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I ran a true myostatin inhibitor and started by injecting it into my left trap. This made my left trap larger than my right one.
Tried injecting the next shot into the right trap but still is not the same size.
What can I do to "balance" this out?
Do I lift heavy on one side? Heavier weights on the smaller muscle than the right?
Synthol or any homolog is not an option for me.
Thanks in advance for your insight and for reading.
I'd say buy more and shoot your other trap, but since there is only one functional myostatin inhibitor, and it's $100 per mg, I'd rather ask how you got any in the first place, and if you're willing to share :0chink:
I am a molecular biologist. I made it.Quote:
Originally Posted by DustMan
It's a myostatin-propeptide expressing plasmid DNA. Technically it is a form of gene therapy or "gene doping".
I will be posting on the full process along with full sequence and a multitude of references. It worked in mice, fish, horse, cow, chicken etc.. big surprise: it works in humans too.
So far I have only tested it in 3 people. 2 males (including myself) and one female (soon to be 2).
I am in the process of making it available. Following all necessary legal routes along with conforming to forum rules.
A large number of questions roll through my head. But, if it worked on one side, why isn't it working the same on the other?
Hopefully you are successful, I am interested to see what comes out of your research.
The plasmid dna transfected the muscle fibers and it then releases it into blood stream. The muscles are then at a certain level of inhibition. A later dose of the same amount will therefore have a lesser effect. The right trap did grow some upon injection but not as much as the left trap did.Quote:
Originally Posted by Amuuzen
What comes out of this research and the decades before it is that gene doping is the future of performance enhancement.
It doesnt affect hpa/hpta, myostatin null humans live full lives, temporary use of it even over years has not shown any statistically significant cardiac hypertrophy, effects can last years, no current test for it, no potential for integration into the genome and therefore no increased chance of cancer, converts white fat cells to brown fat cells, etc etc
Aas are many times more harmful than this true myostatin inhibitor could ever be even if its use "approached abuse".
Some time from now our children or grandchildren will go on these forums and these types of therapies, especially amongst professionals, will be the norm.
Maybe try neglecting the other trap as much as possible. Not only trap work, but with delts and some rowing as well. Damn you’re running this as an experiment on yourself?Quote:
Originally Posted by MaxiMyME
I do not feel that there have been enough studies for long enough periods of time to make any claim if it is safe or not.Quote:
Originally Posted by MaxiMyME
The same way when creatine originally came out. I used it anyway. LOL
I read somewhere about concerns over respiratory effects. I do not remember the reason why.
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Yes I have run on myself and others this experiment.Quote:
Originally Posted by wango
The myostatin inhibitor is actually indicated and went through clinical trials for treating muscular dystrophies. Its efficacy was low for the measure of improving what causes eventual death in individuals with muscular dystrophies: diaphragmatic atrophy to the extent that breathing ceases.Quote:
Originally Posted by charger69
The myostatin inhibitor does have some potential to cause diaphragmatic hypertrophy as well as cardiac hypertrophy but 1. This is orders of magnitude less than majority of aas and 2. Also they occur in people who are born with myostatin disabled. So throughout a lifetime.
Some diaphragmatic, just like cardiac hypertrophy is good for breathing and pumping blood, respectively.
For example cardio causes some cardiac as well as diaphragmatic hypertrophy.
My understanding is the inhibition increases mass but does not necessarily increase strength.
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I would need to see a sizeable person before I believed any claim that it works.
Can you provide any proof that it works?
There are a number of medical studies on myostate inhibitors.Quote:
Originally Posted by The Deadlifting Dog
I do t know about his brew, but if it functions like a myostatic inhibitor it does work. The extent would be the question. Most studies are based off of muscle wasting diseases however there are some out there without the muscle wasting diseases.
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There is an increase in mass and there is an increase in strength (as will come with mass) but it was not proportional to the increase in strength.Quote:
Originally Posted by charger69
This is because myostatin inhibition causes skeletal muscle hypertrophy but not hyperplasia.
Thanks. I will do some searching.Quote:
Originally Posted by charger69
Now if I could just find a new knee and shoulder...
Wondering why you chose to try it on your traps.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4271642/
https://selfhacked.com/blog/myostatin-inhibition/
If building muscle, preserving mass and forcing blood to muscle fibers is the name of the game...I can certainly find many more studies on the role of testosterone and other AAS that are essentially doing the same things, as well as HGH or other secretagogues. It’s not like they’re risk free either and have documented adverse events around respiratory issues, fluid retention and long term risk of muscle imbalance.
I’ll stick with some good old testosterone and some shrugs (maybe going heavy on the underdeveloped side). Perfect symmetry also has a lot to do with genetics, balance, gait and injury as well
The primary benefit it had was maintaining muscle while losing lots of fat. Which makes sense with regards to its mechanism of action.Quote:
Originally Posted by The Deadlifting Dog
Can I post my phone number? Lol. I can explain all you would like.
I have never been big. I have played soccer my whole life. Only been overweight from drinking too much. Lost 30+ pounds (depending on the timing and how much you can attribute to the inhibitor). Hence the 30 plus.
PM me and I will give you all the information you want. But I would rather talk over the phone honestly to make things quicker.
It's about what goes in versus what comes out. I was nearly 200 and overweight. Lost a shit ton of weight maintained all strength.
Think its bs? Try it.
Traps cause I had worked them out that day and I felt they are easy to tell when they grow with an opposite side "control".Quote:
Originally Posted by T-boner
Also my traps are my strongest muscle (yes including my legs). 450 - 3 sets of 4 np. Or for those who like more reps: 420 4+ sets at 7 each.
Aas have been around and in use for a long time. Follistatin has been studied but it can affect many metabolic pathways some of which involve akt and other oncogenic pathways along with some patheays that affect the leydig cells of the testis.Quote:
Originally Posted by SampsonandDelilah
One of the first gene therapies was approved back in 1990.
Go to pubmed and do your own research.
I got pics, references, stats etc I'll share on this. This is one of multiple gene therapies/"gene doping" I have and will continue to make.
It had profound benefits at the modest (200-500ug) dosages I took primarily regarding maintaining gains and losing a lot of fat. Studies use up to a mg/kg.
It's not excessively expensive but it takes a lot of bench work to produce. Have to check for contaminants, use vaccine grade isolation columns, molecular bio grade water and all to yield only about a mg at a time how I have been doing it lately. Can scale up to say 50mg for a substantial cost.
For muscle building effects a longer time at higher dosages would be required.
Look at myostatin null organisms. This is over a lifetime that they look this way. A minimum of years so it is not surprising that a modest effect is found over 8 weeks at a very low end dose.
I'll stop touting its benefits. Just try it in your research experiments free of charge.
Hit me with more questions.
Search pubmed and let me know where I have been inaccurate or exaggerated.
***If I have violated forum rules or even come close, PLEASE tell me and I will adjust accordingly. These forums are my staple for this.
Oh and myostatin inhibition does not force blood to muscle. Myostatin is an evolutionary "brake" on muscle growth to reduce caloric/metabolic requirement.
One of the studies that I saw showed it had no effect on the strength.
The strength increase was equal to the placebo group. Can you provide references where it shows that there was significant increase in strength from the placebo group?
This is the thing about research ... it needs to be compared to a placebo group. Everyone had an increase in strength... that is the result of the workout and not the inhibitors.
I find this a very interesting conversation.
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My bad I thought I posted here but I was mistaken.Quote:
Originally Posted by charger69
It is 100% true no statistically significant (relative to control) increase in strength happens due to myostatin inhibition only causing skeletal muscle hypertrophy and not hyperplasia.
It has been studied with controls.. just not in humans. Anyone know any identical twins of same age height weight bf etc willing to test it? :-P
My control was my opposing muscle. Best I could think of.
I am going to turn this conversation a little.. it has been said that creatine acts similar to a myostaten inhibitor however there is also an increase in strength. Why?
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Off the top of my head I believe creatine provides not only myostatin inhibition (albeit at a nearly negliable level) but it also increases ATP available to muscles thus increasing primarily endurance but also strength.Quote:
Originally Posted by charger69
I am not sure if creatine causing increased cell volume is sufficient to account for an increase in strength.
I have read that creatine has a direct effect on myonuclei which can lead to increased force contraction, thus producing additional strength increases, or at least augmenting them.
I would have to dig deeper to know for sure but the data is available.
Phosphorylation is improved in muscles. Energy for contractions is supplied by ATP (3 P’s or phosphate). When you contact a myofibril the ATP is used but is converted to ADP (a P is removed). Phosphorylation helps convert the ADP back to ATP.Quote:
Originally Posted by charger69
This one I had to check for, but I’m pretty sure it helps calcium release in the myofibril, allowing more to bind to the myosin. Again, improved muscle fiber contraction for greater strength.
NSCA certification was tough.
I like nicknames- so I am going to call you the wango-tango after Ted Nugent.Quote:
Originally Posted by wango
Thanks for the answer.
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My pleasure. And thanks for the nick name, I like Ted Nugent too.Quote:
Originally Posted by charger69
I hope that you do t speak Spanish. Wan go in Spanish means loose. More or less.Quote:
Originally Posted by wango
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And here I just thought it WAS a cool sounding name. Loose? Great, my wife is going to get a laugh out of that.Quote:
Originally Posted by charger69
OK, I’m changing my name to phosphorylation, I think that’s safe.
LMAO!Quote:
Originally Posted by wango
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El myostatin inhibitadore es bueno para Los musculos y tambien Los muchachas queiren el pena de los hombres que estan grandes.Quote:
Originally Posted by charger69
Soy un medio mexicano y puedo hablar en espanol cuando quieres.
Pudo amor.
They call me the reverse wetback. Lived and worked in Mexico for 26 years.Quote:
Originally Posted by MaxiMyME
I can offend anyone in Spanish. LOL
Wife is 100% Cachanilla.
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Mi familia es de Mexico. But the shady stuff some people work with there.. or anything else.. ain't worth dying for!Quote:
Originally Posted by charger69
Are inhibitors available to the public?
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Gene therapy is available to the public for certain conditions however the cost is astronomical (dozens of thousands of dollars).Quote:
Originally Posted by charger69
It is kind of a gray area. Just like "research purposes only". If there is a demand for something you can always get it somewhere.
God bless America!!!