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Physical Exercise Prevents Cellular
Senescence in Circulating Leukocytes and in the Vessel Wall
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Download the PDF here
full pdf of article attached, from Jules: I can tell you I have been a runner for 25 years & I think this is true.
"Peripheral blood leukocytes isolated from endurance athletes showed increased telomerase activity, expression of telomere-stabilizing proteins, and downregulation of cell-cycle inhibitors compared with untrained individuals. Long-term endurance training was associated with reduced leukocyte telomere erosion compared with untrained controls.
Conclusions-Physical activity regulates telomere-stabilizing proteins in mice and in humans and thereby protects from
stress-induced vascular apoptosis."
"Our animal data show that physical exercise upregulates telomere-stabilizing proteins in the vascular wall and in MNCs. The underlying mechanism is the increase in endothelial NO, which synergizes with activation of telomerase to protect against cellular senescent and apoptotic signaling events. In mice, these effects are observed after only 3 weeks of voluntary running. Circulating leukocytes of track and field athletes show similar changes in telomerase activity, telomere-stabilizing proteins, and senescence markers compared with untrained individuals."....."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."
Exercise May Slow Telomere Shortening, Aging
MedPage Today
Published: November 30, 2009
Endurance training appears to have anti-aging effects at the molecular level, researchers found.
Middle-aged marathoners and triathletes who had been training for decades had significantly less telomere erosion than their more sedentary counterparts, according to Ulrich Laufs, MD, of Saarland University in Hamburg, Germany, and colleagues.
Both younger track-and-field athletes and the older runners had upregulation of telomere-stabilizing proteins and decreased expression of vascular apoptosis regulators in circulating leukocytes compared with individuals who did not exercise frequently, the researchers reported online in Circulation: Journal of the American Heart Association.
"This is direct evidence of an anti-aging effect of physical exercise," Laufs said in a statement.
"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," he and colleagues wrote.
The researchers explored the effects of physical activity on telomere biology using both mice and humans.
They randomized mice to voluntary exercise on a running wheel or no exercise for three weeks, and found significant effects on their telomeres.
Those who exercised had increased telomerase activity in the thoracic aorta and in circulating mononuclear cells, increased expression of telomere-stabilizing proteins, and reduced expression of apoptosis regulators.
Telomere length, however, did not differ between the two groups.
These animal results were generally confirmed in a study in humans.
A group of professional track-and-field athletes (mean age 20.4) and middle-age endurance runners (mean age 51.1), who had been training for an average of 35 years, were compared with controls of similar ages who rarely exercised.
As expected, fitness levels were higher in both groups of athletes.
Both groups of athletes had increased telomerase activity, upregulation of telomere-stabilizing proteins, and downregulation of cell-cycle inhibitors compared with the controls.
The older controls had significantly shorter telomeres than the younger controls and both groups of athletes (P<0.001).
The age-dependent telomere erosion in circulating leukocytes was significantly lower in older runners who had trained for decades than in sedentary controls (P<0.001), although not among younger runners.
"Our study population may have been too small and too young to detect subtle differences in telomere length, but the data show that beneficial antisenescent effects of physical activity are observed more rapidly than effects on telomere length itself," the researchers said.
They acknowledged that they could not exclude the possibility that the extent of telomere shortening in the older group was partly due to an unknown selection bias.
Also, they could not determine to what extent exercise's beneficial effects on metabolism, heart rate, and blood pressure influenced telomere biology, as opposed to the physical activity itself.
The study was supported by the Deutsche Forschungsgemeinschaft, the Universitat des Saarlandes (HOMFOR), and the Ministerium fur Wirtschaft und Wissenschaft des Saarlandes.
The authors made no financial disclosures.
Physical Exercise Prevents Cellular Senescence in Circulating Leukocytes and in the Vessel Wall
Circulation, Jnl of the Americamn Heart association, Nov 30 Advance online publication
Christian Werner MD, Tobias Furster MD, Thomas Widmann MD, Janine Poss MD, Cristiana Roggia MD, Milad Hanhoun MD, Jurgen Scharhag MD, Nicole Buchner DBBSc, Tim Meyer MD, Wilfried Kindermann MD, Judith Haendeler PhD, Michael Bohm MD, and Ulrich Laufs MD*
From the Klinik fur Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin (C.W., T.F., J.P., M.H., M.B., U.L.), Klinik fur Innere Medizin I, Onkologie, Hamatologie, Klinische Immunologie und Rheumatologie (T.W.), and Institut fur Pathologie (C.R.), Universitatsklinikum des Saarlandes, Homburg/Saar, Germany; Institut fur Sport und Praventivmedizin, Universitat des Saarlandes, Saarbrucken (J.S., T.M., W.K.); and Institut fur Umweltmedizinische Forschung at the Universitat Dusseldorf gGmbH, Dusseldorf (N.B., J.H.), Germany.
Background-The underlying molecular mechanisms of the vasculoprotective effects of physical exercise are incompletely understood. Telomere erosion is a central component of aging, and telomere-associated proteins regulate cellular senescence and survival. This study examines the effects of exercising on vascular telomere biology and endothelial apoptosis in mice and the effects of long-term endurance training on telomere biology in humans.
Methods and Results-C57/Bl6 mice were randomized to voluntary running or no running wheel conditions for 3 weeks. Exercise upregulated telomerase activity in the thoracic aorta and in circulating mononuclear cells compared with sedentary controls, increased vascular expression of telomere repeat-binding factor 2 and Ku70, and reduced the expression of vascular apoptosis regulators such as cell-cycle-checkpoint kinase 2, p16, and p53. Mice preconditioned by voluntary running exhibited a marked reduction in lipopolysaccharide-induced aortic endothelial apoptosis. Transgenic mouse studies showed that endothelial nitric oxide synthase and telomerase reverse transcriptase synergize to confer endothelial stress resistance after physical activity. To test the significance of these data in humans, telomere biology in circulating leukocytes of young and middle-aged track and field athletes was analyzed. Peripheral blood leukocytes isolated from endurance athletes showed increased telomerase activity, expression of telomere-stabilizing proteins, and downregulation of cell-cycle inhibitors compared with untrained individuals. Long-term endurance training was associated with reduced leukocyte telomere erosion compared with untrained controls.
Conclusions-Physical activity regulates telomere-stabilizing proteins in mice and in humans and thereby protects from stress-induced vascular apoptosis.
Exercise Increases Aortic Telomerase Activity and
Telomere-Stabilizing Proteins in Mice
Voluntary running for 3 weeks had no effect on lipid levels, body weight, blood pressure (controls, 116/91 mm Hg; exercise, 119/92 mm Hg; n=10 per group), or resting heart rate (controls, 478 bpm; exercise, 474 bpm) in C57/Bl6 mice but induced a 2.9-fold increase in aortic telomerase activity as determined by the telomere repeat amplification protocol
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