Exercise Physiology Laboratory, School of Kinesiology, Universidad Finis Terrae, Santiago, Chile.
Department of Neurobiology, Physiology and Behavior, University of California, Davis, CA, USA.
Physiol Rep. 2020 May;8(9):e14429. doi: 10.14814/phy2.14429.
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 (n = 7; 50.3 ± 4.1 y; 69.1 ± 7.2 kg); Obese (n = 6; 49.8 ± 4.1 y; 92.9 ± 19.5 kg); and Obese with type 2 diabetes (n = 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 < .01) in lean compared to obese and type 2 diabetic adults, while the protein levels of the remaining force transfer and membrane integrity proteins were similar between groups. After training, obese individuals decreased (-53%; p < .01) the levels of the muscle ankyrin repeat protein and lean individuals decreased dystrophin levels (-45%; 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.
导致肥胖和 2 型糖尿病患者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。一个重要但尚未得到充分关注的肌肉因素是涉及纵向和横向力传递的蛋白质机制。本研究旨在比较瘦、肥胖和肥胖 2 型糖尿病成年人在 12 周耐力训练前后的力传递和膜完整性蛋白水平。19 名久坐的受试者（男性 8 名，女性 11 名）分为三组：瘦组（n=7；50.3±4.1 岁；69.1±7.2kg）；肥胖组（n=6；49.8±4.1 岁；92.9±19.5kg）；肥胖 2 型糖尿病组（n=6；51.5±7.9 岁；88.9±15.1kg）。参与者每周训练 150 分钟，强度为 55%至 75%的 VO2，持续 12 周。在训练干预前后采集骨骼肌活检标本。瘦组的抗肌萎缩蛋白和肌肉 LIM 蛋白水平基线较高（~50%，p<0.01），而肥胖和 2 型糖尿病成年人的其余力传递和膜完整性蛋白水平相似。训练后，肥胖个体的肌锚蛋白重复蛋白水平下降（-53%；p<0.01），瘦个体的抗肌萎缩蛋白水平下降（-45%；p=0.01），而其余力传递和膜完整性蛋白水平不受训练影响。这些结果表明，中年个体在 12 周的生活方式和训练干预后，力传递和膜完整性蛋白会发生适度变化。
