Kemppainen Jukka, Stolen Kira, Kalliokoski Kari K, Salo Tiina, Karanko Hannu, Viljanen Tapio, Airaksinen Juhani, Nuutila Pirjo, Knuuti Juhani
Turku PET Centre, University of Turku, PO Box 52, 20521 Turku, Finland.
J Card Fail. 2003 Aug;9(4):286-95. doi: 10.1054/jcaf.2003.35.
The purpose of the present study was to investigate the effects of a 5-month exercise training program on skeletal muscle perfusion and insulin sensitivity at rest and during exercise in patients with idiopathic dilative cardiomyopathy (DCM).
Patients with chronic heart failure are characterized by impaired insulin sensitivity and endothelial function. It is hypothesized that exercise training improves metabolism by enhancing perfusion in patients with heart failure.
Fifteen DCM patients (New York Heart Association I-III) on stable medical therapy participated in the study. Patients were divided to receive either supervised strength and aerobic training (n=9, left ventricular ejection fraction [LVEF]=34 +/- 8%) for 5 months (3 times per week at an intensity of 70% of peak oxygen uptake [VO2]) or standard care (n=7, LVEF=36 +/- 6%) based on their living proximity to the exercise training site. Muscle blood flow, oxygen consumption, and glucose uptake were quantified using [15O]-water, [15O]-oxygen, [18F]FDG, and positron emission tomography (PET) during euglycemic hyperinsulinemia and 1-legged isometric exercise. PET studies were performed twice for each patient at the same individual workloads.
Exercise training improved exercise capacity by 27% (P<.001). Whole body insulin-stimulated glucose uptake enhanced by 23% (P<.05) and muscle glucose uptake by 53% (P<.05) in the trained group but tended to decrease in the untrained group. When studied using identical workloads, muscle glucose uptake in exercising muscles was enhanced by 55% (P<.05), whereas no changes were observed in muscle blood flow and oxygen uptake.
Exercise training counteracts the impaired insulin sensitivity caused by DCM. Training improves exercise capacity with a concomitant enhancement in whole body, resting, and exercising skeletal muscle glucose uptake. The improved insulin sensitivity is not explained by changes in muscle perfusion suggesting enhanced cellular glucose extraction.
本研究旨在调查为期5个月的运动训练计划对特发性扩张型心肌病（DCM）患者静息及运动时骨骼肌灌注和胰岛素敏感性的影响。
慢性心力衰竭患者的特征为胰岛素敏感性和内皮功能受损。据推测，运动训练可通过增强心力衰竭患者的灌注来改善代谢。
15例接受稳定药物治疗的DCM患者（纽约心脏协会心功能分级I-III级）参与了本研究。根据患者与运动训练地点的居住距离，将患者分为两组，一组接受为期5个月（每周3次，强度为峰值摄氧量[VO2]的70%）的有监督的力量和有氧运动训练（n = 9，左心室射血分数[LVEF]=34±8%），另一组接受标准护理（n = 7，LVEF=36±6%）。在正常血糖高胰岛素血症和单腿等长运动期间，使用[15O] - 水、[15O] - 氧气、[18F]FDG和正电子发射断层扫描（PET）对肌肉血流量、耗氧量和葡萄糖摄取进行定量。每位患者在相同的个体工作量下进行两次PET研究。
运动训练使运动能力提高了27%（P<0.001）。训练组全身胰岛素刺激的葡萄糖摄取增加了23%（P<0.05），肌肉葡萄糖摄取增加了53%（P<0.05），而未训练组则有下降趋势。在相同工作量下进行研究时，运动肌肉的肌肉葡萄糖摄取增加了55%（P<0.05），而肌肉血流量和摄氧量未观察到变化。
运动训练可抵消DCM导致的胰岛素敏感性受损。训练可提高运动能力，同时增强全身、静息及运动时骨骼肌的葡萄糖摄取。胰岛素敏感性的改善并非由肌肉灌注的变化所解释，提示细胞葡萄糖摄取增强。
