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Q1: sir , you suggest best way of GH use is to inject it directly in the muscle group trained that day , this is site specific application u say (page 116) , now we know all the conversion of GH to IGF-1 is done in the liver, so what benefits are u mentioning here cos site increase og-1, or MGF is not going to happen , so what’s the use of this method ?
2)u also suggest post workout GH injects (page 117) , now , frank is using Humulin post workout which is active I think for 6 hrs or so , now ure suggesting gh shot an hour after the slin shot , he wudve also got in his huge protein shake, carbs etc with his post workout slin shot , simply means insulin levels are very high . its common knowledge gh doesnt work in high insulin environment , as they contradict each other , so arent we wasting a gh shot here ??
Q2: sir , in most of ur writings , u mention the hepatic liver production a lot and seem to give it a lot of importance , recent studies show that increased hepatic-1 is linked with cancer development(growth of unwanted cells ) and it seems like localised-1 and mgf is much more important , also , in a study done in rats that are engineered not to produce hepatic IGF, growth of the rats, including skeletal muscle development, is still normal. This sugggests that liver produced IGF is not very significant for muscle development.
this itself is enough to show liver-1 is playing very lil role, if any in muscle hypertrophy , isnt it sir ?
A: Interesting contradictive questions to say the least. You appear to be suggesting that localized IGF-1 formation is non-existent yet more effective for building muscle as well. Hmmm. Okay!
In truth research has validated on several occasions that GH and insulin do indeed have a site-specific response of anabolism on target tissues. The fact remains that it is the interaction between GH and insulin that allows for the formation of somatomedins such as IGF-1…which is part of the synergistic response.
The issue concerning cancer is moot as we are discussing a single source of origin for IGF-1 as if it were actually a fact to come to this supposition. Cancer cells produce a great deal of IGF-1 themselves.
We will talk about rats in a moment but I think it is time for a basic review of factual information.
The Latest Research on IGF, Growth Hormone, Insulin…and Site Specific Response
A Brief Lesson To Help Catch Up First
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.
Q1: sir , you suggest best way of GH use is to inject it directly in the muscle group trained that day , this is site specific application u say (page 116) , now we know all the conversion of GH to IGF-1 is done in the liver, so what benefits are u mentioning here cos site increase og-1, or MGF is not going to happen , so what’s the use of this method ?
2)u also suggest post workout GH injects (page 117) , now , frank is using Humulin post workout which is active I think for 6 hrs or so , now ure suggesting gh shot an hour after the slin shot , he wudve also got in his huge protein shake, carbs etc with his post workout slin shot , simply means insulin levels are very high . its common knowledge gh doesnt work in high insulin environment , as they contradict each other , so arent we wasting a gh shot here ??
Q2: sir , in most of ur writings , u mention the hepatic liver production a lot and seem to give it a lot of importance , recent studies show that increased hepatic-1 is linked with cancer development(growth of unwanted cells ) and it seems like localised-1 and mgf is much more important , also , in a study done in rats that are engineered not to produce hepatic IGF, growth of the rats, including skeletal muscle development, is still normal. This sugggests that liver produced IGF is not very significant for muscle development.
this itself is enough to show liver-1 is playing very lil role, if any in muscle hypertrophy , isnt it sir ?
A: Interesting contradictive questions to say the least. You appear to be suggesting that localized IGF-1 formation is non-existent yet more effective for building muscle as well. Hmmm. Okay!
In truth research has validated on several occasions that GH and insulin do indeed have a site-specific response of anabolism on target tissues. The fact remains that it is the interaction between GH and insulin that allows for the formation of somatomedins such as IGF-1…which is part of the synergistic response.
The issue concerning cancer is moot as we are discussing a single source of origin for IGF-1 as if it were actually a fact to come to this supposition. Cancer cells produce a great deal of IGF-1 themselves.
We will talk about rats in a moment but I think it is time for a basic review of factual information.
The Latest Research on IGF, Growth Hormone, Insulin…and Site Specific Response
A Brief Lesson To Help Catch Up First
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.
