i am into bodybuilding. i don't wanna say whether i have tried LongR3 or not. Lets just say that i think it has promise for connective tissue rehabilitation

Yes there is a lot of speculation on such, but no supporting data.

All cells have the potential to grow out of control. Organisms have evolved limits on such activity a several levels and hormones are used to try to control things. Cancers have freed themselves of these built in limits and are, at least in fast growing cancers, not going to respond to GH or IGF-1 as they are already at full throttle already.
 
The following post I put up on another thread with few changes but Grunt wanted to get your take on it.

I plan to use igf-1lr 3 as a long term anti aging drug instead of hgh which could get you busted like Stallone. The plan is 30mcg every other day for 8 weeks on 2 weeks off indefinetly. I'm going for duplication of using 2 IUs of GH 5 days on 2 off.

Not really going for local muscle gains so I want to inject sub-q in the belly fat b/c it's much easier. Would this regimen lead to organ intestinal or jawbone growth down the line? Would 10 or 20 mcg be a safer longterm dose?

Want to clarify also how to compare IUs for GH to mcg for igf-1lr3. Anthony Roberts says 120 mcg igf-1lr3 are the same as 3-4 IUs GH but some people on this forum say 10 mcg igf equals to 1 IU gh.

Would appreciate your opinion on this stuff. Thanks.
 
The following post I put up on another thread with few changes but Grunt wanted to get your take on it.

I plan to use igf-1lr 3 as a long term anti aging drug instead of hgh which could get you busted like Stallone. The plan is 30mcg every other day for 8 weeks on 2 weeks off indefinetly. I'm going for duplication of using 2 IUs of GH 5 days on 2 off.

Not really going for local muscle gains so I want to inject sub-q in the belly fat b/c it's much easier. Would this regimen lead to organ intestinal or jawbone growth down the line? Would 10 or 20 mcg be a safer longterm dose?

Want to clarify also how to compare IUs for GH to mcg for igf-1lr3. Anthony Roberts says 120 mcg igf-1lr3 are the same as 3-4 IUs GH but some people on this forum say 10 mcg igf equals to 1 IU gh.

Would appreciate your opinion on this stuff. Thanks.



longR3 is certainly no replacement for GH therapy. I would avoid it for long term use due to its physiologically unnatural pharmacodynamic characteristics. straight old IGF-1 might be preferable but even that is no true replacement.

the GH secretagogue peptides and the GHRH analogs would be the way to go if you wanna have your GH and stay above the law
 
longR3 is certainly no replacement for GH therapy. I would avoid it for long term use due to its physiologically unnatural pharmacodynamic characteristics. straight old IGF-1 might be preferable but even that is no true replacement.

the GH secretagogue peptides and the GHRH analogs would be the way to go if you wanna have your GH and stay above the law

Good info PA....
 
longR3 is certainly no replacement for GH therapy. I would avoid it for long term use due to its physiologically unnatural pharmacodynamic characteristics. straight old IGF-1 might be preferable but even that is no true replacement.

the GH secretagogue peptides and the GHRH analogs would be the way to go if you wanna have your GH and stay above the law

You cannot find IGF-1, all that is available is Lr3 IGF-1.

"physiologically unnatural pharmacodynamic characteristics" exist because the product was developed to have a greater active half life in serum than [natural] IGF-1. I don't see where these different characteristics are a negative issue.

"the GH secretagogue peptides and the GHRH analogs" all seen to have a limited length of effective use, so these are not any good for long term use.

"GHRH analogs" have "physiologically unnatural pharmacodynamic characteristics"?

Are you also telling body builders that Lr3 IGF-1 should be avoided?
 
You cannot find IGF-1, all that is available is Lr3 IGF-1.

"physiologically unnatural pharmacodynamic characteristics" exist because the product was developed to have a greater active half life in serum than [natural] IGF-1. I don't see where these different characteristics are a negative issue.

"the GH secretagogue peptides and the GHRH analogs" all seen to have a limited length of effective use, so these are not any good for long term use.

"GHRH analogs" have "physiologically unnatural pharmacodynamic characteristics"?

Are you also telling body builders that Lr3 IGF-1 should be avoided?

first of all, longR3 was not developed to have a longer half life in the body, in fact it has a shorter half life in the body than IGF-1. longR3 was developed for in-vitro use to study the effects of IGF-1 on cell cultures without the interference of binding proteins

It is very important to remember that IGF-1 binding proteins serve important functions. IGF-1BP3 for instance protects IGF-1 from degradation (greatly extending its half-life) and delivers it to specific tissues in a regulated fashion. An IGF-1 that does not bind to binding proteins (LongR3) will run amok in the body, stimulating tissues in a potentially haphazard fashion.

I wrote an article on this and it was published in muscular development. The science of IGF-1 is very complicated and alot of its association with cancer is closely tied to its relationship with binding proteins.

I think longR3 in the short term might have benefits (healing of connective tissue in particular) but for long term use you are really rolling the dice. This is a potent growth factor that can do as much bad is it can do if things don't go right

GH releasers are much farther upstream in the whole GH/IGF-1 cascade from IGF-1 and the farther upstream you provide the artificial influence the more naturally balanced the end outcome will be.

a combination of a GHRP and a GHRH analog can actually provide a stimulation of GH release that is as good as you can get with GH itself, perhaps better. At least the literature indicates this.

I don't know of anything in the literature indicating that these GH releasing drugs have diminishing effects over time.
 
first of all, longR3 was not developed to have a longer half life in the body, in fact it has a shorter half life in the body than IGF-1. longR3 was developed for in-vitro use to study the effects of IGF-1 on cell cultures without the interference of binding proteins

It is very important to remember that IGF-1 binding proteins serve important functions. IGF-1BP3 for instance protects IGF-1 from degradation (greatly extending its half-life) and delivers it to specific tissues in a regulated fashion. An IGF-1 that does not bind to binding proteins (LongR3) will run amok in the body, stimulating tissues in a potentially haphazard fashion.

I wrote an article on this and it was published in muscular development. The science of IGF-1 is very complicated and alot f its association with cancer is closely tied to its relationship with binding proteins.

I think longR3 in the short term might have benefits (healing of connective tissue in particular) but for long term use you are really rolling the dice. This is a potent growth factor that can do as much bad is it can do if things don't go right

GH releasers are much farther upstream in the whole GH/IGF-1 cascade from IGF-1 and the farther upstream you provide the artificial influence the more naturally balanced the end outcome will be.

a combination of a GHRP and a GHRH analog can actually provide a stimulation of GH release that is as good as you can get with GH itself, perhaps better. At least the literature indicates this.

I don't know of anything in the literature indicating that these GH releasing drugs have diminishing effects over time.

:goodpost:
 
first of all, longR3 was not developed to have a longer half life in the body, in fact it has a shorter half life in the body than IGF-1. longR3 was developed for in-vitro use to study the effects of IGF-1 on cell cultures without the interference of binding proteins

It is very important to remember that IGF-1 binding proteins serve important functions. IGF-1BP3 for instance protects IGF-1 from degradation (greatly extending its half-life) and delivers it to specific tissues in a regulated fashion. An IGF-1 that does not bind to binding proteins (LongR3) will run amok in the body, stimulating tissues in a potentially haphazard fashion.

I wrote an article on this and it was published in musculardevelopment. The science of IGF-1 is very complicated and alot of its association with cancer is closely tied to its relationship with binding proteins.

I think longR3 in the short term might have benefits (healing of connective tissue in particular) but for long term use you are really rolling the dice. This is a potent growth factor that can do as much bad is it can do if things don't go right

GH releasers are much farther upstream in the whole GH/IGF-1 cascade from IGF-1 and the farther upstream you provide the artificial influence the more naturally balanced the end outcome will be.

a combination of a GHRP and a GHRH analog can actually provide a stimulation of GH release that is as good as you can get with GH itself, perhaps better. At least the literature indicates this.

I don't know of anything in the literature indicating that these GH releasing drugs have diminishing effects over time.

Anthony Roberts wrote: "Unlike GH, however, some attenuation to Hexarelin occurs by week 4, and continues on up to 16 weeks of use. By separating Hexarelin cycles by 4 week off periods, this attenuation can be totally reset, (9) and the next cycle of Hexarelin will produce the same level of results as the first cycle." from:Invalid Link Removed

It does not mater what the intent was when first creating a drug. Guys take AIs, SERMs and HCG which were not created as products for guys.

Binding proteins extend the serum half life, but probably do not increase the receptor delivery. Lr3 will find more receptors. If too many receptors are affected, change the dose. Actually, a short half life in serum can be a non-issue if the drug has docked in receptors... then the cellular activity will take place.

Long term use will shut down ones own GH&IGF-1 production, but GH replacement would do the same. If one really needs GH replacement, use of lr3-IGF-1 might be a reasonable affordable alternative. 10mcg is thought to be as effective as 1 iu of HG.

I don't know what delivery to the cells in a regulated fashion means. Receptors are binary, either activated or not. Once a receptor is activated, the drug cannot dock there twice. The receptors will be re-expressed later.

Do you see that long term use of lr3 IGF-1 would present more issues than GH replacement if comparing doses that have the same IGF-1 receptor activation effects [assuming that one knew the dosage equivalents]?

With those seeking a cost effective alternative to GH, stimulation of the pituitary to release more HG might not be viable for those who have pituitary glands that are aged or damaged.

Growth Hormone Releasing Peptide- 6 (GHRP-6) can cause intense hunger, and resultant weight gain. Many wanting GH replacement or an alternative are wanting to loose weight, not gain. It can also drive down blood sugars, a dangerous mix for a diabetic.

I tried 1000mcg; 50 days of lr3 IGF-1 40mcg EOD (thought to be equal to 2iu of HG per day). I felt better, but the effects were not huge, subtle would be a good description. I felt a bit tired afterwards in comparison. Some of that would be suppression of endogenous GH release which would be time limited. If I do this again, I might feel "that's what I felt like before". But such judgements can be difficult and sometimes things are never clear cut. I have no GH experience to compare to. I have been trying to learn about these things. It is easy to think that these things are all new, but they are all in "Growing Young with HGH", Klatz 1997. But that book does not get into details or usage for these alternatives.
 
longR3 is certainly no replacement for GH therapy. I would avoid it for long term use due to its physiologically unnatural pharmacodynamic characteristics. straight old IGF-1 might be preferable but even that is no true replacement.

the GH secretagogue peptides and the GHRH analogs would be the way to go if you wanna have your GH and stay above the law

Seems to me like gh secretagogue peptides and ghrh analogs are illegal without a precription. Am I wrong?
 
I don't know what delivery to the cells in a regulated fashion means. Receptors are binary, either activated or not. Once a receptor is activated, the drug cannot dock there twice. The receptors will be re-expressed later.

OK. most of the IGF-1 circulating in your body is bound to IGF-1BP3. This bound complex will find its way rhought the bloodstream to target tissues, and when it finds the appropriate target tissues it will encounter localized proteases that will then free up the IGF-1 for receptor interaction - AT THAT PARTICULAR TISSUE

This is what i mean by regulated. This is the function of the binding protein, or it appears to be a very important function of this binding protein. It protects it and delivers it to where it is needed, and nowhere else

Now there are also other binding proteins that serve to sequester and permanently deactivate IGF-1 - speeding up its elimination. These apparently serve as protectors and are secreted by certain cells under certain conditions.

Bottom line? The body has a very complex and highly regulated system of checks and balances to make sure IGF-1 is active where it is needed and inactive where it may cause problems.

When you use a form of IGF-1 that is engineered to avoid binding to IGF1-BPs (such as longR3) you circumvent these checks and balances and invite all kinds of unforeseen problems
 
check out the GHRH analog cjc1295 ksman if you have not already

it apparently will elevate endogenous GH substantially with injections as infrequent as once a week, and its efficacy apparently does not diminish over long term usage
 
check out the GHRH analog cjc1295 ksman if you have not already

it apparently will elevate endogenous GH substantially with injections as infrequent as once a week, and its efficacy apparently does not diminish over long term usage

But also the reccomended doses I saw (totally forgett them offhand) would cost more than running GH so it would have to be a matter of legality or there would be no advantage.
 
Bottom line? The body has a very complex and highly regulated system of checks and balances to make sure IGF-1 is active where it is needed and inactive where it may cause problems.

When you use a form of IGF-1 that is engineered to avoid binding to IGF1-BPs (such as longR3) you circumvent these checks and balances and invite all kinds of unforeseen problems

That is nice for a young vital person, but now we don't die in our 30's from disease and starvation. We live into old age and our hormones all seem to decline. If my GH and IGF-1 levels are low enough to be a major cause of decline, do I give a rat's ass about a wonderfully balanced mechanism that is now broken and my tissue systems are in decline, causing cascading degeneration?

Our T levels fall over time, so does DHEA but SHBG also increases with age. So TT drops and %FT drops as well, providing a double impact. Do I care about the wonderful balancing effects of SHBG when I have hypogonadism?

When the machine breaks, the intervention can be inconsistent with the original design.

In the context of TRT/HRT, when the mechanism breaks, you don't worry about affecting something that just does not work anymore. When you do TRT, it is because your HPTA does not work anymore and you don't worry about shutting the HPTA down because you are better off on TRT.
 
That is nice for a young vital person, but now we don't die in our 30's from disease and starvation. We live into old age and our hormones all seem to decline. If my GH and IGF-1 levels are low enough to be a major cause of decline, do I give a rat's ass about a wonderfully balanced mechanism that is now broken and my tissue systems are in decline, causing cascading degeneration?

Our T levels fall over time, so does DHEA but SHBG also increases with age. So TT drops and %FT drops as well, providing a double impact. Do I care about the wonderful balancing effects of SHBG when I have hypogonadism?

When the machine breaks, the intervention can be inconsistent with the original design.

In the context of TRT/HRT, when the mechanism breaks, you don't worry about affecting something that just does not work anymore. When you do TRT, it is because your HPTA does not work anymore and you don't worry about shutting the HPTA down because you are better off on TRT.

you are completely missing the point. in fact when you are older this balance is perhaps even more crucial.

your body has tissues for which regeneration is important and of course growth factors are integral for this process. However there can be abnormal cell systems popping up and these do pop up all the time, especially as you age. the body has mechanisms to recognize these anomalies and to suppress them so they do not grow into something like a malignant cancer. These mechanisms can involve interventions to protect them from IGF-1 via manipulation of localized binding protein expression. If you introduce longR3 you quite possibly can circumvent such protective mechanisms in the body and the consquences can be serious
 
T

In the context of TRT/HRT, when the mechanism breaks, you don't worry about affecting something that just does not work anymore. When you do TRT, it is because your HPTA does not work anymore and you don't worry about shutting the HPTA down because you are better off on TRT.

the consequences we are talking here are much more severe than HPTA shutdown
 
But also the reccomended doses I saw (totally forgett them offhand) would cost more than running GH so it would have to be a matter of legality or there would be no advantage.

Some people are reporting good results with as little as 500 mcg/wk. The doses used in clinical studies are perhaps way too high.
 
OK so how does this sound. 1295 has a very long half life (>7 days). Let's say it is exactly 7. Now studies were done showing pretty serious increases in GH and related stuff with one dose in the 30-60 mcg/kg of bodyweight range. Or 3-6 mg/wk for a 100 kg person. If one were to dose at 1 mg/wk, for a 100 kg person (10 mcg/kg) after 4 weeks serum levels would be at a steady state near 20 mcg/kg (roughly double the initial single dose, or 1 + 1/2 + 1/4 + 1/8). Or a steady-state level equivalent to a single 2 mg dose.

So if you can find this stuff for around $25/mg, $100/mo for two or three months is not that bad. Enough to last through a decent androgen cycle and pct. Plus you'll have elevated levels for a month+ after stopping. The longer the half life really is the better this gets.

Keep in mind the half life of real GH is not very long, the nature of endogenous production is pulsatile, so consistently elevated steady-state levels over months might be pretty cool.
 
Keep in mind the half life of real GH is not very long, the nature of endogenous production is pulsatile, so consistently elevated steady-state levels over months might be pretty cool.

gh injections by subcutaneous have pharmacokinetic properties such that it is released into the system over a few hours. of course each bit that gets released only has a half life of 20 minutes or so. bottom line is a gh injection will keep gh elevated maybe 3 or so hours and no more

anyway, while it is elevated it is stimulating the liver to release IGF-1 and IGF-1 has a half life of 8 to 18 hours (because most of it is bound to IGF-1BP3). So you don't necessarily need elevated GH all the time to have constant activity, since most activity is expressed by IGF-1

However GH has potent fat burning properties that IGF-1 does not have. Keeping GH high all the time with CJC might enhance the fat loss effects versus direct daily GH injections
 
gh injections by subcutaneous have pharmacokinetic properties such that it is released into the system over a few hours. of course each bit that gets released only has a half life of 20 minutes or so. bottom line is a gh injection will keep gh elevated maybe 3 or so hours and no more

anyway, while it is elevated it is stimulating the liver to release IGF-1 and IGF-1 has a half life of 8 to 18 hours (because most of it is bound to IGF-1BP3). So you don't necessarily need elevated GH all the time to have constant activity, since most activity is expressed by IGF-1

However GH has potent fat burning properties that IGF-1 does not have. Keeping GH high all the time with CJC might enhance the fat loss effects versus direct daily GH injections

This is good to know. I was thinking more about area under-the-curve effects from steady state elevated GH concentrations vs. pulsitile (either endogenous or by GH inj.). If one GH injection lasting three hours produces a certain amount of IGF-1, and that IGF-1 once bound lasts 8-18 hrs, what amount of IGF1 production might continuously elevated GH stimulate? Well if the 1295 keeps it up 24/7, then that's like 8 or more doses of peak-equivalent GH evenly spaced out per day plus whatever IGF1 that produces. I do not know enough about feedback mechansims or limiting amounts of binding proteins, but it seems like that would mean proportionally much greater elevated levels of bound IGF1 due to its longer half life.
 
This is good to know. I was thinking more about area under-the-curve effects from steady state elevated GH concentrations vs. pulsitile (either endogenous or by GH inj.). If one GH injection lasting three hours produces a certain amount of IGF-1, and that IGF-1 once bound lasts 8-18 hrs, what amount of IGF1 production might continuously elevated GH stimulate? Well if the 1295 keeps it up 24/7, then that's like 8 or more doses of peak-equivalent GH evenly spaced out per day plus whatever IGF1 that produces. I do not know enough about feedback mechansims or limiting amounts of binding proteins, but it seems like that would mean proportionally much greater elevated levels of bound IGF1 due to its longer half life.

i am guessing that you really are not gonna see any more IGF-1 if the GH is spread throughout the day as opposed to being more of a bolus. I know that studies have shown that multiple daily injections of GH don't hold any advantage over once daily injection.
 
i am guessing that you really are not gonna see any more IGF-1 if the GH is spread throughout the day as opposed to being more of a bolus. I know that studies have shown that multiple daily injections of GH don't hold any advantage over once daily injection.

Ah well, there goes that hypothesis. Better not quit my day job.
 
And this ladies and gentlemen brings us back to the idea that pinning LR3 right in the last muscle trained, right after training, should lessen any systemic effect which PA rightly denounces as potentially dangerous.

IGF-1 receptors are greatly upregulated by resistance exercise but that effect is transient. By applying my dosing guidelines you diminish the likelihood of any adverse effects greatly.

That this is not as good as injecting 10mg of hIGF-1/IGFBP3 complex every day is IMO besides the point since that remains pretty unavailable and only interesting to white coats with big research budgets and not bodybuilders on a quest for size and somewhat more limited means, most of the time.
 
i got to page 15 but i have to go. Grunt or anyone that has read and is familiar with this thread.......can you tell me what Grunts thoughts were on receptor vs. media grade igf1lr3?
 
i got to page 15 but i have to go. Grunt or anyone that has read and is familiar with this thread.......can you tell me what Grunts thoughts were on receptor vs. media grade igf1lr3?

From page 16 ;)

Originally Posted by jonesboy
in regards to media grade vs receptor grade igf. Would you keep the dosage the same for receptor as you would for the media grade? i.e. 40mcg bi lat 3x's a week in my case?

thanks...
Nope, I would reduce it in half and see. You may get the same effects with 20mcg receptor as you do with 40mcg media, but not twice the effects with 40mcg receptor as you do with 40mcg media. There is a fairly low saturation point IMO.
 
From page 16 ;)

Originally Posted by jonesboy
in regards to media grade vs receptor grade igf. Would you keep the dosage the same for receptor as you would for the media grade? i.e. 40mcg bi lat 3x's a week in my case?

thanks...
Nope, I would reduce it in half and see. You may get the same effects with 20mcg receptor as you do with 40mcg media, but not twice the effects with 40mcg receptor as you do with 40mcg media. There is a fairly low saturation point IMO.

So receptor grade is better?
 
And this ladies and gentlemen brings us back to the idea that pinning LR3 right in the last muscle trained, right after training, should lessen any systemic effect which PA rightly denounces as potentially dangerous.

The local effects may increase, but most of the product may still go systemic. So while the local muscle may see an improvement, systemic effects may have very little change.

I suggest that one do a local IM injection after pulse and respiration have fully recovered. Otherwise the local injection may wash out too quickly. Rest 20 minutes perhaps?
 
The local effects may increase, but most of the product may still go systemic. So while the local muscle may see an improvement, systemic effects may have very little change.

I suggest that one do a local IM injection after pulse and respiration have fully recovered. Otherwise the local injection may wash out too quickly. Rest 20 minutes perhaps?

can you restate or explain that last paragraph better? im using 50mcg in each muscle with receptor post workout only.


Too much? this is my first time with Igf1lr3...
 
can you restate or explain that last paragraph better? im using 50mcg in each muscle with receptor post workout only.


Too much? this is my first time with Igf1lr3...

Too much for what? 50mcg is more than the muscle can use, so more than the muscle needs. From a gains point of view, this could be wasteful.

If you inject when your heart rate is still high, the blood flow through the muscle will wash the IGF-1 out faster than injecting after your body calms down.

So you inject 2X50mcg? 100mcg might be excessive from the point of view of unwanted systemic effects to the gut.

I am no expert. Take these thoughts and integrate them into [or discard] other things that you have learded and read.
 
ill cut it down to 40mcg bilat...2x20mcg.

when you say the blood flow will wash out the igf how would you get the site benefiets from it then? would you then think that it would be best to do 2x10mcg immedietly post wo then follow with 2x10mcg once the heart rate goes to normal? in my situation of 2x20mcg...?

reps for the continuance of this subject.
 
50mcg divided among your muscles, is quite different than "50mcg per muscle" which is what you stated before.

Knowing that you have some size to you, 50mcg total should be allright.

Receptor MAY be better than media grade, depending on the media grade.
 
last time i pinned i did 20mcg split (10mcg each) about 5-10minutes post. then i did the same dose about 20-30 mins after that one. Do you think that would prevent washout rather then doing the 40mcg split at once or does this delay kill the spot enhancing effects.

So receptor vs media is up in the air, depending on the source. SO from the same source recpetor advantage is just more igf absorbed or what?
 
The one time that I tried something which was called "receptor grade IGF-1" I did not like the results at all.
 
ill cut it down to 40mcg bilat...2x20mcg.

when you say the blood flow will wash out the igf how would you get the site benefiets from it then? would you then think that it would be best to do 2x10mcg immedietly post wo then follow with 2x10mcg once the heart rate goes to normal? in my situation of 2x20mcg...?

reps for the continuance of this subject.

Most of the IGF-1 injected IM will become systemic in time. If the objective to maximize IGF-1 exposure in the injected muscle, one needs to extend the time that the IGF-1 remains in the muscle. Injecting right after training will create the least amount of exposure before the IGF-1 washes out. Perhaps the muscles are primed to react to IGF-1 right after training, but is there really any data to suggest that that effect is strongly diminished after 20 minutes?
 
Most of the IGF-1 injected IM will become systemic in time. If the objective to maximize IGF-1 exposure in the injected muscle, one needs to extend the time that the IGF-1 remains in the muscle. Injecting right after training will create the least amount of exposure before the IGF-1 washes out. Perhaps the muscles are primed to react to IGF-1 right after training, but is there really any data to suggest that that effect is strongly diminished after 20 minutes?

The receptors return to baseline after 60 minutes... Waiting 5 minutes, which would be about long enough to drop the weights, pick up your stuff, go to the locker room, take the IGF and go somewhere quiet, swab and pin. After 5 minutes, blood flow is already down by a lot.
 
igf1 lr3 and caner

if you were taking igf1 lr3 and a girl swallowed ur cum and she had cancer b4 and might still have some cancer cells would it grow her cancer cells?
 
The receptors return to baseline after 60 minutes... Waiting 5 minutes, which would be about long enough to drop the weights, pick up your stuff, go to the locker room, take the IGF and go somewhere quiet, swab and pin. After 5 minutes, blood flow is already down by a lot.

How do we know this? A series of muscle biopsies starting just as lifting starts, then plotting to find the peak receptor expression and the time of drop off? I don't think that this has been done. How do we know that this is not web-lore? And I don't think that biopsied tissue would maintain its receptor state long enough to get whatever analytical work needed to measure receptor expression. You can't train muscle tissue in-vitro either.
 
i still think hitting the gym.

going home within 15-30mins. workout more. then igf it up could product exactly same results?
 
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