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Abstract
Endurance exercise increases mitophagy in skeletal muscle through the AMPK/PGC-1α signaling pathway.
- Different exercise modalities uniquely influence mitochondrial quality control mechanisms in skeletal muscle.
- Endurance exercise promotes mitochondrial turnover and enhances metabolic efficiency by upregulating mitophagy.
- High-intensity exercise is associated with a greater increase in mitophagy compared to traditional endurance exercises in humans.
- Resistance exercise may trigger alternative mechanisms for mitochondrial quality control, including the potential ejection of mitochondria.
- Specific molecular pathways regulating mitophagy and mitochondrial quality control appear to differ among exercise types.
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