Type 2 diabetes mellitus and exercise impairment.

Type 2 diabetes mellitus and exercise impairment.
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DOI:
10.1007/s11154-012-9234-4
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发表时间:
2013-03
影响因子:
8.2
通讯作者:
Regensteiner JG
Regensteiner JG
中科院分区:
医学2区
文献类型:
--
作者:
Reusch JE;Bridenstine M;Regensteiner JG

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在I型和2型糖尿病患者中,体能限制是一个一致的发现,与心血管和全因死亡率密切相关。这些限制可能会显著导致影响这一群体的持续过高的心血管死亡率。即使血糖控制良好且无临床明显并发症,运动对VO2峰值和VO2动力学的损害也在糖尿病早期表现出来。亚临床心功能不全是常见的,但不能完全解释糖尿病患者运动能力的缺陷。在某种程度上,心脏限制是继发于运动负荷灌注减少。这是一种可逆缺陷。类似地,在骨骼肌中,营养性血流的损伤与运动动力学减慢(或低效)和运动能力降低相关。几种相关性强调了内皮特异性损伤作为糖尿病运动功能障碍的介导物的可能性,包括胰岛素抵抗、内皮功能障碍、心肌灌注减少、组织血红蛋白氧饱和度降低和线粒体功能受损。运动训练和针对改善胰岛素敏感性和内皮功能的治疗都能改善2型糖尿病受试者的体能。优化糖尿病患者的运动功能对预防糖尿病和降低死亡风险具有重要意义。了解糖尿病内皮功能障碍的分子细节可能为修复这种缺陷提供特定的治疗靶点。目前正在研究测试这一假设的大鼠模型。
Limitations in physical fitness, a consistent finding in individuals with both type I and type 2 diabetes mellitus, correlate strongly with cardiovascular and all-cause mortality. These limitations may significantly contribute to the persistent excess cardiovascular mortality affecting this group. Exercise impairments in VO2 peak and VO2 kinetics manifest early on in diabetes, even with good glycemic control and in the absence of clinically apparent complications. Subclinical cardiac dysfunction is often present but does not fully explain the observed defect in exercise capacity in persons with diabetes. In part, the cardiac limitations are secondary to decreased perfusion with exercise challenge. This is a reversible defect. Similarly, in the skeletal muscle, impairments in nutritive blood flow correlate with slowed (or inefficient) exercise kinetics and decreased exercise capacity. Several correlations highlight the likelihood of endothelial-specific impairments as mediators of exercise dysfunction in diabetes, including insulin resistance, endothelial dysfunction, decreased myocardial perfusion, slowed tissue hemoglobin oxygen saturation, and impairment in mitochondrial function. Both exercise training and therapies targeted at improving insulin sensitivity and endothelial function improve physical fitness in subjects with type 2 diabetes. Optimization of exercise functions in people with diabetes has implications for diabetes prevention and reductions in mortality risk. Understanding the molecular details of endothelial dysfunction in diabetes may provide specific therapeutic targets for the remediation of this defect. Rat models to test this hypothesis are under study.
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