Research Progress on Senile Sarcopenia and Its Sutritional Intervention
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摘要: 肌少症是一种与年龄相关的肌肉质量和功能下降疾病，极大增加了老年人骨折、摔伤和死亡风险。其发病机制主要涉及运动神经元缺失、激素失衡和炎症因子与胰岛素抵抗等因素。补充蛋白质、氨基酸、n-3、n-6多不饱和脂肪酸以及维生素等营养素可以有效防治肌少症。文章着重对肌少症的发病机制和营养干预进行了阐述，以期为老年肌少症研究提供参考。Abstract: Sarcopenia, an age-associated loss of muscle mass and function, greatly increases the risk of fractures, falls, and death in older adults. The pathogenesis of which is mainly involves motor neuron loss, hormone imbalance, inflammatory factors, and insulin resistance, etc. Supplementing nutrients such as protein, amino acid, n-3, n-6 polyunsaturated fatty acids and vitamin and other nutrients can effectively prevent and treat the sarcopenia. This paper focuses on the pathogenesis and nutritional intervention of sarcopenia to provide a reference for the research of sarcopenia.
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Keywords:
- old age /
- sarcopenia /
- nutritional intervention /
- protein /
- fatty acid
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肌少症又称肌肉减少症，是指与年龄相关的肌肉质量减少，同时存在肌肉力量和/或躯体功能下降的老年综合征[1]。随着老龄化问题日益严重，老年病患者越来越多，该症作为发病率较高的骨骼肌运动系统疾病，近年来已成为研究重点[2]。Liu等[3]通过荟萃分析（Meta）明确了肌少症是社区老年人全因死亡率的一个重要预测因子。然而现阶段我国对肌少症的了解还处于初步阶段，对老年肌少症的风险认知不够深入，防治不够规范[4]。提高民众对肌少症的认知率并对其进行有效防治，是当下亟待解决的问题。
肌少症的发病机制与运动神经元丢失、胰岛素抵抗、炎症因子、线粒体功能障碍及营养不足等因素有关[5−10]。其防治方式主要有运动干预、药物治疗和营养补充[11]。研究表明，基于阻力的运动对受试者的肌肉力量和功能有积极影响[12]。Hsu等[13]的分析显示运动可以改善肌少症肥胖患者的肌肉力量和身体功能。老年患者肌肉力量不足，行动不便，难以有效完成运动训练，因此运动干预并非防治肌少症的最佳办法。药物治疗则应根据老年人多重用药安全管理专家共识和用药指南进行科学、规范的药品知识宣教，且多重用药会对健康造成严重影响[14]。而营养干预在提供充足能量的同时，又可以通过营养补充改善老年人肌肉质量，安全方便。因营养素缺乏是导致肌少症的重要原因之一，临床上的治疗方案有补充蛋白质、氨基酸和维生素D，也有研究发现其他营养素如多不饱和脂肪酸[15]和矿物质[16]等与肌少症防治有着密切联系。近年来，肌少症研究现状的探讨或着重发病机制，或着重干预方式，本文整合了肌少症发病机制和营养干预的相关资料并进行探讨，以期分析其危害和营养因素来提高民众认知，并为肌少症的防治提供参考。
1. 老年肌少症及其发病机制研究进展
1.1 老年肌少症
肌少症首次由Rosenberg于1989年命名。2010年欧洲老年肌少症工作组首先发表了肌少症共识[17]，建议对于肌少症的诊断同时使用肌肉质量下降和肌肉功能或强度下降两个指标，并应用这些特征进一步将其概念定义为“骨骼肌前减少症”、“肌少症”和“严重肌少症”。2011年国际肌少症工作组对肌少症进行了明确定义[1]。2014年亚洲肌少症工作组在发表的共识报告中推荐了一种动态的肌少症研究方法，通过测量肌肉质量、力量和功能、身体表现、虚弱状态、日常生活活动、在给定时间内的日常生活基本活动、害怕跌倒以及尿失禁作为肌少症研究的结果指标，为亚洲人提供了肌少症的有效诊断[18]。2018年11月国际肌少症与衰弱工作组发布了国际肌少症临床实践指南，内容包括肌少症的筛查、诊断及管理，指出可侧重蛋白质与维生素D的研究，适度的蛋白质摄入可作为一种非药物干预的治疗方案[19]。2019年中华医学会老年医学分会发布了老年人肌少症口服营养补充中国专家共识（2019）[20]，指出营养缺失的肌少症患者可进行口服营养补充。2021年中华医学会老年医学分会、《中华老年医学杂志》编辑委员会编写了适合我国老年人肌少症患者的诊疗规范共识[4]。分别对肌少症定义、流行病学、诊断参数、诊断切点值、筛查和诊断流程以及预防和治疗发表了十五条推荐。
1.2 发病机制
肌少症是年龄增加相关性疾病，其危险因素与发病机制多种多样。源于组织学、生物化学和分子生物学的研究证实，神经元丢失、激素水平变化、线粒体功能障碍、营养素缺乏或摄入改变等均与肌少症有关，这些均是衰老相关的多因素综合作用的结果。探明肌少症发生与发展的机理有助于其临床干预，但目前尚无明确的首要致病因素。
1.2.1 衰老与运动神经元丢失
随着年龄增长，老年人机体骨骼肌逐渐萎缩，患肌少症概率增大。老年人肌肉质量的减少，主要是由于运动神经元尤其是α运动神经元（α-MNs）的逐渐丧失导致肌纤维数量下降。α-MNs丢失，神经肌肉连接（NMJs）改变，特别是II型肌纤维向I型肌纤维转变可导致肌纤维的萎缩，同时伴有肌内和肌间脂肪浸润导致的骨骼肌结构异常，最终发展为肌少症[5−6]。在骨骼肌再生过程中起主要作用的卫星细胞由于衰老而数量减少，导致肌肉的修复和再生能力降低[21]。还有研究表明衰老引起的线粒体损害可以加速活性氧和细胞能量缺乏，损伤的线粒体不断累积可触发运动神经元死亡[22]。
1.2.2 激素失衡
人体内多种激素可通过不同方式影响骨骼肌。研究表明，雌激素是一种抗氧化剂和肌膜稳定剂，可以积极影响骨骼肌的收缩特性并防止肌肉损伤。雌激素替代疗法可能间接影响骨骼肌蛋白质的更新，从而降低人体肌肉质量和力量损失[23]。Brioche等[24]发现生长激素替代治疗可导致骨骼肌蛋白合成、线粒体生物发生途径的增加和骨骼肌再生、蛋白质降解抑制因子的降低来预防肌少症。另有研究比较了肌少症患者和非肌少症患者血液和激素指标，发现生长激素（growth hormone，GH）和胰岛素样生长因子（insulin-like growth factor，IGF-1）与老年肌少症有关，且IGF-1与骨骼肌质量的减少独立相关，IGF-1表型是激活骨骼肌卫星细胞以启动骨骼肌细胞修复并促进其增殖的主要因素[25]。
1.2.3 胰岛素抵抗与炎症因子增多
胰岛素抵抗通过影响蛋白质合成途径以及激活蛋白质降解途径，最终导致肌肉损失[26]。Kim等[7]通过人群实验得出胰岛素抵抗指数HOMR-IR与骨骼肌质量指数SMI呈负相关的结论。
炎症因子增多是推进肌少症发生发展的重要机制之一。随着年龄增大，炎症因子肿瘤坏死因子α（tumor necrosis factor，TNF-α）、白细胞介素-6（interleu-kin-6，IL-6）和C反应蛋白（C-creactive protein，CRP）表达增加影响蛋白质的合成，促进蛋白质的分解，最终导致骨骼肌质量减少[27]。研究发现较高水平的循环炎症标志物（包括CRP、TNF-α和IL-6）与较低水平的骨骼肌力量及质量显著相关[8]。另有研究通过测定受试者的IL-6、CRP、下肢肌肉质量和肌肉蛋白水解量，证实了炎症增加了骨骼肌蛋白水解，降低了骨骼质量和力量[28]。
1.2.4 线粒体功能障碍
肌细胞中线粒体完整性的丧失是导致肌肉退化的主要因素。线粒体功能的调节可诱导衰老细胞死亡，进而改善肌肉骨骼的健康、质量和功能。有证据表明，线粒体干预电子传递链的多个调控步骤，诱导了促炎衰老相关分泌表型元件的表达，如IL-6和IL-8，这些促炎细胞因子已被发现可以改变卫星细胞的基因表达程序，深刻影响肌肉再生，并导致肌肉功能的年龄依赖性下降[9]。还有研究表明，老年人线粒体膜通透性转换孔功能的失调导致线粒体活性氧（ROS）的过量产生、线粒体DNA释放增加参与肌肉萎缩的泛素连接酶的表达和促凋亡因子的释放等促进肌肉质量下降和功能丧失[29]。
1.2.5 营养素缺乏
Shan等[10]在调研中发现营养素缺乏是肌少症发病的一个重要预测因子。蛋白质合成、降解和自噬参与肌少症的分子机制，老年人营养素摄入不足时，如蛋白质的缺乏使肌肉蛋白质的降解速率超过合成速率时，肌肉质量损失、肌肉功能逐渐减退[30]。维生素D缺乏也会因转录因子FOXO1持续激活，诱导胰岛素抵抗从而降低肌肉质量[31]。营养与老年人的肌肉质量、力量和功能有密切联系，这表明营养在肌少症的预防和管理方面发挥着重要作用，应充分补充蛋白质、维生素D、抗氧化营养素和长链多不饱和脂肪酸以确保老年人的能量和营养需求[32]。
虽然老年肌少症发病机制的研究已经取得长足进步，但目前许多研究仍停留在探索阶段，新型特异性指标的发现，对诊断标准的制订及针对性治疗的开展都将具有重要意义，基因组学、蛋白组学、代谢组学等多组学的研究及大数据分析能为老年肌少症的发病机制研究及特异指标挖掘提供保障。
2. 老年肌少症的营养干预
肌少症的病因与营养素的摄入不足密切相关。有效正确的营养补充对肌肉质量有着积极的影响，是预防肌少症最有效的方法。补充蛋白质、脂肪酸和多种维生素等营养素有益于肌肉组织合成，对抗肌少症效果显著。在难以通过膳食满足肌少症患者营养需求的情况下，额外的营养补充是必不可少的干预手段。
2.1 蛋白质对肌少症的干预
蛋白质代谢是营养问题的核心，蛋白质摄入不足也是肌少症患者营养不良的首要因素。研究表明，有效的蛋白摄入，可显著增加肌肉蛋白储备，减少肌肉量流失，从而有效控制老年肌少症病情发展[33]。Morifuji等[34]研究发现与膳食酪蛋白相比，膳食乳清蛋白增加了肝脏葡萄糖激酶和骨骼肌糖原合酶的活性，研究也首次证明了基于乳清蛋白的饮食增加大鼠骨骼肌中的糖原含量，还观察到乳清蛋白通过不同的机制调节糖原代谢。最佳蛋白质摄入量与肌肉功能测定结果有关，如骨量、骨骼肌量、力量和患病风险[35]。欧洲肠外肠内营养学会推荐：对于身体状况良好的老人每日蛋白质适宜摄入量为1.0～1.2 g/kg；急慢性病老年患者1.2～1.5 g/kg，其中优质蛋白质如动物蛋白和乳清蛋白的比例最好占一半[36]。Elisabet等[37]通过实验得出，增加乳清蛋白的摄入量比单独的碳水化合物会更有效地促进肌肉蛋白的合成。还有文章指出，在老年肌少症的营养配方中乳清蛋白的比例应占60%及以上[38]。
2.2 肽及氨基酸对肌少症的干预
肽是由两个或者两个以上氨基酸组成的化合物，作为蛋白质的水解中间产物和发挥活性作用的基团，肽与肌少症也有着密切联系。尤莉蓉[39]通过长达6个月的人群对照实验确定了大豆水解蛋白肽可以使人体肌肉含量显著增加。有研究通过动物实验得出低分子量的核桃蛋白水解肽具有显著的抗氧化（增强超氧化物歧化酶（SOD）、GSH-Px和过氧化氢酶（CAT）活性，降低丙二醛（MDA）含量）和免疫调节（提高免疫器官指数，促进肠道T淋巴细胞增殖和sIgA分泌）等预防肌肉衰减的功能[40]。汪云凤等[41]也通过动物实验证实玉米低聚肽通过降低肌环指蛋白-1和肌萎缩F盒蛋白的mRNA表达量，抑制肌肉萎缩。目前，德国公司嘉利达开发了一款可帮助肌少症患者改善肌肉状况的胶原蛋白肽（BODYBALANCE®），且经实验证明，产品中的蛋白肽可使受试者的肌力增加[42]。
氨基酸是蛋白质营养与代谢的基本单位。补充部分必需氨基酸、支链氨基酸或氨基酸代谢产物均有助于肌少症患者身体机能的改善。亮氨酸、缬氨酸和异亮氨酸统称为支链氨基酸（BCAA），支链氨基酸通过促进胰岛素和生长激素的释放来加快合成代谢和肌肉增长。Hernández等[43]对32名经诊断的肝硬化和肌少症患者进行了为期12周的安慰剂和BCAA营养干预，结果显示BCAA组的锌水平高于安慰剂组，白蛋白水平也显著提高。因此补充BCAA可改善肝硬化伴随肌少症患者的肌肉质量。Park等[44]对54名患者进行营养干预实验，单因素分析结果显示，受试者在补充BCAA和强化康复治疗后具有更高的骨骼肌指数。Izumi等[45]对肌少症老年人进行为期8周的BCAA干预，结果显示BCAA可以改善患者的肌肉状态。王蕾等[46]的动物实验表明亮氨酸和谷氨酰胺的联合可以延缓肌少症。我国青岛一项1140受试者参与的调查研究结果表明：较高的BCAA摄入量与较低的肌少症风险有关，这可能有益于预防肌少症并改善老年人的身体机能[47]。此外，其他氨基酸也对肌少症有着积极影响。补充瓜氨酸能增加氧化能量周转，降低pH功率比和ATP成本，改善骨骼肌代谢和/或收缩效率[48]。研究发现，天冬氨酸可以抑制脂多糖诱导的肌肉萎缩相关基因的表达，从而抑制蛋白质降解，改善肌肉状态[49]。还有动物实验表明，赖氨酸的补充也可以通过抑制蛋白水解提高骨骼肌质量[50]。
亮氨酸改善肌肉质量和力量的关键之一就是转化为代谢产物β-羟基-β-甲基丁酸（β-hydroxy-β-methylbutyrate，HMB）。研究[51]表明，HMB诱导急性肌肉合成代谢，增加肌蛋白的合成。Ellis等[52]研究表明，HMB可通过刺激蛋白质合成和减少蛋白质降解，同时减少炎症，从而改善肌肉损失。还有文章通过归纳分析法汇总了HMB可以通过调节靶蛋白的表达水平、激活丝氨酸-苏氨酸激酶（MAPK）和磷脂酰肌醇3-激酶（PI3K）的信号通路、影响半胱天冬酶和ROS的产生以及转化为HMG-CoA来抑制骨骼肌蛋白质的降解[53]。美国雅培开发了一款类似的乳清蛋白固体饮料——安补素，其中添加了两大有助肌肉健康的成分CaHMB和乳清蛋白。
与年轻人相比，老年人的代谢效率下降，因此需要更多的蛋白质摄入，以保证蛋白质合成。作为综合治疗的一部分，补充足量的优质蛋白质或肽有助于预防甚至逆转肌肉减少症。同时饮食中增加富含亮氨酸的食材或额外补充特殊氨基酸同样对肌少症有较好的干预效果。
2.3 脂肪酸对肌少症的干预
脂肪酸是人类生命活动中的重要物质，不同种类脂肪酸均有其特定功能和用途。多不饱和脂肪酸与人体健康密不可分，在人体生理中起着极为重要的代谢作用，根据其结构分为n-6和n-3两大主要系列。n-3多不饱和脂肪酸、n-6多不饱和脂肪酸和共轭亚油酸（CLA）在肌少症的形成中发挥着不同作用。n-3多不饱和脂肪酸和CLA主要通过降低炎症反应、机体氧化活性，影响睾丸素生物合成、胰岛素敏感性和前列腺素产量和直接参与肌肉蛋白合成与降解来延缓肌少症的形成，同时还可通过增加抗阻力运动的效果及与蛋白质、肌酸等营养物质的联合作用来延缓肌少症的形成。n-6多不饱和脂肪酸主要是促使肌肉蛋白分解，降低炎症反应来抑制肌少症的形成[15,54−60]。Calder等[15]指出n-3和n-6多不饱和脂肪酸的抗炎机制可以抑制促炎转录因子的激活，并提到n-3脂肪酸补充剂可降低内毒素刺激的单核细胞或单核细胞对TNF、IL-1β和IL-6的产生，而炎症可能是骨骼肌蛋白减少和消耗的重要机制。Rahman等[55]研究结果显示CLA可以通过维持衰老过程中的氧化还原平衡来预防肌少症。Cintia等[61]研究表明富含n-3多不饱和脂肪酸的补充剂组能有效提高老年妇女的肌肉激活水平并改善肌肉力量和功能。Mizanur等[59]发现添加CLA可以通过调节炎症和破骨细胞因子的标志物来防止骨骼和肌肉质量的损失。Virtanen等[62]研究发现n-6多不饱和脂肪酸与关键炎症标志物CRP呈强负相关。此外，中链脂肪酸甘油三酯（MCT）对骨骼肌也有着积极影响。MCT通常是由6～12个碳原子的饱和脂肪酸包括己酸（C6:0）、庚酸（C7:0）、辛酸（C8:0）、壬酸（C9:0）、癸酸（C10:0）和月桂酸（C12:0）组成的甘油三酯[63]。Sakiko等[64]研究表明，晚餐时联合补充6 g剂量的MCT，可改善虚弱老年人的肌肉力量和功能，且通过补充MCT，脂肪酸被大量用于骨骼肌的能量生产。MCT供能可达到葡萄糖的两倍多，还可增强人体对钙、镁和氨基酸的吸收，从而促进氨基酸和矿物质对肌少症患者肌肉质量的改善。
目前，脂肪酸与肌少症的关系研究主要集中于多不饱和脂肪酸，但大多是流行病学资料、动物实验以及多不饱和脂肪酸与其他营养物质的联合作用的人群干预实验，单独分析多不饱和脂肪酸作用的人群干预实验报道较少。单类脂肪酸或不同比例脂肪酸复配与老年肌少症在临床应用的组效、量效、构效关系及其作用机制仍需要更进一步的研究。
2.4 维生素与微量元素对肌少症的干预
维生素可通过不同机制参与肌少症的预防和治疗。维生素D是目前具备最多理论研究和临床实践支撑的能有效防治肌少症的维生素。Girgis等[65]发现维持正常的维生素D信号传递是防止肌肉功能和肌肉大小丧失的有效策略。维生素D也可通过基因组和非基因组机制精细控制骨骼肌细胞[66]。25（OH）D3是维生素D的重要中间代谢产物，也是维生素D在人体内储存的重要形式。相关研究表明，其水平降低将导致肌肉质量下降，进而增加肌少症患病风险[67]。《老年人肌少症口服营养补充中国专家共识（2019）》推荐老年肌少症患者维生素D的补充剂量为15~20 μg/d（600~800 U/d）[20]。维生素E可以通过增强抗氧化能力、抑制炎症反应、减轻氧化磷脂和稳定胰岛素结构等来增加损伤骨骼肌的存活率和增强肌肉再生能力[68]。研究表明维生素E的膳食摄入量与骨骼肌质量呈正相关[69]。Bo等[70]还发现补充维生素E可以有效改善老年肌少症患者的肌肉质量和力量。一项针对55~56岁的成年人观察研究结果揭示在女性人群中，较低的维生素K水平与较弱的握力、小腿围及躯体功能相关[71]。但维生素K在骨骼肌中的具体作用机制目前还有待进一步研究。维生素B12在外周神经和中枢神经的整合过程中起着重要的作用。Bulut等[72]通过观察记录403位患者的行走速度、肌力和肌肉质量，分别对每个患者进行4米行走实验、握力实验和生物阻抗实验，并进行维生素B12检测，结果揭示肌少症可能与维生素B12缺乏症有关。维生素C具有很强的还原性，是有效的抗氧化剂，也是生物合成和基因调节酶家族的辅助因子。研究发现饮食中的维生素C与中、老年人骨骼肌质量呈正相关，表明膳食维生素C摄入可能有助于减少与年龄相关的肌肉损失[73]。Welch等[69]研究表明，维生素C可以降低衰老过程中骨骼肌质量和力量的损失，进而防治肌少症。
血清低水平微量元素是老年衰弱的独立危险因素，并且衰弱风险会随微量元素缺乏而增大。一项研究探讨了老年人血清硒与骨骼肌质量的关系，发现通过调整年龄、性别、生活方式、身体和代谢因素，较低血清硒水平与低骨骼肌质量的高风险相关[74]。另有研究对331名受试者的数据分析结果显示，与非肌少症受试者相比，肌少症受试者消耗的许多微量营养素（钾、镁、铁、钙等）显著减少，表明不平衡的饮食可能与肌少症和肌肉骨骼健康不良有关，但还需要前瞻性研究来确认这些因素[16]。
维生素广泛参与细胞增殖、骨骼肌蛋白质合成、氧化损伤及修复等过程，与人体肌肉健康密切相关，但其对肌肉减少症的相关作用机制尚未完全明确。今后需进一步深入探讨维生素及微量元素影响肌肉减少症发生发展的机制。
3. 总结与展望
肌少症主要引起老年人运动功能障碍，生活质量下降，增加家庭及社会的经济负担。因其发病可能性强、人群广，目前已经被社会逐渐重视，治疗这种疾病对提高老年人生活质量有很重要的意义。老年肌少症的发病机制涉及衰老、激素和营养缺失等多个方面。充足的优质蛋白、维生素D和脂肪酸等营养干预可以提前预防或及时改善肌肉减少症。
从肌肉减少症概念的提出开始，国际上对此综合征的研究已有二十多年，在定义、发病机制、诊断和营养干预措施方面都有一定的积累，但还是存在许多空白亟需相关学科专业或产业的重视和投入。一是发病机制的研究仍应进一步深入。通过基因组学、蛋白组学、代谢组学等多组学的研究及大数据分析，挖掘新型特异性指标，对诊断标准的制订及针对性治疗的开展都将具有重要意义。二是营养干预手段应进一步完善。营养干预等是对肌少症干预的重要手段，其相关研究将是今后预防和治疗肌少症的重要研究方向，后续仍需拓展并完善单一营养素或复合营养素对老年肌少症的发病机制及防治作用研究。三是针对肌少症的多元化营养健康食品产业需要大力发展。随着经济发展和健康型消费模式的出现，营养健康食品的产业规模年均增幅也达到了10%~15%，已成为未来食品行业的重要发展方向。针对肌肉减少症人群的特殊营养需求，开展多营养素互作、营养素随加工工艺的动态变化规律的研究，最终开发出适合肌少症人群专用的特殊医学用途配方食品、营养强化食品或功能性食品等多元化产品，大力促进我国营养健康产业发展，助力国民健康。
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