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x30001
Kraken
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- Jan 9, 2019
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Actenin Alpha 3 activation is what you need to maximize your chances of making it as someone who can excel in athletics, college football, having the genetics to pack on muscle naturally and stay lean; ie, have a higher chance of becoming a "Chad". 75%+ of all top flight professional sports stars have an active ACTN3, ranging across many many sports such as soccer, American football, basketball, tennis, swimming, sprinting etc. Under 17% of already athletically fit athletes have an active ACTN3.
Activation of ACTN3 is relatively straight forward and clean in the sense that it is so specific to enhancing skeletal muscle growth potential (only skeletal muscle), and giving a better edge in competitive sports.
MSTN (the myostatin gene) on the other hand is not at all specific to enhancing growth of skeletal muscle and can cause many complications if messed with. A functioning MSTN is what most of us have. causing one or more mutations on the gene is not only biologically much harder than simply activating ACTN3, but also only prevents the myostatin gene from doing all it's tasks. Over 97% of ultra successful professional and college athletes have the normal TT homozygous allele pair on MSTN. MSTN polymorphisms do not statistically provide a genetic advantage in success with athletics. In fact there's so few accomplished athletic professionals who even have a hetrozygous or non-default homozygous allele pair on MSTN.
EDIT: Green bar in picture1 is showing Skeletal Muscle
MSTN is a regulatory gene for many very different parts of our biology. It is in no way selective to skeletal muscle modulation like ACTN3 is.
Activation of ACTN3 is relatively straight forward and clean in the sense that it is so specific to enhancing skeletal muscle growth potential (only skeletal muscle), and giving a better edge in competitive sports.
MSTN (the myostatin gene) on the other hand is not at all specific to enhancing growth of skeletal muscle and can cause many complications if messed with. A functioning MSTN is what most of us have. causing one or more mutations on the gene is not only biologically much harder than simply activating ACTN3, but also only prevents the myostatin gene from doing all it's tasks. Over 97% of ultra successful professional and college athletes have the normal TT homozygous allele pair on MSTN. MSTN polymorphisms do not statistically provide a genetic advantage in success with athletics. In fact there's so few accomplished athletic professionals who even have a hetrozygous or non-default homozygous allele pair on MSTN.
EDIT: Green bar in picture1 is showing Skeletal Muscle
MSTN is a regulatory gene for many very different parts of our biology. It is in no way selective to skeletal muscle modulation like ACTN3 is.
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