Krüger Karsten, Seimetz Michael, Ringseis Robert, Wilhelm Jochen, Pichl Alexandra, Couturier Aline, Eder Klaus, Weissmann Norbert, Mooren Frank C
Institute of Sports Science, Department Exercise and Health, Leibniz University Hannover , Germany.
Department of Sports Medicine, University of Giessen , Giessen , Germany.
Am J Physiol Regul Integr Comp Physiol. 2018 Mar 1;314(3):R366-R376. doi: 10.1152/ajpregu.00316.2017. Epub 2017 Nov 1.
Long-term cigarette smoking induces inflammatory processes in the pulmonary system that are suggested to "spill over" into systemic inflammation. Regular exercise has been shown to have anti-inflammatory properties. The aim of the study was to investigate the effects of therapeutic exercise on inflammation and muscle wasting in smoke-exposed mice. C57BL/6J mice ( n = 30) were separated into three groups to receive either 1) no specific treatment (control group), 2) 8-mo exposure to cigarette smoke [smoke-exposed (SE) group], or 3) 8 mo of cigarette smoke combined with exercise training during the last 2 mo (SEex group). The inflammatory status was analyzed by quantifying levels of various plasma proteins using multiplex ELISA and detection of lymphocyte surface markers by flow cytometry. Muscle tissue was analyzed by histological techniques and measurements of RNA/protein expression. SE led to decreased maximal O uptake (V̇o) and maximal running speed ( V), which was reversed by exercise ( P < 0.05). Expression of ICAM-1, VCAM-1, and CD62L on T cells increased and was reversed by exercise ( P < 0.05). Similarly, SE induced an increase of various inflammatory cytokines, which were downregulated by exercise. In muscle, exercise improved the structure, oxidative capacity, and metabolism by reducing ubiquitin proteasome system activation, stimulating insulin-like growth factor 1 expression, and the SE-induced inhibition of mammalian target of rapamycin signaling pathway ( P < 0.05). Exercise training reverses smoke-induced decline in exercise capacity, systemic inflammation, and muscle wasting by addressing immune-regulating, anabolic, and metabolic pathways.
长期吸烟会在肺部系统引发炎症反应，这些炎症反应被认为会“扩散”到全身炎症中。有研究表明，规律运动具有抗炎特性。本研究的目的是调查治疗性运动对暴露于烟雾中的小鼠炎症和肌肉萎缩的影响。将30只C57BL/6J小鼠分为三组，分别接受以下处理：1）无特定治疗（对照组）；2）暴露于香烟烟雾8个月[烟雾暴露（SE）组]；3）在最后2个月将8个月的香烟烟雾暴露与运动训练相结合（SEex组）。通过使用多重ELISA定量各种血浆蛋白水平以及通过流式细胞术检测淋巴细胞表面标志物来分析炎症状态。通过组织学技术以及RNA/蛋白质表达测量来分析肌肉组织。SE导致最大摄氧量（V̇o）和最大跑步速度（V）降低，而运动可使其恢复（P<0.05）。T细胞上ICAM-1、VCAM-1和CD62L的表达增加，运动可使其恢复（P<0.05）。同样，SE诱导多种炎性细胞因子增加，而运动可使其下调。在肌肉方面，运动通过减少泛素蛋白酶体系统激活、刺激胰岛素样生长因子1表达以及SE诱导的雷帕霉素哺乳动物靶标信号通路抑制来改善结构、氧化能力和代谢（P<0.05）。运动训练通过调节免疫、合成代谢和代谢途径，逆转了烟雾引起的运动能力下降、全身炎症和肌肉萎缩。
