Findings from a recent study suggest ways to help best manage exercise in individuals with a particular genetic mutation.
According to the study, in mice with the mutated version of desmoplakin—a protein that helps maintain the structure of the heart wall—exercise made the heart walls come apart sooner, leading to the earlier development of arrythmogenic ventricular cardiomyopathy (AVC).
AVC is the most common heart condition that causes sudden cardiac death during intense exercise, explains a media release from the American Physiological Society.
The study’s lead researcher, Jeffrey Towbin, MD, notes in the release that its findings confirm the role of the mutation in the development of AVC and offer insight into how to best manage exercise in individuals with AVC.
The study was published recently in American Journal of Physiology—Heart and Circulatory Physiology.
The release explains that desmosomes are made up of several proteins, including desmoplakin. Defects in the proteins, as in AVC, weaken the cell-cell links. The cells do not withstand the extra stretch from exercise and detach from each other. Scar tissue fills the gaps between the disconnected cells, further reducing the heart wall’s ability to withstand increases in workload such as exercise.
In this new study, researchers at the Cincinnati Children’s Hospital Medical Center discovered endurance exercise led to earlier onset of AVC symptoms in mice with the mutated desmoplakin. Moreover, the desmosomes started coming apart before changes in heart function were detected.
Exercise also changed the signaling in the molecular pathway that promoted growth of new cells and prevented deposition of fat, the Wnt-?-catenin pathway, offering an explanation for the accelerated development of AVC, the release continues.
Towbin notes in the release that the study suggests that changes in the cell-cell links can be detected before alterations in heart function occur. This can help identify individuals with the mutation before they develop AVC symptoms, opening the possibility of better strategies to prevent exercise-induced complications.
The study also suggests that drugs targeting the Wnt-?-catenin pathway may help patients with AVC, Towbin continues in the release.
[Source(s): American Physiological Society, Science Daily]
