Abstract
Physical activity and exercise not only provide health benefits that contribute to the quality of life in healthy subjects, but also mitigate many aspects of disease or chronic conditions, particularly cardiovascular disease (CVD), by reducing risk and controlling disease progress. Atherosclerosis, the underlying pathological process for CVD, occurs as the result of imbalance between endothelial injury resulting from chronic inflammation and production of reactive oxygen species (ROS) and vascular repair induced at least in part by circulating endothelial progenitor cells (EPCs). Importantly, pro-inflammatory cytokines stimulate the production of ROS that in turn activate various intracellular signaling pathways leading to further increase in ROS production, creating a positive feedback loop. Considerable evidence suggests that exercise can disrupt the positive feedback loop, thus suppressing inflammation and ROS production. Exercise also mobilizes EPCs from the bone marrow and improves their self-renewal potential and differentiation capability, although the mechanisms for such effects are less well understood. Acute exercise can, however, trigger a cardiovascular event. Thus, exercise appears to be a double-edge sword, which in the long run can maintain the equilibrium between vascular injury and repair. As with pharmacological approaches, individuals respond to exercise differently. The Genetics, Exercise and Research (GEAR) program at the University of Miami uses genomic and epigenomic approaches to decipher the molecular mechanisms underlying EPC mobilization and the spectrum of responses to various forms of exercise, in an attempt to provide the scientific basis for optimized personalized training programs.
