Could your DNA reveal your Marathon Endurance?

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Marathon Endurance gene explained

The fitness and health industry is exploding thanks to increasing lifestyle-related diseases. Increasingly, people are aware that they need to exercise to stay healthy. As people look for ways to remain motivated and keep exercising, workouts that appeal to a team spirit and a sense of personal accomplishment are becoming increasingly popular. 

As the average age increases and people remain healthier for longer, we are increasingly aware of the importance of developing a healthy skeletal muscle system. Interestingly, it is becoming clear that an exceptional skeletal muscle system may not only enable better health but actually create more success for marathon runners.

Muscle fascicles are bundles of skeletal muscle fibers that form muscle mass. Shorter fascicles are known to be advantageous for long-distance runners. The short length improves mechanical efficiency in the muscle group, enabling runners to run better. However, it has thus far been unknown whether the muscular architecture of elite runners varies because of genetic variation, so-called, “running genes,” or due to training adaptation. 

Of course, it could also be that there is a combination of running genetics and training resulting in these improved muscle groups. Recent studies may have uncovered an endurance gene that results in some of the marathon runner traits that enable exceptional performance. 

The titin gene (TTN) is responsible for encoding the biggest protein that has thus far been described. This protein is the third most abundant in the myofilament of human striated muscle. TTN creates a blueprint on the molecular level, which both builds and organizes thin and thick filaments each time a new generation of muscular fascicles develops. 

Seven variants of TTN exist within human striated muscle, each different in elasticity and size. rs10497520 polymorphisms in TTN might explain why there is so much variability in the isoform expression of TTN in cardiac muscle. This influence may even explain an increase in the volume of strokes and an individual’s maximal oxygen consumption. If this relationship exists within cardiac muscles, then it makes sense that it may exist within skeletal muscle tissue as well.

Researchers hypothesized that recreationally active men would have longer muscle fascicle lengths while trained marathon runners would have shorter fascicle lengths. They found that the genetic polymorphisms in the TTN gene and the fascicle length in recreationally active men (RA, n=137) and their contribution to marathon running performance in habitually trained marathon runners (MR, n=141) had a relationship. MR Participants were drawn from international, national, and Olympic-level marathon runners. They were recruited from London Marathon competitors at the London Marathon Expos during 2013-2015 and regional athletics clubs. 

The strongest and largest muscle in the upper thigh, the vastus lateralis, was measured for fascicle length using ultrasound. Researchers genotyped the participants’ DNA and found that the vastus lateralis fascicle was longer in RA participants with the CC genotype, compared to participants who had the CT genotype. T-allele carriers within the MR group had the best personal times when marathon running. They were, on average, two minutes and 25 seconds faster than participants with CC homozygotes. That said, no difference was observed between genotype frequency in the RA and MR groups. 

Nevertheless, it would appear that the T-allele at rs10497520 in the TTN gene makes it more likely that an individual will have skeletal muscle fascicles that are shorter and need less energy to create the same force. This endurance gene will likely make marathon runners more successful compared to runners without this runner DNA.

This study was limited in some important ways. There weren’t any TT homozygotes in the RA group, which makes sense as Caucasian populations typically have low T-allele frequency. If the study had been more generalized, the fascicle length may have been even smaller. Another issue is that marathon personal best time may or may not have been enhanced in the MR T-allele carriers due to shorter fascicles since this wasn’t measured directly in the MR group. 

More research is needed into marathon runner traits and runner DNA. However, this study is exciting for the future of running genetics and the influence of genes on human skeletal muscles. 

Read more about the study here:

Are you interested in learning more about your genetic tendency for running a marathon with a personal best time? You can login to your Genomelink dashboard now to see this new genetic trait.

Photo by sporlab on Unsplash

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