Impact of different exercise modalities on mitophagy in human skeletal muscle.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic rodent and human studies without systematic review methodology
PubMed 42303368 · doi:10.1016/bs.ircmb.2025.10.005
What was done
This narrative review examined literature regarding the effects of endurance, resistance, and high-intensity interval training (HIIT) on skeletal muscle mitophagy and mitochondrial quality control pathways in rodents and humans.
What was found
The abstract reports no quantitative data or effect sizes. Qualitatively, it notes that endurance exercise in rodents upregulates mitophagy primarily via AMPK/PGC-1α signaling, high-intensity exercise in humans increases mitophagy more than traditional endurance exercises, and resistance exercise triggers alternative mitochondrial quality control mechanisms such as potential mitochondrial ejection.
Why it matters
This review outlines modality-specific signaling pathways in exercise-induced mitochondrial turnover, helping clarify how different training regimens drive muscle metabolic adaptation.
Limits
As a narrative review, it lacks systematic search methodology, meta-analytic pooling, and risk-of-bias assessment. The abstract reports no quantitative findings, study counts, or human sample sizes.
Cited by
- supports Higher-intensity, more vigorous exercise increases the prevalence of mitophagy relative to lower-intensity exercise.