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Related Experiment Video

Updated: Jan 10, 2026

Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
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Mild hyperbaric oxygen does not attenuate mitochondrial decrease induced by detraining in mice.

Ai Takemura1, Tatsuro Egawa2, Kazuki Uemichi1

  • 1Ritsumeikan Global Innovation Research Organization, Ritsumeikan University, Shiga, Japan.

Biochemistry and Biophysics Reports
|November 24, 2025
PubMed
Summary

Mild hyperbaric oxygen (MHO) did not prevent muscle loss or reduced mitochondrial function after detraining in mice. This study found MHO did not attenuate negative adaptations from exercise cessation.

Keywords:
DetrainingMild hyperbaric oxygenMitochondriaVoluntary wheel running

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Area of Science:

  • Exercise Physiology
  • Hyperbaric Medicine
  • Mitochondrial Biology

Background:

  • Muscle disuse leads to atrophy, and training cessation causes loss of adaptations.
  • Mild hyperbaric oxygen (MHO) is known to attenuate muscle atrophy from disuse.

Purpose of the Study:

  • To investigate if MHO exposure post-running training could prevent detraining-induced adaptations.
  • To assess MHO's effect on muscle weight, mitochondrial enzyme activity, and antioxidant protein expression.

Main Methods:

  • Mice underwent four weeks of voluntary wheel running, followed by two weeks of detraining.
  • Detraining occurred under normal conditions or with MHO (1.3 atm, 38% oxygen).
  • Soleus muscle weight, citrate synthase activity, mitochondrial complex IV, and antioxidant proteins were measured.

Main Results:

  • Detraining significantly decreased soleus muscle weight (approx. 30%) in both normal and MHO groups compared to the trained group.
  • Citrate synthase activity, mitochondrial complex IV, catalase, and HO-1 expression decreased in detraining groups versus the trained group.
  • MHO did not significantly attenuate these detraining-induced decreases.

Conclusions:

  • Mild hyperbaric oxygen did not prevent muscle mass loss after exercise cessation in mice.
  • MHO did not preserve mitochondrial enzyme activity or antioxidant protein levels during detraining.