肌–腦軸線是一種關鍵的雙向調控機制，連結骨骼肌與中樞神經系統，涵蓋神經、免疫、代謝與循環等系統的整合。在其核心概念中，骨骼肌不僅被視為運動執行的器官，更是具內分泌功能的器官，能在收縮過程中分泌多種肌肉激素，例如腦源性神經滋養因子、白介素-6（IL-6）、乳酸及其他細胞激素。這些分子能穿越血腦屏障，參與神經可塑性、突觸傳遞、神經發育及抗發炎反應等生理過程。因此，維持活躍的骨骼肌功能可促進神經健康與認知穩定，有助於預防神經退化性疾病。
本研究結合功能性近紅外光譜儀與血清生物標誌分析，探討肌少症對肌–腦軸線功能的影響。我們共招募 36 名年長受試者（18 位為肌少症患者，18 位為健康對照組），進行一項以最大自主收縮70% 強度執行的膝關節等長伸展任務。使用NIRScout 1624 同步量測大腦皮質與骨骼肌的血流動力變化。頭皮探頭依據 EEG 10–10 系統安置於前額皮質區，形成 20 個通道；另於右側股直肌中央配置單一光源–接收器對。研究中同步記錄前額皮質與右側股直肌的血氧動力變化，並由含氧血紅素(HbO)、去氧血紅素(HbR)、總血紅素濃度(HbT) 資料中，透過曲線函數模型擷取時間常數、拐點時間、反應強度與曲線下面積等參數。
血液樣本則用以分析血清中 BDNF 與 IL-6 濃度。為控制晝夜節律與活動影響，所有受試者皆於早上 8:00 至中午 12:00 期間由合格醫療人員進行採血，並於採血前 24 小時內避免劇烈身體活動。血清生物標誌物濃度透過 MILLIPLEX® （Millipore）多重免疫檢測系統進行分析，並使用Luminex® MAGPIX® 平台讀取數據。
結果顯示，肌少症組在肌肉與循環參數方面表現出延遲且反應強度較低的特徵，包括骨骼肌質量指數（SMI）較低、SARC-Calf 得分較高，且 SMI 與最大扭力（r = 0.379, p = 0.023）、SARC-Calf 與扭力（r = –0.377, p = 0.023）間皆呈現中等程度的顯著相關性。血清分析顯示，肌少症組的 BDNF 濃度顯著較低（p = 0.002），而 IL-6 雖略高，但差異未達統計顯著（p = 0.134）。功能性近紅外光譜儀結果亦發現，肌少症組於肌肉層級的 HbO、HbR 與 HbT 的 AUC 顯著較低（p = 0.006、0.041、0.004），顯示其氧氣提取與灌流效率受損。在大腦層級方面，雖然 HbO 與 HbR 並無達到統計顯著差異，但健康組在前額皮質的反應整體呈現較高趨勢，暗示其大腦血流調控與氧氣利用功能可能較佳。
總而言之，本研究透過結合功能性近紅外光譜神經影像與血清生物標誌物分析，揭示肌少症對肌–腦軸線功能的影響，涵蓋肌肉與大腦層級的變化。結果顯示，肌少症個體在肌肉血流動力學、肌肉激素分泌與肌力表現方面皆呈現受損現象，支持其氧氣代謝與循環功能退化的假設。雖然在皮質層級的差異未達統計顯著，但健康組所展現的血流動力趨勢顯示，維持良好肌肉功能可能對大腦健康具有保護作用。考量功能性近紅外光譜技術具非侵入性、即時性與臨床應用潛力，本研究提供了其作為評估肌–腦交互作用與介入效果的可行性。未來若能導入更高解析度與可攜式的設備，將有助於進一步釐清肌少症與神經退化間的交互機制，並為預防性健康策略建立更堅實的科學基礎。

The muscle–brain axis is a crucial bidirectional regulatory mechanism between skeletal muscle and the central nervous system, integrating neural, immune, metabolic, and circulatory systems. At its core, skeletal muscle is recognized not only as a motor organ but also as an endocrine organ that releases myokines—such as brain-derived neurotrophic factor (BDNF), interleukin-6 (IL-6), lactate, and other cytokines—during contraction. These molecules can cross the blood–brain barrier and participate in neuroplasticity, synaptic transmission, neurodevelopment, and anti-inflammatory processes. Thus, maintaining active skeletal muscle function can promote neurological health and cognitive stability, potentially preventing neurodegenerative diseases.
This study combined functional near-infrared spectroscopy (fNIRS) with serum biomarkers to investigate how sarcopenia affects the muscle–brain axis. A total of 36 elderly adults (18 with sarcopenia and 18 healthy controls) were recruited to perform an isometric knee-extension task at 70% of their maximal voluntary contraction (MVC). A fNIRS system (NIRScout 1624, NIRx) was used to measure cortical and muscular hemodynamics. Optodes were positioned over the prefrontal cortex according to the EEG 10–10 system, forming 20 channels. An additional source-detector pair was placed at the midpoint of the right thigh’s rectus femoris muscle. Hemodynamic responses in the right rectus femoris and prefrontal cortex were recorded using fNIRS simultaneously. From the oxyhemoglobin (HbO), deoxyhemoglobin (HbR), and total hemoglobin (HbT) signals, we extracted parameters such as time constant (TC), inflection time (IT), intensity, and area under the curve (AUC) using sigmoidal modelling. Blood samples were collected to quantify serum concentrations of BDNF and interleukin-6 (IL-6). To control for circadian and activity-related variability, all blood draws were conducted by trained medical personnel between 8:00 AM and 12:00 PM, following a 24-hour restriction on strenuous physical activity. Biomarker levels were measured using a multiplex immunoassay system (MILLIPLEX®, Millipore) and analyzed on a Luminex® MAGPIX® platform.
The results indicated that the sarcopenia group demonstrated delayed and attenuated responses in muscular and circulatory parameters, lower skeletal muscle mass index (SMI), higher SARC-Calf scores, and significant correlations between SMI and peak torque (r = 0.379, p = 0.023), and between SARC-Calf and torque (r = –0.377, p = 0.023), both of which indicate moderate associations. Serum analysis revealed significantly lower BDNF levels in the sarcopenia group (p = 0.002), and although IL-6 levels were higher, the difference was not statistically significant (p = 0.134). fNIRS results showed significantly lower muscle HbO, HbR, and HbT AUCs in the sarcopenia group (p = 0.006, 0.041, and 0.004, respectively), suggesting impaired oxygen extraction and perfusion efficiency. At the cortical level, while no statistically significant differences were found, the healthy group showed generally higher trends in HbO and HbR responses in the prefrontal cortex, indicating better brain blood flow regulation and oxygen utilization.
In conclusion, this study combined fNIRS neuroimaging and serum biomarker analysis to reveal, how sarcopenia affects the function of the muscle–brain axis at both muscular and cortical levels. Our results indicate that individuals with sarcopenia exhibit impairments in muscle hemodynamics, myokine secretion, and muscle performance, supporting the hypothesis of deteriorated oxygen metabolism and circulatory function. Although cortical-level differences were not statistically significant, the favorable hemodynamic trends observed in healthy individuals suggest a potential protective effect of muscle health on brain function. Given its non-invasive, real-time, and clinically feasible nature, fNIRS shows promise as a tool to assess muscle–brain interactions and intervention effects in aging populations. Future research utilizing higher-resolution and more portable devices may offer deeper insights into the interplay between sarcopenia and neurodegeneration, thereby strengthening the scientific foundation for preventive health strategies.

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