Molecular Proof: Exercise Keeps You Young
Intense Activity Keeps Telomeres Long
Reviewed by Elizabeth Klodas, MD, FACC
Dec. 1, 2009 -- People who exercise regularly tend to stay healthier as they age, and now new research may explain why at a cellular level. Compared to people who did not exercise, elite runners in the study had cells that looked much younger under a microscope.
Specifically, investigators measured the length of telomeres -- the DNA on either end of thread-like chromosomes. Just as the plastic tips on the ends of shoelaces keep the laces from fraying, telomeres protect the chromosomes that carry genes during cell division.
Each time a cell divides, telomeres get shorter. When telomeres get too short, cells can no longer divide and they die.
Researchers now believe telomere shortening is critical to aging, making people more vulnerable to diseases such as heart disease, diabetes, and cancer.
“Telomeres can be thought of as a biological clock,” lead researcher Ulrich Laufs, MD, of Homburg, Germany’s Saarland University tells WebMD. “If they are shorter than a critical length, the process of programmed cell death starts.”
Exercise and Telomeres
The new research involved animal and human studies designed to determine how exercise impacts telomere length.In the animal studies, mice that ran on a running wheel for as little as three weeks showed evidence of increased production of telomere-stabilizing proteins, which protected against cell death.
In the human studies, middle-aged professional athletes who ran about 50 miles a week and had done so for many years had longer telomeres than healthy, age-matched non-athletes who did not exercise regularly.
Not surprisingly, the athletes also had slower resting heart rates, lower blood pressures, and less body fat.
The study appears in the Dec. 15 issue of the American Heart Association journal Circulation.
“This is the first time it has been shown at the molecular level that exercising has an antiaging effect on the cardiovascular system,” Laufs says.
American Heart Association spokesman Barry Franklin, PhD, calls the new research "phenomenal."
“In many respects, I think this is a blockbuster study that complements research in twins published last year,” he tells WebMD.
Exercise May Trump Genes
That study suggested exercise might trump genes when it comes to keeping people young. Researchers found that telomere length was related to activity level. People who engaged in the most exercise had telomeres of similar length to inactive people up to 10 years younger.When one twin was largely sedentary and the other was active, the active twin tended to have longer telomeres.
The most active people in the twin study engaged in just a few hours of moderate to vigorous activity a week, suggesting that it is not necessary to run 50 miles a week to achieve the antiaging benefits of exercise.
“In my own lab, I have seen a 3-month conditioning program raise oxygen capacity significantly,” Franklin says. He is director of cardiac rehabilitation and the exercise laboratories at the William Beaumont Hospital in Royal Oaks, Mich.
“In both studies, active people had cells that were measurably younger than inactive people,” he says. “This striking finding may explain how exercise helps prevent heart attacks, diabetes and other degenerative diseases.”
xercise Keep You Young?
By GRETCHEN REYNOLDSWe all know that physical activity is beneficial in countless ways, but even so, Dr. Mark Tarnopolsky, a professor of petrics at McMaster University in Hamilton, Ontario, was startled to discover that exercise kept a strain of mice from becoming gr prematurely.
Mitochrondria have their own DNA, distinct from the cell’s own genetic material, and they multiply on their own. But in the process, mitochondria can accumulate small genetic mutations, which under normal circumstances are corrected by specialized repair systems within the cell. Over time, as we age, the number of mutations begins to outstrip the system’s ability to make repairs, and mitochondria start malfunctioning and dying.
Many scientists consider the loss of healthy mitochondria to be an important underlying cause of aging in mammals. As resident mitochondria falter, the cells they fuel wither or die. Muscles shrink, brain volume drops, hair falls out or loses its pigmentation, and soon enough we are, in appearance and beneath the surface, old.
The mice that Dr. Tarnopolsky and his colleagues used lacked the primary mitochondrial repair mechanism, so they developed malfunctioning mitochondria early in their lives, as early as 3 months of age, the human equivalent of age 20. By the time they reached 8 months, or their early 60s in human terms, the animals were extremely frail and decrepit, with spindly muscles, shrunken brains, enlarged hearts, shriveled gonads and patchy, graying fur. Listless, they barely moved around their cages. All were dead before reaching a year of age. Except the mice that exercised.
Half of the mice were allowed to run on a wheel for 45 minutes three times a week, beginning at 3 months. These rodent runners were required to maintain a fairly brisk pace, Dr. Tarnopolsky said: “It was about like a person running a 50- or 55-minute 10K.” (A 10K race is 6.2 miles.) The mice continued this regimen for five months.
At 8 months, when their sedentary lab mates were bald, frail and dying, the running rats remained youthful. They had full pelts of dark fur, no salt-and-pepper shadings. They also had maintained almost all of their muscle mass and brain volume. Their gonads were normal, as were their hearts. They could balance on narrow rods, the showoffs.
But perhaps most remarkable, although they still harbored the mutation that should have affected mitochondrial repair, they had more mitochondria over all and far fewer with mutations than the sedentary mice had. At 1 year, none of the exercising mice had died of natural causes. (Some were sacrificed to compare their cellular health to that of the unexercised mice, all of whom were, by that age, dead.)
The researchers were surprised by the magnitude of the impact that exercise had on the animals’ aging process, Dr. Tarnopolsky said. He and his colleagues had expected to find that exercise would affect mitochondrial health in muscles, including the heart, since past research had shown a connection. They had not expected that it would affect every tissue and bodily system studied.
Other studies, including a number from Dr. Tarnopolsky’s own lab, have also found that exercise affects the course of aging, but none has shown such a comprehensive effect. And precisely how exercise alters the aging process remains unknown. In this experiment, running resulted in an upsurge in the rodents’ production of a protein known as PGC-1alpha, which regulates genes involved in metabolism and energy creation, including mitochondrial function. Exercise also sparked the repair of malfunctioning mitochondria through a mechanism outside the known repair pathway; in these mutant mice, that pathway didn’t exist, but their mitochondria were nonetheless being repaired.
Dr. Tarnopolsky is currently overseeing a number of experiments that he expects will help to elucidate the specific physiological mechanisms. But for now, he said, the lesson of his experiment and dozens like it is unambiguous. “Exercise alters the course of aging,” he said.
Although in this experiment, the activity was aerobic and strenuous, Dr. Tarnopolsky is not convinced that either is absolutely necessary for benefits. Studies of older humans have shown that weightlifting can improve mitochondrial health, he said, as can moderate endurance exercise. Although there is probably a threshold amount of exercise that is necessary to affect physiological aging, Dr. Tarnopolsky said, “anything is better than nothing.” If you haven’t been active in the past, he continued, start walking five minutes a day, then begin to increase your activity level.
The potential benefits have attractions even for the young. While Dr. Tarnopolsky, a lifelong athlete, noted with satisfaction that active, aged mice kept their hair, his younger graduate students were far more interested in the animals’ robust gonads. Their testicles and ovaries hadn’t shrunk, unlike those of sedentary elderly mice.
Dr. Tarnopolsky’s students were impressed. “I think they all exercise now,” he said.
But shiny fur was the least of its benefits. Indeed, in heartening new research published last week in The Proceedings of the National Academy of Sciences, exercise reduced or eliminated almost every detrimental effect of aging in mice that had been genetically programmed to grow old at an accelerated pace.
In the experiment, Dr. Tarnopolsky and his colleagues used lab rodents that carry a genetic mutation affecting how well their bodies repair malfunctioning mitochondria, which are tiny organelles within cells. Mitochondria combine oxygen and nutrients to create fuel for the cells — they are microscopic power generators.Mitochrondria have their own DNA, distinct from the cell’s own genetic material, and they multiply on their own. But in the process, mitochondria can accumulate small genetic mutations, which under normal circumstances are corrected by specialized repair systems within the cell. Over time, as we age, the number of mutations begins to outstrip the system’s ability to make repairs, and mitochondria start malfunctioning and dying.
Many scientists consider the loss of healthy mitochondria to be an important underlying cause of aging in mammals. As resident mitochondria falter, the cells they fuel wither or die. Muscles shrink, brain volume drops, hair falls out or loses its pigmentation, and soon enough we are, in appearance and beneath the surface, old.
The mice that Dr. Tarnopolsky and his colleagues used lacked the primary mitochondrial repair mechanism, so they developed malfunctioning mitochondria early in their lives, as early as 3 months of age, the human equivalent of age 20. By the time they reached 8 months, or their early 60s in human terms, the animals were extremely frail and decrepit, with spindly muscles, shrunken brains, enlarged hearts, shriveled gonads and patchy, graying fur. Listless, they barely moved around their cages. All were dead before reaching a year of age. Except the mice that exercised.
Half of the mice were allowed to run on a wheel for 45 minutes three times a week, beginning at 3 months. These rodent runners were required to maintain a fairly brisk pace, Dr. Tarnopolsky said: “It was about like a person running a 50- or 55-minute 10K.” (A 10K race is 6.2 miles.) The mice continued this regimen for five months.
At 8 months, when their sedentary lab mates were bald, frail and dying, the running rats remained youthful. They had full pelts of dark fur, no salt-and-pepper shadings. They also had maintained almost all of their muscle mass and brain volume. Their gonads were normal, as were their hearts. They could balance on narrow rods, the showoffs.
But perhaps most remarkable, although they still harbored the mutation that should have affected mitochondrial repair, they had more mitochondria over all and far fewer with mutations than the sedentary mice had. At 1 year, none of the exercising mice had died of natural causes. (Some were sacrificed to compare their cellular health to that of the unexercised mice, all of whom were, by that age, dead.)
The researchers were surprised by the magnitude of the impact that exercise had on the animals’ aging process, Dr. Tarnopolsky said. He and his colleagues had expected to find that exercise would affect mitochondrial health in muscles, including the heart, since past research had shown a connection. They had not expected that it would affect every tissue and bodily system studied.
Other studies, including a number from Dr. Tarnopolsky’s own lab, have also found that exercise affects the course of aging, but none has shown such a comprehensive effect. And precisely how exercise alters the aging process remains unknown. In this experiment, running resulted in an upsurge in the rodents’ production of a protein known as PGC-1alpha, which regulates genes involved in metabolism and energy creation, including mitochondrial function. Exercise also sparked the repair of malfunctioning mitochondria through a mechanism outside the known repair pathway; in these mutant mice, that pathway didn’t exist, but their mitochondria were nonetheless being repaired.
Dr. Tarnopolsky is currently overseeing a number of experiments that he expects will help to elucidate the specific physiological mechanisms. But for now, he said, the lesson of his experiment and dozens like it is unambiguous. “Exercise alters the course of aging,” he said.
Although in this experiment, the activity was aerobic and strenuous, Dr. Tarnopolsky is not convinced that either is absolutely necessary for benefits. Studies of older humans have shown that weightlifting can improve mitochondrial health, he said, as can moderate endurance exercise. Although there is probably a threshold amount of exercise that is necessary to affect physiological aging, Dr. Tarnopolsky said, “anything is better than nothing.” If you haven’t been active in the past, he continued, start walking five minutes a day, then begin to increase your activity level.
The potential benefits have attractions even for the young. While Dr. Tarnopolsky, a lifelong athlete, noted with satisfaction that active, aged mice kept their hair, his younger graduate students were far more interested in the animals’ robust gonads. Their testicles and ovaries hadn’t shrunk, unlike those of sedentary elderly mice.
Dr. Tarnopolsky’s students were impressed. “I think they all exercise now,” he said.
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