Researchers at the Joslin Diabetes Center found an anti-aging treatment that slowed the declines that come with getting older in a model organism. They did this by looking at the effect of a single cellular process involved in getting fitter through exercise training. The results of the study show new ways to improve muscle function as we get older.
Long-term exercise in humans lowers the overall death rate and is often done to improve quality of life and protect against diseases that get worse over time. The new information points to a key regulator of how well the body responds to exercise and a possible therapeutic target for keeping muscles working in older people.
How mitochondria work is important
The organelles inside every cell that make energy, called mitochondria, are always breaking apart and repairing themselves. This is a very important mediator. Disturbances in the way mitochondria work have been linked to the onset and progression of age-related chronic diseases like heart disease and type 2 diabetes. Mitochondrial dynamics is the process of fixing broken mitochondria and reconnecting some of the organelles that make energy.
Because of these mitochondrial dynamic cycles, our muscles get tired and then heal in a predictable way after we work them out. This process helps muscles deal with the metabolic effects of exercise and get their strength and power back.
Scientists watched wild-type C. elegans worms swim and crawl for 15 days and found that the worms' fitness level naturally dropped with age. Also, the researchers showed that as the animals aged, there was a dramatic and progressive change toward fragmented and/or disorderly mitochondria. For example, juvenile worms were tired by the end of their first day as adults after just one workout.
After the 60-minute workout, the mitochondria in the muscles were also more broken up, but both ability and mitochondrial function were back to normal within 24 hours.
In older worms, animals' abilities did not return to normal after 24 hours. Even though older animals' mitochondria also went through a cycle of breaking up and fixing, the networks of the mitochondria were reorganized much less than in younger animals.
They found that the mitochondrial network rebuilds itself in cycles that are the same as the cycles of tiredness and fitness caused by a single workout. The effect of this was lessened by getting older, which also made people less fit. That showed how important mitochondrial dynamics are for keeping fit and getting fitter through exercise.
In a second set of tests, researchers gave wild-type adult worms free reign of the water for ten days. At first, the worms were only allowed to swim for an hour a day. As with people, the researchers saw that by day 10, the training program had greatly improved the middle-aged fitness of the animals, and some of the normal decline in mitochondrial dynamics that comes with getting older had been stopped.
Lastly, the researchers looked at how well known ways to make people live longer affect how well older people can exercise. Worms became more fit when their levels of AMPK, a molecule that changes the structure and metabolism of mitochondria and is a major energy regulator during exercise, went up.
They also showed that their fitness level didn't get better as they got older; it stayed the same. Worms whose genes were missing AMPK as they aged were less fit and took longer to recover. Also, they didn't get the anti-aging benefits of exercise that last a lifetime.