Laboratory of Exercise Sciences, Biomedical Institute, Fluminense Federal University, Niteroi, Rio de Janeiro, Brazil.
Research Center on Morphology and Metabolism, Biomedical Institute, Fluminense Federal University, Niteroi, Rio de Janeiro, Brazil.
Physiol Rep. 2024 May;12(9):e16025. doi: 10.14814/phy2.16025.
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.
肥胖会过度激活肾素-血管紧张素系统(RAS)的经典途径,损害骨骼肌重塑。我们旨在比较运动训练和依那普利(一种血管紧张素转换酶抑制剂)对肥胖动物骨骼肌中 RAS 调节的影响。因此,我们将 C57BL/6 小鼠分为两组:标准饲料(SC)和高脂肪(HF)饮食 16 周。在第八周时,HF 喂养的动物被分为四个亚组-安静(HF)、依那普利治疗(HF-E)、运动训练方案(HF-T)和联合干预(HF-ET)。经过 8 周的治疗,我们评估了体重和体重指数(BMI)、身体成分、运动能力、肌肉形态和骨骼肌分子标志物。所有干预措施都导致 BMI 降低和经典途径过度激活的减弱,同时有利于缓激肽受体 B2R 途径。这与肥胖骨骼肌中凋亡标志物的减少有关。HF-T 组表现出肌肉质量增加和合成代谢标志物表达增加,以及肥胖导致的降解标志物表达减少和肌肉纤维萎缩减少。这些发现表明,联合干预对肥胖引起的肌肉重塑没有协同作用。此外,依那普利的使用会损害肌肉对运动训练的生理适应。