Sachlichkeit
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K boys
Muscle Hyperplasia is a phenomenon observed in the musculature of animals under intense physical stress. Instead of getting stronger, the muscle fibers SPLIT, creating new, permanent strands.
There are no studies on hyperplasia in humans because of ethical concerns. idk I forgot how they measure it but apparently you'd have to saw somebodys pec in half or something retarded
Only human account of hyperplasia taking place in adults is an abnormal amount of unique muscle fibers in bodybuilders when compared to normal people.
What this means is, your capacity to build muscle, and your muscular architecture can be permanently altered similar to how pro osteogenic drugs irreversibly effect bone development.
Primary trigger
Mechanical overload. That is, reps until failure, and then the eccentric contraction post failure. You lift weights, then after failure, you control the lowering of the weight. The LOWERING of the weight specifically is the best bet to induce hyperplasia. The other alternatives witnessed in animal studies are non practical or more risky (chronic musculature stress, resistance stretching,) these are more prone to injuries and require a separate training regimen. Whereas if u alrd go 2 gym just lower the weight good.
We have now split our muscle fibers, now we need to create an abnormally "pro split" environment so the fibers don't die off.
MECHANO GROWTH FACTOR MGF is an IGF insulin like growth factor analog. HGH produces IGF-1 >>> IGF-1 binds to protein in the body and is then shuttled around systemically. IGF-1, NOT HGH, is the primary cause of growth
MGF is an IGF-1 analog that is originally produced locally in areas of the body post mechanical stress. It's primary purpose is to activate muscle satellite cells post workout for repair and proliferation. Only word that comes to mind is "substrate," fibers split >>>> no satellite cell activation >> growth can't be supported >> split fiber breaks down instead of becoming separate permanent muscle fiber.
The half life of MGF is few minutes, wakes up cells, dies off.
PEG MGF pegylated MGF is man made derivative of IGF-1 that extends half life of MGF from Couple minutes to 12-24hours. So the chance that our hyperplasia fiber splits get enough support is much higher. This creates a pro hyperplasia environment.
Note; seen people use MGF in puberty for bones, idk anything about it, might be worth looking into given that it deals with epigenetic mechanical side of physical development (which is underrated on .org)
Nvm lmao but I alrd wrote all this so gonna post it anyways.
The threshold for hyperplasia is contingent on being huge, thats why bodybuilders have more individual muscle fibers (I think,) so u guys need to be huge. Probably IFBB pro bodybuilding tier. If u DNR'd, good. Rn the most viable way looks like years of blasting and lifting until you push the muscle fibers to genetic limit and cause splitting (AND THEN) creating pro-split environment
We can theoretically trigger premature splitting by going BEYOND FAILURE (as previously stated,) and using standard gear (HGH, Testosterone, + PEG-MGF) to sustain the splits while using other drugs for cell plasticity but im tired and no longer interested
FUCK I just wasted 2 hours of my life
Muscle Hyperplasia is a phenomenon observed in the musculature of animals under intense physical stress. Instead of getting stronger, the muscle fibers SPLIT, creating new, permanent strands.
There are no studies on hyperplasia in humans because of ethical concerns. idk I forgot how they measure it but apparently you'd have to saw somebodys pec in half or something retarded
Only human account of hyperplasia taking place in adults is an abnormal amount of unique muscle fibers in bodybuilders when compared to normal people.
What this means is, your capacity to build muscle, and your muscular architecture can be permanently altered similar to how pro osteogenic drugs irreversibly effect bone development.
Primary trigger
Mechanical overload. That is, reps until failure, and then the eccentric contraction post failure. You lift weights, then after failure, you control the lowering of the weight. The LOWERING of the weight specifically is the best bet to induce hyperplasia. The other alternatives witnessed in animal studies are non practical or more risky (chronic musculature stress, resistance stretching,) these are more prone to injuries and require a separate training regimen. Whereas if u alrd go 2 gym just lower the weight good.
We have now split our muscle fibers, now we need to create an abnormally "pro split" environment so the fibers don't die off.
MECHANO GROWTH FACTOR MGF is an IGF insulin like growth factor analog. HGH produces IGF-1 >>> IGF-1 binds to protein in the body and is then shuttled around systemically. IGF-1, NOT HGH, is the primary cause of growth
MGF is an IGF-1 analog that is originally produced locally in areas of the body post mechanical stress. It's primary purpose is to activate muscle satellite cells post workout for repair and proliferation. Only word that comes to mind is "substrate," fibers split >>>> no satellite cell activation >> growth can't be supported >> split fiber breaks down instead of becoming separate permanent muscle fiber.
The half life of MGF is few minutes, wakes up cells, dies off.
PEG MGF pegylated MGF is man made derivative of IGF-1 that extends half life of MGF from Couple minutes to 12-24hours. So the chance that our hyperplasia fiber splits get enough support is much higher. This creates a pro hyperplasia environment.
Note; seen people use MGF in puberty for bones, idk anything about it, might be worth looking into given that it deals with epigenetic mechanical side of physical development (which is underrated on .org)
Nvm lmao but I alrd wrote all this so gonna post it anyways.
The threshold for hyperplasia is contingent on being huge, thats why bodybuilders have more individual muscle fibers (I think,) so u guys need to be huge. Probably IFBB pro bodybuilding tier. If u DNR'd, good. Rn the most viable way looks like years of blasting and lifting until you push the muscle fibers to genetic limit and cause splitting (AND THEN) creating pro-split environment
We can theoretically trigger premature splitting by going BEYOND FAILURE (as previously stated,) and using standard gear (HGH, Testosterone, + PEG-MGF) to sustain the splits while using other drugs for cell plasticity but im tired and no longer interested
FUCK I just wasted 2 hours of my life
