Tuberc Respir Dis > Volume 44(5); 1997 > Article
Tuberculosis and Respiratory Diseases 1997;44(5):1040-1050.
DOI: https://doi.org/10.4046/trd.1997.44.5.1040    Published online October 1, 1997.
Assessment of Effect of Pulmonary Rehabilitation on Skeletal Muscle Metabolism by 31P Magnetic Resonance Spectroscopy.
Won Kyung Cho, Dong Soon Kim, Kang Hyeon Choe, Young Joo Park, Tae Hwan Lim, Tae Sun Shim, Chae Man Lim, Sang Do Lee, Youn Suck Koh, Woo Sung Kim, Won Dong Kim
Department of Internal Medicine, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.
Abstract
Pulmonary rehabilitation has been known to improve dyspnea and exercise tolerance in patients with chronic lung disease, although it does not improve pulmonary function. The mechanism of this improvement is not clearly explained till now ; however some authors suggested that the improvement in the skeletal muscle metabolism after the rehabilitation could be a possible mechanism. The metabolc changes in skeletal muscle in patients with COPD are characterized by impaired oxidative phosphorylation which causes early activation of anaerobic glycolysis and excess lactate production with exercise. In order to evaluate the change in the skeletal muscle metabolism as a possible cause of the improvement in the exercise tolerance after the rehabilitation, noninvasive 31P magnetic resonance spectroscopy(MRS) of the forearm flexor muscle was performed before and after the exercise training in nine patients with chronic lung disease who have undertaken intensive pulmonary rehabilitation for 6 weeks. 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 voluntary contraction(MVC) force of the muscle was measured before the isometric exercise, and then 30% of MVC force was constantly loaded to each patient during the isometric exercise. After the exercise training, exercise endurance of upper and lower extremities and 6 minute walking distance were significantly increased(p<0.05). There were no differences of baseline intracellular pH (pHi) and inorganic phosphate/phosphocreatine(Pi/PCr). After rehabilitation pHi at the exercise and the exhaustion state showed a significant increase(6.91+/-0.1 to 6.99+/-0.1 and 6.76+/-0.2 to 6.84+/-0.2 respectively, p<0.05). Pi/PCr at the exercise and the recovery rate of pHi and Pi/PCr did not show significant differences. These results suggest that the delayed intracellular acidosis of skeletal muscle may contribute to the improvement of exercise endurance after pulmonary rehabililtation.
Key Words: Pulmonary rehabilitation, Skeletal muscle metabolism, Chronic lung disease


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