R3 IGF-1 Administration-workout days only or?

[T-Biggs]

I plan on running my IGF on Monday (20mcg/am and 20mcg/post-workout) but and have one last question before I start and that would be about administration-how should IGF be administrated during non-workout days? The same as if I was working out w/am-pm shot? Or should I follow a 5 days on 2 days off as I currenty workout M-F (5 days)....
In other words should IGF only be used on workout days?

[flexshack]

I plan on running my IGF on Monday (20mcg/am and 20mcg/post-workout) but and have one last question before I start and that would be about administration-how should IGF be administrated during non-workout days? The same as if I was working out w/am-pm shot? Or should I follow a 5 days on 2 days off as I currenty workout M-F (5 days)....
In other words should IGF only be used on workout days?

no, igf-1lr3 should be used 7 days a week. the only reason not to would be to save some money, imo. i would also run it post workout only and on non workout days, shoot in the morning in the same muscle group worked the previous day.

[T-Biggs]

Ok I gotcha on the 7 days a week makes sense (I run my GH the dame way), but the consciences on the boards seems to be 2x injections because of the half life of R3 Long IGF-1, which seems be be around 12 hours so split injections would make sense.......
However some guys seem to have done injections 2x a day (am/post-workout) and others have done just 1x a day (post-workout) and both parties seem to have recevied good results, but I have yet to find anyone would has done both and compared the two results

[flexshack]

Ok I gotcha on the 7 days a week makes sense (I run my GH the dame way), but the consciences on the boards seems to be 2x injections because of the half life of R3 Long IGF-1, which seems be be around 12 hours so split injections would make sense.......
However some guys seem to have done injections 2x a day (am/post-workout) and others have done just 1x a day (post-workout) and both parties seem to have recevied good results, but I have yet to find anyone would has done both and compared the two results

i have heard 16-20 for the half-life, but could be wrong though. i will be starting my igf-1lr3 cycle soon and will be opting for the one/day injection post w/o. you are right about not being able to find anyone who compared the two methods. that will come with time. this is all still too new.

[T-Biggs]

i have heard 16-20 for the half-life, but could be wrong though. i will be starting my igf-1lr3 cycle soon and will be opting for the one/day injection post w/o. you are right about not being able to find anyone who compared the two methods. that will come with time. this is all still too new.

I have heard 6-8, 8-12 and 20-30 for the half life, however my theory of thinking is this......just IGF-1 (not R3 long) has a half-life of 6-10 min and as I am not sure of the bio-technology behind making the longer version 20-30 or 16-20 it seems like an extremely dramatic increase in longevity of a delicate compound so 8-12 would seem more practical (this is all my opinon though), however as I start on Monday with am/post workout shots continuing with my current cycle I am in fact going to also try just post-workout also during the second time around and try to come up with a comparison...


All this reminds me of the questions that where circulating (as more guys starting doing GH) in reguards to the timing of GH shots in coralation with ones natural GH production Ex: am shots vs afternoon shots vs bedtime shots etc....

[einstein1905]

I have heard 6-8, 8-12 and 20-30 for the half life, however my theory of thinking is this......just IGF-1 (not R3 long) has a half-life of 6-10 min and as I am not sure of the bio-technology behind making the longer version 20-30 or 16-20 it seems like an extremely dramatic increase in longevity of a delicate compound so 8-12 would seem more practical (this is all my opinon though), however as I start on Monday with am/post workout shots continuing with my current cycle I am in fact going to also try just post-workout also during the second time around and try to come up with a comparison...


.

Regular IGF-1 has a short half-life, but it's also dependent upon the levels of IGFBP3, as higher levels will make for a longer half-life of IGF-1. IGFBP3 protects IGF-1 from degradation but also prevents it from being able to readily bind its receptors. The LR3 version has a porcine (pig) region of GH, I believe, at the N terminal end of IGF-1, which serves as a pseudo IGFBP by not allowing it to be easily degraded...it also prevents actual IGFBPs from binding it. These additional amino acids do not, however, prevent LR3 from binding IGF receptors, so the half life actually is considerably longer...by how much, I don't know for sure.

[flexshack]

Regular IGF-1 has a short half-life, but it's also dependent upon the levels of IGFBP3, as higher levels will make for a longer half-life of IGF-1. IGFBP3 protects IGF-1 from degradation but also prevents it from being able to readily bind its receptors. The LR3 version has a porcine (pig) region of GH, I believe, at the N terminal end of IGF-1, which serves as a pseudo IGFBP by not allowing it to be easily degraded...it also prevents actual IGFBPs from binding it. These additional amino acids do not, however, prevent LR3 from binding IGF receptors, so the half life actually is considerably longer...by how much, I don't know for sure.

are you saying that igf-1lr3 can bind to igfbp3 and become useless? if so, then does the body produce more and more of these binding proteins to form a homeostasis? and is this why it seems to stop working after 6 weeks or so?

[einstein1905]

are you saying that igf-1lr3 can bind to igfbp3 and become useless? if so, then does the body produce more and more of these binding proteins to form a homeostasis? and is this why it seems to stop working after 6 weeks or so?

No, the LR3 form is not able to be bound by IGFBPs. However, that doesn't mean that IGFBPs may not still be overexpressed in response to high levels of the LR3 form of IGF-1. Of course, this will only affect endogenous IGF-1.

[flexshack]

No, the LR3 form is not able to be bound by IGFBPs. However, that doesn't mean that IGFBPs may not still be overexpressed in response to high levels of the LR3 form of IGF-1. Of course, this will only affect endogenous IGF-1.

i see. and i assume that the increase will come back down to normal upon cessation of exogeneous igf-1lr3, right?

[einstein1905]

i see. and i assume that the increase will come back down to normal upon cessation of exogeneous igf-1lr3, right?

Yes, well, if they are upregulated in response to LR3 at all...I don't know. IGFBP levels are also influenced by insulin, which "preserves" IGFBPs and also by T3 as well as many other factors I'm sure.

[flexshack]

Yes, well, if they are upregulated in response to LR3 at all...I don't know. IGFBP levels are also influenced by insulin, which "preserves" IGFBPs and also by T3 as well as many other factors I'm sure.

when you say preserves, do you mean allows more to accumulate in the body, therefore, lessening one's free or available igf-1? if so, then is insulin a bad thing?

[einstein1905]

when you say preserves, do you mean allows more to accumulate in the body, therefore, lessening one's free or available igf-1? if so, then is insulin a bad thing?

Insulin is trickey. It "preserves" IGFBPs by preventing proteolytic enzymes from functioning to break down IGFBPs, similar to slin being anticatabolic and preventing muscle "breakdown". Insulin being present can also increase IGF-1 expression in the presence of GH at the liver. Some say IGFBPs are good because they prolong the half life of IGF-1....yes, but at the expense of the IGF-1 not being bioavailable until released from the IGFBPs. I assume IGFBP levels ebb and flow very rapidly in response to all the various influences on thier synthesis and degradation.

[flexshack]

Insulin is trickey. It "preserves" IGFBPs by preventing proteolytic enzymes from functioning to break down IGFBPs, similar to slin being anticatabolic and preventing muscle "breakdown". Insulin being present can also increase IGF-1 expression in the presence of GH at the liver. Some say IGFBPs are good because they prolong the half life of IGF-1....yes, but at the expense of the IGF-1 not being bioavailable until released from the IGFBPs. I assume IGFBP levels ebb and flow very rapidly in response to all the various influences on thier synthesis and degradation.

thanks, great explanation. btw, i realized you said that igf-1 can release from it's binding protein to become bioavailable. this is unlike testosterone, right? when test binds to shbg it is done for good, right?

[einstein1905]

thanks, great explanation. btw, i realized you said that igf-1 can release from it's binding protein to become bioavailable. this is unlike testosterone, right? when test binds to shbg it is done for good, right?

No, it's very similar actually. Test too can and is released from SHBG. SHBG prolongs the life of test too but prevents it from binding ARs until it's released. Serum albumin also binds test this same way. You have to think of things as being very dynamic. These bindings are relatively weak....there is enough affinity for eachother (test:SHBG or IGF-1:IGFBP) so that they associate with one another, but they are constantly coming apart and going back together as they move through the system. When an AR is in close enough proximity and everything is aligned right, test will have greater affinity for the AR than for the SHBG. That's just one scenario. There is also test that happens not to be associated with SHBG, which is free to bind ARs at any time. Then there are test:SHBG complexes that will never come apart, due to several factors (not being in close enough proximity to an AR....not being in the right orientation when near an AR.....or simply is degraded).
It's all, more or less, stochastic.

[flexshack]

No, it's very similar actually. Test too can and is released from SHBG. SHBG prolongs the life of test too but prevents it from binding ARs until it's released. Serum albumin also binds test this same way. You have to think of things as being very dynamic. These bindings are relatively weak....there is enough affinity for eachother (test:SHBG or IGF-1:IGFBP) so that they associate with one another, but they are constantly coming apart and going back together as they move through the system. When an AR is in close enough proximity and everything is aligned right, test will have greater affinity for the AR than for the SHBG. That's just one scenario. There is also test that happens not to be associated with SHBG, which is free to bind ARs at any time. Then there are test:SHBG complexes that will never come apart, due to several factors (not being in close enough proximity to an AR....not being in the right orientation when near an AR.....or simply is degraded).
It's all, more or less, stochastic.

i appreciate this explanation, thank you.
it is interesting to me that insulin can preserve igfbp3, but lessen shbg, from what i have heard.

[einstein1905]

i appreciate this explanation, thank you.
it is interesting to me that insulin can preserve igfbp3, but lessen shbg, from what i have heard.

Yes, insulin is both good and bad. If you want to read up on the insulin:SHBG interactions, these 2 papers are good:
Pasquali R, et al. Insulin regulates testosterone and sex hormone-binding globulin concentrations in adult normal weight and obese men. J Clin Endocrinol Metab 1995 Feb;80(2):654-658.

Strain G, et al. The relationship between serum levels of insulin and sex hormone-binding globulin in men: the effect of weight loss. J Clin Endocrinol Metab 1994 Oct;79(4):1173-1176.

[flexshack]

Yes, insulin is both good and bad. If you want to read up on the insulin:SHBG interactions, these 2 papers are good:
Pasquali R, et al. Insulin regulates testosterone and sex hormone-binding globulin concentrations in adult normal weight and obese men. J Clin Endocrinol Metab 1995 Feb;80(2):654-658.

Strain G, et al. The relationship between serum levels of insulin and sex hormone-binding globulin in men: the effect of weight loss. J Clin Endocrinol Metab 1994 Oct;79(4):1173-1176.

awesome, thanks.