It stimulates tissue repair better than drugs, study finds
WEDNESDAY, Nov. 7 (HealthDay News) -- Exercise boosts the number of progenitor cells in people with heart failure, and those cells in turn repair and rebuild weakened muscle and blood vessels, researchers report.
According to two studies that were to be presented Wednesday at the American Heart Association annual meeting in Orlando, Fla., that response can dramatically enhance patients' ability to move and work out.
"Both studies point to the beneficial effect of exercise on patients with heart failure," said Dr. Sidney Smith, past president of the American Heart Association and director of the Center for Cardiovascular Science and Medicine at the University of North Carolina School of Medicine.
"These observations provide some understanding into the mechanisms which [make exercise helpful]," Smith said.
More than 5 million people in the United States have heart failure, a condition that affects the heart's ability to pump blood throughout the body.
However, researchers are beginning to understand that heart failure woes come not only from this pumping disorder but from changes in the legs and other parts of the body.
"The muscle of the leg starts to shrink, so there is less muscle mass," explained Dr. Axel Linke, a co-author on both studies and assistant professor of medicine at the University of Leipzig in Germany. "The endothelium and the vessels supplying blood to the muscles deteriorate, so they are less flexible, elasticity is reduced," he said. The endothelium is a layer of cells that lines blood vessels.
However, exercise opens up the vessels and improves their flexibility and elasticity.
In the first study, investigators looked at whether exercise training could activate progenitor cells -- immature cells that can divide into other cells and help repair tissue.
Fifty men with moderate-to-severe heart failure were randomized to receive either six months of exercise training under the supervision of a physician, or to be sent to a control group that remained inactive.
Exercise consisted of riding a stationary bicycle at least 30 minutes a day (usually in two sessions).
At the end of six months, biopsies of the patients' thigh quadriceps revealed that the number of progenitor cells in the exercise group increased by 109 percent, progenitor cells turning into muscle cells increased by 166 percent, and progenitor cells actively dividing to form new cells and repair damage to the muscle increased sixfold.
For the second study, 37 men with severe heart failure were randomly assigned to receive three months of exercise or to remain inactive.
The exercisers experienced dramatic changes: Circulating progenitor cells increased 47 percent, progenitor cells beginning to mature into endothelial cells increased almost 200 percent, and the density of capillaries in skeletal tissue increased 17 percent. There were no changes in the control group.
When they began, the exercising patients had peak oxygen uptake in the range of other patients needing heart transplants. But regular exercise was linked to an average 35 percent increase in exercise capacity, giving the men about 75 percent of the capacity seen in healthy people of the same age.
"Your heart is like an engine with six cylinders, and when we started the exercise program in those patients, about 3.5 cylinders were just not working," Linke explained. "After three to six months of exercise training, two of the cylinders started working again."
"It's a tremendous improvement, and no medication is able to do it," he noted.
But patients with heart failure should only embark on an exercise regimen under the supervision of a physician, Linke added.
"We recommend exercise once a day for up to 20 minutes five days a week for patients with heart failure, but clearly an exercise program should be initiated in in-hospital conditions or an outpatient setting, because you never know how an individual patient might react to initiation of a training program," he explained.
For more on exercise and fitness, head to the American Heart Association.
SOURCES: Axel Linke, M.D., assistant professor, medicine, University of Leipzig, Germany; Sidney Smith, M.D., past president, American Heart Association, and director, Center for Cardiovascular Science and Medicine, University of North Carolina School of Medicine, Chapel Hill; Nov. 7, 2007, presentations, American Heart Association annual meeting, Orlando, Fla.
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