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Updated: Oct 4, 2025
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Activating Autophagy by Aerobic Exercise in Mice
Published on: February 3, 2017
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Acute exercise rapidly activates hepatic mitophagic flux
Colin S McCoin1,2,3, Edziu Franczak1, Fengyan Deng4
1Department of Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas City, Missouri.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 10, 2022
Summary
Acute exercise activates hepatic mitophagy, the process of degrading damaged mitochondria in the liver. This mitochondrial quality control mechanism is enhanced 2 hours post-exercise, involving specific signaling pathways.
Area of Science:
- Exercise physiology
- Mitochondrial biology
- Cellular quality control
Background:
- Exercise improves metabolic health by maintaining mitochondrial quality.
- Hepatic mitochondrial biogenesis is known to be induced by exercise.
- The effect of acute exercise on hepatic mitophagy remains unclear.
Purpose of the Study:
- To investigate if acute exercise activates hepatic mitophagy.
- To determine the time course of mitophagy activation post-exercise.
- To identify molecular mechanisms underlying exercise-induced mitophagy.
Main Methods:
- Mice underwent acute treadmill running exercise.
- Hepatic mitophagy flux was assessed 2 hours post-exercise.
- Mitochondrial-associated ubiquitin and LC3-II/p62 accumulation were measured.
Main Results:
- Acute exercise did not immediately increase autophagic flux markers.
- Mitophagy flux was activated 2 hours post-exercise, indicated by LC3-II and p62 accumulation.
- Mitochondrial polyubiquitination and p62 recruitment were significantly increased post-exercise.
Conclusions:
- Acute exercise activates hepatic mitophagy in a time-dependent manner.
- Exercise-induced mitophagy involves polyubiquitination and receptor-mediated signaling.
- This study reveals key proteins involved in exercise-mediated mitochondrial quality control in the liver.
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