Age is the greatest risk factor for cardiovascular disease. Telomere length is shorter in the hearts of aged mice compared to young mice, and short telomere length has been associated with an increased risk of cardiovascular disease. One year of voluntary wheel running exercise attenuates the age-associated loss of telomere length and results in altered gene expression of telomere length maintaining and genome stabilizing proteins in heart tissue of mice. Understanding the early adaptive response of the heart to an endurance exercise bout is paramount to understanding the impact of endurance exercise on heart tissue and cells. To this end we studied mice before (BL), immediately post (TP1) and one-hour following (TP2) a treadmill running bout. We measured the changes in expression of telomere related genes (shelterin components), DNA damage sensing (p53, Chk2) and DNA repair genes (Ku70, Ku80), and MAPK signaling. TP1 animals had increased TRF1 and TRF2 protein and mRNA levels, greater expression of DNA repair and response genes (Chk2 and Ku80), and greater protein content of phosphorylated p38 MAPK compared to both BL and TP2 animals. 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.
Monday, March 13, 2017
Exercise slows the aging of heart cells.
Ludlow et al. find (in female rats) that exercise slows the loss of caps (telomeres) on the end of chromosomes that prevent damage or fraying of DNA. (Shorter telomeres indicate biologically older cells. If they become too short, the cells can die.) Even a single 30 min treadmill period elevates the level of proteins that maintain telomere integrity. This elevation diminishes after an hour, but the changes might accumulate with repeated training. Here is the technical abstract: