Abstract：
Exercise has been recognized as an effective intervention in the treatment of pulmonary arterial hypertension (PAH), supported by numerous studies. However, the precise effects of exercise on pulmonary function remain to be fully elucidated. In this study, using a rat model of swimming exercise training and monocrotaline-induced PAH, we aimed to explore its impact on pulmonary morphology and function. Our investigations revealed that MCT-treated rats exhibited augmented mean pulmonary arterial pressure (MPAP) and pulmonary vascular remodeling, which can be attenuated by 4 weeks of swimming exercise training (60 min/day, 5 days/week). Notably, MCT-treated rats showed impaired pulmonary function, as manifested by decreased tidal volume and dynamic compliance, which were reversed by exercise training. Assessment of pulmonary substrate in PAH rats indicated a prominent pro-inflammatory substrate, evidenced by macrophage accumulation through quantitative immunohistological analysis of macrophage-like cell expression (CD68), and extracellular matrix remodeling, evaluated by Masson staining. Importantly, both the pro-inflammatory substrate and extracellular matrix remodeling were ameliorated by swimming exercise training. Additionally, serum biochemical analysis demonstrated elevated levels of low-density lipoprotein cholesterol and Apolipoprotein B following MCT treatment, which were reduced with exercise intervention. Moreover, exercise enhanced systemic insulin sensitivity in both MCT-treated and untreated rats. Notably, MCT and exercise treatment both decreased fasting blood glucose (FBG) levels in rats, whereas exercise training reinstated FBG levels to normal in MCT-treated rats. In summary, our study suggests that swimming exercise confers a pulmonary protective effect in MCT-induced PAH rats, highlighting the potential importance of exercise-based rehabilitation in the management of PAH.
摘要：
运动已被认为是治疗肺动脉高压（PAH）的有效干预措施，在众多研究的支持下。然而,运动对肺功能的确切影响仍有待充分阐明。在这项研究中,使用游泳运动训练和野百合碱诱导的PAH的大鼠模型，我们旨在探讨其对肺形态和功能的影响。我们的研究表明，MCT治疗的大鼠表现出增加的平均肺动脉压（MPAP）和肺血管重塑，可以通过4周的游泳运动训练(60分钟/天，5天/周）。值得注意的是,MCT治疗的大鼠显示肺功能受损，表现为潮气量下降和动态顺应性，运动训练逆转了。对PAH大鼠肺底物的评估表明有明显的促炎底物，通过定量免疫组织学分析巨噬细胞样细胞表达（CD68）的巨噬细胞积累证明，和细胞外基质重塑，通过Masson染色评价。重要的是,游泳运动训练改善了促炎基质和细胞外基质重塑.此外,血清生化分析显示MCT治疗后低密度脂蛋白胆固醇和载脂蛋白B水平升高，运动干预减少了。此外，运动可增强MCT治疗和未治疗大鼠的全身胰岛素敏感性.值得注意的是,MCT和运动治疗均降低了大鼠空腹血糖（FBG）水平，而运动训练使MCT治疗大鼠的FBG水平恢复正常。总之,我们的研究表明，游泳运动对MCT诱导的PAH大鼠具有肺保护作用，强调基于运动的康复在PAH管理中的潜在重要性。
