by Jonathan Galland
You know exercise is good for you.
Physical activity burns calories, promotes metabolism and weight loss, and helps reduce the risk of many diseases.
Exercise is also a powerful mood booster and helps fight depression.
Now there is even more good news: exercise makes cells younger.
Researchers in the United States and Germany are looking at the benefits of exercise on the cellular level. Their findings indicate that exercise has a potent anti-aging effect on the cells.
When researchers in Germany compared older runners with sedentary people of the same age, the difference was dramatic. The older runners had cells that had stayed much more youthful than those of their less active contemporaries.
In another study from the University of Colorado at Boulder, researchers noted the positive anti-aging effects upon the cells of people maintaining a high level of aerobic fitness. The researchers conclude: “This may represent a novel molecular mechanism underlying the "anti-aging" effects of maintaining high aerobic fitness.” (Larocca et. al)
References and Abstracts:
Beneficial Effects of Long-term Endurance Exercise on Leukocyte Telomere Biology
Christian Werner1; Tobias Fürster1; Cristiana Roggia1; Jürgen Scharhag2; Michael Böhm3; Ulrich Laufs3
1 Universitätsklinikum des Saarlandes, Homburg/Saar, Germany
2 Universität des Saarlandes, Saarbrücken, Germany
3 Universitätsklinikum des Saarlandes, Homburg/Saar, Germany
Background: Epidemiological data show that physical activity is associated with reduced cardiovascular morbidity and mortality. Age is the major cause of cardiovascular disease. Telomeres and telomere-regulating proteins determine the aging process on the cellular level. This study examines telomere biology and senescence-associated factors in endurance athletes and matched controls without physical activity.
Methods: Leukocytes where isolated from the peripheral blood of professional young track & field athletes (n=32, age 20.4 years, running 73±5 km/week), aged athletes performing regular endurance training (n=25, age 51.1 years, running 80±8 km/week, 35 years training history) and two control groups of age-matched, physically inactive healthy volunteers (26 young and 21 aged subjects).
Results: Telomere repeat amplification protocols revealed an activation of leukocyte telomerase in young athletes to 256±19% and in elderly athletes to 182±11% compared to controls. Western blots showed an up-regulation of the telomere-capping protein TRF2 in young (179±1%) as well as in aged athletes (176±10%). FlowFISH assays and real-time PCR measurements of leukocyte telomere length showed no difference between young athletes and young controls. Sedentary elder controls exhibited a significant reduction of leukocyte telomere length (FF: 53±3%; PCR: 70±8%; vs. young controls). Importantly, there was a striking conservation of telomere length in aged athletes (FF: 88±4%; PCR: 84±7%; vs. young controls). Further analysis of telomere-associated proteins and cellular senescence regulators demonstrated an increase of TRF2, Ku70 and Ku80 mRNA and a reduced protein expression of Chk2, p16 and p53 in aged athletes compared to untrained elder controls.
Conclusions: Our data suggest that beneficial effects of exercise on telomere proteins and senescence-associated factors occur in leukocytes of young track & field athletes. In elderly athletes with a history of long-term continuous exercising we found a potent activation of leukocyte telomerase and conservation of telomere length. These findings improve the molecular understanding of beneficial vascular effects of physical activity and implicate an "anti-aging" effect of physical exercise.
Mech Ageing Dev. 2010 Jan 11.
Leukocyte telomere length is preserved with aging in endurance exercise-trained adults and related to maximal aerobic capacity.
Larocca TJ, Seals DR, Pierce GL.
Department of Integrative Physiology, University of Colorado, Boulder, CO 80309, USA.
Telomere length (TL), a measure of replicative senescence, decreases with aging, but the factors involved are incompletely understood. To determine if age-associated reductions in TL are related to habitual endurance exercise and maximal aerobic exercise capacity (maximal oxygen consumption, VO(2)max), we studied groups of young (18-32 years; n=15, 7 male) and older (55-72 years; n=15, 9 male) sedentary and young (n=10, 7 male) and older endurance exercise-trained (n=17, 11 male) healthy adults. Leukocyte TL (LTL) was shorter in the older (7059+/-141bp) vs. young (8407+/-218) sedentary adults (P<0.01). LTL of the older endurance-trained adults (7992+/-169bp) was approximately 900bp greater than their sedentary peers (P<0.01) and was not significantly different (P=0.12) from young exercise-trained adults (8579+/-413). LTL was positively related to VO(2)max due to a significant association in older adults (r=0.44, P<0.01). Stepwise multiple regression analysis revealed that VO(2)max independently explained approximately 60% of the variance in LTL. Our results indicate that LTL is preserved in healthy older adults who perform vigorous aerobic exercise and is positively related to maximal aerobic exercise capacity. This may represent a novel molecular mechanism underlying the "anti-aging" effects of maintaining high aerobic fitness.