Roughly two million to three million years ago, a primate moved from the forest to the savanna. It grew longer legs, larger muscles and wider feet. It developed sweat glands that allowed it to remain cool under the blazing African sun. It was also around this time, according to recent research, that a mutation in a single gene called CMAH spread throughout the species. Now a study in mice supports the idea that this genetic tweak enabled humans to run long distances and hunt their prey to exhaustion.

According to biologist Ajit Varki of the University of California, San Diego, the mutation rendered the CMAH gene completely inactive. Varki wondered if there was a link between this genetic event and a knack for long-distance running. Because all humans share the same nonfunctional gene, he could not simply compare the running abilities of people with different versions of it. But he had spent years studying mice bred to have the same CMAH inactivation as humans to gain insight into diabetes, cancer and muscular dystrophy. Varki's work suggested a link between CMAH loss and muscle biology, but he needed proof.

“For about 10 years I've been trying to convince somebody in my lab to put these mice on a treadmill,” Varki says. When he finally did the experiment, “lo and behold, without any training, [the CMAH-deficient mice] were one and a half times better at running.” The rodents' muscles—especially those in their hind limbs—used oxygen more efficiently and were more resistant to fatigue. The results were published in September in the Proceedings of the Royal Society B.

In 2004 Harvard University biologist Daniel Lieberman had hypothesized that running—as opposed to bipedal locomotion alone—played a major role in human evolution. Lieberman, who was not involved in the new mouse research, says it is “the first really good, careful genetic study that fits our predictions” about running's role in the rise of modern humans.