Related Experiment Video
Updated: Sep 10, 2026

Non-invasive Skeletal Muscle Quantification in Small Animals Using Micro-computed Tomography
Published on: November 8, 2024
Integrating EMG and plasma biomarkers to characterize neuromuscular remodeling in sarcopenia
Rizwan Qaisar1, Mashal Javed2, Imran Muhammad Khan2
1Basic Medical Sciences, College of Medicine, University of Sharjah, Sharjah, 27272, United Arab Emirates; Space Medicine Research Group, Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates; Cardiovascular Research Group, Research Institute of Medical and Health Sciences, University of Sharjah, Sharjah, 27272, United Arab Emirates.
Abstract:
Sarcopenia involves progressive muscle weakness driven by neuromuscular junction (NMJ) degradation, axonal injury, and diminished neurotrophic support. Electromyography (EMG) and plasma biomarkers can reveal these mechanisms, but integrated analyses remain scarce. We examined associations between EMG parameters and plasma biomarkers in older men with and without sarcopenia. We studied 146 men aged ≥60 years, classified as sarcopenic (n=72) or controls (n=74) using standardized criteria. Intramuscular EMG of the biceps brachii and vastus lateralis measured motor unit potential (MUP) amplitude, duration, and recruitment. Plasma C-terminal agrin-fragment 22 (CAF22), neurofilament light-chain (NfL), and brain-derived neurotrophic factor (BDNF) were quantified. Sarcopenic men exhibited higher amplitude and longer MUP duration with reduced recruitment in vastus lateralis. Plasma CAF22 and NfL were elevated, while BDNF was reduced. CAF22 was positively associated with MUP amplitude and duration, whereas NfL with prolonged duration, reflecting NMJ degradation and axonal damage. BDNF showed a negative association with amplitude but a positive association with recruitment, indicating its neuroprotective role. Integrated EMG and biomarker profiling identifies a convergent signature associated with NMJ instability, axonal degeneration, and reduced neurotrophic support in sarcopenia. These findings suggest links between electrophysiological and molecular alterations in sarcopenia.
