肌肉力量衰退与运动干预对老年慢性病共病的影响

赵雅婧 ,  张培珍

中南大学学报(医学版) ›› 2025, Vol. 50 ›› Issue (05) : 897 -906.

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中南大学学报(医学版) ›› 2025, Vol. 50 ›› Issue (05) : 897 -906. DOI: 10.11817/j.issn.1672-7347.2025.240509
综述

肌肉力量衰退与运动干预对老年慢性病共病的影响

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Impact of muscle strength decline and exercise intervention on multimorbidity of chronic diseases in older adults

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摘要

慢性病共病是老年人常见的健康问题之一,其对长期医疗和护理管理的需求给医疗系统造成了极大压力。肌肉力量是反映整体健康状况的核心身体素质,肌肉力量衰退与老年慢性病共病的发生风险密切相关,肌肉力量衰退通过与慢性病共病的相互作用引起共病负担加剧,存在慢性病共病的老年人肌肉力量衰退会影响身体功能和生活质量,引起疾病发展恶化与躯体功能丧失的恶性循环。肌肉强化训练有助于预防慢性病共病发生,促进抗炎效应和增强线粒体能量代谢是运动改善慢性病共病的可能机制。总结肌肉力量衰退对老年人慢性病共病的影响及运动干预对慢性病共病的改善效果和可能机制,可为延缓老年人肌肉力量衰退及预防慢性病共病的发生与发展提供依据,有助于改善老年人的生活质量。

Abstract

Multimorbidity of chronic diseases is one of the most common health issues among older adults, and the resulting demand for long-term medical care and management imposes a considerable burden on healthcare systems. Muscle strength, a core indicator of overall health status, is closely associated with the risk of developing multimorbidity of chronic diseases in older adults. Decline in muscle strength not only increases the risk of multimorbidity of chronic diseases but also interacts with it to exacerbate disease burden. In older adults with existing multimorbidity of chronic diseases, muscle strength decline can impair physical function and quality of life, leading to a vicious cycle of disease progression and physical disability. Strength training can help prevent multimorbidity, with potential mechanisms including the promotion of anti-inflammatory effects and enhancement of mitochondrial energy metabolism. This review summarizes the impact of muscle strength decline on multimorbidity of chronic diseases in older adults and the effectiveness and potential mechanisms of exercise interventions, providing evidence to delay muscle strength decline, prevent the occurrence and progression of multimorbidity of chronic diseases, and improve quality of life in older adults.

关键词

运动医学 / 老年人 / 慢性病共病 / 肌肉力量 / 运动干预

Key words

sports medicine / older adults / multimorbidity of chronic diseases / muscle strength / exercise intervention

引用本文

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赵雅婧,张培珍. 肌肉力量衰退与运动干预对老年慢性病共病的影响[J]. 中南大学学报(医学版), 2025, 50(05): 897-906 DOI:10.11817/j.issn.1672-7347.2025.240509

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老年人慢性病共病是指老年人同时存在2种及以上慢性健康问题[1]。在构建老年健康服务体系中,慢性病共病对医疗资源造成的压力不可忽视。中国健康与养老追踪调查(China Health and Retirement Longitudinal Study,CHARLS)第4轮调查[2]结果显示60岁以上老年人慢性病共病患病率为56.4%。在中国成年人中,患有心血管代谢性共病和呼吸共病者具有较高的死亡风险,每增加1种疾病,死亡风险增加36%[3]
近年研究[4-6]发现肌肉力量衰退与多种慢性病的发生、发展及病死率相关,可能是慢性病共病发生的重要风险因素。握力测量是评估老年人全身整体肌肉力量的一种简便、有效且可行性高的方法[7-8]。研究[9]显示握力与所有部位的骨骼肌质量之间均具有高相关性,因此握力测量可用于反映全身骨骼质量变化情况。握力下降不仅是反映老年人肌肉力量衰退的重要指标,还是肌少症诊断的核心指标之一。肌少症被定义为与年龄相关的骨骼肌减少、肌肉力量和/或躯体功能下降,亚洲肌少症工作组(Asian Working Group for Sarcopenia,AWGS)与欧洲老年人肌少症工作组(European Working Group on Sarcopenia in Older People,EWGSOP)分别发布的AWGS2019与EWGSOP2报告一致推荐以握力评估肌肉力量水平[10-12],握力下降和肌少症是肌肉力量衰退的重要预警信号。
运动干预对于改善慢性病患者的疾病进展及生活质量、降低死亡风险均有积极影响[13-16],但目前关于运动干预对慢性病共病的影响及其机制的研究不足。本文分析肌肉力量衰退与慢性病及慢性病共病之间的相互作用,以临床常用的握力下降和肌少症作为反映肌肉力量衰退的指标,整合运动干预改善慢性病共病的证据与可能机制,以期为老年慢性病共病管理提供理论依据。

1 肌肉力量衰退对慢性病共病的影响

肌肉力量是衡量身体素质和整体健康状况的关键指标,而与衰老有关的肌肉力量衰退与耐力差、步态缓慢和活动能力下降有关,可能导致不良健康结局[17],失用性骨骼肌流失的速度每天约为总肌肉质量的0.5%,同时伴随每天0.3%~4.2%的力量下降[18],糖尿病、冠心病、心力衰竭和其他器官功能衰竭等多种慢性病都会影响与年龄相关的肌肉衰退速度[19]。握力下降是反映肌肉力量衰退的重要指标,而肌少症的发生也反映了肌肉力量衰退发展的负面结果,二者均与慢性病共病发生相关。

1.1 肌肉力量衰退与慢性病及慢性病共病的相互作用

肌肉力量衰退已被证明与多种慢性病的发生及死亡风险相关。作为人体摄取葡萄糖的主要器官,肌肉萎缩会导致胰岛素受体减少,并引发胰岛素抵抗。一项对1 713 468名研究对象进行的荟萃分析[5]结果显示:肌肉力量每增加1个标准差,2型糖尿病的发生风险降低13%。Ding等[4]研究显示握力水平与老年人群心力衰竭及冠心病发生风险存在独立且稳定的强相关,其预测效能显著优于传统风险因素指标;Celis-Morales等[20]的研究显示握力每降低5 kg,女性和男性呼吸系统疾病病死风险分别增加31%和24%。

多种慢性病的发展与肌肉功能减退存在显著相关性,其潜在的病理生理学机制可能通过交互作用介导慢性病共病的发生[21]。肌肉功能减退与慢性病发展相互影响,以糖尿病为例,研究[22]发现与年龄相关的胰岛素抵抗与肌肉葡萄糖处理受损有关,肌肉葡萄糖处理受损会损害细胞内能量产生并导致肌肉收缩减弱,进而使胰岛素抵抗程度逐渐加重;并且由于运动神经传导速度与肌肉质量显著相关,糖尿病患者的神经病变可能通过运动神经元功能障碍降低肌肉力量[23],进一步导致肌肉力量下降。与未患2型糖尿病的老年人相比,2型糖尿病老年患者的肌肉力量随年龄增长流失的速度快28%~33%[24]。而肌少性肥胖伴胰岛素抵抗可能导致动脉粥样硬化、慢性心力衰竭、代谢综合征等多种心血管代谢疾病的发生,从而引起慢性病共病[25]

此外,以低肌肉力量为特征的肌少症和可能肌少症(即符合肌肉力量低、躯体功能差中的任意1条)会加剧慢性病共病发生。在英国生物数据库的499 096名研究对象中,近半数(44.5%)存在慢性病共病状态,可能肌少症患者的慢性病共病患病率(64.8%)明显高于非肌少症人群(43.4%)[26]。而对于存在严重慢性病共病的衰弱老年患者而言,肌肉力量衰退不仅会影响预后及死亡率,还可能是引起衰弱的主要生物学基础[27-28],并进一步导致肌肉力量下降和慢性病共病的相互加重。

1.2 握力下降与慢性病共病的双向关联

握力不仅能评估老年人核心身体素质水平,而且与慢性病共病状态相关,具有与健康相关的预测价值[29-30]。握力水平与慢性病共病状态存在双向关联,既受慢性病数量的影响,又对慢性病共病风险具有预测作用,同时还存在着性别和不对称性差异。

1.2.1 慢性病数量与握力下降的关系

近年来许多国家和地区的学者都针对慢性病共病患者的患病数量及其握力测量结果进行了分析。一项横断面研究[31]显示与没有慢性病的成年人相比,患有3种及以上慢性病者的握力下降;Hurst等[32]的研究显示与未患慢性病者相比,患有超过3种慢性病者更容易出现握力下降[相对风险比(relative risk ratio,RRR)=1.18]。多项研究发现慢性病共病数量与握力呈负相关。研究[33]对2008年美国健康与养老调查(Health and Retirement Survey,HRS)中的877人进行分析,结果显示:随着患者所患慢性病数量的增加,其握力会逐渐下降,并且当所患慢性病超过3种时,这种下降更加明显。对世界卫生组织的全球老龄化与成人健康研究中50岁及以上人群的分析[34]显示:与未患慢性病者相比,患有1、2、3和≥4种慢性病者的握力下降风险分别增加1.22、1.29、1.41和1.78倍。张泽正等[35]研究显示:老年住院患者的握力与查尔森共病指数(Charlson comorbidity index,CCI)评分呈负相关,随着慢性病共病状态的加重,肌肉整体功能下降,且在握力上表现更明显。

心血管代谢性共病是最常见、危害最大的老年慢性病共病模式[36]。与未患心血管代谢疾病者相比,患有1、2、≥3种心血管代谢性疾病者握力下降的风险增加;未患心血管代谢性疾病者,以及患有1、2、≥3种心血管代谢性疾病者的标准化握力预测值逐渐下降,分别为0.50、0.48、0.47和0.45,差异有统计学意义[37]

1.2.2 握力下降对慢性病共病风险的影响

慢性病共病数量与握力呈负相关,而握力下降同样可导致慢性病共病患病风险与患病率增加。韩国国民健康和营养调查相关研究[38]显示男性和女性握力均与共病患病风险之间存在显著的负相关。Balogun等[39]研究发现相对握力(握力/体重)较高者慢性病共病发生风险较低,并且较低的相对握力与较高的慢性病共病发生风险呈线性相关,但绝对握力与慢性病共病发生风险无显著相关性。刘佳佳等[40]的研究发现随着握力和握力指数(握力/体重×100)的增加,老年人慢性病共病发病率呈下降趋势,握力每增加1 kg,慢性病共病风险降低12%,握力指数每增加1,慢性病共病风险降低7%。Peterson等[41]发现≥51岁中老年人相对握力每降低0.05,男性和女性慢性病共病风险均增加14%。

握力对心血管代谢性共病发生风险的影响也与上述相似。Lu等[42]研究发现:基线无心血管代谢性疾病或有单一心血管代谢性疾病的个体中较低的握力与心血管代谢性共病的风险呈正相关。此外,在有心血管代谢性共病的人群中,较低的握力与全因死亡率呈正相关。Zhang等[43]研究发现在9 200名平均年龄为59.49岁的研究对象中,相对肌肉力量每增加1个单位,心血管代谢性共病的发生风险降低40%。

1.2.3 性别差异与握力不对称性对慢性病共病发生的影响

1.2.3.1 握力下降与慢性病共病关联的性别差异

握力对慢性病共病发病风险的影响存在性别差异。巴西的一项研究[44]显示:与上四分位数老年男性和老年女性相比,握力下四分位数的老年男性和老年女性慢性病共病患病率分别高50%和16%;在未患肌少症的男性中,肌力减退会增加慢性病共病的发生率;在肌少症患者中,肌力减退仅导致女性慢性病共病患病率增加10%。董潇杨等[45]基于CHARLS数据进行了老年人慢性病共病与握力的纵向研究,结果显示:与高握力者相比,低握力者在基线时慢性病共病患病率更高,随着年龄的增长,慢性病共病患病率增长更快;握力与慢性病共病(共病数量≥3或者≥5)发生风险的关联在男性研究对象中均显著,而在女性研究对象中较不稳定。造成这种性别差异的原因可能是由于女性在绝经期间以及绝经后雌激素水平显著降低,雌激素或与孕激素联合的激素治疗对65岁及以上绝经后女性的握力下降没有明显改善作用,但对血清睾酮水平较低的老年男性单独使用睾酮或与非那雄胺联合治疗能够显著提升其肌肉力量水平[46-47]

1.2.3.2 握力不对称与慢性病共病发生风险

肌肉力量不对称是反映肌肉功能下降的另一个指标,表明与年龄相关的肌肉协调能力下降[48],握力不对称同样与慢性病共病有关。一项研究[49]比较了3 977名研究对象(≥50岁)的握力大小及对称性与慢性病共病发生率的关系,将握力不对称量化为双手最大握力的比值(非优势侧握力/优势侧握力),该比值<0.90或>1.10视为存在握力不对称,结果显示:低握力与老年男性[风险比(hazard ratio,HR)=1.20]和女性(HR=1.19)慢性病共病发生风险相关,但握力不对称仅增加了女性的慢性病共病发生风险(HR=1.23)。对≥40岁人群的研究[50]显示:慢性病共病患者中握力不对称的比例明显高于非慢性病共病者,差异有统计学意义;与握力对称者相比,握力不对称者慢性病共病发生风险增加31%,累积发病率风险增加22%。因此,在进行社区老年人体质检查时可以对握力不对称提出针对性健康建议,提升其肌肉功能,预防慢性病和慢性病共病的发生。

1.3 肌少症与慢性病共病的关系

肌少症是一种以随年龄增长而发生的以骨骼肌质量下降,骨骼肌力量和功能减退为特征的综合性退行性疾病,与老年人身体功能下降、残疾、跌倒和高死亡率密切相关[51],它也是肌肉力量衰退的临床表现。老年慢性病共病患者发生肌少症和严重肌少症的风险更大,且慢性病共病数量越多肌少症发生率越高。一项英国老年人的大样本研究[52]发现:基线时的慢性病共病与12年随访期间肌少症的发生风险增加相关。Smith等[53]以中低收入国家的14 585名65岁及以上老年人为研究对象进行分析,结果发现:与未患慢性病者相比,患有≥2种慢性病的老年人肌少症和严重肌少症的发生率分别高1.49和2.52倍。郑燕蓉等[54]的研究显示:在1 026例老年慢性病共病患者中,患有2种、3种、≥4种慢性病者的肌少症发生率分别为15.90%、31.78%、65.06%,差异有统计学意义。

对于老年住院患者的研究进一步揭示了共病与肌少症的关系。贡歌等[55]的研究显示老年住院患者肌少症组的CCI评分显著高于非肌少症组,高龄老年患者的CCI评分与肌少症发生风险呈正相关,即CCI评分越高,患肌少症的风险越高。Pacifico等[56]以549名年龄为(82.2±4.88)岁的老年住院患者为对象进行研究,结果显示高CCI评分的肌少症患者与低CCI评分的肌少症患者的住院率和病死率均高于低CCI评分且非肌少症的患者。因此对高CCI评分住院患者应早期筛查肌少症,将肌肉功能保护纳入慢性病共病管理,以改善临床预后。

为实现早期生活方式干预,AWGS2019还引入了“可能肌少症”的概念。可能肌少症的发生同样与慢性病共病及其数量相关,与非肌少症老年人相比,可能肌少症的老年人更容易出现新发慢性病共病[57]。慢性病共病患者发生可能肌少症的风险更高。Dodds等[58]基于英国生物数据库的研究显示:40~70岁人群可能肌少症的总体患病率为5.3%,且随着年龄的增长而增加,慢性病共病患者肌少症发生率是非慢性病共病者的近2倍。中国的一项研究[59]结果与之相似,可能肌少症与大多数慢性病和慢性病共病显著相关,与未患慢性病共病者相比,患慢性病共病者发生可能肌少症的发生风险更高。

2 运动干预对慢性病共病的改善效果

老年人慢性病共病加重会导致身体整体功能退化加速,体力活动也会随之减少。美国国家健康和营养检查调查(National Health and Nutrition Examination Survey,NHANES)[60]发现:对于≥30岁的成年人,慢性病数量增多与总运动量降低相关,慢性病数量越多,24 h总运动量越低。在存在慢性病共病的墨西哥裔美国老年人中,高握力者跌倒风险较低握力者降低30%,通过运动增加肌肉力量可能有助于防止慢性病共病患者跌倒[61]。为稳定身体功能明显下降、衰弱老年人的慢性病状态,《老年共病管理中国专家共识(2023)》[1]推荐采取整合照护措施,结合适宜的运动锻炼、营养支持等方法,维护慢性病共病患者的内在能力,促进其功能发挥,延缓向失能进展。

运动干预可改善身体功能,降低多种疾病的发病率和病死率,已成为多种慢性病的重要干预措施。尽管运动干预对于改善慢性病患者的疾病进展、死亡风险及生活质量均有积极影响[13-16],但由于慢性病共病患者招募困难,且存在高脱落率及交通问题,因此与运动干预相关的高质量研究并不多见,同时由于老年慢性病共病患者身体衰弱,限制了运动干预在这类人群中的推广[62]

目前的研究结果显示对慢性病共病患者进行运动干预可提升其生活质量和整体身体功能。一项包含3 363例慢性病共病患者、23项随机对照试验的荟萃分析[63]探讨了有氧运动、抗阻运动及联合运动对慢性病共病的益处,结果显示:运动干预改善了慢性病共病患者健康相关的生活质量和躯体功能,并减少了抑郁和焦虑症状,患者在6 min步行试验中的步行距离增加了42.96 m,且运动干预与非严重不良事件[相对危险度(relative risk,RR)=0.96]的发生风险增加无关,与严重不良事件(RR=0.62)的发生风险降低有关。因此,运动干预作为一种安全有效的干预方式,对于慢性病共病患者的管理有很大价值。

提升肌肉力量可能是运动干预延缓慢性病共病发生与发展的重要驱动因素。研究[64]显示对继发性肌少症老年患者进行抗阻运动(resistance exercise,RE)能够有效提升其握力,但涉及慢性病共病患者的单一抗阻训练证据十分有限[65-66]。Hurst等[67]分析认为老年慢性病共病患者普遍缺乏对RE的认识和理解,因此有必要设计和提供适合老年慢性病共病患者的RE方案。包含RE的多元训练提供了解决该问题的模式,它是针对慢性病共病患者或存在慢性病共病风险者的基于身体能力的个性化训练。研究[68-69]显示:经过24周的多元运动干预,慢性病共病患者或存在慢性病共病风险者的心肺耐力、伸膝肌力等均有显著改善,且干预依从性良好(总体运动依从性77%),无严重不良事件发生。对于慢性病共病患者或存在慢性病共病风险者而言,应考虑其疾病状况与身体功能,在确保安全的前提下制订个性化运动方案,延缓疾病进展,改善生活质量。

对于还未发生慢性病与慢性病共病的老年人来说,提升肌肉力量可能是预防慢性病共病的有效途径。RE是有效降低慢性病共病发生风险的运动方式。Dankel等[70]基于美国健康和营养调查数据,探讨了成年人肌肉强化训练(muscle strengthening activities,MSA)对慢性病共病发生风险的影响,结果发现:进行MSA的个体慢性病共病发生风险降低了26%,每周MSA每增加2次,慢性病共病发生风险降低8%。进一步的研究[71]显示:同时符合MSA和体力活动指南的个体发生慢性病共病的风险低于只符合其中1项或都不符合的个体。

由于证据有限,目前尚缺乏对于慢性病共病运动处方的具体建议[72],但运动是至少26种慢性病的核心治疗方法,因此无论慢性病共病的患病模式如何,都可以通过每周锻炼2~3次来改善慢性病共病患者的社会心理和身体健康[73]。慢性病共病患者的运动干预包括:健康状态评估、适合慢性病共病患者运动方案的制订、行为改变技术的应用及临床推广(其目的是促进运动方案的临床应用)[74]。可根据患者的共病模式及不同慢性病运动处方指南,为患者制订个性化的运动能力评估方案和运动处方。可通过改变有氧运动、抗阻运动和平衡柔韧性运动的时间来调整运动方案。例如,对慢性心衰合并衰弱前期的慢性病共病患者,其运动处方可采用抗阻运动20 min/次[80% 1次最大重复重量(one-repetition maximum,1RM)强度,每周2~3次],结合平衡运动(20 min/次,每周2~3次)和有氧运动10 min/次;对慢性心衰合并衰弱者,总运动时间缩减至45 min/次,其中有氧运动 20 min/次,抗阻运动减至10 min/次,其余15 min/次为平衡/柔韧性运动[75]

3 运动改善慢性病共病的机制

3.1 运动的抗炎效应

慢性炎症是衰老的标志之一,循环中的C-反应蛋白(C-reactive protein,CRP)、白细胞介素(interleukin,IL)-6、IL-1β和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)等炎症因子水平升高在衰老过程中比较常见[76]。美国中年人调查(Survey of Mid-Life in the United States,MIDUS)数据[77]显示:慢性病共病数量与血液IL-6和CRP水平呈线性相关,炎症部分介导了慢性病与躯体功能受限之间的联系。一项包含9年随访数据的研究[78]也表明老年慢性病共病患者的IL-6水平较高,且随着时间推移,较高的IL-6基线水平和IL-6快速增加与老年患者慢性病共病数量增加呈显著独立相关。这表明高水平IL-6和IL-6快速升高可作为慢性病共病发生的早期预警信号。此外,Garrafa等[79]发现老年人CRP、脂蛋白(a)和胱抑素C水平越高,其慢性病共病数量越多。

慢性低度炎症(low-grade inflammation,LGI)可能与最常见的慢性病,特别是心血管疾病的发病机制有关[80],较少的体力活动时间与较高的血清低度炎症评分显著相关[81]。Poulsen等[82]发现成年慢性病共病患者每日低强度体力活动(light intensity physical activity,LPA)量越少,发生LGI的可能性越大,每天中高强度体力活动(moderate-to-vigorous-intensity physical activity,MVPA)少于15 min和每天LPA小于90 min者发生LGI的风险最高。

运动可通过提升体力活动水平改善身体炎症水平。对于慢性病共病患者而言,运动是促炎和抗炎状态平衡的有效途径。一项研究[83]对精神疾病和肥胖共病患者进行了12周中等强度训练(运动组),对照组不进行运动训练,结果显示运动组IL-10水平在12周运动干预后显著上升。Pedrosa等[84]研究发现:对年龄为(82±6.3)岁的老年慢性病共病女性进行持续28周的渐进运动(每周2~3次)干预后,与不运动者相比,其抗炎因子IL-10水平显著升高,促炎因子TNF-α水平显著降低,TNF-α/IL-10比值降低。提示运动对减轻全身LGI有益。

3.2 运动增强肌肉线粒体能量代谢

原发性衰老是渐进性进行且不可避免的,而疾病和不良生活方式引起的继发性衰老会加剧年龄增长引起的骨骼肌质量和肌肉线粒体能量(muscle mitochondrial energetics,MME)下降[85]。MME的作用机制比较复杂,它的破坏是多种疾病发病的核心[86]。随着骨骼肌的衰老,MME代谢过程中线粒体氧化磷酸化(oxidative phosphorylation,OXPHOS)的激活显著减少[87],可能导致与年龄相关的肌肉性能和心肺耐力降低[88],因此MME较差的老年人往往心肺耐力较差,这与心血管疾病、癌症和痴呆的发生风险有关[89]。Mau等[90]研究发现:老年人较低的OXPHOS水平与较高的共病指数评分相关[比例比值比(proportional odds ratio,POR)=1.32],并与糖尿病(OR=1.62)、抑郁症状(OR=1.45)和慢性肾脏病(OR=1.57)相关。提示MME下降增加老年人慢性病共病发生风险的可能性。研究[89]探讨了MME与老年人(>70岁)慢性病共病指数的关联,结果发现:老年男性线粒体呼吸功能降低与更高共病计数发生呈正相关,具体为质子渗漏每降低1个标准差,更高共病计数发生率增加47%(POR=1.47,P<0.001);最大氧化磷酸化每降低1个标准差,更高共病计数发生率增加35%(POR=1.35,P<0.001);ATPmax每降低1个标准差,更高共病计数发生率增加22%(POR=1.22,P=0.08);但在女性中并不存在上述差异。导致这一差异的原因有待于进一步探究。

运动能有效延缓衰老对老年人MME代谢的负面影响。一项横断面研究[91]显示:有运动锻炼的老年人氧化磷酸化复合物I和III蛋白的表达水平显著高于普通老年人;且有运动锻炼的老年人的氧化磷酸化复合物II和复合物IV蛋白的表达水平显著高于普通老年人和活动功能受损的老年人。提示有运动锻炼老年人的线粒体能量代谢能力增强。有运动锻炼的老年人与年轻人的线粒体呼吸、最大线粒体容量、最大ATP生成氧耗比及线粒体工作效率等MME代谢核心指标水平相似,且均显著高于无运动锻炼的老年人[92]

4 结 语

肌肉力量衰退与多种慢性病及慢性病共病互相影响,引起肌肉力量下降和慢性病共病的相互恶化作用。握力与老年人慢性病共病的发生率存在显著的负相关,可用于有效识别慢性病共病高风险人群,慢性病共病患者肌少症发生率随患病数量增加而升高。运动干预通过抗炎效应和增强肌肉线粒体能量代谢,提升慢性病共病患者的躯体功能和生活质量。针对未患病老年人进行肌肉强化训练可以有效降低慢性病共病风险。未来实践中应重视握力对慢性病共病发生风险的预警作用和慢性病共病患者肌少症的早期筛查,可进一步开展多中心随机对照试验探索针对肌肉力量提升的抗阻运动对不同慢性病共病组合(如代谢-心血管、呼吸-骨骼肌共病)的运动干预策略,明确剂量效应与安全性,为制订精准化运动处方指南提供高等级证据支持。

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