Eight weeks of voluntary running exercise significantly increased the birth of new diploid, mononucleated cardiomyocytes in adult mice by approximately 4.6-fold compared to sedentary controls.
Does running exercise induce new cardiomyocyte generation in adult mice?
Exercise stimulates endogenous cardiomyocyte generation in both normal and injured adult mouse hearts, a process dependent on miR-222.
Odds Ratio: 4.695 (95% CI 1.44–15.53)
Absolute Event Rate: 1.15% vs 0.25%
p-value: p=0.01
Abstract Loss of cardiomyocytes is a major cause of heart failure, and while the adult heart has a limited capacity for cardiomyogenesis, little is known about what regulates this ability or whether it can be effectively harnessed. Here we show that 8 weeks of running exercise increase birth of new cardiomyocytes in adult mice (~4.6-fold). New cardiomyocytes are identified based on incorporation of 15 N-thymidine by multi-isotope imaging mass spectrometry (MIMS) and on being mononucleate/diploid. Furthermore, we demonstrate that exercise after myocardial infarction induces a robust cardiomyogenic response in an extended border zone of the infarcted area. Inhibition of miR-222, a microRNA increased by exercise in both animal models and humans, completely blocks the cardiomyogenic exercise response. These findings demonstrate that cardiomyogenesis can be activated by exercise in the normal and injured adult mouse heart and suggest that stimulation of endogenous cardiomyocyte generation could contribute to the benefits of exercise.
Vujić et al. (Thu,) conducted a other in Healthy and myocardial infarction. Voluntary wheel running vs. Sedentary activity was evaluated on Frequency of diploid/mononucleated 15N-thymidine-labeled cardiomyocytes (OR 4.695, 95% CI 1.44-15.53, p=0.01). Eight weeks of voluntary running exercise significantly increased the birth of new diploid, mononucleated cardiomyocytes in adult mice by approximately 4.6-fold compared to sedentary controls.