Working on a Title The sports industry has reached incredible heights over the last few decades, leading to a push for stronger and faster athletes. However, when parents try train their children to become great athletes, they have to notice there are limitations on how good someone can get just from practice. Of course, not just anyone can win seven consecutive tour de Frances like Lance Armstrong, and not everybody can shoot the ball like Michael Jordan. The fact that practice is not enough to succeed at a sport means that something else has to contribute to one’s ability. Recently, scientists have been finding more and more evidence that links a person’s genes to athletic performance. Humans have tens of thousands of genes, each coding for different proteins that act as the workers of the body. Scientists have noted over 150 different genes that contribute to athletic performance. Collaboratively, these genes help determine how good an athlete is. In order for muscles to contract they require a protein found in muscle cells called actin. However, actin needs to be stabilized in order to function. A protein called α-actinin 3 stabilizes actin so that it can work properly. (Yang, et al., 2009). Despite α-actinin-3’s seemingly critical function, scientists noted the lack of the protein in more than one billion people worldwide (North, 2008). Eventually the reason for the proteins deficiency in the population was uncovered. In the people who lack the protein there is a change in their genes, causing a non-functioning version of α -actinin-3 to be produced. Therefore, two groups are created: a group of people that makes a-actinin-3, and another group of people that creates a nonfunctioning protein. (Yang, et al., 2009). The increasing prevalence of those who do not make the protein (especially in European and Asian populations), have led some to question if having the non-functioning protein is beneficial to athletics, and if so, why would this advantageous relationship exist (North, 2008). Scientists have conducted much research identifying the characteristics of people who produce the protein, and those who don’t make the protein since the identification of the two groups in 1999. The research has been conducted in elite athletes because the influence of α-actinin-3 on muscle function should be most noticeable in these subjects. According to Enyon, et al., (2009) there is a link between those who make the protein and elite sprint and power performance, and a link between those who don’t produce the protein and endurance. Since Enyon’s experiment, many other experiments have been conducted in different types of athletes. However it has been found that even though other scientist’s research supports the link between those who make the protein and sprint and power performance, much research conducted on these genes finds no link between people who do not make the protein and endurance. In one of these other experiments that branched off from Enyon's, scientists studied whether or not having the protein provided an advantage to artistic gymnastic performance. As hypothesized, the authors noted a higher degree of gymnasts that made the protein (Massida, et al, 2009). Although this experiment supports Enyon’s conclusion that having the protein contributes to power performance, it also refuted Enyon’s link between people who didn’t make the protein and endurance. In Massida’s experiment testing gymnastics, there was an equal number of gymnasts and controls, or ordinary people, that didn’t make the protein. In addition, two more experiments testing soccer players and triathlon runners have linked people that make α –actinin-3 to sprint and power performance, while haven’t neither have linked those who don’t produce the working protein to endurance running. Scientists recorded that a higher degree of professional soccer players make the protein compared to endurance athletes and controls; nevertheless, the experiment also indicated an extremely similar amount of endurance runners and controls that don’t make the protein ( Santiago, et al., 2009). This shows that the production of the nonfunctioning protein may not be linked to endurance running. Finally, according to Saunders et al., (2007) there was no link between those who don’t make the protein and any “ultra-endurance performance”. So, although Enyon concluded that people who don’t make a functioning α-actinin-3 have an advantage in endurance activities, most other experiments do not support this conclusion. Recently, a Colorado based company, ATLAS Sports Genetics, opened plans to screen for the protein. The company says if you make α-actinin-3 you have an advantage in sprint and power events, but if you don’t make a working version of αactinin-3 then you have an advantage in endurance events. By determining whether or not you have the protein, the company thinks that enables them to give parents an idea of how good a child can be a sports, and what sport their child is predisposed to excel in (Lite, 2008). However, experiments conducted over the past eight years show a non-functioning protein is not linked or additive to endurance performance. The research on this topic is still relatively new, but there is not enough evidence supporting these claims by ATLAS Genetics to purchase these tests. The evidence recorded by scientists over the years may in fact help parents determine which sport their child would be best in, but it cannot ensure how good a child can be at that sport. 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