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.

Acute hypoxia causes skeletal muscle dysfunction in vitro, but little is known about its effect on muscle function in vivo. In 10 healthy male subjects, isometric contractile properties and fatigue resistance of the quadriceps muscle were determined during normoxia and hypoxia using electrically evoked and voluntary contractions. The oxygen saturation (SaO(2); 96.9 +/- 0.7 vs. 79.9 +/- 3.0%; P < 0.001) was reduced during hypoxia. The maximal voluntary contraction (MVC), force-frequency relation, and contraction and relaxation times were unaffected by hypoxia. The endurance time of a sustained 30% MVC was reduced in hypoxia (248 +/- 104 vs. 217 +/- 76 s; P < 0.05), but not that of a sustained 70% MVC. Fatigue induced by electrically evoked intermittent contractions was unaltered. Thus, acute hypoxia has no significant impact on contractile properties of skeletal muscle in vivo but causes reduced endurance during low-level sustained voluntary contractions. This indicates that skeletal muscle dysfunction during conditions associated with prolonged hypoxemia, except for limited endurance, is not due to acute effects of hypoxemia.