Telomeres are DNA fragments that are located at the ends of chromosomes, hence the name. They have a decisive role in avoiding the loss of information during chromosomal duplication. With each cell division they become shorter. Our skin cells as well as those of immunity lose them faster than those of the heart or brain. A cell without telomeres may either age or die. It is therefore logical that research tends to find ways to extend the life of telomeres. The erosion of telomeres is a central component of aging, and telomere-associated proteins regulate cellular aging and survival.
The presence of telomeres can be considered not only a sign of longevity, but also a sign that influences the quality of old age and life in general. A Japanese study currently in progress shows that a population living at a high elevation (near Nagano) has excellent telomere preservation.
The lifestyle of this population has been studied and it has been noted that it has a great influence in telomeric conservation. They live in a community of several generations gathered under the same roof, where the elders cultivate and prepare vegetables for their family, they practice moderate daily exercise and are nurtured with natural food and water. It would seem that the most important factor for telomeric preservation is the quality of their social relationships.
But exercise has also proved to be significant in stimulating the production by our body of a very important enzyme, telomerase. Ulrich Laufs, one of the authors of the study, states that long-term physical exercise reduces telomere loss due to the activation of telomerase in leukocytes.
Peripheral blood leukocytes isolated from athletes showed an increase of telomeric activity, expression of telomere-stabilizing proteins and down-regulation of cell cycle inhibitors compared with those from untrained individuals.
The long-term resistance training was associated with reduced leukocyte telomere erosion compared with untrained individuals.
In conclusion, physical activity and life-style regulate telomere stabilization of proteins in both mice and humans and thus protect from apoptosis induced by vascular stress.