Some have it in their blood... jogging and running, I mean. Now scientists have also found why: because of a mutation that increases muscle endurance and which has become common in some human populations.

The skeletal muscles contain two types of fibers (cells): fast fibers, which can burn sugars without oxygen (anaerobic fibers, employed in sports like body building), and deliver maximum force for rapid action, like sprinting.

Slow fibers use oxygen (they are aerobic), and accomplish endurance activities, like long-distance running.

The protein alpha-actinin-3 is synthesized mainly by fast fibers, being involved in their ability for rapid force outbreak. About 18% of the Europeans do not synthesize this protein because they carry two mutated ACTN3 genes, encoding for alpha-actinin-3.

Previous researches have discovered that endurance athletes like marathon runners are more likely to carry this mutation, but sprinters and athletes in sports requiring rapid muscle strength rather carry the original genes.

A team led by geneticist Kathryn North of the Institute for Neuromuscular Research in Sydney, Australia, analyzed the effect of ACTN3 on muscle activity. On engineered mice missing the functioning gene, the researchers detected significantly higher amounts of enzymes connected with aerobic metabolism, pointing that the lack of alpha-actinin-3 induced the fast fibers to act more like slow fibers.

On treadmill tests, the engineered mice could ran 33% more before turning exhausted than control individuals did, carrying the unmutated ACTN3, showing the mutation boosts endurance.

The team analyzed the ACTN3 in 96 people from Europe, Asia, or Africa. Previous researches showed that the percentage of the mutated variant differed in human populations, ranging from 10% in African populations to about 50% in the case of Europeans and Asians.

The team discovered that the DNA region surrounding the mutation had less variability than other parts of the DNA did, pointing towards a positive natural selection. The Australian team believes that the mutation could have brought an adaptive advantage for Homo sapiens, which moved out of Africa into Europe and Asia for the first time about 60,000 years ago.

"The team's experiments are a great test of ACTN3's role and support the conclusion that the mutation affects some kind of athletic ability," said Michael Nachmann, a geneticist at the University of Arizona, Tucson.