Enterococcus Faecium Strain R30 Prevents Capillary Regression through Increasing Red Blood Cell Velocity in Rat Soleus Muscle under Disuse Condition

Abstract

Inactivity leads to capillary regression in skeletal muscle. Angiogenesis is promoted by shear stress via endothelial nitric oxide synthase (eNOS)‐vascular endothelial growth factor (VEGF) pathway, and the shear stress correlates to blood flow velocity. Enterococcus faecium strain R30 (R30) has been shown to increase exercise tolerance and muscle sympathetic activity. Therefore, the aim of this study was to determine the effect of administration of R30 on hemodynamics and preventive effects via angiogenesis pathway on hindlimb unloading (HU) induced capillary regression in rat soleus muscle. Firstly, the red cells velocity in the soleus muscle was measured for assessment of the hemodynamics by single administration of R30 in rats. Secondly, chronic effects of R30 supplementation on HU‐induced capillary regression in skeletal muscle of rats were determined. Twenty‐five male SD rats were divided and administrated either saline or R30; control+saline, control+R30, HU+saline, and HU+R30. HU groups were unloaded for 2 weeks. The red cells velocity was increased by single administration of R30 compared to saline and the response was inhibited by beta‐blocker; propranolol (2 mg/kg i.v.). In addition, HU resulted in capillary regression compared to control, indicated by decreases in capillary‐to‐fiber ratio and capillary volume. However, the capillary‐to‐fiber ratio and the capillary volume in HU+R30 were higher than those in HU+saline. In addition, both the levels of eNOS and VEGF protein expression in HU+R30 were higher than those in HU+saline. These results indicated that R30 administration attenuated the capillary regression via eNOS/VEGF pathway by increasing red blood cell velocity in atrophied muscle.