Smoking-induced Skeletal Muscle Dysfunction From Evidence to Mechanisms
Smoking-induced Skeletal Muscle Dysfunction From Evidence to Mechanisms
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DOI：
10.1164/rccm.201410-1830pp
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发表时间：
2015-03-15
影响因子：
24.7
通讯作者：
van Hees, Hieronymus W. H.
中科院分区：
文献类型：
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作者：
Degens, Hans;Gayan-Ramirez, Ghislaine;van Hees, Hieronymus W. H.
吸烟是慢性阻塞性肺疾病（COPD）发展的最重要的危险因素。COPD患者通常患有骨骼肌功能障碍，有研究表明，即使在出现明显的肺部病变之前，香烟烟雾暴露也会导致骨骼肌功能障碍的发展。这篇综述总结了无症状吸烟者的肌肉比不吸烟者更弱，抗疲劳性更差的证据。虽然许多吸烟者的身体不活动导致骨骼肌中观察到的一些改变，但暴露于香烟烟雾本身也可诱导骨骼肌功能障碍。香烟烟雾成分和全身炎症介质增强蛋白质水解并抑制蛋白质合成，导致肌肉质量损失。吸烟者骨骼肌收缩耐力降低可能是由于一氧化碳与血红蛋白、肌红蛋白和呼吸链组分相互作用导致向线粒体的氧输送受损以及线粒体产生ATP的能力受损。除了阻碍收缩功能，吸烟可能对运动技能有直接的有益影响，这可归因于尼古丁。与肺部病理学相反，吸烟对骨骼肌的许多影响很可能通过戒烟逆转。
Smoking is the most important risk factor for the development of chronic obstructive pulmonary disease (COPD). Patients with COPD commonly suffer from skeletal muscle dysfunction, and it has been suggested that cigarette smoke exposure contributes to the development of skeletal muscle dysfunction even before overt pulmonary pathology. This review summarizes the evidence that muscles of nonsymptomatic smokers are weaker and less fatigue resistant than those of nonsmokers. Although physical inactivity of many smokers contributes to some alterations observed in skeletal muscle, exposure to cigarette smoke per se can also induce skeletal muscle dysfunction. Cigarette smoke constituents and systemic inflammatory mediators enhance proteolysis and inhibit protein synthesis, leading to loss of muscle mass. Reduced skeletal muscle contractile endurance in smokers may result from impaired oxygen delivery to the mitochondria and ability of the mitochondria to generate ATP due to interaction of carbon monoxide with hemoglobin, myoglobin, and components of the respiratory chain. Besides hampering contractile function, smoking may have immediate beneficial effects on motor skills, which are attributable to nicotine. In contrast to pulmonary pathology, many of the effects of smoking on skeletal muscle are most likely reversible by smoking cessation.