Chest
Volume 133, Issue 1, January 2008, Pages 13-18
Journal home page for Chest

Original Research
Smoking and Skeletal Muscles
Peripheral Muscle Alterations in Non-COPD Smokers

https://doi.org/10.1378/chest.07-1592Get rights and content

Background

Although tobacco smoke is the main cause of COPD, relatively little attention has been paid to its potential damage to skeletal muscle. This article addresses the effect of smoking on skeletal muscle.

Methods

The vastus lateralis muscle was studied in 14 non-COPD smokers (FEV1/FVC, 78 ± 5%) and 20 healthy control subjects (FEV1/FVC, 80 ± 3%). Muscular structure, enzyme activity, constitutive and inducible nitric oxide (NO) synthases (endothelial NO oxide synthase [eNOS], neuronal NO synthase [nNOS] and inducible NO synthase [iNOS]), nitrites, nitrates, nitrotyrosine, and the presence of macrophages were analyzed.

Results

In smokers, type I muscle fibers cross-sectional area was decreased, and a similar trend was found in type IIa fibers. Lactate dehydrogenase levels and the percentage of fibers with low oxidative and high glycolytic capacity were increased in smokers. nNOS (96.9 ± 11.7 vs 125.4 ± 31.9 ng/mg protein; p < 0.01) and eNOS (38.9 ± 11.0 vs 45.2 ± 7.7 ng/mg protein [± SD]; p < 0.05) were lower in smokers, while fiber type distribution, capillarity measures, β-hydroxy-acyl-CoA-dehydrogenase levels, iNOS, nitrite, nitrate, and nitrotyrosine levels, and macrophage number in the muscle tissue were similar to the nonsmoker subjects.

Conclusions

Smokers presented some alterations of skeletal muscle such as oxidative fiber atrophy, increased glycolytic capacity, and reduced expression of the constitutive NO synthases (eNOS and nNOS). The findings support some muscular structural and metabolic damage but not the presence of local inflammation in the smokers. In addition, they suggest a possible effect of tobacco smoke impairing the normal process of NO generation.

Section snippets

Study Subjects

The study group consisted of 14 current smokers subjects (30 ± 10 pack-years), with normal spirometry results who were recruited from the smoking cessation clinic of the Hospital Universitario de Caracas. Twenty healthy sedentary nonsmoking subjects served as control subjects. The committee on human research approved the study, and all subjects signed the informed consent.

A non-COPD smoker was defined as a postbronchodilator FEV1/FVC ratio > 0.7, and a smoking history > 20 pack-years. Smokers

Results

The clinical characteristics and spirometric data of the non-COPD smokers and controls subjects are detailed in Table 1. There were no differences in age, weight, height, body mass index, and pulmonary function between the groups.

The smokers and control subjects fiber type distribution, mean CSA of the fibers, CSA of the different fiber types, capillarity measured as capillaries per square millimeter, capillaries per fiber, and the number of capillary contacts with the different fiber types are

Discussion

There were several important findings in this study of non-COPD smoker skeletal muscle. Smoker subjects had reduced CSA of type I fibers and a similar trend in type IIa fibers compared with control subjects. LDH levels and the percentage of fibers with low oxidative and high glycolytic capacity were increased in smokers. Muscular eNOS and nNOS concentrations were decreased in smokers, and there was no evidence supporting the presence of local inflammation in the skeletal muscle of these

References (33)

  • J Orlander et al.

    Skeletal muscle metabolism, morphology and function in sedentary smokers and nonsmokers

    Acta Physiol Scand

    (1979)
  • I Rahman et al.

    Systemic oxidative stress in asthma, COPD, and smokers

    Am J Respir Crit Care Med

    (1996)
  • A Aycicek et al.

    Decreased total antioxidant capacity and increased oxidative stress in passive smoker infants and their mothers

    Pediatr Int

    (2005)
  • S Petruzzelli et al.

    Effects of nicotine replacement therapy on markers of oxidative stress in cigarette smokers enrolled in a smoking cessation program

    Nicotine Tob Res

    (2000)
  • P Rytila et al.

    Increased oxidative stress in asymptomatic current chronic smokers and GOLD stage 0 COPD

    Respir Res

    (2006)
  • WZ Zhang et al.

    Adverse effects of cigarette smoke on NO bioavailability: role of arginine metabolism and oxidative stress

    Hypertension

    (2006)
  • Cited by (125)

    View all citing articles on Scopus

    Grant support was provided by Fondo Nacional de Ciencia, Tecnología e Innovación, S1-2005000149, G-2005000389, Consejo de Desarrollo Científico y Humanístico, Universidad Central de Venezuela, 09.33.4367.2005.

    The authors have no conflicts of interest to disclose.

    View full text