Author: Ludlow AT1, Ludlow LW2, Roth SM3.
1Department of Cell Biology, UT Southwestern Medical Center, Dallas, TX 75309, USA. 2Department of Applied Physiology and Wellness, Southern Methodist University, Dallas, TX 75206, USA. 3Department of Kinesiology, School of Public Health, University of Maryland, College Park, MD 20742-2611, USA.
Conference/Journal: Biomed Res Int.
Date published: 2013
Other: Volume ID: 2013 , Pages: 601368 , Word Count: 192
Aging is associated with a tissue degeneration phenotype marked by a loss of tissue regenerative capacity. Regenerative capacity is dictated by environmental and genetic factors that govern the balance between damage and repair. The age-associated changes in the ability of tissues to replace lost or damaged cells is partly the cause of many age-related diseases such as Alzheimer's disease, cardiovascular disease, type II diabetes, and sarcopenia. A well-established marker of the aging process is the length of the protective cap at the ends of chromosomes, called telomeres. Telomeres shorten with each cell division and with increasing chronological age and short telomeres have been associated with a range of age-related diseases. Several studies have shown that chronic exposure to exercise (i.e., exercise training) is associated with telomere length maintenance; however, recent evidence points out several controversial issues concerning tissue-specific telomere length responses. The goals of the review are to familiarize the reader with the current telomere dogma, review the literature exploring the interactions of exercise with telomere phenotypes, discuss the mechanistic research relating telomere dynamics to exercise stimuli, and finally propose future directions for work related to telomeres and physiological stress.