We’ve all been told that exercise is good for us. It reduces stress, keeps our muscles and bones healthy, and makes our hearts stronger. But the exact cardiovascular benefits are less clear. A big question has always been whether the heart can generate new cells once it had reached peak maturity. If it can, that could mean that exercise might be crucial for people who have certain cardiac diseases like heart failure.
In a new study out this month in the journal, Nature Communications, researchers found that over a period of eight weeks, healthy mice that ran about three miles a day on a hamster-type running wheel generated four times as much new heart tissue as those that didn’t run. They also did the same running test in groups of mice shortly after inducing a heart attack on the rodents. Even after a heart attack, the ones who ran consistently on the wheel showed signs of developing new heart tissue. The ones that didn’t showed no sign of creating new cells. Because that sounded promising, the researchers wanted to understand the mechanisms at play: What cellular or chemical changes in the body allowed them to regenerate this heart tissue? They identified one possible route by which the body might create these new heart cells, but now they must ask whether they can induce that change without exercise—or amplify its effects.
So, why is this so important? Researchers previously understood that the adult heart has a limited ability to generate new cells. In fact, scientists studying our cardiovascular system once thought that we had no ability whatsoever to create new heart tissue. We now know that, on average, young adults can renew a small amount—about 1 percent—of all of their heart cells every year, and that amount goes down gradually as we age.
At the same time, however, researchers have also found that in humans, heart failure can result from just a small amount of dying cells. So if exercise can provide resilience by generating new cells (even a small number) and keeping the balance, that could prevent heart failure.
“Repetitive exercise protects the heart from disease, with an impact similar to many drug interventions, although the basis for these benefits is incompletely understood,” the researchers say in the study. We know exercise increases the heart’s functioning as well as its overall size. In the past, though, researchers have always attributed that to an increase in the size of each cell and not to an increase in the total number of cells.
The researchers say this hints at a basis for understanding why regular exercise is so good for the heart. And, more importantly, why it could be crucial to prevent heart failure, and help those who just experienced a heart attack.
But the study obviously has limitations. While all mammalian hearts share many similarities, they are not all identical, and neither is the overall physiology of each species. Big and subtle differences could mean that the conclusions in a mouse study don’t translate to humans at all.
The researchers next plan is to examine the mechanistic pathway involved and how else they can turn it on. Initiating the pathway means more cardiac cell production, which could tip the balance in the right direction for someone with heart failure or who has just suffered from a heart attack.
“If we can turn on these pathways at just the right time, in the right people, then we can improve recovery after a heart attack,” Richard Lee, a cardiovascular disease researcher at Harvard and co-author of the study, said in an accompanying release.
For, now though, it looks like regular exercise is probably the best way to maximize your heart’s capacity and potential ability to generate some new cells.