High-intensity exercise training induces mitonuclear imbalance and activates the mitochondrial unfolded protein response in the skeletal muscle of aged mice

The impairment of mitochondrial metabolism is a hallmark of aging. Mitonuclear imbalance and the mitochondrial unfolded protein response (UPRmt) are two conserved mitochondrial mechanisms that play critical roles in ensuring mitochondrial proteostasis and function. Here, we combined bioinformatics,...

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Bibliographic Details
Published in:GeroScience 2021-06, Vol.43 (3), p.1513-1518
Main Authors: Cordeiro, André Victor, Peruca, Guilherme Francisco, Braga, Renata Rosseto, Brícola, Rafael Santos, Lenhare, Luciene, Silva, Vagner Ramon Rodrigues, Anaruma, Chadi Pellegrini, Katashima, Carlos Kiyoshi, Crisol, Barbara Moreira, Barbosa, Lucas Torres, Simabuco, Fernando Moreira, da Silva, Adelino Sanchez Ramos, Cintra, Dennys Esper, de Moura, Leandro Pereira, Pauli, José Rodrigo, Ropelle, Eduardo Rochete
Format: Article
Language:English
Subjects:
Aging
Bioinformatics
Biomedical and Life Sciences
Cell Biology
Geriatrics/Gerontology
Life Sciences
Metabolism
Mitochondria
Molecular Medicine
Musculoskeletal system
Physical training
Physiology
Protein folding
Short Communication
Skeletal muscle
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Summary:The impairment of mitochondrial metabolism is a hallmark of aging. Mitonuclear imbalance and the mitochondrial unfolded protein response (UPRmt) are two conserved mitochondrial mechanisms that play critical roles in ensuring mitochondrial proteostasis and function. Here, we combined bioinformatics, physiological, and molecular analyses to examine the role of mitonuclear imbalance and UPRmt in the skeletal muscle of aged rodents and humans. The analysis of transcripts from the skeletal muscle of aged humans (60–70 years old) revealed that individuals with higher levels of UPRmt-related genes displayed a consistent increase in several mitochondrial-related genes, including the OXPHOS-associated genes. Interestingly, high-intensity interval training (HIIT) was effective in stimulating the mitonuclear imbalance and UPRmt in the skeletal muscle of aged mice. Furthermore, these results were accompanied by higher levels of several mitochondrial markers and improvements in physiological parameters and physical performance. These data indicate that the maintenance or stimulation of the mitonuclear imbalance and UPRmt in the skeletal muscle could ensure mitochondrial proteostasis during aging, revealing new insights into targeting mitochondrial metabolism by using physical exercise.
ISSN:2509-2715
2509-2723
DOI:10.1007/s11357-020-00246-5