In This Article
- Research in animal models finds that exercise increases the generation of new cardiomyocytes
- Healthy mice that exercised were found to generate 4.6 times the number of new cardiomyocytes compared to healthy sedentary mice
- miR-222 is necessary for the exercise-induced cardiomyogenic response
- Enhancing the regenerative capacity of heart muscle cells may be an effective strategy to maintain heart function over time
The rate in which humans renew cardiomyocytes decreases as they age, and losing too many of these cells that are not replaced increases the risk for heart failure. Enhancing the regenerative capacity of heart muscle cells may be an effective strategy to maintain heart function over time.
A recent study, co-led by Anthony Rosenzweig, MD, chief of the Cardiology Division at Massachusetts General Hospital, seeks to test the effects of exercise in increasing cell generation. Their findings in mice, which published in Nature, show that exercise can increase the generation of new cardiomyocytes, which may be the key to maintaining heart cardiovascular health.
As part of the study, the research team, which includes collaborators from the Harvard Department of Stem Cell and Regenerative Biology (HSCRB), Harvard Medical School (HMS) and the Harvard Stem Cell Institute (HSCI), gave groups of healthy adult mice and mice that had recently experienced a myocardial infarction (MI) either access to a running wheel or not. The team tracked the growth of new cardiomyocytes over time by incorporated 15N-thymidine by multi-isotope imaging mass spectrometry.
The healthy mice voluntarily ran about three miles each day, and were found to generate 4.6 times the number of new cardiomyocytes compared to healthy sedentary mice. Similarly, they found that exercise in MI mice showed a ~6.75-fold increase in new cardiomyocytes in an extended border zone of the infarcted area. Based on these results, the team concludes that exercise directly stimulates the generation of new cardiomyocytes in mice.
The researchers also show that exercise-induced increase in cardiomyocytes, as seen by the 15N-thymidine labeling, can be stopped by inhibiting miR-222, which is increased by exercise. Therefore, they conclude that miR-222 is necessary for the exercise-induced cardiomyogenic response.
In a follow-up study, the researchers will attempt to pinpoint biological mechanisms that link exercise with increased cardiomyocyte regeneration to better understand how to apply mechanisms to patient care.
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