T Nation

What does this mean?

I am writing this letter per the request of Flex Wheeler.

I would first like to briefly provide you with some background information regarding BALCO Laboratories. BALCO has been working with elite Olympic and professional athletes for over fifteen years. BALCO has provided testing and consultation for over 250 NFL players including the entire 1998 Super Bowl Champion Denver Broncos team and the entire Miami Dolphins team. BALCO works with professional athletes in many sports including teenis (Michael Chang, Jim Courier, etc.), hockey, bodybuilding (10 of the 16 1998 Mr. Olympia contestants), track and field, soccer and basketball (Seattle SuperSonics).

BALCO Laboratories has been testing and monitoring Flex on a routine basis during the last year. We have performed tests including blood chemistry (SMAC), complete blood count (CBC), PSA, anabolic hormone levels, genotyping as well as comprehensive testing for nutritional elements. Flex’s test results have been compared to twenty-four other professional bodybuilders and overall he has one of the healthiest profiles. Basically, Flex is in excellent health and has demonstrated the discipline necessary to maintain a peak level of conditioning.

Flex was a participant in a study we recently conducted in collaboration with the Department of Human Genetics at the University of Pittsburgh involving 62 men who made unusually large gains in muscle mass in response to strength training (extreme responders). Flex was one of only nine extreme responders that had the very rare "myostatin mutation." Myostatin is the gene that "limits muscle growth." Specifically, Flex had the rarest form of myostatin mutation at the "exon 2" position on the gene. This simply means Flex has a much larger number of muscle fibers compared to the other subjects or the normal population. We believe that these are the very first myostatin mutation findings in humans and the results of this landmark study have already been submitted for publication. Flex was also found to have a very unusual type of the IGF-1 gene. In fact, Flex was the only participant in the study that did not have a "match." All of the other extreme responders had at least three other subjects with a matching IGF-1 gene. Based upon Flex's very unique genetic profile, we plan to expeditiously publish a scientific paper that reveals his complete genotype in specific detail. The publication of his remarkable genetic data should generate an enormous amount of media exposure.

Hope this information will be helpful and please call if I can be of assistance.


Victor Conte

Found that on the net somewhere, does this mean that Flex is a Mutant?LOL. Could anybody translate it in english please.

That information is probably 3 years old. I believe Balco labs is responsible for the original development of ZMA. Regarding the findings on Flex Wheeler it does show that he is a freak of nature…but so were 9 others out of 62.

Yes, this does mean that Flex is a mutant, but so is everyone else. As the human genome becomes more extensively characterized we will find that mutations are quite common. They are quite common in lower organisms, and without mutations we would not have been able to evolve from lower organisms (if you subscribe to that theory. Don’t want to start evo vs creation argument). That being said, if these claims are in fact valid, they might explain an individuals genetic ability for phenomenal growth.

With regard to myostatin specifically. Myostatin is a protein that somehow limits muscle growth. The mechanism has not been determined yet, but in animals, if you remove the gene coding for myostatin, and in effect remove the protein, skeletal muscle growth is increased substantially. In fact, when this phenomenon was first described, it was characterized as muscle doubling, because the mice involved had almost twice the muscle mass of the normals. Now the author's claim is that Flex has a mutation in the myostatin gene that is very rare. I cannot confirm this because I have not seen this study published yet. Pittsburgh does have a stellar molecular genetics program though, and they do a lot of work on skeletal muscle, so it is possible. But... the statement, " This simply means Flex has a much larger number of muscle fibers compared to the other subjects or the normal population" is not correct. Flex very well may have more muscle fibers than the normal population, but having a rare mutation in the myostatin gene does not necessarily explain this. A gene can possess a mutation and still code for a protein which maintains maximal activity or even greater. A study would have to be done to determine if the specific mutations described actually inactivate or attenuate the activity of said protein. Further, there is no mention of the measurement of fiber number, and without measuring it you can't say it. It is possible though that a mutation in the myostatin gene would result in an inactive protein, which might then result in greater "natural" muscle growth.

The ironic thing is that with regard to the IGF-1 gene, the author is arguing contrary to his myostatin reasoning. He is saying the Flex possesses a rare isoform of IGF-1, possibly a mutation. Since IGF-1 is an important player in muscle growth and differentiation, the inference is that this rare “mutation” in Flex confers greater potential for muscle growth. Again, the inference is that the rare isoform present in Flex is more active than the normal isoform, which as I previously stated is contrary to the myostatin argument.

If these claims are, in fact, genuine, then I will be very interested. We will have to wait and see.

To know Victor is to be overwhelmed by Victor. He is a very complex pioneer of health products. He recently released Proglycosym for muscle recovery to be taken 30 minutes after heavy lifting. The stuff is amazing. I have been on it for 3 weeks and can see and feel the results. As for his text on Mutant genes, well my guess is that he will have two categories of people after this gene study to design product for. Those that can really assimilate protein and grow muscle and those that can not. He is a great guy and genius would not be a far off label that fits. In closing, I can say he did not have anything to do with the teenage mutant ninjas turtles muscular developement. Peace

I would just like to correct something I stated in my original response. I wrote that the mechanism of myostatin’s effect was not known. I was kind of rushing it and after I submitted I thought to myself, “that isn’t right.”

The mechanism of the growth inhibitory effect of myostatin on muscle growth most likely happens, for the most part, before we are born. As the fetus is developing, muscle cells proliferate and then fuse to form mature muscle (mature fetal at least). Before the mature muscle can form though, the myoblasts (baby muscle cells) must stop proliferating. Myostatin has been shown in tissue culture to inhibit the process which tells the muscle cells to stop proliferating. Ultimately they will likely be stopped via other mechanisms and then fuse into mature muscle fibers. What this means, is that when baby mutant is born, he has more muscle cells than normal baby. If the mutant has twice as many muscle cells as a normal baby and they both lift weights and hypertrophy to the same extent, the mutant will be much bigger. Kind of like if you and a buddy put money in a mutual fund at the same time, but you put in twice as much, in twenty years you will have a lot more money than your buddy even though both accounts grew at the same rate.

Will myostatin also have an effect on the adult over and above the prenatal effect. Maybe, but likely not as substantial. When you lift weights there are many other factors involved other than myostatin (inflammation, mechanotransduction etc.), further, adult myofibers are not going to proliferate, just satellite cells. So, there might be an effect, but again, less observable.

A counter argument could also be made that by inhibiting the differentiation signal to occur, actual hypertrophy might be attenuated.

Mac where did you see this Proglycosym?