TUESDAY, Dec. 1 (HealthDay News) -- In mice as well as humans, exercise helps regulate telomere-stabilizing proteins and prevent stress-induced vascular apoptosis, according to a study in the Dec. 1 issue of Circulation.
Christian Werner, M.D., of the Universitätsklinikum des Saarlandes in Homburg/Saar, Germany, and colleagues studied mice which either did or did not have access to a running wheel for three weeks. Compared to the control group, they found that the exercise group had increased telomerase activity in the thoracic aorta and in circulating mononuclear cells, increased vascular expression of telomere repeat-binding factor 2 and Ku70, and decreased expression of vascular apoptosis regulators, all of which were associated with a dramatic reduction in lipopolysaccharide-induced aortic endothelial apoptosis.
These findings prompted the researchers to study young and middle-aged track and field athletes, and compare their telomere biology in circulating leukocytes with that of untrained controls. They found that long-term endurance training was associated with increased telomerase activity and expression of telomere-stabilizing proteins.
"In agreement with the animal data, long-term continuous exercising leads to an attenuation of telomere erosion in the leukocytes of middle-aged athletes," the authors conclude. "Our data improve the molecular understanding of the vasculoprotective effects of exercise and underline the potency of physical training in reducing the impact of age-related diseases."
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