背景:与年龄相关的力量损失不成比例地大于质量损失,提示神经-肌-腱系统的适应不良。肌纤维在衰老和患病的肌肉中经常变形,但缺乏对大型样本集的系统分析。我们的目的是研究肌纤维形状与年龄的关系,锻炼,肌纤维类型,物种和性别
方法:来自197名男性和女性的股外侧肌活检(n=265),年龄跨度为20-97岁,进行了检查。还检查了11+22月龄雄性C57BL/6小鼠的腓肠肌和比目鱼肌。使用肌肉横截面的免疫荧光和ATP酶染色来测量肌纤维横截面积(CSA)和周长。从这些,形状因子指数(SFI)以纤维类型特定的方式计算(人类的I/II型;小鼠的I/IIa/IIx/IIb型),较高的值表明畸形增加。一个亚组(n=59)每周进行3次强阻训练(RT),持续3-4个月。将SFI和CSA与年龄进行相关性分析,肌肉质量,最大自愿收缩(MVC),力发展率和比力(MVC/肌肉质量)。
结果:在人类肌肉中,SFI与I型(R2=0.20)和II型(R2=0.38)肌纤维的年龄均呈正相关。当受试者被分成年龄组时,I型SFI较低(4%,P<0.001)和II(6%,P<0.001)与老年(60-80)相比,年轻(20-36)的肌纤维和I型更高(5%,P<0.05)和II(14%,P<0.001)肌纤维中年纪最老(>80岁)与老年人比拟。在所有大小的肌纤维中都观察到旧肌肉中SFI的增加。在所有三个年龄组中,II型肌纤维SFI高于I型肌纤维(4-13%,P<0.001),老鼠的肌肉也是如此(8-9%,P<0.001)。跨年龄组,I型(P=0.496/0.734)或II型(P=0.176/0.585)肌纤维的SFI在男性和女性之间没有差异。多元线性回归显示,SFI,在调整了年龄和肌纤维CSA后,对肌肉质量和功能的8/10指标具有独立的解释力。RT降低了年轻人和老年人的II型肌纤维的SFI(3-4%,P<0.001)。
结论:这里,我们将人类的I型和II型肌纤维形状确定为肌肉老化的标志,可独立预测肌肉健康的体积和功能评估.RT恢复了II型肌纤维的形状,提示缺乏肌纤维募集可能导致肌纤维畸形。
BACKGROUND: Age-related loss of strength is disproportionally greater than the loss of mass, suggesting maladaptations in the neuro-myo-tendinous system. Myofibers are often misshaped in aged and diseased muscle, but systematic analyses of large sample sets are lacking. Our aim was to investigate myofiber shape in relation to age, exercise, myofiber type, species and sex.
METHODS: Vastus lateralis muscle biopsies (n = 265) from 197 males and females, covering an age span of 20-97 years, were examined. The gastrocnemius and soleus muscles of 11 + 22-month-old male C57BL/6 mice were also examined. Immunofluorescence and ATPase stainings of muscle cross-sections were used to measure myofiber cross-sectional area (CSA) and perimeter. From these, a shape factor index (SFI) was calculated in a fibre-type-specific manner (type I/II in humans; type I/IIa/IIx/IIb in mice), with higher values indicating increased deformity. Heavy resistance training (RT) was performed three times per week for 3-4 months by a subgroup (n = 59). Correlation analyses were performed comparing SFI and CSA with age, muscle mass, maximal voluntary contraction (MVC), rate of force development and specific force (MVC/muscle mass).
RESULTS: In human muscle, SFI was positively correlated with age for both type I (R2 = 0.20) and II (R2 = 0.38) myofibers. When subjects were separated into age cohorts, SFI was lower for type I (4%, P < 0.001) and II (6%, P < 0.001) myofibers in young (20-36) compared with old (60-80) and higher for type I (5%, P < 0.05) and II (14%, P < 0.001) myofibers in the oldest old (>80) compared with old. The increased SFI in old muscle was observed in myofibers of all sizes. Within all three age cohorts, type II myofiber SFI was higher than that for type I myofiber (4-13%, P < 0.001), which was also the case in mice muscles (8-9%, P < 0.001). Across age cohorts, there was no difference between males and females in SFI for either type I (P = 0.496/0.734) or II (P = 0.176/0.585) myofibers. Multiple linear regression revealed that SFI, after adjusting for age and myofiber CSA, has independent explanatory power for 8/10 indices of muscle mass and function. RT reduced SFI of type II myofibers in both young and old (3-4%, P < 0.001).
CONCLUSIONS: Here, we identify type I and II myofiber shape in humans as a hallmark of muscle ageing that independently predicts volumetric and functional assessments of muscle health. RT reverts the shape of type II myofibers, suggesting that a lack of myofiber recruitment might lead to myofiber deformity.