Exercise helps repair muscle damage in heart failure patients
Exercise increased the growth of new muscle cells and blood vessels in the weakened muscles of people with heart failure, according to two studies reported at the American Heart Association’s Scientific Sessions held earlier this month in Orlando, Fla.

“If you have heart failure, exercise training can improve your health status, increase your ability to exercise and reverse patterns of muscle damage that are common in heart failure,” according to Axel Linke, MD, assistant professor of medicine at the University of Leipzig, Germany, and a co-author on both studies.

“In addition to getting out of condition because it becomes difficult to exercise, people with heart failure have cellular-level changes in their muscles that make them weaker, more prone to fatigue, and in later stages results in actual muscle shrinkage,” Linke said.

In one study, researchers investigated whether exercise training could activate progenitor cells, a pool of immature cells in skeletal muscle that can divide into various mature cells that are needed for muscle repair.

Compared with healthy people, heart failure patients have about a 50 percent reduction in the number of progenitor cells in their muscles, Linke said.

The researchers examined biopsies of the vastus lateralis, the largest quadricep muscle in the outer thigh, in 50 men, average age 56, with moderate to severe heart failure. They took biopsies before and after a six-month period in which 25 men remained inactive and the other 25 participated in an individualized, physician-supervised exercise program.

For exercise, the participants rode a stationary bicycle at least 30 minutes a day (usually divided into two sessions) at about half their peak exercise capacity.

After six months, levels of progenitor cells stayed the same in the inactive group, but changed significantly in the exercisers:
  • Total number of progenitor cells increased by 109 percent.
  • Progenitor cells differentiating into muscle cells increased by 166 percent.
  • Progenitor cells actively dividing to form new cells and repair muscle damage significantly increased six-fold.
 said that with exercise, the number of progenitor cells normalized, the cells started to divide again and began to differentiate into muscle cells, exactly what patients with heart failure need. The participants in the exercise program also felt better and increased their exercise capacity 20 percent during the six-month study, he concluded.

In the second study, researchers tracked endothelial progenitor cells that are created in bone marrow and circulate through the bloodstream. The cells help repair damaged blood vessel linings and spur new vessels to form in a process called vasculogenesis.
In heart failure, the linings of blood vessels are damaged, blood vessels in muscle do not dilate normally, and the number of capillaries in muscle tissue is reduced.

The researchers randomly assigned 37 men, average age 65, with severe heart failure to receive either 12 weeks of exercise training or to remain inactive. They took blood tests and biopsies of the quadricep muscle before and after the program, and after 12 weeks, they found no changes in the control group. In contrast, exercisers changed significantly:
  • Circulating progenitor cells increased 47 percent.
  • Circulating progenitor cells beginning to mature into endothelial cells significantly increased -- 199 percent.
  • Functional activity of the circulating progenitor cells increased 149 percent.
  • The density of capillaries in skeletal tissue increased 17 percent.
ther you have moderate or severe heart failure, you can benefit from exercise therapy,” Linke said. “These studies show that the benefits come from both the regeneration of muscle cells and the formation of blood vessels.”

More than 5 million people in the United States have heart failure.

Volker Adams, PhD; Sandra Erbs, MD; Robert Höllriegel, MD; Ephraim B. Beck, MD; Stephan Gielen, MD; Sven Möbius-Winkler, M.D; Rainer Hambrecht, MD; and Gerhard Schuler, MD., co-authored both studies. They were funded by the German Heart Foundation.