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Effect of a 12‐week endurance training program on force transfer and membrane integrity proteins in lean obese and type 2 diabetic subjects

机译:一项为期12周的耐力训练计划对瘦肥胖和2型糖尿病受试者的力传递和膜完整性蛋白的影响

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摘要

The mechanisms accounting for the loss of muscle function with obesity and type 2 diabetes are likely the result of a combination of neural and muscular factors. One muscular factor that is important, yet has received little attention, is the protein machinery involved in longitudinal and lateral force transmission. The purpose of this study was to compare the levels of force transfer and membrane integrity proteins before and after a 12‐week endurance training program in lean, obese, and obese type 2 diabetic adults. Nineteen sedentary subjects (male = 8 and female = 11) were divided into three groups: Lean (  = 7; 50.3 ± 4.1 y; 69.1 ± 7.2 kg); Obese (  = 6; 49.8 ± 4.1 y; 92.9 ± 19.5 kg); and Obese with type 2 diabetes (  = 6; 51.5 ± 7.9 years; 88.9 ± 15.1 kg). Participants trained 150 min/week between 55% and 75% of VO for 12 weeks. Skeletal muscle biopsies were taken before and after the training intervention. Baseline dystrophin and muscle LIM protein levels were higher (~50%  p p = .01), while the levels of the remaining force transfer and membrane integrity proteins were not affected by training. These results suggest that there are modest changes to force transfer and membrane integrity proteins in middle‐aged individuals as a result of 12 weeks of lifestyle and training interventions.
机译:肥胖和2型糖尿病导致肌肉功能丧失的机制可能是神经和肌肉因素共同作用的结果。一个重要但尚未引起人们注意的肌肉因素是参与纵向和横向力传递的蛋白质机制。这项研究的目的是比较瘦,肥胖和肥胖2型糖尿病成年人在12周耐力训练计划前后的力量传递和膜完整性蛋白水平。十九个久坐的受试者(男性= 8和女性= 11)分为三组:瘦(= 7; 50.3±4.1 y; 69.1±7.2 kg);肥胖(= 6; 49.8±4.1 y; 92.9±19.5 kg);肥胖的2型糖尿病患者(= 6; 51.5±7.9岁; 88.9±15.1 kg)。参与者每周训练150分钟,介于VO的55%和75%之间,持续12周。在训练干预之前和之后进行骨骼肌活检。基线肌营养不良蛋白和肌肉LIM蛋白水平较高(〜50%p = 0.01),而其余力传递和膜完整性蛋白的水平不受训练的影响。这些结果表明,由于12周的生活方式和训练干预,中年人的力量传递和膜完整性蛋白发生了适度的变化。

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