• Xin-ming Su, Zhi Liu, Gang Liu, Yu Song, and Run-jiang Yu.
• Institute of the Respiratory Disease, 1st Hospital, China Medical University, Shenyang 110001, China.
• Zhonghua Nei Ke Za Zhi. 2003 May 1; 42 (5): 324-7.

ObjectiveTo investigate the relationships of the rest energy expenditure to the respiratory mechanics and arterial blood gases in chronic obstructive pulmonary disease (COPD) patients.MethodsTwenty six patients with COPD and 21 healthy subjects were involved in the study. The rest energy expenditure (REE), oxygen consumption (VO(2)), carbon dioxide production (VCO(2)) and respiratory quotient (RQ) were measured with indirect energy measurements of canopy test; the arterial blood gases were measured soon after energy measurements; then routine pulmonary function, P(0.1) and P(IMAX) were measured at rest.Results(1) The REE/day, P(0.1)/P(IMAX) and heart rate (HR) in the COPD group [(1,577.69 +/- 311.31) kcal, 0.068 +/- 0.026 and (83.46 +/- 11.36) BPM, respectively] were significantly higher than those in the healthy control group [(1,388.29 +/- 194.89) kcal, 0.039 +/- 0.014 and (69.71 +/- 5.73) BPM, respectively, P < 0.05 for all]; the forced expiratory volume in one second (FEV(1))% of predicted, partial pressure of oxygen in artery (PaO(2)) and arterial oxygen saturation (SaO(2)) in the COPD group [(50.46 +/- 21.35)%, (77.72 +/- 8.84) mm Hg and (92.54 +/- 2.55)%, respectively] were significantly lower than those in the control group [(92.29 +/- 11.91)%, (92.50 +/- 3.82) mm Hg and (96.29 +/- 1.87)%, respectively, P < 0.01 for all]. (2) In COPD group, the REE/day was positively correlated with body height, body weight, body mass index, P(0.1)/P(IMAX) and HR (r = 0.57, 0.65, 0.62, 0.41 and 0.51, respectively, P < 0.05 for all), negatively correlated with FEV(1)%, PaO(2) and SaO(2) (r = -0.43, -0.47 and -0.32, respectively, P < 0.05 for all); the P(0.1) was negatively correlated with PaO(2) and SaO(2) (r = -0.62 and -0.53, respectively, P < 0.01).ConclusionThe rest energy expenditure of COPD patients was significantly higher than that of healthy subjects. This increase in REE was not only attributed to the airway obstruction and the damaged gas exchange, but may be related to the elevated respiratory drive and dysfunction of respiratory muscles as well.

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