Authors
Qiaowei Li, Qin Liu, Zhong Lin, Wenwen Lin, Feng Huang, Pengli Zhu
Lab
Journal
Open Life Sciences
Abstract
Exercise training can significantly improve skeletal muscle mitochondrial function and has been proven to be highly relevant to alterations in skeletal muscle DNA methylation. However, it remains unclear whether late-in-life exercise has an effect on promoter methylation of PGC-1Alpha, a key regulator of mitochondrial biogenesis. Here we employed two distinct exercise modalities, constant medium intensity exercise training (CMIT) and high-intensity interval exercise training (HIIT), to investigate their impacts on PGC-1Alpha expression and methylation regulation in skeletal muscle of aged mice. The results revealed a notable decrease in PGC-1Alpha expression in skeletal muscle of aged mice, accompanied by elevated methylation levels of the PGC-1Alpha promoter, and increased DNA methyltransferase (DNMT) protein expressions. However, both forms of exercise training significantly corrected PGC-1Alpha epigenetic changes, increased PGC-1Alpha expression, and ameliorated skeletal muscle reduction. Furthermore, exercise training led to elevated expression of proteins related to mitochondrial biogenesis and energy metabolism in skeletal muscle, improving mitochondrial structure and function. In conclusion, late-in-life exercise improved skeletal muscle function, morphology, and mitochondria biogenesis, which may be associated with hypomethylation in promoters of PGC-1Alpha and increased content of skeletal muscle PGC-1Alpha. Notably, there was no clear difference between HIIT and CMIT in PGC-1Alpha expression and skeletal muscle function. Graphical abstract
Keywords/Topics
exercise ; PGC - 1 ; DNA methylation ; sarcopenia
BIOSEB Instruments Used:
Grip strength test (BIO-GS4)
Source :
https://www.degruyterbrill.com/document/doi/10.1515/biol-2022-0959/html
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