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卧床休息并不会导致健康年轻男性的胰岛素敏感性受损,而骨骼肌中的毛细血管密度增加与这一现象无关。

Increased capillary density in skeletal muscle is not associated with impaired insulin sensitivity induced by bed rest in healthy young men.

机构信息

a Department of Cardiology, University Hospital of Zurich, Switzerland.

b Center for Physical Activity Research, University Hospital of Copenhagen, Denmark.

出版信息

Appl Physiol Nutr Metab. 2018 Dec;43(12):1334-1340. doi: 10.1139/apnm-2018-0195. Epub 2018 Jun 19.

Abstract

Physical inactivity alters glucose homeostasis in skeletal muscle, potentially developing into overt metabolic disease. The present study sought to investigate the role of skeletal muscle capillarization in glucose tolerance and insulin sensitivity (IS) using a classic human model of physical inactivity. Thirteen healthy males (age = 23 ± 2 years) underwent 4 days of full-time supervised and diet-controlled bed rest. Oral glucose tolerance test, indices of IS (quantitative insulin sensitivity check index (QUICKI), Matsuda index), as well as skeletal muscle biopsies with measurement of fiber type distribution, fiber cross-sectional area (FCSA), capillary-to-fiber ratio (C/F ratio), and capillary density (CD) were assessed prior to and after bed rest. Body weight and composition were unaltered by bed rest. Fasting glucose/insulin ratio (G/I ratio) (-25%, P = 0.016), QUICKI (-7%, P = 0.023), and Matsuda index (-24%, P = 0.003) diminished with bed rest. Skeletal muscle FCSA decreased (-737.4 ± 763.2 μm (-12%), P = 0.005) while C/F ratio was preserved, resulting in augmented CD (+93.9 ± 91.5 capillaries·mm (+37%), P = 0.003) with bed rest. No association was detected between changes in skeletal muscle variables and metabolic outcomes. Independently of bed rest-induced effects, a positive linear relationship was detected between C/F ratio and G/I ratio (β = 17.09, P = 0.021). In conclusion, impaired glucose homeostasis with bed rest is not prevented nor associated with enhanced skeletal muscle capillarization in healthy individuals.

摘要

身体活动不足会改变骨骼肌中的葡萄糖稳态,可能会发展为明显的代谢疾病。本研究旨在使用经典的身体不活动人类模型,研究骨骼肌毛细血管化在葡萄糖耐量和胰岛素敏感性(IS)中的作用。13 名健康男性(年龄=23±2 岁)接受了 4 天的全职监督和饮食控制卧床休息。在卧床休息前后评估了口服葡萄糖耐量试验、IS 指数(定量胰岛素敏感性检查指数(QUICKI)、Matsuda 指数)以及骨骼肌活检,测量纤维类型分布、纤维横截面积(FCSA)、毛细血管-纤维比(C/F 比)和毛细血管密度(CD)。卧床休息并未改变体重和身体成分。空腹血糖/胰岛素比(G/I 比)(-25%,P=0.016)、QUICKI(-7%,P=0.023)和 Matsuda 指数(-24%,P=0.003)随卧床休息而降低。骨骼肌 FCSA 减少(-737.4±763.2μm(-12%),P=0.005),而 C/F 比保持不变,导致卧床休息时 CD 增加(+93.9±91.5 个毛细血管·mm(+37%),P=0.003)。骨骼肌变量的变化与代谢结果之间没有关联。独立于卧床休息引起的变化,C/F 比与 G/I 比呈正线性关系(β=17.09,P=0.021)。总之,卧床休息导致的葡萄糖稳态受损,不能预防,也与健康个体骨骼肌毛细血管化的增强无关。

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