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Decreased Peripheral Muscle Oxygen Utilization Reduces Exercise Tolerance in Patients With Chronic Obstructive Pulmonary Disease FREE TO VIEW

Mumtaz Zaman, MD; Jeremy Cumberledge, MD
Chest. 2011;140(4_MeetingAbstracts):871A. doi:10.1378/chest.1116711
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Abstract

PURPOSE: Exercise limitation in chronic obstructive pulmonary disease (COPD) is related to multiple physiological problems including peripheral muscle dysfunction. Unsettled is whether the limitations in peripheral muscle dysfunction are a result of myopathic effects of COPD pathology or muscle inactivity, as in sedentarism due to obesity. In this study we sought to determine whether impaired peripheral muscle oxygen extraction limits the exercise tolerance of patients with COPD.

METHODS: The three study groups comprised 15 adult patients with COPD (forced expiratory volume in one second [FEV1] =1.98±0.20L) (Mean±SE), 19 obese patients (FEV1=2.92±0.17L) and nine normal adults (FEV1 = 3.41±0.25L). All patients performed symptom-limited incremental cardiopulmonary exercise test on cycle ergometer. Measurements included BMI, oxygen uptake, oxygen pulse, anaerobic threshold, calculated stroke volume, heart rate, hemoglobin, oxygen saturation and breathing reserve.

RESULTS: Oxygen uptake was significantly reduced in patients with COPD compared to obese patients (1325±93.2 ml/min vs 1712±112.4 ml/min, p=0.01) and oxygen uptake in obese patients was not different from control patients (1712±112.4 vs 2015±196.2 ml/min, p=0.164). The anaerobic threshold was also reduced in the group with COPD compared to the obese patients (964.5±78.4 ml/min vs 1271.3±98.3 ml/min, p=0.02) but anaerobic threshold was not different between obese patients and normal adults (1271.3±98.3 ml/min vs 1332.8±195.7 ml/min, p=0.75). The oxygen pulse (% predicted) was reduced in the group with COPD when compared to obese individuals (74.8±3.4% vs 92.6±5.4%, p=0.01) although no significant differences in the calculated stroke volume (based on the measured hemoglobin and oxygen pulse) was found among all three groups (COPD, 76.2±5.6 ml/beat; obese, 91±6.6 ml/beat; and, normal 85.1±5.9 ml/beat).

CONCLUSIONS: Our study suggests that COPD causes impaired muscle oxygen utilization due to the systemic myopathic effects in persons with moderate disease and not simply due to sedentary lifestyle alone as in obesity.

CLINICAL IMPLICATIONS: Limitations in exercise capacity of moderate COPD patients are most likely the result of muscle dysfunction and poor lung function, rather than reduced cardiac function. Systematic muscle training and strengthening exercises might act to ameliorate exercise intolerance.

DISCLOSURE: The following authors have nothing to disclose: Mumtaz Zaman, Jeremy Cumberledge

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