Muscle explosiveness vis-à-vis endurance

malaria Carl Lewis is according to the International Athletics Association the best athlete of the 20th century. He won 10 Olympic medals, 9 gold, 1 silver and 10 medals at the world championships and there were 8 gold. He won in sprints on shorter distances as well as in long jump. Between his first and his last gold medal it has passed almost 13 years! In order to achieve top sport results only motivation and quality training are usually not enough. Genetic predisposition is also very important. It is not a coincidence that good sprinters are mostly from the western part of Africa, while the best runners on long distances originate from the eastern part of Africa, which clearly shows a tight correlation between the abilities and the population genetics. At this point a simple question arises - if genetic factors contribute to a big part of athletic success, can we predict them?



Journal: American Journal of Human Genetics

Citations: Yang et al. (2003) . ACTN3 Genotype Is Associated with Human Elite Athletic Performance. Am J Hum Genet 73(3): 627-631

Study size: size graficsize grafic

Your result

You have two working copies of alpha-actinin 3 present in your muscle fibres. Many world sprinters have this genotype but it is it rare in endurance athletes.

ACTN3 gene is connected with endurance or explosive muscle fibres. Lack of this gene`s activity is quite frequent through human population. On the other hand in your case is this gene active. T variation that can be found in this gene is responsible for inactivity of mentioned gene. You have two C variations, each present in one of both gene copies. C form is reason for your gene`s activity and your explosive muscle fibres. This type of muscle fibres gives you good predisposition for being a sprinter. They have explosive fibres in their muscles in contrast with endurance athletes that mostly have endurance muscle fibres.

ACTN3 gene

While researching neuromuscular diseases, Australian scientists have focused on the gene ACTN3, which encodes a protein called the α-actinin-3. This gene is present in primitive as well as in highly developed animals (also in humans). Results showed that a number of healthy individuals do not possess an operating form of the gene ACTN3. How is it possible that a gene which is widespread amongst living organisms is defective in such a large number of individuals?

Even that many individuals do not possess an operating form of the gene ACTN3 they have no health problems and live quite normal life. From that scientists have concluded that the gene ACTN3 must play an important role in the functioning of muscle tissue. Because ACTN3 gene is expressed mostly in fast twitching fibbers they assumed it must be important for sprinters who need explosiveness and speed to succeed. They examined more than 400 Australian, all top athletes, many of them representing Australia at the Olympic Games. The researchers divided the athletes into two groups. In first group there were athletes who need speed and power and in the second group there were those who need to require endurance. In the first group almost every athlete had the functioning gene version (CC). In the second group athletes mostly had the none-functioning gene version (TT). With this experiment, the hypothesis at the beginning was confirmed. The gene ACTN3 is important for sprinters.

Why inactive gene form

The last research even showed that the sprint results are in a negative correlation with the results for jogging 1500 m, which indicates a strong genetic background. Now we can answer the question from the introduction: why do so many individuals have a mutated form of the gene? Obviously selection operated in a balanced way, depending from environmental factors. In some cases, speed was more desired and in other endurance, that is why both forms of the gene were preserved in the world’s population. They have also discovered that ACTN3 gene had a greater impact on the female athletes than on the male athletes. The differences regarding the impact on males and females are explained with compensation for the lack of α- actinin-3 in males by a greater expression of androgens during training.