A half hour’s stroll can give people with hardening of the arteries in their legs or arms a boost in protection from a heart attack or stroke, a study finds.
“The findings overall are encouraging,” said Russell C. Pate, associate dean for research at the University of South Carolina’s School of Public Health. “This class of patient already has atherosclerotic disease. It’s important to do everything possible to slow or stop the progression of that disease.”
The study found walking boosted levels of a natural clot-dissolving chemical called tissue plasminogen activator, known as TPA. The body makes TPA, and genetically engineered versions are used as drugs to treat heart attack and stroke.
The study examined people with peripheral arterial disease, a condition similar to the narrowed vessels in coronary artery disease. In either case, blood clots can develop in the constricted arteries. If a clot travels to the heart, the result is a heart attack. If it travels to the brain, the result is a stroke.
Pate was not involved in the study, which was published in the February issue of the American College of Sports Medicine journal, Medicine and Science in Sports and Exercise. But he said the results are similar to unpublished data from his lab.
The study done at the University of Maryland looked at eight men and one woman with an average age of 70. The condition is more common as people get older, and more common among men than women, said lead author Christopher J. Womack, now at Michigan State University. All nine hurt if they walked too far. The disease reduces blood flow to the legs, leading to cramping and fatigue, although their symptoms subsided with rest. No patient had been an exerciser before taking part in the study.
The researchers had the nine walk for 30 minutes each, not including any rest breaks. The pace would have been gentle for a healthy person, but it was tough for the patients because of the pain it generated, Womack said. The scientists measured changes in TPA and another chemical, plasminogen activator inhibitor, PAI-1, which binds to TPA and neutralizes it. The balance between TPA and PAI-1 helps to regulate the ability to clot.
Before exercise, the patients had only 80 percent of normal TPA levels, so their ability to dissolve clots was reduced, Womack said.
After exercise, however, TPA levels were about the same as those in a non-exercising person of the same age with peripheral arterial disease, the study found. Levels of PAI-1 fell at the same time. And the changes in both remained significant for at least an hour after the walk, the report said. “An increase in TPA is good for you, and a decrease in PAI-1 is good for you,” commented researcher Anna Carter of the University of Leeds in England, who was not a part of the study. “High levels of PAI-1 have been related to heart disease, and low levels of TPA have been related to heart disease.”
The changes were strong enough potentially to reduce the risk of an artery blockage, and the findings add to evidence that should encourage people with peripheral arterial disease to be physically active, Womack said.
Other studies have shown that aerobic activity improves the ability of patients to perform activities of daily life, and trains them to go farther without feeling pain.
There is a risk that exercise can jar loose a clot – causing what the exercise program was aimed at preventing, Womack conceded. But the risk of this is very small, and the benefits of exercise are large, so the benefits generally outweigh the risk, he said.
However, it is not easy to make patients do things that hurt, even if the things are good for them. So another researcher on vascular medicine, Dr. Joe Mills of the University of Leeds, said the unanswered question is whether patients could get a clinically meaningful improvement in their TPA levels with activity that was not so intense.
By IRA DREYFUSS, Associated Press Writer, Sunday February 11, 2001 12:01 PM ET, WASHINGTON (AP)
