Marathon running “helps mend broken hearts”

Regular endurance training such as running marathons helps mend broken hearts and keeps the organ young a new study found.

A hard work out increases the expression of genes used to repair damaged DNA.

And even one session can be as important to maintaining heart health as reducing bad cholesterol and having a health diet.

Mice who exercised had longer telomeres – tiny caps found on the ends of strands of DNA that have been likened to the plastic tips on shoelaces.

These protect chromosomes from deterioration and progressively shorten with age – increasing the risk of disease.

And the findings apply to humans because these genes are regulated in a similar way to those in humans.

Researchers said the findings are important for understanding how exercise provides a protective effect on the heart.

By understanding this process and basic heart biology, future research may lead to increased life expectancy and drug-free cures for chronic heart problems, including high blood pressure.

Age was the number one risk factor in the development of cardiovascular diseases and the positive benefits or ‘cardioprotective’ effects of exercise on reducing risk has long been recognised.

This includes reduced resting blood pressure, lowered basal heart rate, reduced
cholesterol levels and improved vascular health.

They studied the hearts of mice after 30 minutes of running on a treadmill and looked at how genes were being expressed compared to those in hearts of mice that had not been exercised.

Assistant instructor Dr Andrew Ludlow of University of Texas Southwestern Medical Centre said: “Age is the greatest risk factor for cardiovascular disease.

“Telomere length is shorter in the hearts of aged mice compared to young mice, and short telomere length has been associated with an increased risk of cardiovascular disease.

“One year of voluntary wheel running exercise attenuates the age-associated loss of telomere length and results in altered gene expression of telomere length maintaining and genome stabilising proteins in heart tissue of mice. ”

Professor Stephen Roth from University of Maryland’s Department of Kinesiology, said: “The genes that are important for genome stability are upregulated in the heart tissue after a single bout of endurance exercise.

“This may contribute to the protective effects of exercise on cardiovascular health.”

However Dr Ludlow added: “Our data indicate that a single acute bout of exercise does not significantly increase telomerase activity levels and that the effect of exercise on telomerase may be a repeat bout effect, with telomerase adapting after several bouts of exercise.

“Understanding how telomere length is regulated in cardiac tissue with exercise training and how each bout of exercise results in a cardioprotective phenotype is important research for improving the healthspan of humans.

“Telomere length is one aspect of ageing tissues that regulates genomic stability and, as elucidated recently, chromatin structure and gene expression.

“How exercise results in longer telomeres and perhaps influences gene expression with ageing in cardiac tissue and how the altered gene expression effects specific cell types and the increase in fibrotic cells in the heart with ageing makes these findings and future research particularly important to human cardiovascular health.

“Ultimately, understanding the positive benefits of exercise training on these phenotypes may lead to novel therapies in preventative and personalised medicine.”

The study by the University of Maryland, the University of Texas Southwestern Medical Center, East Carolina University, the Catholic University of Brasilia and Southern Methodist University was published in Experimental Physiology.

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