Fightaging – Exercise extends healthy life in laboratory animals, but not maximum life span as is the case for calorie restriction. Present evidence suggests exercise and calorie restriction to have broadly similar – though very different in detail – effects on life expectancy. There is as yet no 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.
Autophagy could the mechanism for the benefits of exercise. 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.
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 SENS (Strategies for Engineered Negligible Senescence) Apoptosens project is related to autophagy. It is a project to removing cells that the body tries but fails to kill.