overview: The findings reveal cellular mechanisms that help improve physical fitness through exercise training and identify one anti-aging intervention that can help slow the decline associated with natural aging.
sauce: Joslyn Diabetes Center
Exercise, which has been proven to protect against a variety of diseases, may be the most powerful anti-aging intervention known to science. Yes, but its beneficial effects are inevitably diminished. 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 Sciencesresearchers at the Joslyn Diabetes Center have investigated the role of one cellular mechanism in improving physical fitness with exercise training and identified one anti-aging intervention that slows age-associated decline in model organisms. findings open the door to new strategies for promoting muscle function during aging.
“Exercise has been widely adopted to improve quality of life and protect against degenerative diseases. In humans, long-term exercise regimens reduce overall mortality,” said co-corresponding author. Senior Research Fellow T. Keith Blackwell, MD, PhD, said. Joslin’s Head of Islet Cell and Regenerative Biology. “Our data identify a key mediator of exercise response and a starting point for interventions to preserve muscle function during aging.”
Its key mediator is the cycle of fragmentation and repair of mitochondria, specialized structures, or organelles in every cell that produces energy. Disruptions in mitochondrial dynamics, the cycle that restores connections between organelles that generate cytotoxicity, are associated with the development and progression of age-related chronic diseases such as heart disease and type 2 diabetes.
“Our muscles experience this mitochondrial dynamic cycle because they perceive themselves to be experiencing patterns of fatigue and recovery after an exercise session,” says Joslin’s head of immunobiology. said Blackwell, who is also “In this process, the muscle manages the aftermath of metabolic demand from exercise and restores functional capacity.”
Blackwell and colleagues (including co-author Dr. Julio Cesar Battista Ferreira, Institute of Biomedical Sciences, University of Sao Paulo) investigated the role of mitochondrial dynamics during locomotion in the model organism C. elegans. A frequently used species in metabolic and aging studies.
Researchers who documented swimming and crawling in wild-type worms observed a typical age-related decline in strength over the 15 days after the animals reached adulthood. Scientists have also shown significant and gradual changes toward fragmented and/or disorganized mitochondria in aging animals. For example, they observed that in a young nematode on his first day of adulthood, one exercise induced fatigue in him one hour later.
A 60-minute session also increased mitochondrial fragmentation in animal muscle cells, but 24 hours was sufficient to restore both performance and mitochondrial function.
In older (days 5 and 10) worms, animal performance did not return to baseline within 24 hours. Similarly, mitochondria in older animals underwent cycles of fragmentation and repair, but the network reorganization that occurred was reduced compared to younger animals.
Juliane Cruz Campos, lead author and postdoctoral fellow at the Joslin Diabetes Center, said:
“Aging attenuated the extent to which this occurred, and at the same time caused a decline in physical fitness. doing.”
In a second set of experiments, scientists allowed wild-type worms to swim for 1 hour a day for 10 consecutive days from the onset of adulthood. The team found that, similar to humans, a long-term training program significantly improved fitness in middle-aged animals on day 10, alleviating the impairments in mitochondrial dynamics typically seen during aging. .
Finally, researchers tested known longevity-prolonging interventions for their ability to improve exercise performance during aging. A molecule that also facilitates modeling), worms showed increased physical strength.
It also showed maintenance of exercise performance with aging, but not enhancement. Worms engineered to lack AMPK showed age-related decline in physical fitness and impaired recovery cycles. They also did not enjoy the aging-slowing effects of exercise over their lifetimes.
“An important goal in the aging field is to identify interventions that not only extend lifespan, but also improve health and quality of life,” said Blackwell, who is also a professor of genetics at Harvard Medical School.
“In human aging, declines in muscle function and exercise tolerance are major concerns leading to substantial morbidity. Our data point to potentially beneficial intervention points to forestall this decline. It is of great interest to determine how mitochondrial network plasticity affects human longevity and physical fitness along with age-related diseases. .”
Additional authors include Takafumi Ogawa of Joslyn Diabetes Center. Luiz Henrique Marchesi Bozi (co-first author); Barbara Krum, Luiz Roberto Grassmann Poor, Nicholas Dresch Ferreira, Gabriel Santos Arini, Wheel Priests Albuquerque, University of São Paulo. Annika Traa of McGill University. Alexander M. van der Brigg, David Geffen School of Medicine, University of California, Los Angeles. Afshin Beheshti of NASA Ames Research Center. and he Jeremy M. Van Raamsdonk of Harvard Medical School.
Funding: This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (Grants 2013/07937-8, 2015/22814-5, 2017/16694-2 and 2019/25049-9). National Council for Research and Development – Brazil (CNPq) (Grants 303281/2015-4 and 407306/2013-7); Coordination for the Improvement of Higher Education Personnel – Brazil (CAPES) Finance Code 001 and National Institute of Science and Technology and Research and development center for redox processes in biomedicine. National Institutes of Health (NIH) (grant R35 GM122610, R01 AG054215, DK123095, AG071966); Joslin Diabetes Center (grant P30 DK036836, and R01 GM121756). FAPESP Postdoctoral Fellowships 2017/16540-5 and 2019/18444-9, 2016/09611-0 and 2019/07221-9. American Heart Association Career Development Award (2022/926512); Claudia Adams Barr Program. Lavine Family Fund. Pew Charitable Trust. William B. Mair (Harvard TH Chan School of Public Health) and her Malene Hansen (Sanford Burnham Prebys Medical Discovery Institute) provided some of the worm strains used in this study. Other strains were provided by CGC funded by NIH (P40 OD010440).
See also
Chouchani is the founder and shareholder of Matchpoint Therapeutics. The other authors declare no competing interests.
About this Aging and Exercise Research News
author: Chloe Meck
sauce: Joslyn Diabetes Center
contact: Chloe Meck – Jocelyn Diabetes Center
image: image is public domain
Original research: closed access.
“Exercise maintains fitness during aging through AMPK and mitochondrial dynamics.” by T. Keith Blackwell et al. PNAS
overview
Exercise maintains fitness during aging through AMPK and mitochondrial dynamics.
Exercise is a non-pharmacological intervention that improves health during aging and is a valuable tool in the diagnosis of aging-related diseases. In muscle, exercise transiently alters mitochondrial function and metabolism. Mitochondrial fission and fusion are key effectors of mitochondrial plasticity, allowing fine tuning of organelle connectivity, size and function.
Here, we investigated the role of mitochondrial dynamics during exercise in model organisms. Caenorhabditis elegansIn body wall muscles, one exercise session induces cycles of mitochondrial fragmentation followed by fusion after a recovery period, and that daily exercise sessions slow age-related mitochondrial fragmentation and loss of strength. is shown.
Maintaining proper mitochondrial dynamics is essential for physical fitness, fortification through exercise training, and exercise-induced remodeling of the proteome. Surprisingly, among the long-lived genotypes we analyzed (isp-1,～6, daf-2, eat-2When CA-AAK-2), constitutive activation of AMP-activated protein kinase (AMPK) uniquely maintains physical fitness during aging that is lost due to impaired mitochondrial fission or fusion. AMPK is also required to enhance physical fitness through exercise, and our findings together suggest that exercise may enhance muscle function through her AMPK regulation of mitochondrial dynamics. .
Our results demonstrate that mitochondrial connectivity and the mitochondrial dynamics cycle are essential for maintaining physical fitness and exercise responsiveness during aging, and that AMPK activation contributes to several exercise effects. It suggests that it can be reproduced.
Targeting mechanisms to optimize mitochondrial fission and fusion and AMPK activation may be promising strategies for promoting muscle function during aging.
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