# IGF-1 10 day blast cycle



## 1982chris1982 (Jan 18, 2011)

Hello I've come across a lot of threads recently on GH blast cycles and people seem to be getting unbelievable results when adopting this protocol. Unfortunately GH is way out of my price range and would remain so no matter what protocol I chose to adopt! My question is could you mimic a GH blast with an IGF-1 blast and expect similar results?Days 1&2: 150mcg/daily.Days 3&4: 200mcg/daily.Days 5&6: 300mcg/daily.Days 7&8: 400mcg/daily.Days 9&10: 500mcg/daily.A couple of questions regarding this;1.Would there be any benefits in running a blast cycle like this with IGF-1 or does it have to be GH when used in such a manor? 2. Has anyone ever ran such a protocol where IGF-1 is concerned?3. Is there any dangers in raising IGF-1 levels so high? 4. As far as I am aware there isn't a saturation point where IGF-1 is concerned am I correct in believing this?5. Would there be a better dose scheme to use in an IGF-1 blast cycle?Please can someone with more experience then me take a little time to answer the above questions as dependent on research I am contemplating on running a blast cycle like above in the not too distant future.Thanx in advance for any replies.


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## 1982chris1982 (Jan 18, 2011)

I did lay the format of the opening post out properly so it was easier to digest.. But its all been squashed together for some reason.


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## 1982chris1982 (Jan 18, 2011)

Anyone?


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## Ragingagain (Sep 4, 2010)

lol getting info like this from the boards, i like tryna squeeze blood out a stone... maybe pscarb will chime in but other than that :no:

but for what little my knowledge is worth;

i lloked into it and decided not to go with it, apparently this kinda stuff is used when aas wont be doing much for you.

apparently the igf-lr3 is better, also i think the doses were more like 50mcg ed, (or maybe thas for peg mgf cant remember). also i read that it is fairly dangerous in the sense that, if you do have any tumours etc it will accentuate growth etc and appparently can therefore lead to cancer and all that..... not sure if its true but i left it cos ive only done 1 aas cycle so it can wait.

if you are gonna do it, i read some use it with peg-mgf

like i say i am totally new to this stuff and have no experience. worst case this is a bump. hopefully someone will give an answer


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## 1982chris1982 (Jan 18, 2011)

Ok thanx for reply normal dosage and cycle duration is advised to be between 30mcg-100mcg for 40-50 days.. I read some people use it as low as 20mcg to help prevent igf-1 receptors from down regulating and run it for longer.

I've searched the internet and carnt find any information on an igf-1 blast cycle and I'm still unsure if there is a good reason why some people don't adopt this protocol.The only thing I can think of as to why it is not attempted is perhaps there would be an igf-1 over spill and the receptors in the intestines would end up utilising the left over igf-1 causing GH gut in the process. But if this was the case surly the same could be said for a GH blast cycle.


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## 3752 (Jan 7, 2005)

1982chris1982 said:


> Hello I've come across a lot of threads recently on GH blast cycles and people seem to be getting unbelievable results when adopting this protocol. Unfortunately GH is way out of my price range and would remain so no matter what protocol I chose to adopt! My question is could you mimic a GH blast with an IGF-1 blast and expect similar results?Days 1&2: 150mcg/daily.Days 3&4: 200mcg/daily.Days 5&6: 300mcg/daily.Days 7&8: 400mcg/daily.Days 9&10: 500mcg/daily.A couple of questions regarding this;1.Would there be any benefits in running a blast cycle like this with IGF-1 or does it have to be GH when used in such a manor? 2. Has anyone ever ran such a protocol where IGF-1 is concerned?3. Is there any dangers in raising IGF-1 levels so high? 4. As far as I am aware there isn't a saturation point where IGF-1 is concerned am I correct in believing this?5. Would there be a better dose scheme to use in an IGF-1 blast cycle?Please can someone with more experience then me take a little time to answer the above questions as dependent on research I am contemplating on running a blast cycle like above in the not too distant future.Thanx in advance for any replies.


No this will not work as the GH blast does, you will be wasting your IGF


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## 3752 (Jan 7, 2005)

1982chris1982 said:


> Ok thanx for reply normal dosage and cycle duration is advised to be between 30mcg-100mcg for 40-50 days.. I read some people use it as low as 20mcg to help prevent igf-1 receptors from down regulating and run it for longer.
> 
> I've searched the internet and carnt find any information on an igf-1 blast cycle and I'm still unsure if there is a good reason why some people don't adopt this protocol.The only thing I can think of as to why it is not attempted is perhaps there would be an igf-1 over spill and the receptors in the intestines would end up utilising the left over igf-1 causing GH gut in the process. But if this was the case surly the same could be said for a GH blast cycle.


no this is not true, it does not work because this is not how IGF-1 works and you will be using either IGF-1LR3 or IGF-1 DES which one will it be?


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## 1982chris1982 (Jan 18, 2011)

Thanx for the reply pscarb firstly I won't be using any if I carnt find any science that would support a blast with igf-1 it is nothing more then an idea at the moment! if I was to go ahead with it I would be using igf1 lr3 though! I was under the impression that GH's main anabolic effect comes from the conversion of gh to igf within the liver? Can you please shine some light on to why an igf-1 blast cycle would not work and also tell me which other mechanisms GH uses to split and recruit new muscle cells!

Thanx


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## 3752 (Jan 7, 2005)

1982chris1982 said:


> Thanx for the reply pscarb firstly I won't be using any if I carnt find any science that would support a blast with igf-1 it is nothing more then an idea at the moment! if I was to go ahead with it I would be using igf1 lr3 though! I was under the impression that GH's main anabolic effect comes from the conversion of gh to igf within the liver? Can you please shine some light on to why an igf-1 blast cycle would not work and also tell me which other mechanisms GH uses to split and recruit new muscle cells!
> 
> Thanx


i am far to tired to explain it mate so read this, it was written by VX1 on Dats Board who knows far more than me on the subject...

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IGF1 and Muscle Growth

IGF1 is thought to induce muscle hypertrophy, by distinct mechanisms. The IGF1 receptor is a tyrosine-kinase receptor which induces cellular signal transduction chains by adding phosphate groups or "phosphorylating" specific proteins within the cell. Activation of the PI3K/AKT kinases cause phosphorylation of the FOXO transcription factors, which prevents them from entering the nucleus and promoting the expression of atrophic factors, like MuRF1. The AKT pathway (often called "PKB" instead of "AKT") also inhibits the secretion of myostatin, thereby increasing both muscle cell differentiation, and protein synthesis.(ref) Myostatin inhibition results in a positive feedback cycle, since myostatin also inhibits the AKT pathway.(ref, ref) IGF1 also activates the mTOR pathway, which is well-known to play a central role in muscle growth. Apparently, PI3K activates mTOR by moving tuberous sclerosis complexes (mTOR inhibitors) from the membrane to the cytosol.(ref) (Independent of growth factors, amino acid availability, especially leucine, regulates mTOR activity, ref.) For a more detailed discussion of the AKT pathway, see: Akt: a nexus of growth factor and cytokine signaling in determining muscle mass

For an overview of transcriptional regulation of muscle growth/atrophy pathways,see: Anabolic and catabolic pathways regulating skeletal muscle mass See, also: Regulation of Muscle Growth

Until recently the exact roles of these pathways and their relationships to IGF1, the effects of resistance exercise (mechanical load/stretch), and developmental stage have remained mysterious. However, current research involving transgenic models is quickly unraveling these mysteries.

Mechanical Stimuli Activate mTOR Independent of IGF1.

It was observed that mechanical stimulation induced local expression of IGF1 and other growth factors.(ref) These were accompanied by an increase in kinase phosphorylation signaling, and muscle growth. It was logical to conclude that IGF1 activated the pathways responsible for muscle growth. Subsequent research has cast serious doubts on this conventional theory. In 2004, it was shown that mechanical stimulation activate mTOR growth pathways, completely independent of IGF1 and the PI3K/AKT pathway. Pharmacologically inhibiting PI3K did not alter activation of mTOR. These results were confirmed with AKT-knockout mice (which lack the AKT gene).

Mechanical stimuli regulate rapamycin-sensitive signalling by a phosphoinositide 3-kinase-, protein kinase B- and growth factor-independent mechanism.

"These surprising results indicate that mechanical stimuli are different from insulin-like growth factors in that mTOR-dependent signalling events are regulated via a PI3K/Akt1-independent mechanism. Furthermore, these results indicate that if mechanical stimuli regulate protein synthesis by the release of locally acting factors, then these factors must activate mTOR through a PI3K/ Akt1-independent mechanism. However, in both the co-incubation and conditioned-media experiments, the release of locally acting factors was not sufficient for the activation of mTOR-dependent signalling events, thus suggesting that mechanotransduction (e.g. mechanoreceptor) rather than ligand binding of autocrine/paracrine growth factors as the cause for the induction of the mTOR-dependent signalling events."

These results were confirmed by a 2009 study, The role of PI3K in the regulation of mTOR following eccentric contractions:

"In summary, the results from this study indicate that resistance exercise contractions, such as ECs (eccentric contractions), activate mTOR through a PI3K-AKT-independent mechanism."

In 2007, another transgenic study using mice with a negative IGF1 receptor (one that binds IGF1, but doesn't transduce signals) showed that the hypertrophic effects of mechanical load were NOT mediated by IGF1.(ref) "We demonstrate that IGF-I receptor-mediated signalling is not necessary for the induction of skeletal muscle hypertrophy in adult mice following a chronic increase in mechanical loading."

This study has previously been discussed by Dat: IGF-1 & receptor aren't even needed post-workout

The results of these studies have been further confirmed by a new transgenic study published last year. Researchers conclude, "Acute resistance exercise did not increase either IGF-1 receptor phosphorylation. . . [Furthermore] these data suggest that physiological loading does not lead to the enhanced activation of the PI3K/Akt/mTORC1 axis and that PI3K activation levels play no significant role in adult skeletal muscle growth."(ref)

mTOR Causes Muscle Hypertrophy, Not IGF1

Additional studies have confirmed that mTOR plays a central role in muscle growth; but they also confirm that this happens independent of the PI3K/AKT pathway. A PI3K-independent Activation of mTOR Signaling Is Sufficient to Induce Skeletal Muscle Hypertrophy "In this study, we demonstrate that the overexpression of Rheb induces mTOR signaling through a PI3K/PKB-independent mechanism and that this event is sufficient to induce a robust and cell autonomous hypertrophic response. Furthermore, it was determined that the hypertrophic effects of Rheb occurred through a rapamycin-sensitive mechanism, that mTOR was the rapamycin-sensitive element in skeletal muscle that conferred the hypertrophic response, and that the kinase activity of mTOR was necessary for this event. Combined, these results strongly indicate that a PI3K/PKB-independent activation of mTOR signaling, in skeletal muscle, is sufficient to induce hypertrophy." The researchers conclude by suggesting that muscle hypertrophy could be induced by the use of mTOR agonists.

What purpose, then, does IGF1 serve?

Obviously it serves many purposes. I would not presume to definitively answer this question. However, it does appear clear from experimental data that the proliferative role of IGF1 is limited to developmental growth and to regenerative repair. IGF1 is necessary for proper development and repair following injury. Young, developing mammals not only need IGF1 for proper development, but overexpression leads to increased growth. The same does not happen in adults overexpressing IGF1. From a transgenic study published in 2010: "In conclusion, these data show that adult non-growing skeletal muscles are refractory to hypertrophy in response to the elevated IGF-1. By contrast, growing muscles respond by activating signalling downstream from the IGF-1 receptor (demonstrated by phosphorylation of Akt, p70S6K) to increase protein accretion by the myofibres. Thus, the IGF-1-mediated hypertrophy evident in adult transgenic muscles results from enhanced increase in muscle mass mainly during the postnatal growth phase." (ref)

Am I wasting my time and money on IGF1?

Yes. Anecdotes are not scientific evidence, no matter how loudly they are proclaimed. The previously accepted theory on the role of IGF1 in muscle hypertrophy has been reversed. Many are apparently slow to get the message. This should not come as a surprise to readers of this forum. I merely wanted to give a concise review of some of the recent, relevant literature. *All currently available scientific evidence based on in vivo studies indicates that IGF1 plays no role in normal, exercise-induced muscle hypertrophy*

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## m118 (Feb 4, 2011)

Pscarb said:


> i am f....... *All currently available scientific evidence based on in vivo studies indicates that IGF1 plays no role in normal, exercise-induced muscle hypertrophy*
> 
> ------------------------------------------------------------------------------------------------------------------------


that's not reassuring. I was under the belief that it not able to make immediate growth likely, but increased hyperplasia allowing for a greater amount of muscle growth in the long term... and also perhaps help with fat loss


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## 1982chris1982 (Jan 18, 2011)

Ok thanx pscarb the majority of that didn't make sence to me I lack the education needed to understand it. I did however grasped a firm understanding of the last paragraph or so. I was never under the impression that igf-1 induced hypertrophy I wasn't aware that people deemed it possible. As m118 has pointed out It was my understanding that igf-1's main role was to produce more muscle cells either by splitting existing cells or by recruiting new satellite cells. Once these cells have been formed they are then matured by exercise induced hypertrophy? Is there a igf-1 saturation point?


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## 1982chris1982 (Jan 18, 2011)

Anyone? Is there a saturation point with igf-1 where as the excess igf-1 is rendered useless? Also how quick would igf-1 receptors down regulate if you were to try a 10 day blast with high doses?

Thanx


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## 3752 (Jan 7, 2005)

m118 said:


> that's not reassuring. I was under the belief that it not able to make immediate growth likely, but increased hyperplasia allowing for a greater amount of muscle growth in the long term... and also perhaps help with fat loss


if used with MGF muscle growth is possible but not by just jabbing it in and hoping as many do



1982chris1982 said:


> Ok thanx pscarb the majority of that didn't make sence to me I lack the education needed to understand it. I did however grasped a firm understanding of the last paragraph or so. I was never under the impression that igf-1 induced hypertrophy I wasn't aware that people deemed it possible. As m118 has pointed out It was my understanding that igf-1's main role was to produce more muscle cells either by splitting existing cells or by recruiting new satellite cells. Once these cells have been formed they are then matured by exercise induced hypertrophy? Is there a igf-1 saturation point?


mate it clearly says that IGF-1 plays no role in muscle growth yet your asking about splitting cells? this is the reason you are doing a blast to create new muscle cells but the science does not lead to this result when used on its own??



1982chris1982 said:


> Anyone? Is there a saturation point with igf-1 where as the excess igf-1 is rendered useless? Also how quick would igf-1 receptors down regulate if you were to try a 10 day blast with high doses?
> 
> Thanx


saturation point is individual and down to frequency more than dose, i would assume if you did what you did you would be saturated by the end of it but apart from the massive pump IGF-1 gives i see no reason for it as you are trying to force the body into creating new muscle cells by just jabbing one drug, it is not that easy mate you have to look at the whole picture combined with pMGF this is possible but timings/dose for both is all taken into account.......in my opinion you need to do alot more reading to understand the mechanics of the drug but it is your money, your body so your choice......


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## m118 (Feb 4, 2011)

Pscarb said:


> if used with *MGF *muscle growth is possible but not by just jabbing it in and hoping as many do
> 
> ...


so without mgf, its worthless running igf in your experienced opinion?


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## 1982chris1982 (Jan 18, 2011)

Ok fanx for taking the time to reply. It appears igf-1 isnt as promising as I originally thought it was. back to the drawing board it is.


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