Telomeres are the caps at the ends of chromosomes, shortening with each cell division in normal cells. When very short a cell self-destructs or falls into a senescent state and ceases further replication. Stem cells maintain long telomeres via the activity of telomerase, and provide fresh new long-telomere daughter cells to replace those lost over time in tissues throughout the body. Average telomere length in a cell sample is thus a reflection of stem cell activity and consequent cell replacement rates, as well as the pace of cell division. It is commonly measured in immune cells from a blood sample, and tends to fall during periods of ill health and be lower for older people. This should not be surprising given that stem cell activity declines with age, one of the contributing causes of frailty and failure of tissue function.
There are considerable limitations inherent in the interpretation of present telomere length measurement techniques, not least of which being the existence of studies such as this one in which study populations known to have longer life expectancies and better health do not demonstrate longer telomere length. It isn't hard to find work that challenges the relevance of this marker as a tool for everyday clinical medicine, or even as a basis for serious studies in aging, at least as presently measured:
A career as an elite-class male athlete seems to improve metabolic heath in later life and is also associated with longer life expectancy. Telomere length is a biomarker of biological cellular ageing and could thus predict morbidity and mortality. The main aim of this study was to assess the association between vigorous elite-class physical activity during young adulthood on later life leukocyte telomere length (LTL). The study participants consist of former male Finnish elite athletes (n = 392) and their age-matched controls (n = 207).
Relative telomere length was determined from peripheral blood leukocytes by quantitative real-time polymerase chain reaction. Volume of leisure-time physical activity (LTPA) was self-reported and expressed in metabolic equivalent hours. No significant difference in mean age-adjusted LTL in late life was observed when comparing former male elite athletes and their age-matched controls. Current volume of LTPA had no marked influence on mean age-adjusted LTL. LTL was inversely associated with age. Our study findings suggest that a former elite athlete career is not associated with LTL later in life.