增加的cGMP提高了饮食诱导的肥胖症中微血管运动训练适应能力
Nathan C Winn1,2, David A Cappel1, Ethan D Pollack1
1Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, United States.
概括
运动训练与PDE5抑制剂西尔德纳菲尔相结合,改善了肥胖小鼠的运动能力和微循环功能. 增强内皮氧化合成酶 (eNOS) /氧化 (NO) /cGMP通路显示,有可能改善循环限制患者的行走能力.
科学领域:
- 心血管生理学心血管生理学
- 运动科学 运动科学
- 药理学 药理学是指药理学的学科.
背景情况:
- 与动脉样硬化和2型糖尿病相关的微血管功能受损,降低了运动能力.
- 内皮氧化合成酶 (eNOS) /氧化 (NO) /cGMP通路对于调节血管度和微循环至关重要.
- 了解这种途径在运动适应中的作用,是改善身体功能的关键.
研究的目的:
- 调查是否加强eNOS/NO/cGMP轴与西德纳菲尔与运动训练的协同作用,以改善饮食诱导肥胖 (DIO) 小鼠的运动能力和微循环功能.
- 为了确定是否减少瘦小鼠的eNOS功能会影响运动训练的适应性.
主要方法:
- 药理学功能的增加:DIO小鼠每天接受西尔代纳菲尔 (一种PDE-5a抑制剂) 或安慰剂,有或没有慢性炼训练.
- 遗传性功能丧失:瘦小鼠具有内皮细胞特异性eNOS敲除 (KD) 被接受运动训练.
- 测量包括运动能力,骨肌肉毛细血管流动速度和通过静脉内显微镜进行的血透气毛细血管密度.
主要成果:
- 慢性西尔代纳菲尔治疗与运动训练协同作用,显著改善了DIO小鼠的运动性能.
- 这种改善与骨肌毛细血管流动速度增加和血透气毛细血管密度增加有关.
- 在瘦小鼠中,内皮细胞eNOS的降低并没有阻止运动训练诱导的耐力能力或微循环的改善.
结论:
- 在与训练相结合的情况下,慢性服用西尔德纳菲尔可以增强微循环功能和运动耐受性.
- eNOS/NO/cGMP路径很重要,但完全废除它并不能阻止运动训练引起的微循环适应.
- 将PDE-5a抑制剂与体育炼相结合,为改善循环限制患者的行走提供了一个潜在的策略.
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