Exercise has been shown to reduce the risk of several illnesses, suggesting that it could be the most effective anti-aging activity currently known. A reduction in the positive benefits of exercise is a natural consequence of aging, despite the fact that exercise may enhance health in later years. Despite extensive research, the molecular pathways connecting exercise, fitness, and aging remain unclear.
Joslin Diabetes Center researchers uncovered an anti-aging intervention that slowed the decreases associated with aging in a model organism by investigating the impact of a single cellular process involved in the enhancement of physical fitness via exercise training. The research results provide new avenues for improving muscular function as we age.
Long-term exercise in humans decreases overall mortality and is commonly practiced to enhance quality of life and guard against degenerative illnesses. The new information pinpoints a key modulator of exercise receptivity and a potential therapeutic target for preserving muscular function in the elderly.
The importance of mitochondrial dynamics
The mitochondria, the organelles inside every cell that are responsible for energy production, undergo a constant cycle of fragmentation and repair; this is a crucial mediator. Disruption of mitochondrial dynamics has been associated with the onset and progression of age-related chronic illnesses including cardiovascular disease and type 2 diabetes. Mitochondrial dynamics is the cycle of mending damaged mitochondria and restoring the connection amongst some of the energy-producing organelles.
These mitochondrial dynamic cycles are what cause our muscles to tire and recover in a predictable fashion after exercise. Through this procedure, muscles deal with the metabolic fallout from exercise and regain their strength and power.
Researchers who monitored the swimming and crawling of wild-type C. elegans worms for 15 days found that the worms’ fitness level naturally declined with age. Additionally, the researchers demonstrated that, as the animals aged, there was a dramatic and progressive transition toward fragmented and/or disorderly mitochondria. A single workout session, for instance, generated exhaustion in juvenile worms by the end of the first adult day.
Muscle mitochondrial fragmentation was also increased after the 60-minute training, although both ability and mitochondrial function were restored within 24 hours.
Animals’ ability did not return to normal after 24 hours in older worms. Although the mitochondria of older animals also went through a cycle of fragmentation and repair, the degree to which the mitochondria’s networks were reorganized was far lower than in younger animals.
They found that the mitochondrial network rebuilds itself in cycles that mirror the fatigue and fitness cycles induced by a single exercise session. This effect was mitigated by aging, which also led to a loss in physical fitness. That pointed to the importance of mitochondrial dynamics in both maintaining and increasing fitness via exercise.
In a second series of tests, researchers gave adult wild-type worms free rein of the water for ten days straight, beginning with an hour of swimming a day. As in humans, the researchers observed that by day 10, the animals’ middle-aged fitness had been much enhanced by the training program, and that the normal decline in mitochondrial dynamics associated with aging had been somewhat offset.
Finally, the researchers looked at the efficacy of established therapies for increasing longevity on exercise performance in the elderly. Elevated levels of AMPK, a molecule that drives remodeling of mitochondrial architecture and metabolism and is a major regulator of energy during exercise, led to enhanced fitness in worms.
They also showed that their exercise performance remained steady rather than improved with age. Aging worms genetically depleted of AMPK showed worse physical fitness and a slowed recovery cycle. In addition, they missed out on exercise’s lifelong anti-aging advantages.