Low- and moderate-intensity exercise improved muscle, heart and breathing function in an animal model of Duchenne muscular dystrophy, according to a Northwestern Medicine study.
The study, published in Scientific Reports, was led by Elizabeth McNally, MD, PhD, the Elizabeth J. Ward Professor of Genetic Medicine and director of the Center for Genetic Medicine.
Duchenne Muscular Dystrophy (DMD) is the most common and severe form of muscular dystrophy, a group of genetic diseases that cause progressive weakness and loss of muscle. There is currently no cure for DMD, which occurs in children, and almost exclusively in boys. Symptoms of the disease began early in childhood, and by the age of 13, most patients require the use of a wheelchair.
The goal of treatment for DMD is to control symptoms and improve quality of life. The impact of exercise in the disease, however, has not been well understood.
“It has long been a question whether exercise is bad for patients with Duchenne Muscular Dystrophy,” said McNally, also a professor of Medicine in the Division of Cardiology and of Biochemistry and Molecular Genetics. “It has been suggested by some that exercise worsens the disease. However, we know that not exercising is bad for the heart and cardiovascular system.”
In the current study, McNally and her collaborators investigated the impact of aerobic exercise using an animal model of DMD. The scientists examined mice with the same genetic disorder as patients with DMD and tested two different levels of exercise, low and moderate. The mice were exercised on a treadmill three times a week, for six months.
The investigators found that both exercise regimens were beneficial in mice and did not increase muscle damage or fibrosis. In particular, the mice showed an improvement in skeletal muscle function, reduction in cardiac decline and increase in respiratory capacity.
“For most measurements, the moderate intensity was generally a little better, but for many measurements even low-intensity exercise was beneficial,” McNally explained. “With exercise, the mice became more active, even when they were not on the treadmill. The exposure to exercise made them move more.”
Furthermore, the scientists found that exercise was associated with a dose-dependent increase in serum levels of adiponectin, indicating that the hormone could serve as a biomarker for favorable response to exercise in DMD.
Although the study’s findings suggest that low-intensity or moderate-intensity exercise may be beneficial in DMD, the authors note that further research in humans is needed to determine appropriate levels of exercise and the impact on muscle, cardiac and respiratory function.
Aaron Zelikovich, ’16 BA, was the first author of the paper. Nancy Kuntz, MD, professor of Pediatrics in the Division of Neurology and Epilepsy and in the Ken and Ruth Davee Department of Neurology; Mattia Quattrocelli, PhD, a postdoctoral fellow in McNally’s laboratory; and Isabella Salamone, a student in Feinberg’s Driskill Graduate Program in Life Sciences (DGP), were also co-authors.
The study was supported by National Institutes of Health grants AR052646, HL061322 and T32 DK007169, the Muscular Dystrophy Association, and Parent Project Muscular Dystrophy.
