Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Department of Chronic Diseases, Metabolism and Ageing (CHROMETA), KU-Leuven, Leuven, Belgium.
Research Group for Rehabilitation in Internal Disorders, Department of Rehabilitation Sciences, KU-Leuven, Leuven, Belgium.
Nicotine Tob Res. 2021 Jan 7;23(1):143-151. doi: 10.1093/ntr/ntaa016.
Apart from its adverse effects on the respiratory system, cigarette smoking also induces skeletal muscle atrophy and dysfunction. Whether short-term smoking cessation can restore muscle mass and function is unknown. We, therefore, studied the impact of 1- and 2-week smoking cessation on skeletal muscles in a mouse model.
Male mice were divided into four groups: Air-exposed (14 weeks); cigarette smoke (CS)-exposed (14 weeks); CS-exposed (13 weeks) followed by 1-week cessation; CS-exposed (12 weeks) followed by 2 weeks cessation to examine exercise capacity, physical activity levels, body composition, muscle function, capillarization, mitochondrial function and protein expression in the soleus, plantaris, and diaphragm muscles.
CS-induced loss of body and muscle mass was significantly improved within 1 week of cessation due to increased lean and fat mass. Mitochondrial respiration and protein levels of the respiratory complexes in the soleus were lower in CS-exposed mice, but similar to control values after 2 weeks of cessation. Exposing isolated soleus muscles to CS extracts reduced mitochondrial respiration that was reversed after removing the extract. While physical activity was reduced in all groups, exercise capacity, limb muscle force, fatigue resistance, fiber size and capillarization, and diaphragm cytoplasmic HIF-1α were unaltered by CS-exposure. However, CS-induced diaphragm atrophy and increased capillary density were not seen after 2 weeks of smoking cessation.
In male mice, 2 weeks of smoking cessation reversed smoking-induced mitochondrial dysfunction, limb muscle mass loss, and diaphragm muscle atrophy, highlighting immediate benefits of cessation on skeletal muscles.
Our study demonstrates that CS-induced skeletal muscle mitochondrial dysfunction and atrophy are significantly improved by 2 weeks of cessation in male mice. We show for the first time that smoking cessation as short as 1 to 2 weeks is associated with immediate beneficial effects on skeletal muscle structure and function with the diaphragm being particularly sensitive to CS-exposure and cessation. This could help motivate smokers to quit smoking as early as possible. The knowledge that smoking cessation has potential positive extrapulmonary effects is particularly relevant for patients referred to rehabilitation programs and those admitted to hospitals suffering from acute or chronic muscle deterioration yet struggling with smoking cessation.
除了对呼吸系统的不良影响外，吸烟还会导致骨骼肌萎缩和功能障碍。短期戒烟是否能恢复肌肉质量和功能尚不清楚。因此，我们在小鼠模型中研究了 1 至 2 周戒烟对骨骼肌的影响。
雄性小鼠分为四组：空气暴露组（14 周）；香烟烟雾暴露组（14 周）；香烟烟雾暴露组（13 周）后戒烟 1 周；香烟烟雾暴露组（12 周）后戒烟 2 周，以检查运动能力、身体活动水平、身体成分、肌肉功能、毛细血管化、线粒体功能和比目鱼肌、跖肌和膈肌肌肉的蛋白质表达。
由于瘦体重和脂肪体重增加，戒烟 1 周内 CS 引起的体重和肌肉质量下降明显改善。与对照组相比，CS 暴露小鼠的比目鱼肌线粒体呼吸和呼吸复合物的蛋白质水平降低，但戒烟 2 周后恢复到对照水平。将分离的比目鱼肌暴露于 CS 提取物中会降低线粒体呼吸，去除提取物后可逆转。虽然所有组的身体活动都减少了，但运动能力、四肢肌肉力量、抗疲劳能力、纤维大小和毛细血管化以及膈肌细胞质 HIF-1α不受 CS 暴露的影响。然而，戒烟 2 周后，CS 诱导的膈肌萎缩和毛细血管密度增加并未出现。
在雄性小鼠中，戒烟 2 周可逆转吸烟引起的线粒体功能障碍、四肢肌肉质量下降和膈肌萎缩，突出了戒烟对骨骼肌的即时益处。
我们的研究表明，在雄性小鼠中，戒烟 2 周可显著改善 CS 引起的骨骼肌线粒体功能障碍和萎缩。我们首次表明，戒烟 1 至 2 周与骨骼肌结构和功能的即时有益影响有关，其中膈肌对 CS 暴露和戒烟特别敏感。这可能有助于激励吸烟者尽早戒烟。了解戒烟对肺外器官有潜在的积极影响，特别是对那些因急性或慢性肌肉恶化而被转介到康复计划或住院治疗的患者，这些患者正在努力戒烟。
