{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Koh JH"],"funding":["NCATS NIH HHS","NIA NIH HHS","NIDDK NIH HHS"],"pagination":["2324"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9050893"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Resistance exercise training (RET) is an effective countermeasure to sarcopenia, related frailty and metabolic disorders. Here, we show that an RET-induced increase in PGC-1α4 (an isoform of the transcriptional co-activator PGC-1α) expression not only promotes muscle hypertrophy but also enhances glycolysis, providing a rapid supply of ATP for muscle contractions. In human skeletal muscle, PGC-1α4 binds to the nuclear receptor PPARβ following RET, resulting in downstream effects on the expressions of key glycolytic genes. In myotubes, we show that PGC-1α4 overexpression increases anaerobic glycolysis in a PPARβ-dependent manner and promotes muscle glucose uptake and fat oxidation. In contrast, we found that an acute resistance exercise bout activates glycolysis in an AMPK-dependent manner. These results provide a mechanistic link between RET and improved glucose metabolism, offering an important therapeutic target to counteract aging and inactivity-induced metabolic diseases benefitting those who cannot exercise due to many reasons."],"journal":["Nature communications"],"pubmed_title":["Enhancement of anaerobic glycolysis - a role of PGC-1α4 in resistance exercise."],"pmcid":["PMC9050893"],"funding_grant_id":["T32 DK007352","UL1 TR000135","R01 AG062859"],"pubmed_authors":["Dasari S","Nair KS","Pataky MW","Kumar AP","Robinson MM","Vuckovic I","Klaus KA","Koh JH","Ruegsegger GN"],"additional_accession":[]},"is_claimable":false,"name":"Enhancement of anaerobic glycolysis - a role of PGC-1α4 in resistance exercise.","description":"Resistance exercise training (RET) is an effective countermeasure to sarcopenia, related frailty and metabolic disorders. Here, we show that an RET-induced increase in PGC-1α4 (an isoform of the transcriptional co-activator PGC-1α) expression not only promotes muscle hypertrophy but also enhances glycolysis, providing a rapid supply of ATP for muscle contractions. In human skeletal muscle, PGC-1α4 binds to the nuclear receptor PPARβ following RET, resulting in downstream effects on the expressions of key glycolytic genes. In myotubes, we show that PGC-1α4 overexpression increases anaerobic glycolysis in a PPARβ-dependent manner and promotes muscle glucose uptake and fat oxidation. In contrast, we found that an acute resistance exercise bout activates glycolysis in an AMPK-dependent manner. These results provide a mechanistic link between RET and improved glucose metabolism, offering an important therapeutic target to counteract aging and inactivity-induced metabolic diseases benefitting those who cannot exercise due to many reasons.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2024-11-05T18:25:34.059Z","creation":"2024-11-05T18:25:34.059Z"},"accession":"S-EPMC9050893","cross_references":{"pubmed":["35484130"],"doi":["10.1038/s41467-022-30056-6"]}}