MGF Cycle and stack???

aliamini

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hi all

i am new to the board ... i needed some info on MGF and got some ggod results in your from ...iwanted to know how do you cycle and with what do you stack MGF ... Building the perfect beast book wasn't much of a help ... good on IGF-1 but very little on MGF


Appriciate all the help i could get
 
UnicronSpawn

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I wish I could help, but I only know what you allready read in "building the perfect beast", would like to learn more though. :think: :think:
 

Loki

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Wait, WTF... MGF?? Are you referring to a mechano-growth-factor supplement??

MGF is an intracellular growth factor (for which there seem to be specific, as of yet unspecified intracellular receptors for it), part of the adaptive response protein-synthesis interplay with local IGF1/mTOR/ion transfer & the inflammatory/cytokine/prostaglandin response.

But as I see it, there's no way one could viably "supplement" with MGF--the technology simply doesn't exist unless some drastic innovative leap that I'm not aware of has just been made. Are you saying you've seen an MGF supplement? Or are you just looking for more general info on the workings of MGF?
 

Loki

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Just to give you more general information though, while I'm here and the topic is fresh:

As I just said above, MGF is a local, intracellular growth factor that seems to be extremely important in the body's anabolic response. More MGF means better myogenic cell differentiation efficiency, and, subsequently, more potential for contractile protein synthesis. The reasoning is that MGF activates satellite cells, which--whether you're aware of this or not--satellite cell-proliferation is kind of the overall rate-limiting step in the human hypertrophy response. That's because mature myocytes can't divide, which means satellite cells are needed to loan their nuclei, so that--if I understand the dynamic correctly--myoblast fusion can occur, and more contractile proteins can be synthesized.

Bear in mind however that this doesn't mean I necessarily think MGF is really "the answer" (at least based on what I know--I do think it important though). However, Spook has pointed out to me that recombant GH use in one study using elderly subjects found that the GH use increased MGF significantly. Now, we know GH use isn't a good anabolic substance in trained, young athletes, but GH does seem much more anabolic in elderly subjects, and I kind of wonder if it doesn't have something to do with GH's effects on MGF activity (and thus, satellite-cell availability, which definitely declines which age). Such is my hypothesis at least (although, then again, by that logic, assuming GH influences MGF in the young, it may not be as critical--complex subject this be).


Very cool though...
 

aliamini

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yes i meant Mechano Growth factor ... and man Loki you complecated it ... i just want to know how to use ... dosage , frequency, stack and how to inject

anyway thanx for the info.

appriciate what ever else you or anyone posts
 

Loki

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No, that's what I was asking though, can you even get MGF to inject??

Although I will say that, assuming you can, I would have no idea how to administer it. Even a regular IM pin probably wouldn't work, because--as I said--it exerts its effects intracellularly, and I don't know how you would guarantee intracellular delivery; in fact I'm almost positive you couldn't.
 

Loki

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I'm guessing you can't. Not that I've ever really tried to search it down, but it definitely wouldn't be something with the availability of any of the IGF1 analogues.

Although, as I noted, if you really have your heart set on MGF, you could probably stimulate it via the recombant growth hormone route. I don't know whether or not you have experience with inj. GH--I don't think very highly of it, from a cost or a benefit standpoint--but that would be one potential way to increase intracellular MGF, theoretically (based off one study I've seen--so take that for what it's worth).
 

aliamini

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IGF-1 is with no doubt much more better than GH ... but MGF result is similar if not beeter than IGF-1

I know that cause i asked an amature who got the most improved price ... how did he improve that much in one year and he told me MGF ... that is y I am after it now
 

Loki

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Then I don't know what to tell you because I don't think it exists...
 

aliamini

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Mattris ... give me what ever u have on MGF ... and IGF-1
 
UnicronSpawn

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The following is an exert on MGF from Author L Rea's book.
"Many studies support my belief that IGF-1, whether of endogenous or exogeneous origin, was the primary SYNERGY hormone responsible for muscular growth and repair. I have had several clients who had below average endogeneous test production and average or above IGF-1 levels.

Yet most experienced gains near equal to other natural bodybuilders. I believe this was due to the synergy between IGF-1 and another hormone called Mechano growth factor, or MGF.

MGF is a hormone locally produced in muscles in response to both stretching and overload training, especially due to heavy overload training. This is true only when there is an atmosphere of extensive muscle fiber damage from high weight trumatic sets. The more severe the heavy stimuli, the more MGF the muscle fibers produce. This is quite similar to localized endogeneous IGF-1 production and stimuli.

Recent studies used engineered genes that increased the expression of MGF in mice muscles. The researchers injeceted the genes and found a 20% muscle mass increase in only 14 days. MGF is far more potent than IGF-1 or GH.

Currently, MGF research is geared toward treating various muscle diseases and weakened musculature occurring due to the lack of exercise and age. Researchers have found humans who continue to train as they age, may be able to maintain optimum MGF production.

However, some surgery or disabled patients cannot. For this reason, researchers are experimenting with MGF and IGF-1 and or GH for muscle wasting prevention. For now, watch out for big mice.

I think its safe to theorize that MGF will be one of the next genetic expanding chemistries for most sports. I have noted two genetic research companies are presently manufacturing MGF for research use. Soon it will show up on the black market I think.

By the way, researchers have also already created a testing protoccol to detect MGF use."


I'll see what else I can dig up on MGF. As for IGF-1, there are many threads in this section that tell you just about everything you could want to know about IGF-1, including source. Try the muscle-research forum as well, and check out their site muscle-research.com But to briefly recap what I know from memory, IGF-1 is a protien hormone synthesized in the liver and in muscles from the remanents of GH in the presence of insulin. It is responsible for many of the effects associated with GH use including hyperplasia, or muscle fiber splitting. It is similar to insulin in structure and shares many of the same receptor sites. The rIGF-1 variety, is extremely fragile and even loud noises or less than optimal temperatures can deactivate it. It has a very short active life (I think around 20 or 30 minutes) after administration, and is commonly dosed from 60 to 120mcgs a day devided into 3-5 doses, for steadier plasma levels. However, the Long R3 IGF-1 variety (thats the one I use) is much more stable, and less prone to deactivation. LR3 also has a much longer active life, and is stronger mcg for mcg. common LR3 IGF-1 doses are 40-80 mcgs a day (some people take it in devided doses, some take it all at once.) I take at least part of my daily dose right after my workout. If your sensitive to hypoglycemia, you might want to eat some carbs around the same time you take your shot. I've yet to have that problem. BTW IBE has developed an orally active IGF-1 that people on theese boards have been raving about. I've yet to try it, but user feed back seems to be strong. Some of the people whove tried it had allready tried LR3 and said that IBE's product (its called Oratropin-1) was comparable. I cant vouch for it until Ive tried it myself, but it looks like it might actually work. In the past if anyone had claimed to have an oral form of IGF (or any protien hormone for that matter) I would have thought they were full of it, because, protien hormones, being made of amino acids and only functioning when intact in a specific order/formation, would be easily quelled by protylytic enzymes in the stomach. But some reputable cats have tried it with great success, and its a bit cheaper than the injectable to boot. Just something to consider.
 
UnicronSpawn

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Hypertrophy of mature single muscle fibres in culture: different effects of insulin and mechano growth factor E-domain

R.T. Jaspers, J. Weaden, B. Ramesh, P.A. Huijing, G. Goldspink, W.J. van der Laarse

Introduction
Movement op the human body requires optimal adjustment of the muscle’s potential to generate force. The potential to generate mechanical power is largely determined by the cross-sectional area (CSA) of the muscle fibres and the number of sarcomeres in series. These parameters are usually finely adjusted to functional demands in daily live. In contrast, during ageing and under pathological conditions such as cardiac cachexia, chronic obstructive pulmonary disease (COPD), cerebral palsy these parameters are not optimally adapted to functional demands, causing limited mobility in many patients. Development of effective therapy and/or medication requires basic knowledge of the mechanisms underlying the regulation of muscle size. Insulin, insulin like growth factor (IGF-1) and its splice variant mechano growth factor (MGF) have been shown to be important growth factors involved in the induction of muscle hypertrophy. The mechanisms by which these factors induce hypertrophy in mature muscle fibres in poorly understood. Major reason for this, is that in vivo the presence of growth factors in the interstitial fluid cannot be manipulated independently. The aim, of this study is to investigate the individual effects of insulin and MGF E-domain on the induction of hypertrophy and adaptation of the number of sarcomeres in series as well as their interaction. For this purpose we use a culture system for mature single muscle fibres in which muscle fibre strain, hormonal composition of the culture medium and the contractile activity are manipulated independently.

Methods
Mature, single Xenopus muscle fibres were dissected from the m. illiofibularis and attached to a force transducer in a 20 ºC culture chamber (Fig. 1A-C). Fibres were cultured at a mean sarcomere length of 2.3 mm for 12 to 22 days in a serum-free medium (Jaspers et al., 2001, Arch Physiol Biochem 109: 410-417) supplemented with 0.2% albumin. Muscle fibres were cultured with or without bovine insulin (1 mg/ml) and stabilized human mechano growth factor (MGF) E-domain (500 ng/ml). Before and after culture, the number of sarcomeres was determined using laser diffraction as well as the mean fibre CSA, which was calculated by measurement of the largest and smallest diameters at three locations along the length of the muscle fibre. Tetanic force was determined one daily by electrical stimulation (50Hz). After culture the mean volume of cytoplasm per myonucleus was determined (Schmallbruch and Hellhammer, 1971, Anat Rec 189: 169-176).

Results and discussion
The muscle fibres cultured in medium with insulin (n=5) or with insulin and MGF E-domain (n=4), showed an increase in tetanic force of 1.3±0.1% per day (mean±SEM) up to 20.0±2.2% after 17.6±2.3 days of culture, which was accompanied by an increase of the cross-sectional area (CSA) of 40.1±4.5% at the end of culture (p<0.001) (Fig. 1D). Changes in tetanic force correlated with the culture duration and change of CSA (R2=0.93). In culture medium without insulin (n=5) and in medium containing MGF E-domain but no insulin (n=5), tetanic force and CSA of the fibres did not change. The number of sarcomeres in series remained unchanged during culture, indicating that insulin stimulates growth in the radial but not in the longitudinal direction. The volume of cytoplasm per nucleus of fibres exposed to insulin was doubled compared to that of the other fibres (p<0.001). It is concluded that insulin induces hypertrophy in Xenopus muscle fibres without proliferation of nuclei, whereas the MGF E-domain stimulates proliferation of nuclei without inducing hypertrophy. The ability of Xenopus muscle fibres to remain viable in culture for many days, and to respond to human growth factors, offers a very useful method for studying different components involved in molecular regulation of muscle mass.





Fig.1. Culture chamber for mature single muscle fibres and change in tetanic force in response to different growth factors. A Top-view of the culture chamber. B Lateral view of the chamber. C Photograph of a single muscle fibre during culture. D Tetanic force during culture in the presence of BSA with or without insulin, IGF-1, MGF or insulin/MGF.


The above had a picture chart, but I couldnt paste it....Mattris, let me see if I can find anything else of interest.
 
Dwight Schrute

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Bear in mind however that this doesn't mean I necessarily think MGF is really "the answer" (at least based on what I know--I do think it important though). However, Spook has pointed out to me that recombant GH use in one study using elderly subjects found that the GH use increased MGF significantly. Now, we know GH use isn't a good anabolic substance in trained, young athletes, but GH does seem much more anabolic in elderly subjects, and I kind of wonder if it doesn't have something to do with GH's effects on MGF activity (and thus, satellite-cell availability, which definitely declines which age). Such is my hypothesis at least (although, then again, by that logic, assuming GH influences MGF in the young, it may not be as critical--complex subject this be).


Very cool though...
Couple things to think about. The study on elderly men did not measure hepatic IGF-1 levels so it could have easily been the results of increased IGF-1 levels as well (GH>IGF-1>MGF). Several studies on mice have shown increased hepatic IGF-1 led to hyperplasia (which would lead you to believe there was increased MGF levels as well). Since the research in men isn't exactly clear we have to put the pieces together (which doens't make it fact but gives us a general idea of possibly could be going on)

We also have to look at its anti-catabolic effects and the similar action insulin has. Insulin's main action at promoting an anabolic environment (within normal physiological levels) is be reducing protein degradation. IGF-1 is much more potent than insulin and decreases protein degradation substantially more than insulin so there easily could be benefits in that area especially in older men.

Just some things to think about as I've seen one person clearly point out that IGF-1 won't cause hyperplasia. It is quite funny that he makes these bold statements while the leading authorities in this area don't even have the answers.
 

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