身體不活動對年齡相關功能衰退的可能影響 (下) | The Likely Contribution Of Physical Inactivity To Age-Related Functional Decline
人類肌肉結構與新陳代謝的年齡相關變化:身體不活動對年齡相關功能衰退的可能影響
3. 不活動相關的肌肉事件
3.1 不活動模型
缺乏機械洞察對於身體不活動的回應就是肌肉質量、肌肉結構和葡萄糖處力的幅度及比率下降。近期的一項上肢靜止研究表示,靜止後葡萄糖處理變化是快速且特定於非活動肢體上(Burns等人,2021年),但確切的機制尚不清楚。這是我們認知內的主要差異,需要於受控的人類研究當中解決,因與人類相比,囓齒動物泛化能力較差,其因來自較差的代謝穩定性(Demetrius,2005年)。應用不同的不活動模式以研究了解這個差距相當重要,目前已有數種不同研究程度的身體不活動模式,來幫助研究不活動對健康人類受試者的影響。這些模型允許探索短期和長期的身體不活動及能量之間的平衡以及這些對代謝健康的影響,為了解它們的生理機制提供了有用見解(圖 2)。
圖2:針對身體活動範圍的不活動/靜止模型。DI = 乾浸浴,ULLS = 單側下肢懸吊靜止,WHO = 世界衛生組織。
太空飛行或微重力環境是不活動的極端模型。缺乏負重活動會導致肌肉收縮減少,進而導致大量的功能性及代謝適應。然而,基於研究成本和復雜性,研究太空航行期間生理變化的機會有限;因此研究數量很少而且通常持續時間不等。有鑑於樣本量小、飛行時間變化以及飲食和運動缺乏監管,研究數據仍然難以解釋。
臥床休息是一種被廣泛接受的缺乏身體活動模型。通常其所有活動都在水平面或頭朝下-6度的傾斜位置進行,其最大限度地減少所有肌肉使用,並帶來近似於太空飛行期間觀察到的顯著生理適應。目前已經進行了大量臥床休息研究,持續時間自3天到120天不等(LeBlanc等人,1992年;Ferrando等人,1996年;Smorawiński等人,2000年)。這些研究整體顯示出骨骼肌質量、力量和全身胰島素敏感性在不同程度上有所降低,且在7天後就會反應顯示出(Dirks等人,2016年)。與一般人缺乏身體活動的程度相比,臥床休息是一種極端刺激。不過其有利於干預影響檢測於膳食能量含量和成分、運動或藥理學試劑。全身身體不活動的另一種模型是“乾”浸浴,通常用作於失重模型。其包括將受試對象浸入熱中性水當中;不過受試者會被一層薄的彈性防水織物包裹避免與水接觸。”乾”浸浴會產生與臥床休息期間觀察到的生理效應相似的生理效應,但效應通常會更大且發生速度更快(Shenkman等人,1997年;Navasiolava等人,2010年)。
肢體固定和單側下肢懸吊都廣泛地限制了目標肢體的動作,但允許日常活動的維持。肢體固定研究使用石膏來完全固定目標肢體,而在單側下肢懸吊研究中,如Berg等人研究所敘述,其為治療肢體彎曲並使用吊帶懸吊於地面上(Berg等人,1991年)。兩種模型都會引發類似於臥床休息的肌肉適應,但這些適應大多局限於固定的肢體,因此可以研究身體不活動的局部影響。肢體固定的好處是參與者的對側肢體可以作為內部控制,大幅減少了多種潛在的參與者間變量。在研究中使用肢體固定比臥床休息更具有臨床意義,因為其為治療骨折的常用技術,在所有年齡組中都很常見。
有關於步行活動降低的研究通常是透過減少每日步數來進行,也是最為貼近自由生活狀態的模型(Tudor-Locke和Bassett,2004年)。有數個控制良好的降低步術研究案例指出,每日<1500步於14天後肌肉質量、餐後MPS和胰島素敏感性皆降低(Breen等人,2013 年;Krogh-Madsen 等人,1985年)。
3.2 老化的許多生理特徵似乎也是不活動的主要特徵
在步數漸少或固定不動的年輕受試者當中,因老化導致的肌肉質量和力量下降已經再現。這表示我們可以透過使用前面提到的身體不活動模型使他們靜止或不活動,進而使年輕人在生理上變老。年輕男性(18-30 歲)進行為期兩週的全腿固定,導致股四頭肌瘦體重下降-4.7%,等長肌肉力量下降-27%(Jones 等人,2004年)。另一項對12名年輕參與者(年齡平均±SD為32 ±5歲)進行3天的乾浸浴,導致最大自主收縮下降11%,股四頭肌橫截面積下降 2.4%(Demangel等人,2017年)。這種更大程度的自主力量損失與肌肉纖維去神經支配相關,進行了增加的經細胞粘附分子陽性纖維染色,作者發現IIa纖維的比例下降和混合纖維I/IIX的比例增加。
肌肉蛋白質周轉也因年輕組群的靜止而發生改變。一項針對9名健康男性進行 23天單側下肢固定的研究中發現,在第0天到第10天後,MPS的吸收後率減半(0.047 %比0.022 %),並且在第21天前會一直此速率下降(de Boer 等人, 2007年)。但除了到10天粘著斑激酶的磷酸化下降30%(p < 0.01)外,與蛋白質合成代謝信號相關的其他蛋白質皆無改變,這意味著骨骼肌的信號傳導潛力至少沒有減少到處於禁食狀態。此外,無論施用劑量如何,對蛋白質或胺基酸管理的合成代謝抗性,也就是在老化生理研究當中發現的特徵性,都能夠在靜止的年輕受試者當中再現,且其繼發性與靜止天數無關(Glover等人,2008 年)。Kilroe等人則表示MPS變化迅速,發生在年輕健康受試者下肢固定2天後即出現,使用重水量化累積肌原纖維蛋白合成率,發現在固定7天後,與對照腿相比,固定腿MPS的降低幅度更大(Kilroe 等,2020年)。與非固定腿相比,固定腿的MRI衍生股四頭肌體積減少了6.7+/- 0.6%。
在年輕健康成年人的胰島素刺激條件下,固定和不活動已被證明會導致全身和腿部葡萄糖攝取不足。例如,在高胰島素正常血糖箝制技術下測量的全身和腿部葡萄糖攝取在年輕男性臥床7天後下降,腿部的下降幅度最大(Mikines 等,1991年)。此外,在同一研究中,臥床休息對肝臟胰島素敏感性沒有影響。另一個小規模模型指出,將步數從每天約10000步減少到<1500,持續 2週就足以減少年輕健康男性在胰島素箝制技術下的全身葡萄糖攝取(Krogh-Madsen等人,1985年)。導致固定化誘導的葡萄糖處理減少的機制目前尚未釐清,但可能有的候選因素包括GLUT4向質膜的信號傳導和/或易位的改變(Zierath等人人,1996年),固定所誘發的IMCL積累(Manini等人, 2007年;Cree等人, 2010年) 透過過多的游離脂肪酸供應繼發於正能量平衡,最終導致線粒體含量和/或線粒體功能降低,隨後造成碳水化合物代謝發生改變(Abadi等人,2009年)。近期的一項上肢固定報告認為前臂葡萄糖攝取在24小時內下降,這是固定肢體獨有特性,且不能通過增加脂質可用性來解釋(Burns等人,2021年)。有人認為肌肉收縮的減少造成了前面描述的細胞和分子變化,但具體的機制基礎仍所知甚少。
雖然已有明顯證據表明老化對肌肉和代謝健康產生不利影響,但仍未有研究以精確可量化的方式測量受試者的習慣性身體活動程度基線,並使用這些數據來進行研究受試者的習慣性身體活動匹配。事實上,在針對年長者身體活躍的研究中,與年齡相關的肌肉差異並不太明顯(Pollock等人,2015年)。例如,在一項涉及40名年齡在40-80歲的高階年長運動員的橫斷面研究(Wroblewski等人,2011年)中,肌肉橫截面積、瘦體重和力量的變化似乎與年齡無關。一些人認為老年人的肥胖程度預示著與代謝健康不良相關的肌肉質量和質量下降(Koster等人,2011年)。此種所謂的肌少性肥胖在研究當中受到質疑,研究表明老年人肥胖與絕對瘦組織體積或力量的減少無關(Murton等人,2015年),作者認為這是一個合乎邏輯的結果,基於肥胖個體在日常生活的運動活動中所做的收縮功是增加的。事實上,肌少性肥胖可能只是反映了因肥胖而造成的脂肪體積的相對增加大於瘦體重的相對增加,但從絕對值來則是兩者都增加了。
4. 結論
盡管有大量橫斷面證據詳細說明了與老化相關的肌肉體積、肌肉質量、身體成分和胰島素敏感性的差異,但如果沒有準確測量習慣性身體活動程度,很難斷定這些差異確實是由老化過程造成的。此外,在針對年輕健康成年人進行不活動和固定的研究中,表現出許多被歸因於老化的肌肉反應程度。因此,當前的知識斷層包括缺乏身體活動於年長者肌肉代謝健康不良相關的許多特徵過程所引發的相對影響。包括肌肉中心機制將身體不活動和/或久坐時間與代謝健康受損連結起來。此外,也顯示出政府建議的身體活動指南(或實際上與保護健康相關的任何其他身體活動/活動干預)對肌肉特定健康的積極影響,與年長者功能惡化密切相關程度在數據上有極大缺失。這些都是需要解決的重要知識差距,因為這可能會減輕由於不活動或飲食引起的二次老化的部分負面影響,也將有助於確定肌肉老化的主要驅動因素。因此,有必要以人進行縱向干預研究,以闡明衰老和不活動的影響貢獻,以及不活動導致的代謝失調是否會增加老化及疾病發生。
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