Department of Nutrition Therapy, Digestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA.
J Appl Physiol (1985). 2013 Mar 1;114(5):559-65. doi: 10.1152/japplphysiol.01042.2012. Epub 2013 Jan 3.
Patients with cirrhosis have increased gluconeogenesis and fatty acid oxidation that may contribute to a low respiratory quotient (RQ), and this may be linked to sarcopenia and metabolic decompensation when these patients are hospitalized. Therefore, we conducted a prospective study to measure RQ and its impact on skeletal muscle mass, survival, and related complications in hospitalized cirrhotic patients. Fasting RQ and resting energy expenditure (REE) were determined by indirect calorimetry in cirrhotic patients (n = 25), and age, sex, and weight-matched healthy controls (n = 25). Abdominal muscle area was quantified by computed tomography scanning. In cirrhotic patients we also examined the impact of RQ on mortality, repeat hospitalizations, and liver transplantation. Mean RQ in patients with cirrhosis (0.63 ± 0.05) was significantly lower (P < 0.0001) than healthy matched controls (0.84 ± 0.06). Psoas muscle area in cirrhosis (24.0 ± 6.6 cm(2)) was significantly (P < 0.001) lower than in controls (35.9 ± 9.5 cm(2)). RQ correlated with the reduction in psoas muscle area (r(2) = 0.41; P = 0.01). However, in patients with cirrhosis a reduced RQ did not predict short-term survival or risk of developing complications. When REE was normalized to psoas area, energy expenditure was significantly higher (P < 0.001) in patients with cirrhosis (66.7 ± 17.8 kcal/cm(2)) compared with controls (47.7 ± 7.9 kcal/cm(2)). We conclude that hospitalized patients with cirrhosis have RQs well below the traditional lowest physiological value of 0.69, and this metabolic state is accompanied by reduced skeletal muscle area. Although low RQ does not predict short-term mortality in these patients, it may reflect a decompensated metabolic state that requires careful nutritional management with appropriate consideration for preservation of skeletal muscle mass.
肝硬化患者的糖异生和脂肪酸氧化增加，这可能导致呼吸商 (RQ) 降低，当这些患者住院时，这可能与肌肉减少症和代谢失代偿有关。因此，我们进行了一项前瞻性研究，以测量 RQ 及其对住院肝硬化患者的骨骼肌量、生存和相关并发症的影响。通过间接热量法测定肝硬化患者（n=25）和年龄、性别和体重匹配的健康对照者（n=25）的空腹 RQ 和静息能量消耗（REE）。通过计算机断层扫描定量测定腹部肌肉面积。我们还在肝硬化患者中检查了 RQ 对死亡率、再次住院和肝移植的影响。肝硬化患者的平均 RQ（0.63±0.05）明显低于健康匹配对照组（0.84±0.06；P＜0.0001）。肝硬化患者的腰大肌面积（24.0±6.6cm²）明显低于对照组（35.9±9.5cm²；P＜0.001）。RQ 与腰大肌面积减少相关（r²=0.41；P=0.01）。然而，在肝硬化患者中，降低的 RQ 并不能预测短期生存或发生并发症的风险。当 REE 按腰大肌面积标准化时，肝硬化患者的能量消耗明显更高（P＜0.001；66.7±17.8kcal/cm²），而对照组为（47.7±7.9kcal/cm²）。我们得出结论，住院的肝硬化患者的 RQ 明显低于传统的最低生理值 0.69，并且这种代谢状态伴随着骨骼肌面积的减少。尽管低 RQ 不能预测这些患者的短期死亡率，但它可能反映了一种代谢失代偿状态，需要仔细的营养管理，并适当考虑保留骨骼肌量。
