Even a single workout could be good for the heart. That’s the conclusion of a fascinating new study in mice that found that 30 minutes on a treadmill affects gene activity within cardiac cells in ways that, over the long haul, could slow the aging of the animals’ hearts.
Although the study involved mice, the results may help to explain just how, at a cellular level, exercise improves heart health in people as well.
There’s no question that, in general, physical activity is good for hearts. Many studies have found that people who regularly exercise are much less likely to develop or die from cardiac disease than people who are sedentary.
Still, researchers have remained puzzled about just how exercise alters hearts for the better. Exercise is known to improve our blood pressure, pulse rate and cholesterol profiles, all of which are associated with better cardiac health.
But many scientists who study the links between exercise and heart health have pointed out that these changes, considered together, explain only about half of the reported statistical reductions in cardiac disease and death.
Other, more complex physiological modifications must simultaneously be taking place within the heart itself during and after exercise, these researchers have speculated.
And recently, researchers at the University of Maryland in College Park and other institutions have begun to wonder whether some of these changes might involve telomeres.
Telomeres are tiny caps on the ends of chromosomes, often compared to the tips of shoelaces, which help to prevent fraying and damage to our DNA. Young cells have relatively long telomeres. As a cell ages or undergoes significant stress, its telomeres shorten. If they become too abbreviated, the cell stops working well or dies.
But while shorter telomeres indicate biologically older cells, the process is not strictly chronological, scientists have found. Cells can age at different rates, depending on the lifestyle of the body that contains them.
Aerobic exercise, in particular, affects telomeres. In past studies, masters athletes have been shown to have longer telomeres in their white blood cells than sedentary people of the same chronological years, suggesting that at a cellular level, the athletes are more youthful.
But while it is easy to obtain and look inside white blood cells, far less has been known about telomeres within cardiac cells.
So for the new study, which was published this month in Experimental Physiology, the Maryland researchers and their colleagues turned to young, healthy female mice. (They chose females because they tend to run more readily than males.)
The researchers wished to see what happens inside heart muscle cells after a single workout. So they taught some of the animals how to run comfortably on small treadmills and then returned them to their cages for several days so that their bodies would lose any aerobic conditioning. Other mice remained sedentary as a control group.
Then the runners were placed back on the treadmills, where they ran at a tolerable intensity (in mouse terms) for 30 minutes, a workout designed to simulate moderate exercise in people.
Researchers took tissue samples of the animals’ hearts either immediately after they had finished running or an hour later, and also gathered samples from sedentary mice.
The scientists looked for changes within the animals’ cardiac cells in the levels of certain proteins that are known to directly prevent telomeres from shortening. They also looked at the activity of other genes that help to keep DNA in good repair. These genes release proteins that are thought to help cells adapt to the physiological stress of exercise and, in the process, also indirectly maintain telomere health.
It turned out that immediately after a single, 30-minute jog, the runners’ heart cells were noticeably different than those of the animals that had not moved. In particular, they showed higher levels of the proteins directly related to telomere length. These increases were slight but consistent. The runners’ cells also had markers of greater activity in the genes that respond to DNA stress than the nonrunners’ cells.
These findings indicate that a single, moderate workout beneficially alters telomere biology in the heart, says Andrew Ludlow, who was a doctoral candidate at the University of Maryland and lead author of the study. He currently is a postdoctoral researcher at the University of Texas Southwestern Medical Center.
Presumably, such changes would accumulate with repeated training, he says, and over time help to keep cardiac telomeres longer than without the exercise.
That process could be slow, though. In this study, many of the effects seen in the animals’ hearts immediately after the run were beginning to dissipate an hour later, with protein levels dropping back almost to those seen in the sedentary mice.
So it may be necessary, Dr. Ludlow says, to stick with an exercise routine for some time in order to realize the cellular benefits for the heart.
It is also worth repeating that this study involved mice, not people.
But the implications are encouraging. It looks like getting up and moving may start to immediately change how the heart’s cells work, Dr. Ludlow says, in ways that “seem to make gene expression more youthful and keep the heart young.”