Abstract
This study investigated whether regular endurance exercise maintains basal mitophagy and mitochondrial function during aging. Mitochondrial proteins and total mRNA were isolated from vastus lateralis biopsies (n = 33) of young sedentary (YS), old sedentary (OS), young active (YA), and old active (OA) men. Markers for mitophagy, fission, fusion, mitogenesis, and mitochondrial metabolism were assessed using qRT-PCR, Western blot, and immunofluorescence staining. Independently of age, fission protein Fis1 was higher in active vs. sedentary subjects (+80%; P < 0.05). Mitophagy protein PARKIN was more elevated in OA than in OS (+145%; P = 0.0026). mRNA expression of Beclin1 and Gabarap, involved in autophagosomes synthesis, were lower in OS compared to YS and OA (P < 0.05). Fusion and oxidative phosphorylation proteins were globally more elevated in the active groups (P < 0.05), while COx activity was only higher in OA than in OS (P = 0.032). Transcriptional regulation of mitogenesis did not vary with age or exercise. In conclusion, physically active lifestyle seems to participate in the maintenance of lifelong mitochondrial quality control by increasing fission and mitophagy.
Highlights
Loss of muscle mass and strength is a well-known feature of aging in humans (Kim and Choi, 2013)
VO2peak was about 25% higher in young active (YA) compared to young sedentary (YS) (P = 0.035) and about 50% higher in old active (OA) compared to old sedentary (OS) (P = 0.029)
Wmax was about 40% higher in YA compared to YS (P < 0.001) and about 75% higher in OA compared to OS (P < 0.001)
Summary
Loss of muscle mass and strength is a well-known feature of aging in humans (Kim and Choi, 2013). Direct and robust evidence is lacking to unveil the molecular mechanisms of aging in human, in particular in skeletal muscle function. In this perspective, much attention has been paid to mitochondria as skeletal muscle is highly dependent on mitochondrial oxidative phosphorylation to generate energy in the form of ATP (Egan and Zierath, 2013). Accumulation of mutant mitochondrial DNA (mtDNA) and free radicals during aging is both considered to negatively affect mitochondrial function, even though the correlation between those two processes is not clearly established (Pinto and Moraes, 2015). The maintenance of functional mitochondrial machinery is probably decisive for skeletal muscle mass, quality, and function during aging (Seo et al, 2016)
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