A genetic disease called arrhythmogenic cardiomyopathy (ACM), in which healthy heart muscle is replaced by scar tissue and/or fat over time is a leading cause of sudden cardiac death (SCD) in young athletes. According to Stephen Chelko, an assistant professor of biomedical sciences at the Florida State University College of Medicine,arrhythmias ordinarily are non-fatal if managed and treated properly – it is suggested that individuals with ACM avoid exercise to prevent SCD.

“There is some awful irony in that exercise, a known health benefit for the heart, leads to cell death in ACM subjects,” Chelko said.

Several thousand mitochondria are in nearly every cell in the body, processing oxygen and converting food into energy. In the heart, if mitochondria fail to function properly, myocyte cells will die and healthy tissue is replaced by scar tissue and fatty cells.

Eventually, the heart’s normal electrical signals are reduced to an erratic and disorganised firing of impulses, leading to an inability to properly pump blood during heavy exercise. Without immediate medical treatment, death occurs within minutes.

“Now, we know that endurance exercise, in particular, leads to large-scale myocyte cell death due to mitochondrial dysfunction in those who suffer from ACM; mitochondria ultimately become overwhelmed and expel ‘death signals’ that are sent to the nucleus, initiating large-scale DNA fragmentation and cell death.”

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Chelko discovered that myocyte cell death – and possibly SCD – could be prevented by inhibiting two different mitochondrial proteins. One such approach utilises a novel targeting peptide developed for Chelko’s research by the National Research Council in Padova, Italy.