Bell S C, Saunders M J, Elborn J S, Shale D J
Section of Respiratory Medicine, University of Wales College of Medicine, UK.
Thorax. 1996 Feb;51(2):126-31. doi: 10.1136/thx.51.2.126.
Resting energy expenditure (REE) is often increased and may contribute towards energy imbalance in patients with cystic fibrosis. Several mechanisms may lead to increased REE including the gene defect, the effect of chronic infection, and abnormal pulmonary mechanics. Increased oxygen cost of breathing (OCB) has been demonstrated in patients with chronic obstructive pulmonary disease (COPD), but has not been the subject of extensive study in cystic fibrosis.
Ten clinically stable patients with cystic fibrosis and 10 healthy control subjects were studied. OCB was estimated using the dead space hyperventilation method. Mixed expired gas fractions were measured by online gas analysers and ventilation by a pneumotachograph. After measurement of resting ventilation and gas exchange, minute ventilation (VE) was stimulated by 6-10 1/min by the addition of a dead space and OCB calculated from the slope of the differences in oxygen uptake (VO2) and VE. REE and the non-respiratory component of REE were calculated from gas exchange data. To assess the repeatability of OCB all subjects had a further study performed one week later.
The patients had lower weight, fat free mass (FFM), forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and transfer factor for carbon monoxide (TLCO) than controls. Resting respiratory rate, VE, and oxygen uptake per kilogram of FFM (VO2/kg FFM) were higher in patients (20 (7), 10.4 (1.4) 1/min and 5.5 (0.8) ml/kg FFM/min) than in controls (13 (4), 7.0 (1.2), and 4.2 (0.5), respectively.) The error standard deviation for replicated measures of OCB was 0.5 ml O2/l VE in controls and 0.8 ml O2/l VE in patients with coefficients of variation of 24% in controls and 28% in patients. The mean OCB in patients was 2.9 (1.4) ml O2/l VE and 2.1 (0.7) ml O2/l VE in controls. OCB, expressed as ml/min (VO2resp) was 28.5 (11.7) in patients and 14.0 (3.6) in controls. REE was higher in patients (125.9 (14.0)% predicted) than in controls (99.0 (9.4)%). The estimated non-respiratory component of REE was 112.1 (14.9)% for patients and 93.0 (10.0)% for controls.
In clinically stable patients with cystic fibrosis the OCB at rest is increased but is not the sole explanation for increased metabolic rate. This contrasts with the finding in COPD where the increase in REE is largely explained by increased OCB. This study also showed poor repeatability and OCB measurements similar to earlier studies, which indicates that the technique is not suitable for longitudinal studies.
静息能量消耗（REE）在囊性纤维化患者中常升高，可能导致能量失衡。多种机制可导致REE升高，包括基因缺陷、慢性感染的影响以及异常的肺力学。慢性阻塞性肺疾病（COPD）患者的呼吸氧耗（OCB）已被证实升高，但在囊性纤维化中尚未得到广泛研究。
对10例临床稳定的囊性纤维化患者和10名健康对照者进行研究。采用死腔过度通气法估算OCB。通过在线气体分析仪测量混合呼出气分数，用呼吸流速仪测量通气量。在测量静息通气和气体交换后，通过增加死腔使分钟通气量（VE）增加6 - 10升/分钟，并根据氧摄取量（VO₂）和VE差值的斜率计算OCB。根据气体交换数据计算REE及其非呼吸成分。为评估OCB的可重复性，所有受试者在一周后再次进行研究。
患者的体重、去脂体重（FFM）、一秒用力呼气量（FEV₁）、用力肺活量（FVC）和一氧化碳转运因子（TLCO）均低于对照组。患者的静息呼吸频率、VE和每千克FFM的氧摄取量（VO₂/kg FFM）高于对照组（分别为20（7）次/分钟、10.4（1.4）升/分钟和5.5（0.8）毫升/千克FFM/分钟），而对照组分别为13（4）次/分钟、7.0（1.2）升/分钟和4.2（0.5）毫升/千克FFM/分钟。对照组OCB重复测量的误差标准差为0.5毫升O₂/升VE，患者为0.8毫升O₂/升VE，对照组变异系数为24%，患者为28%。患者的平均OCB为2.9（1.4）毫升O₂/升VE，对照组为2.1（0.7）毫升O₂/升VE。以毫升/分钟（VO₂resp）表示的OCB，患者为28.5（11.7），对照组为14.0（3.6）。患者的REE高于对照组（预测值的125.9（14.0）%），对照组为99.0（9.4）%。患者REE的估计非呼吸成分占112.1（14.9）%，对照组为93.0（10.0）%。
在临床稳定的囊性纤维化患者中，静息OCB升高，但不是代谢率升高的唯一原因。这与COPD的情况不同，在COPD中REE升高主要由OCB增加所致。本研究还显示OCB测量的可重复性差，与早期研究相似，这表明该技术不适用于纵向研究。
