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

被引:25
作者
Cordeiro, Andre Victor [1 ]
Peruca, Guilherme Francisco [1 ]
Braga, Renata Rosseto [1 ]
Bricola, Rafael Santos [1 ]
Lenhare, Luciene [1 ]
Rodrigues Silva, Vagner Ramon [1 ]
Anaruma, Chadi Pellegrini [1 ,2 ]
Katashima, Carlos Kiyoshi [1 ]
Crisol, Barbara Moreira [1 ]
Barbosa, Lucas Torres [1 ]
Simabuco, Fernando Moreira [3 ]
Ramos da Silva, Adelino Sanchez [4 ,5 ]
Cintra, Dennys Esper [6 ]
de Moura, Leandro Pereira [1 ,2 ,7 ]
Pauli, Jose Rodrigo [1 ,7 ]
Ropelle, Eduardo Rochete [1 ,7 ,8 ]
机构
[1] Univ Estadual Campinas, Lab Mol Biol Exercise, Limeira, SP, Brazil
[2] Sao Paulo State Univ, Inst Biosci, Dept Phys Educ, Rio Claro, SP, Brazil
[3] Univ Estadual Campinas, Lab Funct Properties Foods, Limeira, SP, Brazil
[4] Univ Sao Paulo, Postgrad Program Rehabil & Funct Performance, Ribeirao Preto, SP, Brazil
[5] Univ Sao Paulo, Sch Phys Educ & Sport Ribeirao Preto, Ribeirao Preto, SP, Brazil
[6] Univ Estadual Campinas, Lab Nutr Genom, Limeira, SP, Brazil
[7] Univ Campinas UNICAMP, CEPECE Ctr Res Sport Sci, Sch Appl Sci, Limeira, SP, Brazil
[8] Univ Campinas UNICAMP, Fac Med Sci, Dept Internal Med, Campinas, SP, Brazil
基金
巴西圣保罗研究基金会;
关键词
Aging; UPRmt; Skeletal muscle; Exercise; Mitonuclear imbalance; LONGEVITY; UPR; INHIBITION;
D O I
10.1007/s11357-020-00246-5
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
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.
引用
收藏
页码:1513 / 1518
页数:6
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