Thursday, July 5, 2007

Of Mice and Men...and Muscle (part 3)

Read my previous posts on myostatin here and here.

Meet the whippets (click for larger version):


Whippets are a breed of dog developed specifically for racing. They were officially recognized as a breed in the late 1800s and can reportedly run up to 35 mph.


Take another look at the photos of whippets above. See anything interesting? If you look close, you might notice that the dogs get bigger from left to right. The heavily muscled dogs in the right column are referred to as ‘bully’ whippets by breeders. Apparently, whippet breeders brought this trait to the attention of the National Human Genome Research Institute at NIH. Knowing about the role of myostatin mutations in producing other examples of double muscling, the researchers went looking for mutations in the myostatin gene of whippets.

The results are pretty nicely summed up by the pictures. Wild type whippets (lacking any mutation in the myostatin gene) are on the far left, heterozygotes (dogs that possess one copy of a normal myostatin gene and one copy with a mutation that produces a malfunctioning protein) in the middle, and individuals (bullies) with two copies of the mutation on the right.

If that was the end of the story, it would be interesting to scientists (and useful to dog breeders), but not much else. What makes this more newsworthy is that the researchers were able to connect the genetics with athletic performance.

I don’t know anything about dog racing, but racing whippets are apparently divided into four classes: A, B, C, D. Think of it like the system used in professional baseball in the US (or like soccer leagues in the rest of the world). The fastest dogs are A, the slowest in D. It turns out that dogs with the mutation make up a disproportionate number of dogs in the faster classes. We now have a quantitative connection between genes and performance. (I should point out that the faster dogs almost always possess only one copy of the mutation, not two. I don’t think dogs with two copies of the mutation generally are raced. Muscle bound perhaps?)

This brings me back to the boy in Germany who also has two mutated copies of the myostatin gene. His mother, who was a professional athlete and comes from a family with several members noted for their strength, has one copy of the mutation.

Given that high level athletes have shown themselves willing to do lots of things to gain an advantage over the competition, and knowing that drugs are in the pipeline that would inhibit myostatin, how long will it be before athletes are trying to build muscle by blocking their myostatin? Or how long before the national Olympic training programs or college scouts start screening for these mutations to guarantee that funds for training are spent on athletes with the best genes?

As the authors of the whippet research note:

“Our findings have implications for competitive and professional sports. Here, we show that a disruption in the function of the MSTN [myostatin] gene increases an individual’s overall athletic performance in a robust and measurable way. …

The potential to increase an athlete’s performance by disrupting MSTN either by natural or perhaps artificial means could change the face of competitive human and canine athletics. Given the poorly understood consequences for overall health and well-being, caution should be exercised when acting upon these results.”

References:

1. Mosher, D.S. et al. (2007). "A mutation in the myostatin gene increases muscle mass and enhances racing performance in heterozygote dogs." PLoS Genetics 3(5): e79 (doi:10.1371/journal.pgen.0030079)


No comments: