Exercise Regulates Mitochondrial Quality Control: Maintenance and Remodeling of Skeletal Muscle Homeostasis.
Level 5 - mechanism / opinion, no new human data
Narrative review describing molecular mechanisms without primary human data or systematic review methodology.
PubMed 42589108 · doi:10.3390/biology15151240
What was done
This review examined the molecular regulatory mechanisms of mitochondrial quality control (MQC)—encompassing biogenesis, fusion/fission dynamics, and mitophagy—in skeletal muscle homeostasis, and evaluated how different exercise modalities (aerobic, high-intensity interval training, and resistance exercise) modulate these pathways.
What was found
The abstract presents mechanistic descriptions without quantitative data. It reports that exercise activates AMPK-PGC-1α to promote mitochondrial biogenesis; regulates MFN1/2, OPA1, and DRP1 to balance mitochondrial fusion and fission; and stimulates the PINK1/Parkin and receptor-mediated pathways to facilitate mitophagy. Distinct exercise modalities exerted varying effects: aerobic exercise primarily promoted biogenesis and fusion, high-intensity interval training more efficiently induced mitophagy, and resistance exercise required longer durations to modulate dynamic proteins.
Why it matters
Understanding how specific exercise types differentially alter mitochondrial maintenance pathways helps inform targeted exercise programming aimed at mitigating muscle atrophy and metabolic dysfunction.
Limits
The abstract describes a narrative review without reporting primary clinical or experimental data, sample sizes, search strategy, or quantitative effect sizes. In addition, specific dose-response relationships and optimal modality combinations remain undefined.
Cited by
- supports Exercise stimulates the production of new mitochondria.