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Updated: Jan 10, 2026

Supramaximal Intensity Hypoxic Exercise and Vascular Function Assessment in Mice
Published on: March 15, 2019
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.
Abstract:
Mild hyperbaric oxygen (MHO) attenuates the muscle atrophy caused by muscle disuse. Training cessation results in the partial or complete loss of training-induced adaptations, including mitochondrial enzyme activities. The present study aimed to determine whether exposure to MHO after running training attenuated negative adaptation induced by detraining. We allocated eight-week-old mice into training (Tr), detraining after the training period (DeTr), and detraining + mild hyperbaric oxygen (DeTr + MHO, 1.3 atm absolute with 38 % oxygen) groups. Mice underwent voluntary wheel running for four weeks, followed by a two-week detraining period under normal or MHO conditions. The soleus muscle weight (mg/g BW) decreased by approximately 30 % in the DeTr and DeTr + MHO groups compared to the Tr group (P < 0.001 and 0.01, respectively). Citrate synthase (CS) activity, the expression of mitochondrial complex IV, antioxidant-related proteins, catalase, and heme oxygenase 1 (HO-1), decreased in the DeTr and DeTr + MHO group compared to the Tr group (P < 0.05). In summary, MHO did not attenuate the detraining-induced decrease in soleus muscle weight relative to body weight, mitochondrial enzyme activity, protein, or antioxidant protein expression level in the plantaris muscle after a four-week training period using voluntary wheel running in mice.

