Key result
Resistance training in middle-aged mice reverses age-altered gene expression in satellite cells via PI3K-Akt pathways.
Why the study?
Resistance training can prevent muscle loss in sarcopenia, but the underlying mechanisms of its effects on satellite cells are not well understood.
Does resistance training alter the transcriptome of satellite cells to prevent age-induced muscle loss in mice?
Does resistance training alter the transcriptome of satellite cells to prevent age-induced muscle loss in mice?
Resistance training may rejuvenate the self-renewing ability of satellite cells by recovering age-influenced genes, offering a potential mechanism for preventing sarcopenia.
Hypothesis-generating for sarcopenia; leaves open translation of mouse satellite cell changes to human muscle outcomes.
Aims The decrease in the number of satellite cells (SCs), contributing to myofibre formation and reconstitution, and their proliferative capacity, leads to muscle loss, a condition known as sarcopenia. Resistance training can prevent muscle loss; however, the underlying mechanisms of resistance training effects on SCs are not well understood. We therefore conducted a comprehensive transcriptome analysis of SCs in a mouse model. Methods We compared the differentially expressed genes of SCs in young mice (eight weeks old), middle-aged (48-week-old) mice with resistance training intervention (MID+ T), and mice without exercise (MID) using next-generation sequencing and bioinformatics. Results After the bioinformatic analysis, the PI3K-Akt signalling pathway and the regulation of actin cytoskeleton in particular were highlighted among the top ten pathways with the most differentially expressed genes involved in the young/MID and MID+ T/MID groups. The expression of Gng5, Atf2, and Rtor in the PI3K-Akt signalling pathway was higher in the young and MID+ T groups compared with the MID group. Similarly, Limk1, Arhgef12, and Araf in the regulation of the actin cytoskeleton pathway had a similar bias. Moreover, the protein expression profiles of Atf2, Rptor, and Ccnd3 in each group were paralleled with the results of NGS. Conclusion Our results revealed that age-induced muscle loss might result from age-influenced genes that contribute to muscle development in SCs. After resistance training, age-impaired genes were reactivated, and age-induced genes were depressed. The change fold in these genes in the young/MID mice resembled those in the MID + T/MID group, suggesting that resistance training can rejuvenate the self-renewing ability of SCs by recovering age-influenced genes to prevent sarcopenia. Cite this article: Bone Joint Res 2022;11(2):121–133.
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A 2022 study studied Sarcopenia. Resistance training vs. No exercise was evaluated on Differentially expressed genes in satellite cells. Resistance training in middle-aged mice reactivated age-impaired genes and depressed age-induced genes in satellite cells, particularly in the PI3K-Akt and actin cytoskeleton pathways.
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