Exposure to cigarette smoke causes muscular degradation, especially in oxidative (aerobic) muscle fibers. Understanding the mechanism of this muscle degradation will aid in providing treatment to those suffering from COPD.
A competitive athlete is wary of cigarette smoke because of its established negative pulmonary effects. However, recent research has found that cigarette smoke also causes muscle degradation. A team of researchers from the University of California, San Diego is searching for possible biological mechanisms by which cigarette smoke affects muscle.
People suffering from smoking-induced chronic obstructive pulmonary disease (COPD) exhibit changes independent from the pulmonary system in their muscles. These changes include loss of muscle strength and mass, receding capillaries in the muscle, muscle transition from oxidative fibers to glycolytic fibers and impaired muscle energy metabolism.
To assess the biological pathway that links cigarette smoke exposure with muscle degradation, the researchers exposed mice to cigarette smoke for 8 and 16 weeks (TNF-alpha Mediated Reduction in PGC-1alpha may Impair Skeletal Muscle Function After Cigarette Smoke Exposure, 2009, Kechun Tang, et al.). The soleus and extensor digitorum longus (EDL) muscles were then analyzed. Because the EDL is composed of glycolytic muscle fiber it showed, as the researchers expected, a smaller change in oxidative associated enzymes and cytokines as a result of cigarette smoke. In the soleus, aerobic oxidative fibers were converted to anaerobic glycolytic fibers. The decrease in capillary density in the soleus can be seen in the figure below.
Reduced soleus and EDL capillarity in mice exposed to cigarette smoke for 8 and 16 weeks bouts. Measured in capillary number/sq mm.
Cigarette smoke was found to increase levels of the inflammatory cytokine TNF-alpha. The transcriptional co-factor PGC-1alpha has been shown to control capillarity density in the muscle fiber through the angiogenic factor VEGF. TNF-alpha was found to mediate the levels of PGC-1 in vitro. Therefore, mediating the inflammatory cytokine TNF-alpha may result in normal expression of the co-factor PGC-1alpha providing COPD patients with a means of combating the muscular degradation associated with cigarette smoke. As the figure below demonstrates, TNF-alpha levels were raised significantly with cigarette smoke exposure. This elevation in TNF-alpha saw a major decrease in the VEGF transcription factor PGC-1alpha in the oxidative heavy soleus muscle.
In summary, cigarette smoke exposure causes muscular degradation in addition to the adverse pulmonary effects. Athletes, therefore, can expect to see damage to both their pulmonary and muscular systems as a result of exposure to cigarette smoke. Cgarette smoke is found to elevate levels of inflammatory cytokine TNF-alpha which lowers the transcription factor PGC-1alpha. TNF-alpha may be a target for patients with chronic obstructive pulmonary disease.