eli5: I read that every time cells divide, they loose a bit of DNA. So shouldn’t that mean that when we exercise, we would actually be shortening our lifespans?
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Not really, if you lived as long as wolverine it would eventually show but that takes hundreds of years. That is because the ends, that is the parts get gets lost, is “filler” so a normal human lifespan isn’t long enough to experience it. So no, because training lessens the chance of cancer, and cancer would develop far earlier than any negative effects of dna being cut this way.
TLDR: no you are not shortening your lifespan by exercising
Humans have linear chromosomes, meaning our DNA in each chromosome is a long string with 2 ends. When DNA is copied an RNA primer is added at the beginning to start copying but then removed at the end so the DNA gets shorter each time a cell divides ([Diagram](https://cdn.kastatic.org/ka-perseus-images/543664d6b0d7dde9627d6dc342d209291cf71133.png)). To combat this the ends of our chromosomes have regions called [telomeres](https://en.m.wikipedia.org/wiki/Telomere) which are essentially expendable DNA so we don’t loose anything important.
Telomere shortening is one of the [hallmarks of aging](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836174/#abstract-1title), however it is most likely not the primary cause of aging. And there is an enzyme called telomerase active in some cells that can repair the telomeres. There is a large body of evidence showing exercise can reduce many of the hallmarks of aging and when you exercise any decrease in telomere length is either negligible (for a variety of reasons) or counteracted by stem cells/progenitor cells with active telomerase.
In this context you’re referring to *Telomeres* which are loops of DNA found at the end of chromosomes containing several repeating sequences. These are found in most kinds of eukaryotic, multicellular life forms. Such as fungi, plants, algae, and animals.
Each time a cell divides one of the repeats in the telomeres is removed due to the particulars of the way in which chromosomes are duplicated. This is a complex subject beyond the scope of this post. Thus, after a certain number of divisions, usually 5-10 divisions, the telomeres invariably become too shortened. This prevents the chromosome from being able to be duplicated again, thus a further division cannot occur. This is like turning a screw with a screwdriver. After a certain number of rotations you run out of threads, the screw bottoms out and end up damaging the drive recess in the head of the screw rather than turning the screw another rotation.
In practice cells with severly shortened telomeres are called *Somatic* cells, or fully differentiated cells. This is actually true of the majority of cells in the body. As the body ages, the fraction of cells in the body with truncated telomeres increases. (As do the number of stem cells) This can be used a a marker for aging.
This sounds like a huge problem, but actually this mechanism exists as a kind of emergency *fail-safe switch* against cancer development in an adult animal. This ensures that the vast majority of cells in the body simply can’t multiply endlessly and grow out of control of their own devices.
Most tissues and organs in the body contain small numbers of specialized *stem cells.* Stem cells produce proteins called *Telomerases*. These enzymes, working together as a cluster, splice one additional repeat to the telomeres during the copying process, preventing them from shortening.
This is one of several mechanisms allowing stem cells to be effectively immortal, at least compared to most other cell types.
When cancerous tumors form, it is usually a result of stem cells malfunctioning. Because of their telomeres it’s extraordinarily unlikely for non-stem cells to turn cancerous.
The point of this mechanism is to reduce the potential *points of failure.* That is, reduce the number of opportunities for cancer to happen.
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