Activating autophagy by aerobic exercise in mice

Altea Rocchi, Congcong He*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


Autophagy is a lysosomal degradation pathway essential for cell homeostasis, function and differentiation. Under stress conditions, autophagy is induced and targets various cargos, such as bulk cytosol, damaged organelles and misfolded proteins, for degradation in lysosomes. Resulting nutrient molecules are recycled back to the cytosol for new protein synthesis and ATP production. Upregulation of autophagy has beneficial effects against the pathogenesis of many diseases, and pharmacological and physiological strategies to activate autophagy have been reported. Aerobic exercise is recently identified as an efficient autophagy inducer in multiple organs in mice, including muscle, liver, heart and brain. Here we show procedures to induce autophagy in vivo by either forced treadmill exercise or voluntary wheel running. We also demonstrate microscopic and biochemical methods to quantitatively analyze autophagy levels in mouse tissues, using the marker proteins LC3 and p62 that are transported to and degraded in lysosomes along with autophagosomes.

Original languageEnglish (US)
Article numbere55099
JournalJournal of Visualized Experiments
Issue number120
StatePublished - Feb 3 2017


  • Autophagy
  • Brain
  • Cellular biology
  • Chloroquine
  • Exercise
  • Issue 120
  • LC3
  • Microscopy
  • Mouse
  • Muscle

ASJC Scopus subject areas

  • General Chemical Engineering
  • General Biochemistry, Genetics and Molecular Biology
  • General Immunology and Microbiology
  • General Neuroscience


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