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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Skeletal muscle contractility is preserved in COPD patients with normal fat-free mass.

AIM: Peripheral muscle dysfunction often occurs in patients with chronic obstructive pulmonary disease (COPD). The muscle dysfunction may be caused by a loss of force-generating capacity, resulting from a loss of muscle mass, as well as by other alterations in contractile properties of skeletal muscle. METHODS: The maximal isometric voluntary strength and fatigability were determined in hand-grip and quadriceps muscles from nine male COPD patients (FEV(1) 30-50% predicted) and control subjects matched for fat-free mass (FFM), physical activity level and age. Contractile properties and fatigability of the quadriceps muscle were also studied with electrically evoked isometric contractions. RESULTS: The maximal voluntary force (MVC) and fatigability of the handgrip muscle did not differ between the COPD patients and control subjects. Also the MVC of the quadriceps muscle and the rate of force rise, contraction time, force-frequency relationship and fatigability, as determined with electrically evoked contractions, were similar in patients with COPD and control subjects. CONCLUSION: Skeletal muscle strength, contractile properties and fatigability are preserved in patients with moderate COPD and a normal FFM and activity level. This suggests that skeletal muscle dysfunction does not take place during moderate COPD until cachexia and/or a decline in physical activity occur.[1]


  1. Skeletal muscle contractility is preserved in COPD patients with normal fat-free mass. Degens, H., Sanchez Horneros, J.M., Heijdra, Y.F., Dekhuijzen, P.N., Hopman, M.T. Acta Physiol. Scand. (2005) [Pubmed]
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