School of Human Movement Studies, University of Queensland, Brisbane, Australia; Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
School of Medicine, University of Queensland, Brisbane, Australia.
Metabolism. 2014 Sep;63(9):1104-14. doi: 10.1016/j.metabol.2014.05.007. Epub 2014 May 15.
Autonomic dysfunction may contribute to the etiology and exercise intolerance of subclinical diabetic heart disease. This study sought the efficacy of exercise training for improvement of peak oxygen uptake (VO₂(peak)) and cardiac autonomic function in type 2 diabetic patients with non-ischemic subclinical left-ventricular (LV) dysfunction.
MATERIALS/METHODS: Forty-nine type 2 diabetic patients with early diastolic tissue Doppler velocity >1 standard deviation below the age-based mean entered an exercise intervention (n=24) or usual care (n=25) for 6-months (controlled, pre-/post- design). Co-primary endpoints were treadmill VO₂(peak) and 5-min heart-rate variability (by the coefficient of variation of normal RR intervals [CVNN]). Autonomic function was additionally assessed by resting heart-rate (for sympathovagal balance estimation), baroreflex sensitivity, cardiac reflexes, and exercise/recovery heart-rate profiles. Echocardiography was performed for LV function (systolic/diastolic tissue velocities, myocardial deformation) and myocardial fibrosis (calibrated integrated backscatter).
VO₂(peak) increased by 11% during the exercise intervention (p=0.001 vs. -1% in controls), but CVNN did not change (p=0.23). Reduction of resting heart-rate in the intervention group (p<0.05) was associated with an improvement in the secondary endpoint of heart-rate variability total spectral power (p<0.05). However, baroreflex sensitivity, cardiac reflexes, and exercise/recovery heart-rate profiles showed no significant benefit. No effects on LV function were observed despite favorable reduction of calibrated integrated backscatter in the intervention group (p<0.05).
The exercise intolerance of subclinical diabetic heart disease was amenable to improvement by exercise training. Despite a reduction in resting heart-rate and potential attenuation of myocardial fibrosis, no other cardiac autonomic or LV functional adaptations were detected.
自主神经功能障碍可能导致亚临床糖尿病性心脏病的病因和运动不耐受。本研究旨在探讨运动训练对改善 2 型糖尿病伴非缺血性亚临床左心室（LV）功能障碍患者峰值摄氧量（VO₂(peak)）和心脏自主神经功能的疗效。
材料/方法：49 名早期舒张组织多普勒速度超过年龄相关平均值 1 个标准差的 2 型糖尿病患者进入运动干预组（n=24）或常规护理组（n=25），进行 6 个月的治疗（对照，前后设计）。主要终点为跑步机 VO₂(peak)和 5 分钟心率变异性（通过正常 RR 间期变异系数 [CVNN]评估）。自主神经功能还通过静息心率（用于评估交感神经和副交感神经平衡）、压力反射敏感性、心脏反射和运动/恢复心率曲线进行评估。超声心动图用于评估 LV 功能（收缩/舒张组织速度、心肌变形）和心肌纤维化（校准积分反向散射）。
运动干预组 VO₂(peak)增加了 11%（p=0.001，而对照组为-1%），但 CVNN 没有变化（p=0.23）。干预组静息心率降低（p<0.05）与次要终点心率变异性总频谱功率改善相关（p<0.05）。然而，压力反射敏感性、心脏反射和运动/恢复心率曲线没有明显获益。尽管干预组校准积分反向散射有有利降低，但 LV 功能没有观察到效果（p<0.05）。
亚临床糖尿病性心脏病的运动不耐受可通过运动训练改善。尽管静息心率降低和潜在的心肌纤维化减弱，但未检测到其他心脏自主神经或 LV 功能的适应性改变。
