You are going to learn a fantastic new word in this post: autophagy. “This process, whose name is derived from the Greek for “self-eating”, is a mechanism by which surplus, worn-out or malformed proteins and other cellular components are broken up for scrap and recycled.”
Exercise and longevity
Worth all the sweat
Just why exercise is so good for people is, at last, being understood
Jan 21st 2012 | from the print edition
ONE sure giveaway of quack medicine is the claim that a product can treat any ailment. There are, sadly, no panaceas. But some things come close, and exercise is one of them. As doctors never tire of reminding people, exercise protects against a host of illnesses, from heart attacks and dementia to diabetes and infection.
How it does so, however, remains surprisingly mysterious. But a paper just published in Nature by Beth Levine of the University of Texas Southwestern Medical Centre and her colleagues sheds some light on the matter.
Dr Levine and her team were testing a theory that exercise works its magic, at least in part, by promoting autophagy. This process, whose name is derived from the Greek for “self-eating”, is a mechanism by which surplus, worn-out or malformed proteins and other cellular components are broken up for scrap and recycled.
To carry out the test, Dr Levine turned to those stalwarts of medical research, genetically modified mice. Her first batch of rodents were tweaked so that their autophagosomes—structures that form around components which have been marked for recycling—glowed green. After these mice had spent half an hour on a treadmill, she found that the number of autophagosomes in their muscles had increased, and it went on increasing until they had been running for 80 minutes.
To find out what, if anything, this exercise-boosted autophagy was doing for mice, the team engineered a second strain that was unable to respond this way. Exercise, in other words, failed to stimulate their recycling mechanism. When this second group of modified mice were tested alongside ordinary ones, they showed less endurance and had less ability to take up sugar from their bloodstreams.
There were longer-term effects, too. In mice, as in people, regular exercise helps prevent diabetes. But when the team fed their second group of modified mice a diet designed to induce diabetes, they found that exercise gave no protection at all.
Dr Levine and her team reckon their results suggest that manipulating autophagy may offer a new approach to treating diabetes. And their research is also suggestive in other ways. Autophagy is a hot topic in medicine, as biologists have come to realise that it helps protect the body from all kinds of ailments.
The virtues of recycling
Autophagy is an ancient mechanism, shared by all eukaryotic organisms (those which, unlike bacteria, keep their DNA in a membrane-bound nucleus within their cells). It probably arose as an adaptation to scarcity of nutrients. Critters that can recycle parts of themselves for fuel are better able to cope with lean times than those that cannot. But over the past couple of decades, autophagy has also been shown to be involved in things as diverse as fighting bacterial infections and slowing the onset of neurological conditions like Alzheimer’s and Huntington’s diseases.
Most intriguingly of all, it seems that it can slow the process of ageing. Biologists have known for decades that feeding animals near-starvation diets can boost their lifespans dramatically. Dr Levine was a member of the team which showed that an increased level of autophagy, brought on by the stress of living in a constant state of near-starvation, was the mechanism responsible for this life extension.
The theory is that what are being disposed of in particular are worn-out mitochondria. These structures are a cell’s power-packs. They are where glucose and oxygen react together to release energy. Such reactions, though, often create damaging oxygen-rich molecules called free radicals, which are thought to be one of the driving forces of ageing. Getting rid of wonky mitochondria would reduce free-radical production and might thus slow down ageing.
A few anti-ageing zealots already subsist on near-starvation diets, but Dr Levine’s results suggest a similar effect might be gained in a much more agreeable way, via vigorous exercise. The team’s next step is to test whether boosted autophagy can indeed explain the life-extending effects of exercise. That will take a while. Even in animals as short-lived as mice, she points out, studying ageing is a long-winded process. But she is sufficiently confident about the outcome that she has, in the meantime, bought herself a treadmill.