Transcutaneous carbon dioxide application inhibits muscle atrophy after fracture in rats.

Abstract

Muscle atrophy causes difficulty in resuming daily activities after a fracture. Because transcutaneous carbon dioxide (CO₂) application has previously upregulated oxygen pressure in the local tissue, thereby demonstrating its potential in preventing muscle atrophy, here we investigated effects of CO₂ application on muscle atrophy after femoral shaft fracture. Thirty fracture model rats were produced and randomly divided into a no treatment (control group) and treatment (CO₂ group) groups. After treatment, the soleus muscle was dissected at post-fracture days 0, 14, and 21. Evaluations were performed by measuring muscle weight and performing histological examination and gene expression analysis. Muscle weight was significantly higher in the CO₂ group than in the control group. Histological analysis revealed that the muscle fiber cross-sectional area was reduced in both groups. Nevertheless, the extent of atrophy was lesser in the CO₂ group. Muscle fibers in the control group tended to change into fast muscle fibers. Vascular staining revealed that more capillary vessels surrounded the muscle fibers in the CO₂ group than in the control group. Messenger RNA (mRNA) analysis revealed that the CO₂ group had a significantly enhanced expression of genes that were related to muscle synthesis. Transcutaneous CO₂ application may be a novel therapeutic strategy for preventing skeletal muscle atrophy after fracture.