Routine exercise is a simple and affordable means to attenuate the disintegration of chromosomal caps called telomeres during aging to extend health-span and longevity.(kirstypargeter | iStock)
· Exercising induces enzyme (telomerase) activity that protects against age-associated chromosome end (telomere) deterioration.
· Short-term and chronic exercising regimens have similar immediate telomerase activation effectiveness.
· In endurance athletes, strenuous training invigorates telomerase activity, possibly accounting for their longer telomeres.
The erosion of repetitive DNA sequences at the ends of chromosomes called telomeres constitutes a telltale sign of cellular aging. And as telomeres disintegrate with time, cells reach a limit where they can’t replicate and start releasing inflammatory substances that drive age-related diseases like type 2 diabetes and Alzheimer’s. To overcome the attrition of these “guardians of the genome” and associated diseases of aging, researchers have turned to gene therapy trials. But combating human aging with gene therapy is still a long way in the future. So, are there simpler and more affordable telomere-preserving strategies within reach like exercise?
Since past research has shown that athletes possess longer telomeres than sedentary people, Denham and Sellami analyzed multiple studies to see how training slows telomere disintegration. In an article published in Ageing Research Reviews, the duo from the School of Health and Biomedical Sciences in Australia looked at telomere preserving enzymes. The two researchers show that single bout and long-term exercise drive the function of a telomere-protecting enzyme called telomerase in rodents and humans. These data point to exercise as a means to subdue the ravaging effects of passing time on telomere length and age-associated disease onset.
To link physical activity and fitness with telomere maintenance, Denham and Sellami stringently whittled down the number of studies for their analysis from 1700 to 24 high-quality human and rodent reports about exercise’s influence on telomerase. From these studies, the tandem researchers extracted two key measurements: the telomere protecting activity of telomerase and the abundance of telomerase reverse transcriptase (TERT). The level of TERT, the component of the enzyme that maintains chromosome ends, correlates with telomerase activity. Their analysis showed that rejuvenated telomerase activity and TERT abundance after physical training correlated with longer telomeres in endurance athletes, signaling that working out safeguards telomeres.
To get an idea of how much training is required to stimulate telomerase, the two colleagues looked at whether a single bout of physical activity augments its activity along with TERT levels. They found that a single round of 30- to 35-minute working out at low to moderate intensities increased these two parameters in white blood cells and heart muscle.
Since their results signaled that a single session of physical exertion stimulates telomerase activity, Denham and Sellami went on to examine what effects long-term training has. Their findings recapitulated the telomerase invigoration from the single training session. Since their long-term exercise analysis also examined more tissues, they uncovered a tissue-specific effect where physical exertion stimulates telomerase in all tissues except for skeletal muscle. These findings suggest that one training session is as good as multiple to drive immediate telomerase enzyme function and that exercise stimulates its activation to different degrees depending on the tissue.
Since endurance athletes have longer telomeres, Denham and Sellami wanted to see if this could come from higher telomerase activation. They found significantly increased telomerase activity and TERT abundance compared to those with sedentary lifestyles in all athletes analyzed except those over the age of about 70. These findings suggest that increased telomerase stimulation and TERT abundance over long periods with training promote lengthier telomeres up to about age 70.
Denham and Sellami thoroughly reviewed the current literature on physical training’s effects on telomerase activity that correlates with telomere preservation. However, the report didn’t explain why exercise didn’t improve skeletal muscle telomerase activity. Another limitation that future research can confront is the optimal amount of exercise suitable to maintaining telomere length, especially for individuals over age 70 who may not reap telomerase-activating benefits from working out as easily.
One of the biggest questions that remain is whether TERT gene therapy can ever replace exercise’s anti-aging influence in humans. Researchers need to establish beyond a doubt that genetically increasing TERT levels extends telomeres and boosts lifespan. Until then, we’ll need to continue exercising regularly to protect our telomeres in our attempts to stave off age-related diseases.