| Patients with chronic obstructive pulmonary disease ( COPD) commonly demonstrate a reduced exercise capacity. It is generally believed that the limitation of exercise performance is associated with impaired pulmonary and cardiovascular function. Weakness and deconditioning of respiratory muscle ( RM ) are currently recognized in these patients as additional factors implicated in reduction of exercise capacity as well as in the quality of life. However, in a study of 417 subjects, Killian et al found that dyspnea was the most prominent symptom limiting exercise performance in only 26% of patients with COPD and 22% of normal subjects. There is a similar percentage of healthy subjects and patients with COPD whose exercise is limited by leg effort. The recent investigations indicated that the majority of patients with moderately severe COPD did not develop diaphragm fatigue after high - intensity constant workload cycle rx-ercise; the rate of leg fatigue after maximal exercise was significantly higher in COPD than the normal control. These evidences implicate the effect of RM on exercise performance in COPD is complex and unclear.It is well known that exercise performance dependents on production and utilization of energy (ATP) in skeletal muscle cells. Aerobic metabolism, uptake and utilization of oxygen in mitochondria to synthesis ATP, is the dominant mean of ATP production. 90% of oxygen consumption is responsible for 90% of ATP synthesis. Therefore, during incremental exercise the oxygen uptake (VO2) is going higher until reaches the maximal. When the anaerobic threshold (AT) is achieved, muscle metabolism, which was principally oxida-tive, becomes principally glycolytic because oxidative energy supply is inadequate to meet energy demands. The imbalance between supply and demandmust be competing for the available energy supply, Presumably ,ceasing of ex-ercise results from neither the RM required to breathe, nor the skeletal locomo-tor muscles receive sufficient oxygen to continue metabolizing aerobically. Nev-ertheless, until recently it has not been possible to test oxygen consumption of RM or skeletal locomotor separately, Because of the importance of knpwing the effect of oxygen consumption of RM on exercise performance, we developed a novel and simple method to estimate the oxygen consumption of RM. We assume increasing the stress on the respiratory system by using addition of dead space ( VD) could increase oxygen consumption in RM. Thedifference of VO2 between VD loading and unloading ( VO2) should be the oxygen consumption of RM for the demands of increased ventilation.The objective of this study was to investigate the effect of VD loading on ventilation and RM function, to test the new method for measuring oxygen consumption of RM, and to evaluate the ffect of oxygen consumption of RM on xer-cise performance in different intensity exercise in patients with COPD.MethodsSubjects26 patients with moderate COPD [ forced expiratory volume in 1 second (FEV1) <69% and >50% predicted] , 19 men and 7 women 40 to 72 yr of age ( mean ± SE, 62 ±3 yr) were studied. Diagnosis was based on the medical history, clinical manifestations and pulmonary function tests (PFT). All patients were in a clinically stable condition for at least 4 weeks, and without treatment of corticosteroids for at least 2 weeks. 29 age - matched healthy control subjects (22 men and 7 women) were recruited from the hospital staff and their relatives. All were in excellent health and had normal EGG and PFT. All control subjects denied any medicine administration for at least 2 weeks. Bothpatients and control subjects were random arranged into lower or moderate intensity exercise groups. The standard and VD loading PFT and constant work (CW) exercise were performed in all subjects. The sequence of VD loading was random selected individually.Pulmonary function testsBefore and within 3 minutes after completing the CW exercise test, all participants underwent standard and VD loading PFT using a spirometric sy...
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