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IGF-1r3 usage Theory, need some help??

Juice Freak

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I have read many different things all relevant to the use of IGF1 long, which is understandable since it's fairly new and catching on. My questions are as follows:

1.)What is the real half life of IGF-1r3 long?

2.)Combining IGF-1r3 long with insulin allows the drug to stay
active for how long?

3.)I read on a thread which I cannot find anymore that by taking
Growth hormone along side IGF-1r3 long that the down
regulation that occurs after a month of IGF-1r3 long use does
not happen, and can be taken for many months at a time.

My theory is that if insulin is taken 40minutes before admistration of each IGF-1r3 long shot, that IGF-1r3 long could be in the body in large amounts for 24hrs a day. The hypo could be warded off by eating a large amount of low glycemic complex carbs before bed and then a quick snack mid sleep. Combined with Growth hormone this 24hr IGF-1 environment could be used for many months without having to stop or take a break....????

What do you guys think???
 

weight77

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I just came off IGF about 3 weeks ago and had good results..Just the appetite increase alone is worth it for me..

Igf as far as I know stays active for 12 hours..I am not sure that insulin makes last any longer..I know that IGF will increase insulin sensitivity..I went from 10 ius down to 6iu a day..

also I believe that the igf can be run longer than 4 weeks..it is mainly up to the person because everyone's body will produce the binding proteins at different times..
 

big_byrd52

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I dont know that insulin will make it active longer, but it will make IGF more potent by attaching to IGH-BPs allowing for more uptake.

I have a question: How long after injection does the IGF become active? does anyone have a chart that show peak times like with all the diff. types of slin?
 

Juice Freak

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Type of slin in Humulin-R, what do you think of the added GH use along side the IgF, I heard that on paper is seems overkill but in real life it actually works quite well???
 

weight77

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This might help you.

It talks about IGF, GH, Insulin...

-It seems reasonably certain the almost every hard-core and serious athlete is aware of the paramount importance of testosterone and growth hormone (GH) for actualizing gains in lean mass tissue. Unfortunately it seems that not as many are aware of insulin's powerful and symbiotic anabolic effects. This is especially so in regards to its synergistic role in producing one of the body's most potent growth factors called IGF-1 (Insulin-like Growth Factor-1).


Any enhanced athlete could employ the best coaches and training protocols while utilizing polypharmacology yet realize only a fraction of their muscle mass potential unless they realize the facts about interaction between GH, insulin and IGF-1.


The amount of hepatic and site specific IGF-1 the body secretes is dependent upon insulin management.

The ratio and interaction between GH, insulin and IGF-1 is paramount for correct and maximum protein and glucose metabolism.

Many do not realize that IGF-1 is so powerful that it has even been documented to reverse age related metabolic inhibitors such as insulin resistance and muscle loss while improving muscular contractile force.

Hepatic and tissue specific IGF-1 formation is optimized by a more steady tide effect circulatory exchange/interaction between GH and insulin.

Intense training increases testosterone, GH and IGF levels. However it also decreases insulin levels and increases cortisol (the catabolic muscle breakdown hormone)

Whenever insulin is low the life of GH-IGF secretion is short lived.

Heavy, eccentric weight training causes the highest increases in circulating bioactive IGF-1.

GH release via sleep, supplements or exogenous administration is useless without sufficient circulating insulin and blood amino acids.


Huh?


Human secretion of GH occurs from the pituitary gland (which is found at the base of the brain). Some travels the vascular system to muscle and bone tissue resulting in direct initiation of anabolism through alternate growth factor/somatomedin formation (IGF-1&2 are formed due to cascade responses). Some travels to the liver where it interacts with insulin and other factors to form hepatic introduced circulatory growth factors/somatomedins.


Once in circulation both IGF-I and IGF-2 have very short lives. IGF-II is predominantly responsible for nerve growth. IGF-I exerts most of its profound growth effects on muscle. Unless an individual actuates both insulin and IGF circulating in the correct amounts, muscle growth will be about zero.


Consider the Obvious…


It was from research performed on diabetics that initially provided the earlier examples. Insulin-dependant diabetics have chronic low IGF levels both circulatory and site-specific. They also commonly have a very bad time when attempting to increase muscle mass. Realize that diabetes is a disease of inconsistent, ineffective insulin secretion by the pancreas. A diabetic's circulatory insulin level is always going up and down depending on how much they administer and what they eat…and always mistimed to GH release. It's almost impossible to keep constant during the right periods thus resulting in little IGF formation.


Intense Training and local IGF-1 response…


Previous research has shown conflicting results with regard to IGF-1 secretion and exercise of various types. However, recent research has demonstrated that that a large amount of IGF-1 is secreted within the first 12 minutes of intense training protocols.

Properly designed current research also has shown that muscle tissue employed in weight training produced a great deal more bioactive IGF-1 (locally) and that IGF-1 circulates in a sort of "system" consisting predominantly of a group of six binding proteins, free IGF-1 and an acid-labile unit. Did you know that these six binding proteins in blood and muscle alike regulate the biological activity (usability) of IGF-1? (Say what?)


The latest body of research on IGF-1 validates that intense weight training induces a signal within muscle causes a rearranging effect to the ratio of these binding proteins that results in increased activity and availability of IGF-1. This appears to be essential to the growth and repair process…or Action/Reaction Factors.


In fact, he total amount of IGF-1 secreted by any means is not as important as the rearrangement of the IGF-1 binding protein ratio itself. Heavy resistance training triggers this rearrangement quite nicely of course as it is one of the strongest adaptive response actions there is. By the way, big issue here, this modulation of the IGF-1 binding proteins to create active IGF-1 is not fully realized until six to 12 hours after training. Hmmmm, and this just happens to be about the same time that peak muscle protein synthesis rates occur. Are you starting to see the timing and connection?


So What have we (Hopefully) learned so far?


Without proper timing of the insulin supply, kept within a narrow physiological range, GH levels are quickly destroyed and the active-life of IGF-I is sadly short lived. Precisely prolonged circulatory insulin levels prolong the active life of IGF and GH secretion so their powerful effects on muscle likely last longer.


Even though there is a great deal of IGF-1 present a maximum growth stimulus is require to alter the binding proteins ratio as a means of optimizing the amount of bio-active IGF-1.


Without proper timing of insulin and GH introduction IGF formation is reduced or lost and we look like a weenie-boy.


Now that we have the basics out of the way let’s look at some other points of consideration.

It appears that for some the question of hepatic vs. local IGF formation and GH utilization is still a question. Though several exist the studies below eliminate this misperception.


Effects of local administration of GH and IGF-1 on longitudinal bone growth in rats

J Isgaard, A Nilsson, A Lindahl, J O Jansson, O G Isaksson

AMERICAN JOURNAL OF PHYSIOLOGY , 250(4 Pt 1):E367-E372 1986


The effect of local administration of growth hormone (GH) and insulin-like growth factor 1 (IGF-1) on longitudinal bone growth was studied in the proximal tibia of hypophysectomized rats, by using the tetracycline method. Human GH (hGH) stimulated local bone growth when administered into the epiphysial growth plate, into the epiphysis through an implanted cannula, or into the knee joint intraarticularly. In contrast, hGH administration into the metaphysis did not cause such a stimulation. The effect of hGH was dose dependent, and the lowest daily dose of hGH that caused a stimulation was 50 ng. hGH produced by cloned bacteria was as effective as pituitary-derived hGH, excluding the possibility of a pituitary growth factor being the active compound. GH from other mammalian species (rat GH, ovine GH, and bacterially produced bovine GH) also stimulated local bone growth. Ovine prolactin (oPRL) stimulated local bone growth but the threshold dose of oPRL was approximately 100 times higher than that of hGH, suggesting that contamination of this preparation by GH may account for the stimulation. Reduced carboxymethylated human GH, that has a greatly reduced anabolic activity, did not stimulate local bone growth. Local administration of 5 micrograms of bacterially produced human IGF-1 per day produced a small but significant effect on unilateral bone growth. Simultaneous administration of hGH had no additive effect with, nor did it potentiate, the stimulatory effect of IGF-1. The present study confirms and extends earlier investigations, showing that local injection of GH at the site of the epiphysial growth plate stimulates unilateral bone growth. The study also shows that local administration of IGF-1 stimulates longitudinal bone growth.


So we have rat bones that grow in response to IGF-1 and GH administered locally (site-specific)? Ya, but what about the humans that are not rats? Is it the same reaction to the same action? And is IGF-1 formed in places other than the liver?


Autocrine regulation of cell proliferation and secretion of insulin-like growth factor I (IGF-I) in osteoblastic cell line MC3T3-E1]

F Trémollières, S Mohan, C Ribot

ANNALES D ENDOCRINOLOGY , 55(2):95-102 1994


Bone cells maintained in culture produce different growth factors which modulate cell growth via a mechanism of auto/paracrine regulation. IGF-1 is abundantly produced by murine bone cells where it acts as a mitogenic agent. The aim of this work was to study the effect of IGF-II, TGF beta 1, basic FGF (FGFb) and PDGF on cell growth and production of IGF-1 in the murine osteoblastic clonal cell line MC3T3-E1. IGF-1 was assayed by RIA after elimination of the IGF binding proteins. After 24th of treatment in culture conditions without serum, incorporation of [3H] methylthymidine increased significantly in MC3T3-E1 treated with IGF-II, FGFb and PDGF. The effect was dose-dependent. At low cell density (2.5 X 10(4) cemm/cm2) and after 24 h treatment, IGF-II at 10 ng/ml led to a 220% increase in IGF-I production in MC3T3-E1 cells (9.5 +/- 1.5 vs 4.2 +/- 0.44 ng/micrograms protein, p < 0.001) while TGF beta 1, FGFb and PDGF at 1 ng/ml led to a significant decrease (65, 95 and 85% respectively) in IGF-I (TGF beta 1: 1.5 +/- 0.3 ng/micrograms; FGBb: 0.21 +/- 0.04 ng/micrograms; PDGF: 0.66 +/- 0.1 ng/micrograms; p < 0.001). Production of IGF-I was controlled by a dose-dependent relationship and varied as a function of incubation time and cell density. IGF-II led to an increase in mRNA coding for IGF-1 as early as the first hour after IGF-II addition with a maximal effect at 6 hours.

So other cells in the body do produce growth factors. But is it due to GH and Insulin exposure locally (site-specific) Oh, and where are the humans?


Regulation and action of insulin-like growth factors at the cellular level

L S Phillips, J B Harp, S Goldstein, C I Pao

Proceedings of the Nutrition Society , 49(3):451-458 1990


Present understanding of IGF-1 as a growth factor mediating integration of nutritional-hormonal interactions indicates that IGF-1 acts in both an endocrine mode on distant targets and an autocrine-paracrine mode on local targets. In the liver, the combined presence of GH, insulin, and critical metabolic fuels such as essential amino acids results in increased levels of IGF-1 messenger RNA, increased production of a high-MW IGF-1 precursor, and increased release of IGF-1 into the circulation, permitting action on distant target tissues bearing specific receptors for IGF-1. The net effect is distant amplification of anabolic hormone action via IGF-1 acting in an endocrine mode. In extrahepatic tissues, both 'general' anabolic hormones (insulin and GH) as well as 'specific' hormones (e.g. gonadotropins) acting on a wide variety of targets (including fibroblasts and chondrocytes as well as granulosa and Leydig cells) promote both local secretion of IGF-1 and an increase in IGF-1 receptors. Local actions of IGF-1 then result in a secondary increase in both hormone receptors and hormone responses. The net effect is local amplification of hormone action via IGF-1 acting as a growth factor in an autocrine-paracrine mode
 

rippedboy

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i think ill be taking slin my next lean mass bulking cycle. ive been thinking about it, like 10iu post workout. but no gh or igf1 im not ready for that and dont even want to take it.
 

rugbythug

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rippedboy said:
i think ill be taking slin my next lean mass bulking cycle. ive been thinking about it, like 10iu post workout. but no gh or igf1 im not ready for that and dont even want to take it.
I would take IGF before I took slin if it was me. Slin is more unforgiving-Permenant kind
 

rippedboy

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JohnnyB said:
I agree

JohnnyB
hey guys, why is slin more unforgiving? does it have other side effects i dont know of? if you take in carbs post-workout with 10iu slin, what can go wrong as long as you have the carbs?
 

balplayer

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rippedboy,

please do not take insulin. you do not need it. your not missing out on anything ok. unless your going to be a nationally competitive bb do not fuck with slin. i cant emphasize this to you enough
 

Mr_Magoo

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the igf r3 does what insulin needs to do for regular igf-1, meaning slin is used with gh and things of that short to prolong the half life of igf-1, when one is suing igf-1 r3, the extra 3 molecules allow u to use it with no need for slin, those three molecules are doing exactly what the slin is meant to do
 

weight77

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Mr_Magoo said:
the igf r3 does what insulin needs to do for regular igf-1, meaning slin is used with gh and things of that short to prolong the half life of igf-1, when one is suing igf-1 r3, the extra 3 molecules allow u to use it with no need for slin, those three molecules are doing exactly what the slin is meant to do
I did not know that..good info..but would the slin with the igf r3 make it even longer if taken at the right times??
 

rocketman

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question

so what would be the ideal time/s to take it & in what order ? ifg, gh, slin that is.

can slin & igf-1 r3 be combined in the same rocket ?

thanks
 

rippedboy

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well! great info magoo and the rest of you guys. does igf have any side effects like GH? im not interested in using GH because of the enlarged organs, like the gut, jaw, forehead, im not into that.
 

JohnnyB

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Re: question

rocketman said:
so what would be the ideal time/s to take it & in what order ? ifg, gh, slin that is.

can slin & igf-1 r3 be combined in the same rocket ?

thanks
I wouldn't, igf-1 makes you more sensitive to slin, so the problems could be amplified, easier to go hypoglycemic.

JohnnyB
 

JohnnyB

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Mr_Magoo said:
the igf r3 does what insulin needs to do for regular igf-1, meaning slin is used with gh and things of that short to prolong the half life of igf-1, when one is suing igf-1 r3, the extra 3 molecules allow u to use it with no need for slin, those three molecules are doing exactly what the slin is meant to do
Great info Bro

JohnnyB
 

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