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Aerobic Exercise Ameliorates Muscle Atrophy Induced by Methylglyoxal via Increasing Gastrocnemius and Extensor Digitorum Longus Muscle Sensitivity

  • Seong-Min Hong (College of Pharmacy, Gachon University) ;
  • Eun Yoo Lee (College of Pharmacy, Gachon University) ;
  • Jinho Park (Department of Exercise Rehabilitation, Gachon University) ;
  • Jiyoun Kim (Department of Exercise Rehabilitation, Gachon University) ;
  • Sun Yeou Kim (College of Pharmacy, Gachon University)
  • Received : 2023.07.17
  • Accepted : 2023.07.30
  • Published : 2023.09.01

Abstract

Muscle atrophy is characterized by the loss of muscle function. Many efforts are being made to prevent muscle atrophy, and exercise is an important alternative. Methylglyoxal is a well-known causative agent of metabolic diseases and diabetic complications. This study aimed to evaluate whether methylglyoxal induces muscle atrophy and to evaluate the ameliorative effect of moderate-intensity aerobic exercise in a methylglyoxal-induced muscle atrophy animal model. Each mouse was randomly divided into three groups: control, methylglyoxal-treated, and methylglyoxal-treated within aerobic exercise. In the exercise group, each mouse was trained on a treadmill for 2 weeks. On the last day, all groups were evaluated for several atrophic behaviors and skeletal muscles, including the soleus, plantaris, gastrocnemius, and extensor digitorum longus were analyzed. In the exercise group, muscle mass was restored, causing in attenuation of muscle atrophy. The gastrocnemius and extensor digitorum longus muscles showed improved fiber cross-sectional area and reduced myofibrils. Further, they produced regulated atrophy-related proteins (i.e., muscle atrophy F-box, muscle RING-finger protein-1, and myosin heavy chain), indicating that aerobic exercise stimulated their muscle sensitivity to reverse skeletal muscle atrophy. In conclusion, shortness of the gastrocnemius caused by methylglyoxal may induce the dynamic imbalance of skeletal muscle atrophy, thus methylglyoxal may be a key target for treating skeletal muscle atrophy. To this end, aerobic exercise may be a powerful tool for regulating methylglyoxal-induced skeletal muscle atrophy.

Keywords

Acknowledgement

This research was supported by a grant from the Basic Science Research Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF-2022R1I1A4068917). We are also thankful to Myoung Gyu Park, MetaCen Therapeutics Co., Ltd for his valuable support.

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