February 14, 2017

The positive effects of exercise on cardiovascular health are widely known. Not many studies, however, have explored the molecular pathways related to aging in the heart.

 A study led by Dr. Stephen Roth, professor of kinesiology and School of Public Health Associate Dean, found that exercise training can protect cardiac tissue and slow the degeneration of the heart’s DNA structure.

 “We know that the DNA of an exercised heart muscle is healthier than in a sedentary heart, so this study was starting to decipher why is that the case,” Dr. Roth said. “We identified part of the pathway that results in healthier DNA in the exercised heart.”

 The study focused on the effects of exercise on the ends of the heart chromosomes, known as telomeres. As the heart ages, the telomere length in chromosomes becomes shorter, Dr. Roth explains. Longer chromosome ends in the heart are associated with younger, healthier hearts, while shorter ends are a sign of aging and can increase the risk of cardiovascular disease.

 “As we get older, our telomeres shrink until finally it affects the whole DNA,” Dr. Roth said. “They are affected as soon as you’re born. They are a marker of aging, like tree rings. If we can slow the shrinking process, then presumably the heart tissue would be healthier over time.”

 To measure the effects of exercise on the heart, the researchers studied how an acute bout of wheel running exercise affected telomere length in lab mice.  The experiments revealed that running altered the gene expression of telomere length-maintaining and genome-stabilizing proteins in the heart. Exercise also stimulated a greater expression of DNA repair and response genes, according to the paper.

 “These data provide insights into how physiological stressors remodel the heart tissue and how an early adaptive response mediated by exercise may be maintaining telomere length/stabilizing the heart genome through the up-regulation of telomere protective genes,” the study read.

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Acute exercise activates p38 MAPK and increases the expression of telomere protective genes in cardiac muscle

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Stephen Roth