The long-observed association between exercise and a slightly longer life span may have its origins in DNA maintenance, a new study finds. Researchers report that the ends of chromosomes hold up better in active people than in sedentary individuals, possibly extending cell life and contributing to overall survival.
Those ends, called telomeres, consist of repeating DNA segments that guard the ends of chromosomes much as plastic tips preserve shoelaces. Telomeres keep chromosomes from degrading or forming aberrant bonds with other chromosomes, but they shorten each time a cell divides. While there is a raging scientific debate over the possible connection between truncated telomeres and aging, it’s known that shrinking them to a critically short length can mean the death of a cell.
Since regular exercise is known to add a few years on average to the typical person’s life span, Tim Spector, a physician and epidemiologist at King’s College London, and his colleagues set out to measure what effect exercise might have on telomere length. The team tapped into a British health registry of 2,401 adult twins who had filled out questionnaires detailing their medical histories, personal habits, and nonwork activities. Participants had also donated blood samples, from which the scientists determined the length of the telomeres in the volunteers’ white blood cells.
Those who reported regular moderate-to-vigorous exercise of more than 3 hours per week had telomeres markedly longer than did the least active individuals, researchers report in the Jan. 28 Archives of Internal Medicine.
“Really active people had the telomeres of someone 10 years younger,” says Spector. He notes that “gentle walking wouldn’t count as exercise.”
In this study, Spector’s team accounted for differences in age, gender, socioeconomic status, body mass, and smoking.
In a different analysis, the researchers identified 67 sets of twins—some identical and some fraternal—in which one sibling exercised considerably more than the other. The active siblings had longer telomeres.
“I think this would explain why sedentary lifestyle is linked to so many age-related diseases,” Spector says, citing associations with hip fractures, type 2 diabetes, heart disease, stroke, and dementia. These ailments may arise when the body fails to repair itself adequately at the cellular level.
Maybe, maybe not, says biologist Steven Austad of the University of Texas Health Science Center in San Antonio: “I’m intrigued but not overly excited about these results.” For starters, he says, past studies have shown that, other things being equal, the longevity effect of exercise on aging is modest. It’s never been established that people die from too-short telomeres, he adds.
But while the link to longevity may be tentative, Austad says, exercise does impart a considerable quality-of-life improvement.
Meanwhile, Spector says telomeres could serve as markers of biological aging.
“That’s a very provocative idea,” says epidemiologist Jack Guralnik of the National Institute on Aging in Bethesda, Md. But telomeres in this study were measured only in white blood cells. “It’s hard to know the true effect that telomere length has in other organs of the body,” he says.