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Theoretical Dosing Protocols / Stacks / Explanation
There are many various types of MGF, MGF+IGF-1, IGF-1 stacks that have been attempted and although many of them have been successful, there hasn?t, yet, been a standalone winner. This is due to many factors including availability, price, and little experimental evidence on topics such as down regulation of receptors, antibody production, and suppression of natural hormones/growth factors. There are a lot of people on various boards attempting to ?figure out? the scattered scientific data that is spread throughout the internet but it is doing only a small amount of good since most studies conducted on MGF and IGF-1 are done on rats and almost all of the studies done using IGF-1 use rhIGF-1, which mimics the naturally occurring growth factor. There are a lot of doctors and users who question the safety of exogenous IGF-1 use, however. The prime reason surrounding this questionability is due to the fact that IGF-1 has been shown to increase the growth rate of cancerous tumors, enlargement of organs, and various other lurking variables. It must be noted, however, IGF-1 does not directly cause cancer, however, if a cancerous cell culture is already forming then IGF-1 can increase the rate of growth.
In your body IGF-1 is spliced into many different variants that have different anabolic properties. IGF-1Ea and Mechano Growth Factor (IGF-1Ec or MGF) make up the more important spliced variants of the IGF-1 when referring to muscle growth. IGF-1 receptors are increased greatly following exercise due to lactosis (lactic acid buildup from resistance training), which causes muscle damage to the area. The lactic acid is currently thought to be the culprit as well for other irregular spliced variants of IGF-1, such as des 1-3 IGF-1, which is said to be 10 times more potent than that of IGF-1Ea. The most common variant seen in bodybuilding is Long Chain R3 IGF-1 or LR3 IGF-1. This is because LR3 IGF-1 cannot be bound to the IGF-1 Binding Protein 3 (IGF-1 BP3). IGF-1 and IGF-1 BP3 levels are released based off circulating levels of each. As concentrations of IGF-1 in the body rise so do IGF-1 BP3 and as IGF-1 concentrations fall so do IGF-BP3 levels. Recent scientific evidence points out that the reason for IGF-1 BP3 levels rising due to increased levels of IGF-1 is to increase the half-life of circulating IGF-1. Unbound IGF-1 has a half life of around 20 minutes, where as when it?s bound to IGF-1 BP3 the half life is extended to around ~6-12 hours depending on who you ask. This is why there is so much excitement surrounding LR3 IGF-1, since the effects can be seen at much lower dosages than rhIGF-1 due to the longer circulating half life and higher potency.
Although the exact pathways for muscle growth through the IGF-1 axis aren?t directly known or fully understood, a basic understanding has been established and common mechanisms are currently being discovered. Although the pathways go into a great deal of detail we will be sticking to the main IGF-1 and spliced variant pathways and not into MyoD or M-Cadherin related material/gene expression. It is thought that following muscle damage, circulating levels of IGF-1 are partially spliced towards MGF, which in turn proliferates (increasing in amount) myoblasts, which are stem cells that are used for creating muscle fibers. Muscles do not undergo mitosis like other cells, instead they must have myoblasts fuse to the area and be activated (given an identity). As seen in the graph below MGF levels are at their peak 1-2 days following muscle activity and begin to decline rapidly afterwards. IGF-1Ea levels begin to rise at the same time MGF levels begin to fall rapidly, around day 4. MGF proliferates cells in their mononucleated states (muscle stem cells), which is an important piece of the recovery puzzle since without these new stem cells there can be no new growth. This is seen in people with muscular dystrophy and although their bodies still produce IGF-1, their muscles do not exhibit MGF expression, showing the importance for MGF in recovering damaged muscles. Although MGF does proliferate these new stem cells as well as increase protein synthesis to a slight degree, MGF also inhibits differentiation in muscle cells (differentiation can be defined as: myoblast alignment, elongation, and fusion into multinucleate myotubes, basically giving them a new identity). IGF-1Ea completes the repairs by drastically increasing protein synthesis and differentiating these newly brought stem cells. Another possibility for IGF-1 is muscle hyperplasia. Although hypertrophy, which is seen with anabolic steroids usage and normal training, is the enlargement of the muscle fiber, due to maturing myofibrils within, while hyperplasia is the actual increase in muscle fibers (refer to Figure 8 below to see a picture). Hyperplasia will not be discussed in detail in this manual until it is more fully understood given scientific evidence based off of studies conducted by trusted scientists. Although many have stated that hyperplasia is impossible without exogenous use of IGF-1, this is a somewhat false statement; a better statement would be that IGF-1 induced hyperplasia occurs at a VERY slow rate naturally since at any given time less than 1% of all IGF-1 circulating in the blood is unbound from IGF-1 BP3. One must also know that despite IGF-1?s effects on muscle hyperplasia and the increased rate at which it occurs when using exogenous LR3 IGF-1, the overall results that are seen can often be seen at their greatest a fair amount of time after using LR3. This occurs due to the fact that newly made muscle fibers are not matured instantly during the process of hyperplasia. Instead, these cells must go through the process of hypertrophy before they mature and become enlarged, another exciting reason to use a combination of MGF and LR3 IGF-1. This is the process of body recomposition that people talk so much about on bodybuilding forums throughout the internet, as you can technically work around your genetic limit and move past it. It must also be noted that in recent studies caloric restriction had no significant effect on MGF, IGF-1, or IGF-1Ea (systemic, liver form of IGF-1) receptor count, making the possibility for exogenous LR3 IGF-1/MGF as a potent, muscle sparing cutter, a great idea.
Now that all of this basic knowledge of IGF-1 and MGF has been given to you, we can attempt to set up cycles based off of it. Actual dosing protocols for these growth factors (not including hGH) is quite difficult because unlike hormones such as T3 that can be tested for and, therefore, dosed according to circulating levels, it is almost impossible to detect how much MGF is released following muscle loading or how much of a spliced variant such as LR3 IGF-1 needs to be dosed to prevent antibody production or down regulation of receptors, since LR3 IGF-1 doesn?t occur naturally in the body and all studies done are based off of the naturally occurring hIGF-1. This leads us into human testing based off abstract results by brave guinea pigs looking for that extra edge. Although great results have been seen dosing LR3 IGF-1 at 60-120mcg daily following intense exercise, results begin to taper off after around 4 weeks and down regulation of IGF-1 receptors and IGF-1 antibody production is currently thought to be the culprit. Another theory that is being looked into is the possibility that due to LR3 IGF-1?s ability to suppress natural hGH levels, this in turn inhibits MGF levels, which could be the reason people continue to feel effects such as hunger and vascularity on LR3 IGF-1 but no longer see great gains. This leads one to believe that following a lower dosage scheme for a longer amount of time would be the way to go. It seems that not many people are willing to attempt a cycle consisting of 10-20mcg daily of LR3 IGF-1 due to the cost of LR3 IGF-1 being anywhere from $115-$200/mg depending on the source and many feel that a lower dosage would be a waste since ?instant? results are not seen.
MGF has been shown exhibit its effects even while the IGF-1 receptor was blocked in many studies, proving that MGF works through other various pathways and does not attach to the IGF-1R, making it invulnerable to down regulation of the IGF-1R. Since hGH has been said to contribute most of its effects thanks to increased IGF-1 production, the level of IGF-1 produced by administrating exogenous hGH has to be extremely small compared to the amounts currently being injected, which is probably why exogenous hGH results last indefinitely, as seen by many people who use it year round. These small amounts released are not enough to cause rapid down regulation or antibody production. This would be one reason for lower dosage of IGF-1 to be used. An alternative camp says shorter cycles of higher dosages are more important since they want to rapidly increase the rate of muscle hypertrophy/hyperplasia before side effects and blunting effects are seen.
There are many various types of MGF, MGF+IGF-1, IGF-1 stacks that have been attempted and although many of them have been successful, there hasn?t, yet, been a standalone winner. This is due to many factors including availability, price, and little experimental evidence on topics such as down regulation of receptors, antibody production, and suppression of natural hormones/growth factors. There are a lot of people on various boards attempting to ?figure out? the scattered scientific data that is spread throughout the internet but it is doing only a small amount of good since most studies conducted on MGF and IGF-1 are done on rats and almost all of the studies done using IGF-1 use rhIGF-1, which mimics the naturally occurring growth factor. There are a lot of doctors and users who question the safety of exogenous IGF-1 use, however. The prime reason surrounding this questionability is due to the fact that IGF-1 has been shown to increase the growth rate of cancerous tumors, enlargement of organs, and various other lurking variables. It must be noted, however, IGF-1 does not directly cause cancer, however, if a cancerous cell culture is already forming then IGF-1 can increase the rate of growth.
In your body IGF-1 is spliced into many different variants that have different anabolic properties. IGF-1Ea and Mechano Growth Factor (IGF-1Ec or MGF) make up the more important spliced variants of the IGF-1 when referring to muscle growth. IGF-1 receptors are increased greatly following exercise due to lactosis (lactic acid buildup from resistance training), which causes muscle damage to the area. The lactic acid is currently thought to be the culprit as well for other irregular spliced variants of IGF-1, such as des 1-3 IGF-1, which is said to be 10 times more potent than that of IGF-1Ea. The most common variant seen in bodybuilding is Long Chain R3 IGF-1 or LR3 IGF-1. This is because LR3 IGF-1 cannot be bound to the IGF-1 Binding Protein 3 (IGF-1 BP3). IGF-1 and IGF-1 BP3 levels are released based off circulating levels of each. As concentrations of IGF-1 in the body rise so do IGF-1 BP3 and as IGF-1 concentrations fall so do IGF-BP3 levels. Recent scientific evidence points out that the reason for IGF-1 BP3 levels rising due to increased levels of IGF-1 is to increase the half-life of circulating IGF-1. Unbound IGF-1 has a half life of around 20 minutes, where as when it?s bound to IGF-1 BP3 the half life is extended to around ~6-12 hours depending on who you ask. This is why there is so much excitement surrounding LR3 IGF-1, since the effects can be seen at much lower dosages than rhIGF-1 due to the longer circulating half life and higher potency.
Although the exact pathways for muscle growth through the IGF-1 axis aren?t directly known or fully understood, a basic understanding has been established and common mechanisms are currently being discovered. Although the pathways go into a great deal of detail we will be sticking to the main IGF-1 and spliced variant pathways and not into MyoD or M-Cadherin related material/gene expression. It is thought that following muscle damage, circulating levels of IGF-1 are partially spliced towards MGF, which in turn proliferates (increasing in amount) myoblasts, which are stem cells that are used for creating muscle fibers. Muscles do not undergo mitosis like other cells, instead they must have myoblasts fuse to the area and be activated (given an identity). As seen in the graph below MGF levels are at their peak 1-2 days following muscle activity and begin to decline rapidly afterwards. IGF-1Ea levels begin to rise at the same time MGF levels begin to fall rapidly, around day 4. MGF proliferates cells in their mononucleated states (muscle stem cells), which is an important piece of the recovery puzzle since without these new stem cells there can be no new growth. This is seen in people with muscular dystrophy and although their bodies still produce IGF-1, their muscles do not exhibit MGF expression, showing the importance for MGF in recovering damaged muscles. Although MGF does proliferate these new stem cells as well as increase protein synthesis to a slight degree, MGF also inhibits differentiation in muscle cells (differentiation can be defined as: myoblast alignment, elongation, and fusion into multinucleate myotubes, basically giving them a new identity). IGF-1Ea completes the repairs by drastically increasing protein synthesis and differentiating these newly brought stem cells. Another possibility for IGF-1 is muscle hyperplasia. Although hypertrophy, which is seen with anabolic steroids usage and normal training, is the enlargement of the muscle fiber, due to maturing myofibrils within, while hyperplasia is the actual increase in muscle fibers (refer to Figure 8 below to see a picture). Hyperplasia will not be discussed in detail in this manual until it is more fully understood given scientific evidence based off of studies conducted by trusted scientists. Although many have stated that hyperplasia is impossible without exogenous use of IGF-1, this is a somewhat false statement; a better statement would be that IGF-1 induced hyperplasia occurs at a VERY slow rate naturally since at any given time less than 1% of all IGF-1 circulating in the blood is unbound from IGF-1 BP3. One must also know that despite IGF-1?s effects on muscle hyperplasia and the increased rate at which it occurs when using exogenous LR3 IGF-1, the overall results that are seen can often be seen at their greatest a fair amount of time after using LR3. This occurs due to the fact that newly made muscle fibers are not matured instantly during the process of hyperplasia. Instead, these cells must go through the process of hypertrophy before they mature and become enlarged, another exciting reason to use a combination of MGF and LR3 IGF-1. This is the process of body recomposition that people talk so much about on bodybuilding forums throughout the internet, as you can technically work around your genetic limit and move past it. It must also be noted that in recent studies caloric restriction had no significant effect on MGF, IGF-1, or IGF-1Ea (systemic, liver form of IGF-1) receptor count, making the possibility for exogenous LR3 IGF-1/MGF as a potent, muscle sparing cutter, a great idea.
Now that all of this basic knowledge of IGF-1 and MGF has been given to you, we can attempt to set up cycles based off of it. Actual dosing protocols for these growth factors (not including hGH) is quite difficult because unlike hormones such as T3 that can be tested for and, therefore, dosed according to circulating levels, it is almost impossible to detect how much MGF is released following muscle loading or how much of a spliced variant such as LR3 IGF-1 needs to be dosed to prevent antibody production or down regulation of receptors, since LR3 IGF-1 doesn?t occur naturally in the body and all studies done are based off of the naturally occurring hIGF-1. This leads us into human testing based off abstract results by brave guinea pigs looking for that extra edge. Although great results have been seen dosing LR3 IGF-1 at 60-120mcg daily following intense exercise, results begin to taper off after around 4 weeks and down regulation of IGF-1 receptors and IGF-1 antibody production is currently thought to be the culprit. Another theory that is being looked into is the possibility that due to LR3 IGF-1?s ability to suppress natural hGH levels, this in turn inhibits MGF levels, which could be the reason people continue to feel effects such as hunger and vascularity on LR3 IGF-1 but no longer see great gains. This leads one to believe that following a lower dosage scheme for a longer amount of time would be the way to go. It seems that not many people are willing to attempt a cycle consisting of 10-20mcg daily of LR3 IGF-1 due to the cost of LR3 IGF-1 being anywhere from $115-$200/mg depending on the source and many feel that a lower dosage would be a waste since ?instant? results are not seen.
MGF has been shown exhibit its effects even while the IGF-1 receptor was blocked in many studies, proving that MGF works through other various pathways and does not attach to the IGF-1R, making it invulnerable to down regulation of the IGF-1R. Since hGH has been said to contribute most of its effects thanks to increased IGF-1 production, the level of IGF-1 produced by administrating exogenous hGH has to be extremely small compared to the amounts currently being injected, which is probably why exogenous hGH results last indefinitely, as seen by many people who use it year round. These small amounts released are not enough to cause rapid down regulation or antibody production. This would be one reason for lower dosage of IGF-1 to be used. An alternative camp says shorter cycles of higher dosages are more important since they want to rapidly increase the rate of muscle hypertrophy/hyperplasia before side effects and blunting effects are seen.
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