Exercise may be the most effective anti-aging intervention known to science and has been shown to protect against a variety of diseases.
However, while physical activity can improve health during aging, its beneficial effects inevitably diminish. The cellular mechanisms underlying the relationship between exercise, fitness, and aging are still poorly understood.
In a paper published in Proceedings of the National Academy of Sciences, researchers at the Joslin Diabetes Center investigated the role of a cellular mechanism in physical improvement through exercise and identified an anti-aging intervention that helps delay aging-induced deterioration in the body. model organism.
Together, the scientists’ findings open the door to new strategies to promote muscle function during aging.
“Exercise has been widely used to improve quality of life and protect against degenerative diseases, and in humans, long-term exercise regimens reduce overall mortality,” said co-author. T. Keith Blackwell, MD, PhD, a senior researcher. .and department head of islet cell and regenerative biology at Joslin. “Our data identify an essential mediator of exercise response and a starting point for interventions to maintain muscle function during aging.” The necessary mediator is the cycle of fragmentation and repair of mitochondria, specialized structures or organelles, within each cell responsible for energy production. Mitochondrial function is important for health and disruption of mitochondrial dynamics, the cycle of repairing dysfunctional mitochondria and restoring connectivity between energy-producing organelles — there are implicated in the development and progression of age-related chronic diseases, such as heart disease. disease and type 2 diabetes.
“When we notice that our muscles go through a pattern of fatigue and recovery after an exercise session, they are going through a cycle,” said Blackwell, who is also head of immunology at Joslin. mitochondrial dynamics”. “In this process, muscles manage the consequences of their metabolic demands during exercise and restore their ability to function.” Blackwell and colleagues – including co-author Julio Cesar Batista Ferreira, PhD, Institute of Biomedical Sciences, University of Sao Paulo – investigated the role of mitochondrial dynamics during exercise in organisms sample C. elegans, a simple, well-studied organism. Microscopic worms are commonly used in metabolism and aging research.
Recording wild C. elegans worms as they swam or crawled, the investigators observed typical age-related physical decline in the animals’ 15 days of adulthood. The scientists also showed a significant and progressive shift towards fragmented and/or disorganized mitochondria in aged animals. For example, they observed in young worms on the first day of adulthood, a bout of exercise-induced fatigue after an hour.
The 60-minute session also induced an increase in mitochondrial fragmentation in the animals’ muscle cells, but a 24-hour period was sufficient to restore both mitochondrial performance and function.
In older worms (day 5 and day 10), animal performance did not return to baseline within 24 h. Likewise, the mitochondria of older animals undergo a cycle of fragmentation and repair, but the network reorganization that has occurred is reduced compared with younger animals.
“We determined that a single exercise session induces a cycle of fatigue and physical recovery but not at the same time,” said first author Juliane Cruz Campos, a postdoctoral fellow at the Joslin Diabetes Center. parallel to the mitochondrial network rebuilding cycle. “Aging reduces the extent to which this occurs and causes a parallel decline in physical fitness. That suggests that mitochondrial dynamics may be important for maintaining fitness and possibly for strengthening fitness. through a round of exercise.” In a second series of experiments, the scientists allowed wild worms to swim for one hour a day for 10 consecutive days, starting at the onset of adulthood. The team found that — as in humans — the long-term training program significantly improved the animals’ midlife fitness by day 10 and minimized the decline in mitochondrial activity. commonly seen in the aging process.
Finally, the researchers tested life-prolonging interventions known for their ability to improve exercise capacity during aging. Worms with increased AMPK – a molecule that is a key energy regulator during exercise and also promotes regeneration of mitochondrial morphology and metabolism – showed improved fitness. benevolent. They also demonstrated the ability to maintain, but not enhance, exercise performance during aging. Worms engineered for AMPK deficiency exhibited physical decline during aging as well as impaired recovery cycle. They also didn’t get the age-retarding benefits of exercise over their lifetime.
“An important goal of the aging field is to identify interventions that not only prolong life, but also enhance health and quality of life,” said Blackwell, who is also a professor of genetics at the School of Medicine. Harvard said.
Blackwell added: “In the elderly, declines in muscle function and exercise tolerance are key concerns leading to significant morbidity. Our data point to potential intervention points. effective to prevent this decline — most likely along with other aspects of aging. It will be of great interest to determine how mitochondrial network toughness affects physical with longevity and aging-related diseases in humans.”
ANI