Wilson Genevieve Abigail, Wilson Luke C, Lamberts Regis R, Majeed Kamran, Lal Sudish, Wilkins Gerard T, Baldi James Chris
1Department of Medicine, University of Otago, Dunedin, NEW ZEALAND; 2Department of Physiology, HeartOtago, University of Otago, Dunedin, NEW ZEALAND; and 3Royal Adelaide Hospital, Adelaide, AUSTRALIA.
Med Sci Sports Exerc. 2017 May;49(5):907-914. doi: 10.1249/MSS.0000000000001184.
Type 2 diabetes (T2D) is associated with reduced cardiac reserve and aerobic capacity. Altered myocardial autonomic nervous regulation has been demonstrated in humans with diabetes (indirectly) and animal models (directly).
This study aimed to determine the chronotopic and inotropic response of the type 2 diabetic heart to β-adrenergic stimulation.
Eight people with uncomplicated T2D and seven matched controls performed a dual-energy x-ray absorptiometry scan and V˙O2peak test. Plasma catecholamines were determined at rest and during peak exercise. On a second visit, HR and left ventricular contractility were assessed using echocardiography during supine rest, parasympathetic blockade (atropine), and during incremental β-adrenergic stimulation (dobutamine).
V˙O2peak and HR reserve were lower in T2D (P < 0.05) as expected. Both groups increased norepinephrine comparably (P = 0.23) during peak exercise; however, epinephrine increased less in the T2D group (P < 0.05). The dobutamine dose required to achieve 85% of age-predicted maximal HR was 36% higher in CON (P < 0.05). Resting HR was higher (P < 0.01) and stroke volume indexed to fat free mass was smaller (P < 0.05) in T2D. During dobutamine infusion the response (% change) in HR, end-diastolic volumeFFM, stroke volume, ejection fraction, and cardiac output were not different between the groups. However, HR was higher (P < 0.01) and end-diastolic volume indexed to fat free mass (P < 0.01), stroke volumeFFM (P < 0.01), ejection fraction (P < 0.05), and stroke work (P < 0.01) were lower in T2D.
Although the type 2 diabetic heart worked at smaller volumes, the HR and contractile response to β-adrenergic stimulation were unaffected by diabetes. The reduced cardiac reserve observed in uncomplicated T2D was not explained by impaired myocardial sympathetic responsiveness but may reflect changes in the loading conditions or function of the diabetic left ventricle.
2型糖尿病（T2D）与心脏储备和有氧能力降低有关。在糖尿病患者（间接）和动物模型（直接）中已证实心肌自主神经调节发生改变。
本研究旨在确定2型糖尿病心脏对β-肾上腺素能刺激的变时性和变力性反应。
8例无并发症的T2D患者和7例匹配的对照组进行了双能X线吸收法扫描和最大摄氧量（V˙O2peak）测试。在静息和运动峰值时测定血浆儿茶酚胺。第二次就诊时，在仰卧休息、副交感神经阻滞（阿托品）和递增β-肾上腺素能刺激（多巴酚丁胺）期间，使用超声心动图评估心率（HR）和左心室收缩力。
正如预期的那样，T2D组的V˙O2peak和HR储备较低（P < 0.05）。两组在运动峰值时去甲肾上腺素升高程度相当（P = 0.23）；然而，T2D组肾上腺素升高较少（P < 0.05）。对照组达到年龄预测最大心率85%所需的多巴酚丁胺剂量高36%（P < 0.05）。T2D组静息心率较高（P < 0.01），以去脂体重指数化的每搏量较小（P < 0.05）。在多巴酚丁胺输注期间，两组之间HR、去脂体重指数化的舒张末期容积、每搏量、射血分数和心输出量的反应（%变化）无差异。然而，T2D组HR较高（P < 0.01），去脂体重指数化的舒张末期容积（P < 0.01）、每搏量/去脂体重（P < 0.01）、射血分数（P < 0.05）和每搏功（P < 0.01）较低。
尽管2型糖尿病心脏在较小容积下工作，但对β-肾上腺素能刺激的HR和收缩反应不受糖尿病影响。在无并发症的T2D中观察到的心脏储备降低并非由心肌交感反应受损所致，可能反映了糖尿病左心室负荷条件或功能的变化。
