By now you have realized that perhaps I am an exercise freak. Or, perhaps just an old fart that doesn’t want to be limited by his body. Spent the first part of the day in the attic rerouting wires - and reminding myself how glad I am that I can do things like crawl around in the rafters - and, when needed, lift myself up into the rafters.
But, that is not the reason for this posting.
One of the magazines I read, the Economist, periodically has an article I think is worth sharing, or at least commenting on. Recently they wrote about the impact of exercise on longevity.
It is recognized that a near-starvation diet can boost life spans dramatically. Dr. Beth Levine of the University of Texas Southwestern Medical Center was a member of the team that showed that an increased level of autophagy was the mechanism responsible for this life extension.
Autophagy - if you don’t recognize this one, don’t feel bad - my spell checker didn’t either. Autophagy refers to the process by which our bodies surplus, worn-out or malformed proteins and other cellular components are broken up and recycled. And, just in case you thought Autophagy was a long word, check out autophagosomes - the structures that form around the components that are to be recycled.
Dr. Levine used mice to study the impact of exercise on the number of autophagosomes in muscles. She found that the number of autophagosomes had increased after 30 minutes of exercising, and continued to increase until they had been running for 80 minutes.
OK - well and good - the body responds to exercise by increasing the number of autophagosomes to clean up the detritus from using our muscles. But, does this actually benefit us?
The good doctor then "engineered" a second strain of mice with a recycle system that did not ramp up when exercising. She found that the second strain showed less endurance and had less ability to take up sugar from their bloodstreams.
It is recognized that regular exercise (in humans, and mice) helps prevent diabetes. But, when Dr. Levine’s team fed the second strain of mice a diet designed to induce diabetes, they found that exercise gave no protection at all. Which supports the importance of autophagosomes.
It is theorized that autophagy is an adaptation to cope with a scarcity of nutrients: Critters that can recycle parts of themselves for fuel are better able to cope with lean times. In addition to coping with a lack of food, research has shown over the last couple of decades that autophagy is involved in things as diverse as fighting bacterial infections and slowing the onset of neurological conditions like Alzheimer’s and Huntington’s diseases.
And, it seems that it also slows the process of ageing. The theory is that the autophagosomes are most active in removing worn out mitochondria. Think of mitochondria as your cells primary energy source where glucose and oxygen react to produce energy. While we need this energy, the process can also produce free radicals - which are linked to aging. Getting rid of damaged mitochondria would reduce free radical production and might thus slow ageing.
Things like this fascinate me - and, having just written this, I can safely say I mostly understand it. But a week from now what I will remember is this: Exercise makes you live longer.
OK, enough with the lunch break. Back to playing attic monkey!