A “broken” gene may explain humans’ endurance:
Some clues came 20 years ago, when Ajit Varki, a physician-scientist at the University of California, San Diego (UCSD), and colleagues unearthed one of the first genetic differences between humans and chimps: a gene called CMP-Neu5Ac Hydroxylase (CMAH). Other primates have this gene, which helps build a sugar molecule called sialic acid that sits on cell surfaces. But humans have a broken version of CMAH, so they don’t make this sugar, the team reported. Since then, Varki has implicated sialic acid in inflammation and resistance to malaria.
In the new study, Varki’s team explored whether CMAH has any impact on muscles and running ability, in part because mice bred with a muscular dystrophy–like syndrome get worse when they don’t have this gene. UCSD graduate student Jonathan Okerblom put mice with a normal and broken version of CMAH (akin to the human version) on small treadmills. UCSD physiologist Ellen Breen closely examined their leg muscles before and after running different distances, some after 2 weeks and some after 1 month.
After training, the mice with the human version of the CMAH gene ran 12% faster and 20% longer than the other mice, the team reports today in the Proceedings of the Royal Society B. “Nike would pay a lot of money” for that kind of increase in performance in their sponsored athletes, Lieberman says.
The team discovered that the “humanized” mice had more tiny blood vessels branching into their leg muscles, and — even when isolated in a dish — the muscles kept contracting much longer than those from the other mice. The humanlike mouse muscles used oxygen more efficiently as well. But the researchers still have no idea how the sugar molecule affects endurance, as it serves many functions in a cell.