Institute of Sports Medicine Copenhagen, Department of Orthopedic Surgery M, Bispebjerg Hospital and Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, DENMARK.
Med Sci Sports Exerc. 2018 Feb;50(2):225-235. doi: 10.1249/MSS.0000000000001438.
To investigate the effect of blocking the angiotensin II Type I receptor (AT1R) upon the response to acute heavy-resistance exercise in elderly human skeletal muscle. The hypothesis was that AT1R blocking would result in a superior myogenic response accompanied by down-regulation of transforming growth factor-beta and up-regulation of insulin-like growth factor-1 signaling.
Twenty-eight healthy elderly men (+64 yr) were randomized into two groups, consuming either AT1R blocker (losartan, 100 mg·d) or placebo for 18 d before exercise. Participants performed one bout of heavy-unilateral-resistance exercise. Six muscle biopsies were obtained from the vastus lateralis muscles of each subject: two before exercise and four after exercise (4.5 h and 1, 4, and 7 d). Blood pressure and blood samples were collected at the same time points. Biopsies were sectioned for immunohistochemistry to determine the number of satellite cells associated with Type I and Type II fibers. Gene expression levels of Notch, connective tissue, and myogenic signaling pathways were determined by real-time reverse transcription polymerase chain reaction.
Changes over time were detected for circulating creatine kinase, the number of satellite cells per Type I fiber, and most of the gene targets, with no specific effect of losartan on these. However, when compared with placebo, losartan intake resulted in a greater suppression of myostatin messenger RNA.
In general, there does not seem to be any effect of AT1R blocking on satellite cell number or myogenic pathways in elderly men in the days after one bout of heavy-resistance exercise. However, the greater suppression of myostatin may prove to be beneficial over a long-term intervention designed to induce hypertrophy.
研究阻断血管紧张素 II 型 1 型受体（AT1R）对老年人体骨骼肌对急性大强度抗阻运动反应的影响。假说为 AT1R 阻断会导致更好的肌原性反应，同时下调转化生长因子-β和上调胰岛素样生长因子-1 信号。
28 名健康老年男性（+64 岁）随机分为两组，分别在运动前 18 天服用 AT1R 阻滞剂（氯沙坦，100mg·d）或安慰剂。参与者进行一次单侧大强度抗阻运动。从每个受试者的股外侧肌中获得 6 个肌肉活检：运动前 2 个，运动后 4 个（4.5h 及 1、4、7d）。在相同时间点采集血压和血液样本。活检用于免疫组织化学分析，以确定与 I 型和 II 型纤维相关的卫星细胞数量。通过实时逆转录聚合酶链反应确定 Notch、结缔组织和肌源性信号通路的基因表达水平。
循环肌酸激酶、I 型纤维每个卫星细胞的数量以及大多数基因靶标随时间发生变化，但氯沙坦对这些没有特定影响。然而，与安慰剂相比，氯沙坦摄入导致肌肉生长抑制素 mRNA 的抑制作用更大。
一般来说，在一次大强度抗阻运动后几天内，AT1R 阻断对老年男性的卫星细胞数量或肌源性通路似乎没有任何影响。然而，肌肉生长抑制素的更大抑制可能在旨在诱导肥大的长期干预中是有益的。
