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Aldehyde Oxidase 1 Deficiency Enhances Aerobic Exercise Performance by Promoting Skeletal Muscle Adaptation and

Yan Liu1, Qi-Quan Wang1, Tian-E Huang1

  • 1Metabolic Control and Aging, Human Aging Research Institute and School of Life Science, Nanchang University and Jiangxi Key Laboratory of Aging and Diseases, Nanchang, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|July 17, 2025
PubMed
Summary

Aldehyde oxidase 1 (AOX1) negatively regulates aerobic exercise capacity. Removing AOX1 enhances endurance and muscle oxidative properties, offering insights into exercise adaptation and sarcopenia mitigation.

Keywords:
AOX1aerobic exercisecapillary densitymitochondriasarcopeniaskeletal muscle

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Area of Science:

  • Muscle Physiology
  • Molecular Biology
  • Exercise Science

Background:

  • Aerobic exercise capacity is crucial for health and disease prevention, influenced by muscle fiber type.
  • Molecular mechanisms governing exercise adaptation and endurance remain incompletely understood.
  • Aldehyde oxidase 1 (AOX1) is a non-mitochondrial enzyme with a potential role in muscle metabolism.

Purpose of the Study:

  • To investigate the role of aldehyde oxidase 1 (AOX1) in regulating aerobic exercise capacity and muscle adaptation.
  • To explore AOX1's potential involvement in sarcopenia and stress-induced muscle damage.

Main Methods:

  • Gene expression analysis in mouse skeletal muscle following exercise training.
  • Phenotypic characterization of Aox1 knockout (KO) mice using endurance tests.
  • In vitro studies using C2C12 myotubes to assess AOX1's role in muscle atrophy models.

Main Results:

  • Aox1 mRNA expression was downregulated in skeletal muscle after exercise training.
  • Aox1 KO mice demonstrated significantly enhanced exercise endurance and a shift towards oxidative muscle fibers.
  • KO mice showed increased PGC-1α expression, improved mitochondrial function, and greater capillary density.
  • AOX1 knockdown in myotubes protected against starvation- and TNF-α-induced muscle atrophy.

Conclusions:

  • AOX1 acts as a negative regulator of aerobic exercise capacity and stress resilience.
  • Targeting AOX1 may offer a strategy for improving exercise performance.
  • Understanding AOX1's function is key to developing interventions for sarcopenia.