The functional derangement of skeletal muscles which may be attributed to chronic hypoxia has been accepted as a possible mechanism of exercise impairment in patients with chronic obstructive pulmonary disease (COPD). The metabolc changes in skeletal muscle in patients with COPD are characterized by impaired oxidative phosphorylation early activation of anaerobic glycolysis and excessive lactate and hydrogen ion production with exercise. But the cause of exercise limitation in patients with chronic lung disease without hypoxia has not been known. In order to evaluate the change in the skeletal muscle metabolism as a possible cause of the exercise limitation in chronic lung disease patients without hypoxia, we compared the muscular metabolic data of seven male patients which had been derived from noninvasive 31P magnetic resonance spectroscopy(MRS) with those of five age-matched normal male control persons. 31P MRS was studied during the sustained isometric contraction of the dominant forearm flexor muscles up to the exhaustion state and the recovery period. Maximal voluntatry contraction(MVC) force of the muscle was measured before the isometric exercise, and the 30% of MVC force was constantly loaded to each patient during the isometric exercise. There were no differences of intracellular pH (pHi) and inorganic phosphate/phosphocreatine (Pi/PCr) at baseline, exhaustion state and recovery period between two groups. But pHi during the exercise was lower in patients group than the control group (p<0.05). Pi/PCr during the exercise did not show significant difference between two groups. These results suggest that the exercise limitation in chronic lung disease patients without hypoxia also could be attributed to the abnormalities in the skeletal muscle metabolism.