Nusinovich's
summary in Science Magazine of work by
Lerchenmüller et al.:
Aging-related diseases such as heart failure and other cardiovascular disorders are the leading causes of death in many countries, and they are becoming increasingly common worldwide as the number of older people increases. The ability of the heart to produce new cardiomyocytes decreases with age, which makes it more difficult to repair damage and increases the risk of heart failure. However, a study by Lerchenmüller et al. suggests that exercise may offer some help in this regard even if started late in life. The authors had previously reported that voluntary exercise can stimulate the generation of cardiomyocytes in young adult mouse hearts, and now they have also observed this phenomenon in aged animals.
Here is the results statement of the article:
Cardiomyogenesis was observed at a significantly higher frequency in exercised compared with sedentary aged hearts on the basis of the detection of mononucleated/diploid 15N-thymidine–labeled cardiomyocytes. No mononucleated/diploid 15N-thymidine–labeled cardiomyocyte was detected in sedentary aged mice. The annual rate of mononucleated/diploid 15N-thymidine–labeled cardiomyocytes in aged exercised mice was 2.3% per year. This compares with our previously reported annual rate of 7.5% in young exercised mice and 1.63% in young sedentary mice. Transcriptional profiling of young and aged exercised murine hearts and their sedentary controls revealed that exercise induces pathways related to circadian rhythm, irrespective of age. One known oscillating transcript, however, that was exclusively upregulated in aged exercised hearts, was isoform 1.4 of regulator of calcineurin, whose regulation and functional role were explored further.
