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This article reviews the systemic effects of chronic obstructive pulmonary disease in general and the musculoskeletal effects and cachexia in particular.Shift in muscle fiber type from I to II, reduction of capillary/mitochondria ratio, reduction of oxidative enzymes and oxidative capacity, alteration in amino acid profile, changes in respiratory muscle dynamics, activation of the ubiquitin–proteosome pathway with loss of contractile proteins are some of the factors found to cause muscle dysfunction in chronic obstructive pulmonary disease. Chemotaxis and capability to produce more reactive oxygen species and to cause extracellular proteolysis are enhanced in neutrophils of chronic obstructive pulmonary disease patients. Tumor necrosis factor-α is shown to cause loss of myosin chains in a time and dose-dependent fashion and to induce production of reactive oxygen species through activation of the cyclooxygenase pathway. Inflammation and oxidative stress caused by reactive oxygen species fuel each other. Weight loss due to muscle wasting (cachexia) in chronic obstructive pulmonary disease is not solely related to malnutrition and is an independent predictor of mortality. Causative factors for cachexia include cytokine effects, protein degradation enhanced by increased ubiquination, upregulation of mRNA for key enzymes, increased energy expenditure and neurohormonal effects such as leptin production and an imbalance in anabolic and catabolic hormone homeostasis.The findings noted above may well have the common link of inflammation in and beyond the lungs.