PDF(Pubmed)
Abstract：
Obesity over-activates the classical arm of the renin-angiotensin system (RAS), impairing skeletal muscle remodeling. We aimed to compare the effect of exercise training and enalapril, an angiotensin-converting enzyme inhibitor, on RAS modulation in the skeletal muscle of obese animals. Thus, we divided C57BL/6 mice into two groups: standard chow (SC) and high-fat (HF) diet for 16 weeks. At the eighth week, the HF-fed animals were divided into four subgroups-sedentary (HF), treated with enalapril (HF-E), exercise training protocol (HF-T), and combined interventions (HF-ET). After 8 weeks of treatment, we evaluated body mass and index (BMI), body composition, exercise capacity, muscle morphology, and skeletal muscle molecular markers. All interventions resulted in lower BMI and attenuation of overactivation in the classical arm, while favoring the B2R in the bradykinin receptors profile. This was associated with reduced apoptosis markers in obese skeletal muscles. The HF-T group showed an increase in muscle mass and expression of biosynthesis markers and a reduction in expression of degradation markers and muscle fiber atrophy due to obesity. These findings suggest that the combination intervention did not have a synergistic effect against obesity-induced muscle remodeling. Additionally, the use of enalapril impaired muscle\'s physiological adaptations to exercise training.
摘要：
肥胖过度激活肾素-血管紧张素系统（RAS）的经典臂，损害骨骼肌重塑。我们旨在比较运动训练和依那普利的效果，血管紧张素转换酶抑制剂，关于肥胖动物骨骼肌中RAS调制的研究。因此，我们将C57BL/6小鼠分为两组：标准食物（SC）和高脂肪（HF）饮食，持续16周。在第八周，喂食HF的动物分为四个亚组-久坐（HF），用依那普利（HF-E）治疗，运动训练方案（HF-T），和联合干预措施（HF-ET）。治疗8周后,我们评估了体重和指数（BMI），身体成分,锻炼能力,肌肉形态学,和骨骼肌分子标记。所有干预措施均导致经典手臂的BMI降低和过度激活的减弱，同时有利于缓激肽受体中的B2R。这与肥胖骨骼肌中凋亡标志物的减少有关。HF-T组显示出肌肉质量和生物合成标记表达的增加，以及由于肥胖引起的降解标记表达和肌肉纤维萎缩的减少。这些发现表明，联合干预对肥胖诱导的肌肉重塑没有协同作用。此外,采用依那普利对受损肌肉的生理适应进行运动训练。
