Fight Aging!

Exercise extends healthy life in laboratory animals, but not maximum life span as is the case for calorie restriction. In longer lived species such as our own, that difference may be slight: present evidence suggests exercise and calorie restriction to have broadly similar - though very different in detail - effects on life expectancy. The end results are probably in the same ballpark, and quite possibly achieved through an overlapping set of mechanisms. That said, while exercise is certainly good for you, I've yet to see a study on exercise that reproduces similar eye-opening changes in underlying biomarkers of health to those found in human calorie restriction practitioners. Exercise is "merely" great for health, as opposed to amazingly superb for health.

So, obviously, the sensible thing to do is both exercise regularly and practice calorie restriction. Based on the weight of evidence, this is the 80/20 of what can be done today to optimize health for the long term in a basically healthy individual. The complement to this approach is doing your part to ensure that medical technology produces methods of rejuvenation in time to help you in later age when good health practices are no longer enough to stave off significant degeneration and risk of death.

There is a school of thought that places the processes of autophagy front and center when it comes to natural methods of adjusting metabolism for length of health and life. Autophagy is the process by which cells break down damaged components, the first step in recycling and replacement: fewer damaged components at any given time is a good thing, and so more autophagy should also be a good thing. You might recall a demonstration that autophagy is essential to the life span and health benefits of calorie restriction, for example.

I notice that scientists are suggesting that autophagy is similarly important to the health and life span benefits produced by regular exercise:

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.

Autophagy is one of a number of potential mechanisms by which exercise improves long term health. You might look back at a post from the archives for more:

Physical inactivity is increasingly recognized as modifiable behavioral risk factor for cardiovascular diseases. A partial list of proposed mechanisms for exercise-induced cardioprotection include induction of heat shock proteins, increase in cardiac antioxidant capacity, expression of endoplasmic reticulum stress proteins, anatomical and physiological changes in the coronary arteries, changes in nitric oxide production, adaptational changes in cardiac mitochondria, increased autophagy, and improved function of sarcolemmal and/or mitochondrial ATP-sensitive potassium channels. It is currently unclear which of these protective mechanisms are essential for exercise-induced cardioprotection. ... A better understanding of the molecular basis of exercise-induced cardioprotection will help to develop better therapeutic strategies.