As telomere length gets to be more a more popular way of looking into our future to see what will happen to us, some interesting studies are being done. One recent one from Italy looked at the telomere length of tissue in the arms and legs of young and old people.
To make it more telling they looked at the telomere length in old people who were active and robust versus those that were immobilized.
One of the interesting controversies that rages in the field is what tissues we should be looking at. Specifically all the commercial tests measure white blood cell telomere length. Is that good enough?
As I have said before there is a pretty good correlation between aging as seen in the white blood cells (immune compartment) versus the rest of the body. I have also told you in the past that the relationship is not linear- some tissues have longer telomeres but the rate of loss is still a line that goes down with age at least in proliferative tissue.
That raises the question of the role of telomere loss in non proliferative tissue like heart brain and skeletal muscle.
In these cases replacement is usually not possible so does telomere attrition happen and does it matter?
In most cases the answers is yes it happens, albeit more slowly and yes it matters and influence the way the tissue behaves.
Before we go any further into this let’s take a look at what the study showed and what we can learn from it.
Most interesting: arm muscle telomere length was pretty much the same in young and old. This implies that it does not change and does not need telomerase activation to “save it”. Skeletal muscle has the longest telomere length of any cell type in the body. This study correlated that fact when it showed the arms of young and old alike to have an average telomere length of 15,000 base pairs (15kb). This is pretty much what you are born with!
Also interesting: The leg telomere length of the active old and inactive old were reduced versus the telomere length of young people. The loss appears from other studies to become noticeable in middle age. But in the active versus inactive old, leg telomere length was much much shorter in the inactive old.
The final piece of the puzzle was to correlate the degree of muscle free radical damage with telomere length. The idea is that telomeres that are not subject to replicative stress ( get shorter because of cellular replication as they do in white blood cells) must fall victim to other factors. The main one of those other factors may well be free radical damage since the active old had much less damage than the inactive old.
Now here is where the study gets a bit fuzzy. The researchers decided that it was indeed free radical stress that made the inactive old inactive and they concluded that it was due to their inactivity. The next conclusion was that if you stayed active you would not have this happen. If you did not then you’d be in a vicious cycle where you stayed inactive, had more and more free radical damage because of the inactivity and then your muscles telomeres would get shorter and shorter.
They were not able to answer the question of whether the free radical damage was a result of inactivity first, or whether their old inactive people had higher free radical damage first and then got inactive.
So what can we actually take from all this:
The most hopeful thing is that you could potentially use exercise to help stave off the “inevitable weakness” that comes with old age.
Finally even though muscle is “post mitotic” telomere support with telomerase activation is still a really good idea for the rest of the body. And remember 5% of muscle is capable of replication. These “satellite” cells are the stuff that new muscle is made of and this is where telomerase comes in.
As I wrote in the Immortality Edge in 2009 the more you can do the better!