Late-in-life Exercise Training Increases Intracellular Protein Recycling in the Heart

Heart cells (known as myocytes) work hard. Over a human lifetime, the heart beats approximately 2.5 billion times. As myocytes age, and especially in the presence of disease, they accumulate damaged intracellular components such as misfolded proteins. This build-up of damaged cellular material can cause cardiac dysfunction, diminish quality of life, and lead to premature death. Cells have developed a means of identifying and recycling damaged components, through a mechanism termed autophagy (auto=‘self'; phagy=‘eating'). However, these autophagic control processes decline with aging-precisely when heart cells need them the most. Nutrition and Integrative Physiology PhD student Jaemin Cho, together with University of Utah Health researchers J. David Symons, PhD, and Sihem Boudina, PhD, collaborated on an investigation into whether late-in-life exercise in mice enhanced the protein recycling process. They observed that three months of daily treadmill training in very old mice dramatically increased autophagic machinery, enhanced the clearance of damaged proteins, and improved cardiac function. These findings provide the first evidence that late-in-life exercise training can improve cardiomyocyte quality control and function.