The role of exercise-mediated mitochondrial quality control remodeling in aging.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic pathways without systematic review methodology or new empirical data
PubMed 41988385 · doi:10.3389/fcell.2026.1792645
What was done
This narrative review summarizes molecular mechanisms governing mitochondrial quality control (MQC)—including biogenesis, dynamic remodeling, mitophagy, proteostasis, and organelle communication—during aging. It analyzes how different exercise modalities (endurance training, high-intensity interval training, and resistance training) modulate signaling pathways such as AMPK, SIRT1, and p38 MAPK to influence mitochondrial turnover and function.
What was found
The abstract reports no quantitative data, statistics, or numerical effect estimates. It qualitatively describes how age-related disruptions in MQC contribute to bioenergetic decline and chronic low-grade inflammation, and summarizes evidence that regular exercise counteracts these deficits by promoting coordinated mitochondrial renewal and functional remodeling across different training types.
Why it matters
It provides an integrated theoretical framework linking specific exercise training modalities to distinct mitochondrial quality control pathways, highlighting potential targets for personalized, nonpharmacological anti-aging strategies.
Limits
As a narrative review, the paper provides no new empirical human or animal data and lacks systematic search methodology. The abstract provides no quantitative metrics, effect sizes, sample sizes, or clinical trial outcomes.
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