When DNA is copied the machine that does the copying must be already bound to the one of the strands of the two-stranded DNA. Physically, this means that the ve

When DNA is copied the machine that does the copying must be already bound to the one of the strands of the two-stranded DNA. Physically, this means that the very first few bases of the DNA do not get copied by the machine, because the first few bases act instead as a 'handle' for the copying machine to grab onto the data. Imagine if you could not simultaneously read and copy the data of a running program, and you wanted to copy the entire running operating system (you cannot shut down a cell) - you'd have to figure out a kind of 'scratch space' to keep a few versions of the copy program that you knew you would lose during they copy operation. Over time, the amount of scratch space reserved for the DNA to use to bootstrap its copying decreases. Ultimately, if there is not enough room for the DNA copy machine to bind to DNA without actually mis-copying useful DNA (other parts of the operating system outside the scratch space), a cell will shut down and go into a stasis mode called senescence. This is one of the major causes of aging as we know it. Telomerase is a protein machine that adds more blank bases to the ends of DNA so that the DNA copying machinery can act for longer without shorting the DNA to the point of senescence (it increases the size of the scratch partition at the tips of your chromosomes, called 'telomeres'). Because the length of your telomeres is proportional to your age, the protein machine that lengthens your telomeres is likely helping you age less quickly. Here it is found that exercise likely stimulates the production of that lengthening protein, Telomerase, in the heart. This study is a mechanistic study - it provides useful evidence for how various proteins interact under particular conditions. It was not designed to provide proscriptive behavioral advice for how to live longer. But given that heart failure is currently a major cause of death, understanding how to lengthen the heart's useful life would allow us to understand how to lengthen many humans' lives. Current technologies would let us introduce DNA to cells that would direct them to produce more Telomerase, but these techniques are still mostly used in the lab and are only used clinically in the most extreme of cases because though we know exactly what kind of DNA code we would want to inject, we still have a great deal of difficulty injecting the code into a safe location that won't disrupt other critical running programs. But ultimately it is expected that we will be able to adjust the amounts of these proteins in particular tissues outside of their endogenous regulation in an effort to prevent disease, heart failure, and otherwise correct misregulations.