Exercise as a Metabolic Regulator: Targeting AMPK/mTOR-Autophagy Crosstalk to Counteract Sarcopenic Obesity.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic pathways without original human empirical data or systematic search methods.
PubMed 40540722 · doi:10.14336/AD.2025.0419
What was done
The authors synthesized mechanistic evidence on the role of exercise in modulating the AMPK/mTOR-autophagy signaling axis to mitigate muscle atrophy and adipose tissue accumulation in sarcopenic obesity.
What was found
No quantitative findings or empirical metrics were reported in the abstract. Mechanistically, exercise-induced ATP depletion triggers AMPK activation and mTORC1 suppression, stimulating autophagy initiation (ULK1 phosphorylation) and lysosomal biogenesis (TFEB nuclear translocation), while reversing autophagic flux blockade to restore proteostasis and lipid homeostasis in myocytes and adipocytes.
Why it matters
It outlines the molecular framework by which physical activity simultaneously addresses the dual pathologies of muscle loss and fat accumulation in aging.
Limits
The abstract describes a narrative review without new human data, sample sizes, quantitative effect sizes, systematic search methodology, or specific exercise protocols.
Cited by
- supports Rapidly depleting energy reserves triggers mitochondrial biogenesis and stimulates mitophagy.