Genetic advantages article- some people are born lucky some are not

  1. Genetic advantages article- some people are born lucky some are not

    Written by Patrick Arnold
    Friday, 12 June 2009


    I am getting sick of this recent obsession with “fairness in sports.” I have news for everyone: SPORTS ARE INHERENTLY UNFAIR. In fact I will go so far as to say that in many cases performance-enhancing drugs serve to level the playing field of sports.
    OK, you probably are thinking that I am on some drugs right now (and not the performance-enhancing variety). However, I believe my line of thought here is very lucid and rational. Let me ask you…is the person who trains the hardest and puts forth the most effort in competition always the one who wins? Of course not!! In fact, the number one determinant in who will excel in sports is genetics. Characteristics such as large muscle mass, nervous system efficiency, optimal anatomical proportion, blood oxygen carrying capacity and visual acuity can all be vital keys to the making of a champion. And obviously we are not all born with the same gifts. When an athlete takes steroids, EPO, or gets Lasik eye surgery we say that they are enhancing their performance. Many of us go on to say that this enhancement is cheating, or unfair. But what about the person who is already born with greater than average testosterone levels, or extra red blood cells, or 20/10 vision? What the hell is so fair about that? Wouldn’t it be more fair if people were allowed to Make Up for what Mother Nature has neglected? This is all fodder for some pretty cool debates, but that is not what this month’s article is about. I just used this as a lead-in to discuss some of the interesting genetic anomalies that have allowed some people to go on to athletic prominence. I have discussed just a few such mutations here; there are several more that science is aware of and perhaps hundreds more that have not been discovered yet.

    The past decade has seen great advances in our understanding of human biology. Thanks in large part to the power of supercomputers, researchers have been able to analyze and map the blueprint of life known as the human genome. This blueprint represents an extraordinary tool for uncovering mysteries such as the causes of disease and the mechanisms behind the process of aging. DNA consists of specific segments called genes and each gene is basically a code meant for the synthesis of a specific protein. That protein may be a structural protein, a hormone, a cellular messenger, or a host of many other possibilities. In some cases that protein may be something relatively insignificant and in others it could be something very important, such as dystrophin— a protein found in normal muscle that when absent results in the disease of muscular dystrophy (MD). Genes of course determine our physical attributes— whether we will be tall or short, muscular or fat, weak or strong. The genes that allow someone to become a champion weightlifter and the genes that give a legendary marathon runner such great endurance are obviously not the same, but what both of these athletes have in common is the gift of heredity. And it is this athletic gift of heredity that we are learning more and more specific facts about every day. Researchers have speculated that genetic factors determine 20 percent-80 percent of the variation in a wide variety of traits relevant to Athletic Performance, such as oxygen uptake, cardiac output, and the relative proportion of fast and slow fibers in skeletal muscle. In this article, we will examine some of the specific genetic anomalies that science has discovered to be present in and purportedly responsible for the great physical gifts of some extraordinary athletes.

    The myostatin gene is located in skeletal muscle and encodes for the production of the protein hormone myostatin. Myostatin functions in the body as a limiter of muscle growth— the more myostatin you produce, the smaller your muscles will be. Myostatin and the associated myostatin gene were discovered in 1997 by geneticists McPherron and Se-Jin Lee. Soon afterward, Lee produced a strain of mutant mice that lacked the gene and these mice grew twice as big and strong as normal mice. Lee also identified a defective myostatin gene present in so-called “double-muscled” Belgian Blue cattle. It was a goal of Lee’s to seek out myostatin gene mutations in humans to confirm that the protein serves the same muscle-related function in humans as it is known to do in animals. So he underwent a search mission for this abnormality in people, and then finally in 1999 he discovered a German baby boy with remarkably developed musculature. Lee studied the boy from 1999 unitl 2004, when he announced his findings to the world in the New England Journal of Medicine. The child was initially spotted by a neurologist at a hospital in Berlin. Asked to examine the baby, he noticed the infant's bulging thigh and arm muscles. Having just read about myostatin a few weeks earlier, the doctor made the connection and eventually the news made its way to Lee. Lee found no myostatin in the boy’s blood and was also able to demonstrate that the boy had extraordinary strength to match his muscular hypertrophy. He also was able to identify a myostatin gene defect in the boy’s mother, who (not so) coincidentally was a former professional sprinter. Interestingly enough, the mother reported that several of her family members are also stronger than normal— one being a construction worker who used to lift large curbstones unaided.
    Other than the large muscles and accompanying strength, the boy appeared normal and healthy, which was good news for Lee’s team. Lack of side effects invited the possibility of myostatin-based drugs for the treatment of musculoskeletal disorders such as muscular dystrophy (MD) and age-related wasting. Today there actually are such drugs in development. One is called Stamulumab and it is a monoclonal antibody to myostatin. This antibody binds to myostatin and renders it inactive, thereby mimicking the effects seen with myostatin gene defects or deletions. Clinical trials with this drug commenced in February 2005. Scientists believe it is possible that myostatin gene variations can give rise to physical attributes that confer advantages in athletics. Currently, little is known about the prevalence of this mutational advantage. Such is not the case for another known genetic anomaly, which has been clearly characterized and identified in specific populations.

    There is a protein present in fast-twitch muscle fibers called Alpha-Actinin-3. I am not sure if science has quite figured out its exact purpose, but we do know that it is somehow associated with the optimal activity of this explosive muscle fiber type. Alpha-Actinin-3 production is governed by a gene called ACTN3. Apparently, a significant part of the population has a mutated form of this gene which cannot manufacture Alpha-Actinin-3. The appearance of this mutation varies substantially amongst different ethnic groups— about 18 percent of Europeans, 25 percent of Asians and only 1 percent of Bantu-speaking people in Africa carry the mutant form of ACTN3. Now these people are not crippled and their daily lives are not affected at all, so apparently this protein is hardly vital to survival. However, when it comes to Athletic Performance it appears that the presence of either a normal or abnormal ACTN3 can make a substantial difference in what activities you excel in.
    A team of researchers analyzed the effects of ACTN3 muscle physiology and performance. They engineered mice that lacked the gene and found that their muscles contained a lot more of the enzymes known to be associated with aerobic metabolism. Apparently the lack of Alpha-Actinin-3 resulted in their fast-twitch muscle fibers taking on more of the characteristics of slow-twitch fibers. These same ACTN3 knockout mice were able to run 33 percent longer than normal mice on the treadmill, indicating that the metabolic alterations observed carried over into differences in actual muscle performance. To test the theory in humans, Australian researchers analyzed the genes of a large group of world-class athletes as well as a group of nonathletes. They hoped to find a correlation between the ACTN3 gene type and the style of athletic prowess (sprint or endurance-related events) of each athlete. What they found is the athletes who excelled in explosive sprint-type events had 6 percent prevalence of ACTN3 gene mutation, nonathletes had 18 percent and endurance athletes had 24 percent. So there definitely was a measurable connection. So is this mutation just random? Geneticists don’t seem to think so. They found that there was less variability than normal in the DNA surrounding the mutation, which suggests that natural selection was at play. I personally find this intriguing, since the research shows that the farther from Africa an ethnic group resides, the greater the probability of the mutation. Perhaps the muscular endurance once needed for such long migrations away from man’s land of origin was aided by ACTN3 mutations.

    EPO Mutants
    Eero Mantyranta was a phenomenally succesful Finnish cross-country skier. At the 1964 Winter Olympics in Innsbruck, he dominated his competition, winning gold in the 15- and 30-kilometer events. Mantyranta went on to participate in four Winter Olympics, winning a total of seven medals. Was his success due to better training methods, superior work ethic, or maybe even drugs? Or perhaps something else was at play? In 1993, scientists discovered something that may have gone a long way in answering these questions. It appears that Mantyranta came from a family that had a history of polycythemia, which is a condition resulting in an overproduction of red blood cells. This condition can lead to dangerous thickening of the blood, however it can also lead to a greatly increased oxygen-carrrying capacity— something that is obviously of enormous value to a cross-country skier. Mantyranta’s family tree carried a mutation of the gene encoding the EPO receptor. In fact, many members of his family were champion cross-country skiiers as a result. EPO, or erythropoietin, is a peptide hormone which is responsible for the manufacture of red blood cels via stimulation of the development of precursor cells in the bone marrow. EPO works by binding and activating a receptor called the EPO receptor (EPOR). The mutation we are talking about here caused the development of abnormal EPORs. The EPORs of Mantyranta’s family were extremely sensitive to low levels of EPO in the blood, so they kept demanding the production of more and more RBC progenitor cells, even though the body’s feedback mechanism was downregulating the amount of EPO in the blood. It did not matter that Mantyranta’s EPO levels were very low; his EPORs were behaving as though there were large amounts of EPO in his body. This resulted in his red blood cell levels being constantly high (up to 50 percent above normal). As a consequence, his ability to carry oxygen to his muscles was elevated, however he was also under great risk for complications involving hypertension and blood clot formation. In fact, family members with this mutation did not live very long lives. This EPOR mutation is quite rare, however hereditary polycythemia is less rare and there may be other red blood cell mutants out there excelling at endurance events. Scientists are currently studying the subject in greater detail.
    Well that’s enough mutants for this month. I figured you would like this article, since the very fact that you picked up a hardcore bodybuilding magazine means you dig freaks. Or perhaps you just like pictures of men in tight underwear. Either way, it’s cool with me, man. See you next month. APR50 50 % off
    Mind and Muscle Code AM10
    Great Physique fitness, facebook, online coaching

  2. Very interesting. Why can't we all be born with a myostatin deficiency if there are no side effects? lol

  3. thats sweet wish i had the myostain defective gene

    maybee thats the next step in creating a human superrace where everyones jacked out of their minds and strong as a gorrilla

    my question is why would evolution even support a hormone that limits muscle production

  4. Good post.

  5. my question is why would evolution even support a hormone that limits muscle production
    To stop us starving to death during famine times. Muscle is very metabolically active, while fat requires little energy to maintain. That's why It's easier to gain fat that muscle, unfortunately.

  6. Good article.

  7. I wonder if there will be a myostatin-inhibitor product released in the future.. Seems like something you would take for an amount of time to see any results. Perhaps a product that downregulated myostatin production and even digested some of the existing myostatin could be effective for cycles of several months.. If those without myostatin haven't got any severe drawbacks it could be an extremely effective and safe way of increasing muscle growth. Thoughts?

    Edit: google gave me this:

  8. There are a couple of the Myostatin babies now. We've got one that i know of here in the states. He has to eat all day long cause his body doesn't store fat! haha

  9. I read an article last night that stated creatine was a myostatin blocker/reducer.

  10. Actually myostatin inhibition isn't that good. I know some biochemists who were expermenting some chemical that inhibits myostatin expression in rats, but that inhibiton brought two major down sides to it's potential as a medicine to some muscle-wasting diseases (and of course to us as a neat "supplement"): first is that that myostatin inhibitor doesn't distinguish what kind of muscle fibers it does inhibit, thus creating enlarged muscles including cardiac muscle (heart) and stomach as well as the muscles that make us move (don't remember the technical name of them), and it also created a proliferation of cancerigenous cells by uncontrolled muscle cell growth/multiplication. Wich made this biochemist team to conclude is that it isn't only the myostatin inhibition per si that deactivates our muscle development controlling system but keep those people born with that illness (a good one for us of course) alive without that kind of problems, but it might rather be either a mutation of the gene itself or a combination of its deactivation/lack and another gene mutation that specifies the kind of fibers that aren't stoped to grow.

  11. Quote Originally Posted by Mongo97 View Post
    I read an article last night that stated creatine was a myostatin blocker/reducer.
    nice any chance you can pull it up on a history search on your computer? APR50 50 % off
    Mind and Muscle Code AM10
    Great Physique fitness, facebook, online coaching

  12. Quote Originally Posted by Mongo97 View Post
    I read an article last night that stated creatine was a myostatin blocker/reducer.
    I don't believe it is. As far as my understanding goes, Creatine acts as a single strand, free floating phosphate that binds to adenosinediphosphates to make them adenosinetriphosphates and when the ATP breaks off a phosphate to release the explosive energy, the presence of the creatine phosphate concentrates in the blood allows the Diphosphates to regenerate a phosphate immediately back into a triphosphate, in as cycle-recycle pattern, without having to wait on the Kreb Cycle & Electron Transport System to produce the ATP.

    However, if it is does act as a myostatin blocker/reducer, that's the $hit.

  13. I believe it is possible. I feel I have changed my "genetics for building muscle" since I first started.I used to take heavy creatine doses.

    Yes I saw this. Creatine works for myself. First time I used it was when the first month or couple or months when I got into bodybuilding
    (I lifted weights before this for like a year,only doing my chest though
    yep I used to be one of those kids in the gym that always did chest every day I was there basically)

    so when I started bodybuilding in 2002 I gained 10 lbs in two weeks 175 maybe 178-I forget to185..people were asking what I was taking. Now a days I gain 5 lbs if it has been a while like two months or longer and usually a couple pounds if it has not been that long, like a month break.

    not that no one cares, it is personal, I just wanted to put my thoughts on paper and my experience with creatine

    As far as creatine being reducing myostatin it is very possible and pubmed is great APR50 50 % off
    Mind and Muscle Code AM10
    Great Physique fitness, facebook, online coaching

  14. nice read, i think i have alot of Alpha-Actinin-3, not trying to sound ****y or full of myself but my whole family is big in muscular size and strength, we're not exactly endo's but not meso' either. when i was in high school i did football and my explosion off the line was pretty good, i always got the first hit on the other guy. and junior year i was maxing out at 285lbs on bench. high school everyone called me fat kid on steroids. lol. nice read.
    The difference between who you are and who you want to be is what you do.

  15. Good read I like it.

  16. subbing for a later read


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