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Integrating Electromyography into the Physiology Curriculum

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Title: Integrating Electromyography into the Physiology Curriculum
Language: English
Authors: Cristina M. Sena (ORCID 0000-0002-0889-2977)
Source: Advances in Physiology Education. 2026 50(1):261-279.
Availability: American Physiological Society. 9650 Rockville Pike, Bethesda, MD 20814-3991. Tel: 301-634-7164; Fax: 301-634-7241; e-mail: webmaster@the-aps.org; Web site: https://www.physiology.org/journal/advances
Peer Reviewed: Y
Page Count: 19
Publication Date: 2026
Document Type: Journal Articles
Reports - Descriptive
Education Level: Higher Education
Postsecondary Education
Descriptors: Physiology, Curriculum Development, Human Body, Teaching Methods, Learning Activities, Motor Reactions, Muscular Strength, Clinical Diagnosis, Neurological Impairments, Lesson Plans, Fatigue (Biology), College Students, Science Instruction
DOI: 10.1152/advan.00237.2024
ISSN: 1043-4046
1522-1229
Abstract: Muscle physiology is included in the core curriculum in the biomedical, health, and exercise science fields. It is always challenging to understand the dynamic nature of motor unit (MU) functioning, neuromuscular activity, or muscle contractions. Different teaching instruments can be used during a didactic lecture to make it more engaging for the students, including the use of electromyography (EMG) and dynamometry techniques. EMG serves as a clinical and educational tool to evaluate skeletal muscle activity, enhancing the understanding of muscle physiology. This activity aims to describe several sessions where EMG is used as a tool to teach muscle physiology. EMG demonstrates muscle activation and MU recruitment, bridging theory and practice in physiology education. Surface EMG measures electrical activity in muscles, providing real-time data during rest, contraction, and fatigue. At rest, muscles exhibit minimal electrical activity. During contraction, increasing MU recruitment raises the amplitude and frequency of EMG signals. Fatigue is shown by altered patterns, reflecting declining muscle force and changes in MU activation. These principles highlight Henneman's size principle, where smaller motor units are activated first, followed by larger, stronger ones as contraction strength increases. Clinically, EMG distinguishes between neuropathies and myopathies. Neuropathies show delayed or reduced MU activation, spontaneous discharges, and impaired nerve-muscle communication. Myopathies display low-amplitude signals and rapid MU recruitment due to intrinsic muscle weakness. EMG also tracks denervation and reinnervation, revealing fibrillations or polyphasic MU potentials during nerve recovery. Integrating EMG with nerve conduction studies enhances diagnostics, clarifying whether issues stem from nerve or muscle pathology.
Abstractor: As Provided
Entry Date: 2026
Accession Number: EJ1497578
Database: ERIC
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  Value: <anid>AN0192623345;apu01mar.26;2026Apr01.05:47;v2.2.500</anid> <title id="AN0192623345-1">Integrating electromyography into the physiology curriculum </title> <sbt id="AN0192623345-2">INTRODUCTION</sbt> <p>Muscle physiology is included in the core curriculum in the biomedical, health, and exercise science fields. It is always challenging to understand the dynamic nature of motor unit (MU) functioning, neuromuscular activity, or muscle contractions. Different teaching instruments can be used during a didactic lecture to make it more engaging for the students, including the use of electromyography (EMG) and dynamometry techniques. EMG serves as a clinical and educational tool to evaluate skeletal muscle activity, enhancing the understanding of muscle physiology. This activity aims to describe several sessions where EMG is used as a tool to teach muscle physiology. EMG demonstrates muscle activation and MU recruitment, bridging theory and practice in physiology education. Surface EMG measures electrical activity in muscles, providing real-time data during rest, contraction, and fatigue. At rest, muscles exhibit minimal electrical activity. During contraction, increasing MU recruitment raises the amplitude and frequency of EMG signals. Fatigue is shown by altered patterns, reflecting declining muscle force and changes in MU activation. These principles highlight Henneman's size principle, where smaller motor units are activated first, followed by larger, stronger ones as contraction strength increases. Clinically, EMG distinguishes between neuropathies and myopathies. Neuropathies show delayed or reduced MU activation, spontaneous discharges, and impaired nerve-muscle communication. Myopathies display low-amplitude signals and rapid MU recruitment due to intrinsic muscle weakness. EMG also tracks denervation and reinnervation, revealing fibrillations or polyphasic MU potentials during nerve recovery. Integrating EMG with nerve conduction studies enhances diagnostics, clarifying whether issues stem from nerve or muscle pathology. NEW & NOTEWORTHY Electromyography (EMG) is a powerful tool to visualize muscle coordination, synergy, and fatigue, making it invaluable for teaching neuromuscular physiology and diagnosing neuromuscular conditions like carpal tunnel syndrome or muscular dystrophy. EMG effectively connects physiology concepts to clinical applications, helping students comprehend the intricate mechanisms that are subjacent to muscle physiology.</p> <p>"Tell me and I forget, teach me and I may remember, involve me and I learn."</p> <p>This quote obtained from the <emph>Xunzi</emph>, a compilation of Confucian philosophical works published by Xun Kuang ([<reflink idref="bib1" id="ref1">1</reflink>]), has been used in physiology classes at the Faculty of Medicine, University of Coimbra.Physiology is the cornerstone of all biological sciences and includes muscle physiology in the core curriculum. Teaching muscle physiology is demanding, and novel approaches aiming at incrementing student engagement are very important ([<reflink idref="bib2" id="ref2">2</reflink>], [<reflink idref="bib3" id="ref3">3</reflink>]). Skeletal muscles represent 40% of our body mass and are essential to preserving normal human physiology. Skeletal muscles are the fundamental organs that control force generation and movement. The neuromuscular system, which is a complicated interaction between the neural system and the skeletal muscle, controls muscle movement. According to a recent review of Global Burden of Disease data, roughly 1.71 billion individuals worldwide suffer from long-term neuromuscular diseases, causing significant and long-term suffering for them and their caregivers ([<reflink idref="bib4" id="ref4">4</reflink>]). As a result, understanding the physiology and electromechanical properties of the neuromuscular system is critical for diagnosing and monitoring neuromuscular diseases, for motor therapy, and in robotics and prosthetics fields ([<reflink idref="bib5" id="ref5">5</reflink>]).Electromyography (EMG) evaluates skeletal muscle electrical activity, serving as a key clinical and research tool. Surface EMG (sEMG) and intramuscular EMG (iEMG), combined with nerve conduction studies (NCSs), form electrodiagnostic methods to diagnose and localize neuromuscular disorders ([<reflink idref="bib5" id="ref6">5</reflink>]). In physiology education, EMG demonstrates muscle function, nerve conduction, and neuromuscular coordination, connecting theory to practical application ([<reflink idref="bib8" id="ref7">8</reflink>], [<reflink idref="bib9" id="ref8">9</reflink>]). Students learn bioelectric signal acquisition, processing, and analysis, preparing for clinical exposure.This activity uses EMG to illustrate skeletal muscle physiology, engaging students through hands-on demonstrations ([<reflink idref="bib10" id="ref9">10</reflink>]). Three lesson plans integrate EMG to teach motor unit (MU) recruitment, fatigue, abnormal signals, and nerve conduction.</p> <hd id="AN0192623345-3">Electromyography Overview</hd> <p>EMG records electrical activity from skeletal muscles, assessing motor unit (MU) and neuromuscular system integrity.</p> <hd id="AN0192623345-4">Surface EMG.</hd> <p>Surface EMG (sEMG) noninvasively records muscle activity via skin electrodes (Fig. 1), providing insights into MU recruitment and muscle contraction ([<reflink idref="bib11" id="ref10">11</reflink>], [<reflink idref="bib12" id="ref11">12</reflink>]). It is widely used in clinical neurophysiology, rehabilitation, sports science, and kinesiology ([<reflink idref="bib5" id="ref12">5</reflink>]). Limited spatial resolution restricts its use for detailed single-MU analysis in neuromuscular disease diagnosis ([<reflink idref="bib13" id="ref13">13</reflink>]).</p> <p></p> <p>PHOTO (COLOR): Figure 1. Surface electromyography (EMG) and bipolar signal acquisition configuration. Representation of a motor unit and the different layers through which the electrical signal must travel to reach the recording electrodes on the skin.</p> <hd id="AN0192623345-5">Intramuscular EMG.</hd> <p>Intramuscular EMG (iEMG) uses intramuscular needle electrodes to record muscle fiber action potentials, enabling precise MU assessment ([<reflink idref="bib14" id="ref14">14</reflink>], [<reflink idref="bib15" id="ref15">15</reflink>]). It is highly selective for diagnosing myopathies and motor neuron disorders but is invasive and monitors fewer MUs simultaneously ([<reflink idref="bib16" id="ref16">16</reflink>], [<reflink idref="bib17" id="ref17">17</reflink>]). Advances in noninvasive techniques are enhancing MU analysis.</p> <hd id="AN0192623345-6">Physiological Basis of EMG</hd> <p>Muscles enable voluntary (e.g., gripping) and involuntary (e.g., heart beating) movements, controlled by central and peripheral neural systems ([<reflink idref="bib18" id="ref18">18</reflink>], [<reflink idref="bib19" id="ref19">19</reflink>]). The MU, comprising a motor neuron and its innervated muscle fibers, is the smallest functional unit ([<reflink idref="bib20" id="ref20">20</reflink>], [<reflink idref="bib21" id="ref21">21</reflink>]) (Fig. 2). Motor neurons in the spinal cord's ventral horn receive excitatory and inhibitory inputs from the cortex, brain stem, and sensory receptors, determining MU activation ([<reflink idref="bib22" id="ref22">22</reflink>], [<reflink idref="bib23" id="ref23">23</reflink>]).</p> <p></p> <p>PHOTO (COLOR): Figure 2. A: small and large motor units differ in the amount of force they generate. Large motor units produce more force because of the greater number of fibers they contain. B: motor neuron recruitment occurs sequentially as a function of the force exerted. The recruitment sequence typically starts with small motor units (MUs), followed by progressively larger units: first the fatigue-resistant (FR) units and then the fast-fatigable (FF) units, which are activated only at very high force outputs.</p> <hd id="AN0192623345-7">Motor unit and action potential.</hd> <p>When excitatory inputs exceed a motor neuron's threshold, an action potential propagates to the neuromuscular junction, triggering muscle fiber action potentials that form a motor unit action potential (MUAP). The EMG signal is the spatial and temporal sum of MUAP trains from active MUs, recorded via surface or intramuscular electrodes ([<reflink idref="bib24" id="ref24">24</reflink>]). Small muscles (e.g., hand) have ∼100 motor neurons, whereas large muscles (e.g., quadriceps) have ∼1,000 ([<reflink idref="bib22" id="ref25">22</reflink>]).MUs are recruited per Henneman's size principle, from smaller to larger MUs as force increases ([<reflink idref="bib25" id="ref26">25</reflink>]). The CNS modulates force via spatial recruitment (more MUs) and temporal recruitment (higher firing frequency, ∼8–50 pulses/s, up to 100–200 pulses/s in maximal contractions) ([<reflink idref="bib22" id="ref27">22</reflink>], [<reflink idref="bib26" id="ref28">26</reflink>]).</p> <hd id="AN0192623345-8">ELECTROMYOGRAPHY IN PHYSIOLOGY TEACHING</hd> <p>EMG effectively demonstrates muscle activation, MU recruitment, and neuromuscular coordination in educational settings ([<reflink idref="bib27" id="ref29">27</reflink>]). Practical demonstrations provide real-time feedback, linking physiological concepts to muscle movement. The three lesson plans presented below integrate EMG into a physiology curriculum, covering MU recruitment, fatigue, abnormal signals, and nerve conduction. Each lesson is intended for second-year students and will have a duration of 90 min.</p> <hd id="AN0192623345-9">LESSON PLAN 1: MOTOR UNIT RECRUITMENT AND MUSCLE FATIGUE</hd> <p>(Format: Lecture + Practical + Case-Based Discussion)</p> <hd id="AN0192623345-10">Learning Objectives</hd> <p>By the end of this session, students should be able to:1) Explain the size principle of motor unit recruitment.2) Demonstrate how increasing contraction strength leads to sequential recruitment of motor units.3) Define muscle fatigue and describe its central vs. peripheral mechanisms.4) Interpret EMG patterns that reflect motor unit recruitment and fatigue.</p> <hd id="AN0192623345-11">Lesson Structure</hd> <p></p> <hd id="AN0192623345-12">1. Introduction and motivation (10 min).</hd> <p>•Start with a relatable question: "Why does holding a heavy grocery bag become harder the longer you hold it?"•Introduce motor unit recruitment and fatigue as two sides of neuromuscular control.</p> <hd id="AN0192623345-13">2. Normal recruitment practical demonstration (20 min).</hd> <p>Activity: Students record EMG from forearm muscles (see Fig. 3 and appendix).•Light contraction: shows activation of small, low-threshold motor units.•Increasing contraction: more units recruited, higher amplitude, more interference in EMG.•Maximal effort: full interference pattern.</p> <p></p> <p>PHOTO (COLOR): Figure 3. Left: recruitment of motor units as a function of increasing force. Force levels of 10, 20, 30, and 40 kg (blue graph, increasing clench force) were performed, and motor unit recruitment was observed. Right (after dotted line): hand gripper isometric test: a sustained clench at maximal force (40 kg) was performed, and fatigue was observed (Biopac MP36 System). The original electromyographic (EMG) signal is shown in red, and the integrated EMG after rectification is shown in green. Blue graphic represents force generated (in kg, determined by the hand dynamometer). The time to reach 50% of maximal force (an indicator of fatigue) was ∼32 s.</p> <p>Discussion prompt: "What principle explains why small motor units are recruited before large ones?"•Introduce the size principle (Henneman's principle).</p> <hd id="AN0192623345-14">3. Mini-lecture: muscle fatigue (20 min).</hd> <p>Explain the types and mechanisms of fatigue:•Central fatigue: reduced neural drive (CNS origin).•Peripheral fatigue: metabolic and ionic changes at the muscle (e.g., ATP depletion, lactic acid accumulation, ion imbalance).Show EMG features of fatigue:•Decreased median frequency of EMG signal.•Increased amplitude as more motor units are recruited to compensate.•Eventual decline in force despite continued activation.</p> <hd id="AN0192623345-15">4. Fatigue practical demonstration (20 min).</hd> <p>Activity: Sustained maximal grip or repeated handgrip contractions (see Fig. 3).Students observe:•EMG amplitude may increase initially (extra recruitment).•Frequency shifts lower over time (slowing conduction velocity).•Subjective fatigue felt by students.Discussion prompt: "Why does the EMG amplitude rise even though force eventually declines?"Link to compensatory recruitment versus true fatigue.</p> <hd id="AN0192623345-16">5. Case-based discussion (15 min).</hd> <p>Provide case handouts or show examples:1) Endurance athlete vs. sprinter: differences in recruitment and fatigue resistance.2) Clinical fatigue (e.g., chronic fatigue syndrome): compare to physiological fatigue.3) Occupational fatigue (repetitive strain, static postures): central + peripheral contributions.Task: Students identify whether the fatigue is primarily central, peripheral, or mixed and justify their reasoning.</p> <hd id="AN0192623345-17">6. Wrap-up and synthesis (5–10 min).</hd> <p>Recapitulate:•Motor units recruited according to size principle.•Fatigue = progressive loss of force, with both central and peripheral mechanisms.•EMG provides clues: recruitment pattern + frequency shifts.Clinical pearl: "Understanding recruitment and fatigue is essential for training athletes, designing rehab, and diagnosing neuromuscular disease."</p> <hd id="AN0192623345-18">Materials Needed</hd> <p>•EMG recording device (e.g., BIOPAC or PowerLab system).•Electrodes and conductive gel.•Computer with data acquisition software.•Hand dynamometer (for grip strength test).•Exercise equipment (e.g., handgrip, resistance bands).•Excel for data analysis.•Case handouts with fatigue examples.</p> <hd id="AN0192623345-19">Assessment Ideas</hd> <p>•Quick quiz in class: Show EMG traces at rest, increasing force, and fatigue → ask students to identify each stage.•Short-answer question: "Explain why muscle fatigue leads to a shift to lower EMG frequencies."•Practical exam task: Have students record a short fatigue trial and explain their findings.</p> <hd id="AN0192623345-20">Expected Results</hd> <p></p> <hd id="AN0192623345-21">1. Motor unit recruitment—ramp contraction (light → strong).</hd> <p>In Fig. 3, the EMG, integrated EMG, and force (obtained from the hand grip dynamometer) when the muscle is at rest and after are represented: 10 kg, 20 kg, 30 kg, 40 kg of contraction. Table 1 illustrates how electromyographic activity changes with increasing levels of voluntary muscle contraction, from rest to maximal effort. Each stage shows characteristic EMG patterns and the underlying physiological explanations.</p> <p>Table 1. Sequential activation of motor units: from rest to maximal contraction</p> <p> <ephtml> <table><thead><tr><th>Contraction Level</th><th>EMG Trace Features</th><th>Physiological Explanation</th></tr></thead><tbody><tr><td><p>Rest</p></td><td><p>Flat baseline, no activity (0 mV amplitude)</p></td><td><p>No MU activation; muscle at rest</p></td></tr><tr><td><p>10 kg (∼20% MVC)</p></td><td><p>Low amplitude (∼0.5–1 mV), sparse interference, high median frequency (∼80–100 Hz)</p></td><td><p>Small, low-threshold MUs recruited; low firing rate (∼8–20 pulses/s)</p></td></tr><tr><td><p>20 kg (∼40% MVC)</p></td><td><p>Moderate amplitude (∼1–2 mV), moderate interference, stable median frequency</p></td><td><p>Additional MUs recruited; firing rate increases (∼20–30 pulses/s)</p></td></tr><tr><td><p>30 kg (∼60% MVC)</p></td><td><p>High amplitude (∼2–4 mV), dense interference, slight frequency decrease (∼70–90 Hz)</p></td><td><p>More MUs recruited; increased firing rate (∼30–50 pulses/s)</p></td></tr><tr><td><p>40 kg (∼80% MVC)</p></td><td><p>Very high amplitude (∼4–6 mV), near-full interference, further frequency decrease (∼60–80 Hz)</p></td><td><p>Larger MUs recruited; high firing rate (∼50–100 pulses/s)</p></td></tr><tr><td><p>Maximal Effort</p></td><td><p>Maximal amplitude (∼6–10 mV), full interference pattern, lowest frequency (∼50–70 Hz)</p></td><td><p>All available MUs recruited; maximal firing rate (∼100–200 pulses/s)</p></td></tr></tbody></table> </ephtml> </p> <p>Key teaching point: Students should see sequential recruitment (small → large) demonstrating Henneman's size principle. EMG, electromyography; MU, motor unit; MVC, maximal voluntary contraction.</p> <hd id="AN0192623345-22">2. Muscle fatigue—sustained contraction (e.g., 30–60 s at ∼50% maximal voluntary contraction)...</hd> <p>Table 2 describes how EMG signals evolve during a sustained isometric contraction as the muscle becomes fatigued. Students typically perform a task (like gripping a dynamometer or holding a weight) at ∼50% of their maximal voluntary contraction (MVC) for 30–60 s. EMG is recorded throughout.</p> <p>Table 2. Observation of EMG responses across phases of a fatigue activity (∼50% maximal voluntary contraction)</p> <p> <ephtml> <table><thead><tr><th>Phase of Activity</th><th>EMG Signal Features</th><th>Physiological Explanation</th></tr></thead><tbody><tr><td><p>Early (0–10 s, ∼0–20% duration)</p></td><td><p>Moderate amplitude (∼1–2 mV), stable median frequency (∼80–100 Hz), moderate interference pattern</p></td><td><p>Initial recruitment of small MUs; normal conduction velocity due to adequate ATP and ion balance. Firing rate ∼20–30 pulses/s.</p></td></tr><tr><td><p>Middle (10–30 s, ∼20–60% duration)</p></td><td><p>Increased amplitude (∼2–4 mV), slight frequency decrease (∼70–90 Hz), denser interference pattern</p></td><td><p>Compensatory recruitment of additional progressively larger MUs to maintain force; early peripheral fatigue from lactic acid buildup and potassium efflux. Firing rate increases to ∼30–50 pulses/s.</p></td></tr><tr><td><p>Late (30–60 s, ∼60–100% duration)</p></td><td><p>High amplitude (∼4–6 mV), reduced median frequency (∼50–70 Hz), full interference pattern, force decline (measurable via dynamometer)</p></td><td><p>Maximal recruitment of larger MUs; peripheral fatigue dominates (ATP depletion, lactic acid accumulation, ion imbalances). Possible central fatigue (reduced neural drive). Force drops ∼10%–20% below target.</p></td></tr></tbody></table> </ephtml> </p> <p>Key teaching point: Students should observe force decline over time despite high EMG amplitude, highlighting the difference between recruitment and actual muscle output. EMG, electromyography; MU, motor unit.</p> <hd id="AN0192623345-23">3. Quantitative/semiquantitative EMG metrics.</hd> <p>Table 3 summarizes the evaluation of key EMG and performance metrics, including EMG amplitude, motor unit firing rate, EMG median frequency, and force, along with their expected trends during a fatigue-inducing sustained isometric contraction (e.g., maintaining a handgrip at ∼50% maximal voluntary contraction). The table illustrates the physiological processes underlying muscle fatigue, such as reduced firing efficiency and decreased force production despite sustained neural drive. These parameters can be obtained with standard analysis software such as LabChart (ADInstruments) or BIOPAC AcqKnowledge. For the assessment of motor unit firing rates, the Spike Analysis or Spike Histogram module can be used to detect individual motor unit spikes by applying an appropriate threshold. The software automatically extracts spike times, calculates interspike intervals (ISIs), and determines the firing rate as the inverse of the mean ISI (in Hz). This information can also be visualized as an instantaneous firing rate plot over time. This approach enables students to observe how firing rate increases with contraction strength and decreases with fatigue, thereby providing a clear, hands-on understanding of neural drive to muscle.</p> <p>Table 3. Standard metrics and expected trends during muscle fatigue</p> <p> <ephtml> <table><thead><tr><th>Metric</th><th>Expected Trend during Fatigue</th><th>Explanation</th></tr></thead><tbody><tr><td><p>EMG amplitude (mV)</p></td><td><p>Increases initially (∼1–3 mV early, 3–6 mV middle), plateaus or decreases late (∼2–4 mV).</p></td><td><p>Early fatigue prompts recruitment of additional MUs to maintain force, increasing amplitude. In late fatigue, amplitude may plateau or decrease because of reduced MU synchronization, impaired fiber conduction, or central fatigue reducing neural drive.</p></td></tr><tr><td><p>Motor unit firing rate (Hz)</p></td><td><p>Decreases from ∼20–50 Hz to ∼10–20 Hz.</p></td><td><p>Central fatigue reduces corticospinal excitability, lowering MU firing rates. Peripheral feedback (e.g., metabolite accumulation) may further inhibit neural drive, contributing to reduced force output.</p></td></tr><tr><td><p>EMG median frequency (Hz)</p></td><td><p>Decreases from ∼80–100 Hz to ∼50–70 Hz</p></td><td><p>Peripheral fatigue slows muscle fiber conduction velocity due to lactic acid buildup, potassium efflux, and reduced ATP availability, shifting the EMG power spectrum to lower frequencies.</p></td></tr><tr><td><p>Force (N, via dynamometer)</p></td><td><p>Declines gradually (∼10–20% drop by 30–60 s at ∼50% MVC)</p></td><td><p>Metabolic changes (e.g., lactic acid accumulation, increased H<sup>+</sup> and Pi, potassium efflux, ATP depletion) impair cross-bridge cycling, reducing force despite sustained neural effort. Central fatigue may exacerbate force decline.</p></td></tr></tbody></table> </ephtml> </p> <p>EMG, electromyography; MU, motor unit; MVC, maximal voluntary contraction.</p> <hd id="AN0192623345-24">4. Variability to expect.</hd> <p>•Interindividual differences: Muscle fiber composition, limb size, and fitness can change amplitude and fatigue onset.•Upper vs. lower limb: Lower limb muscles may fatigue more slowly because of a higher proportion of oxidative fibers.•Sex and age effects: Younger adults may sustain contraction longer; older adults may fatigue sooner.</p> <hd id="AN0192623345-25">5. Illustrative laboratory observations.</hd> <p>•Students may record small discrete spikes at light effort → progressively merge into interference pattern.•During sustained effort: EMG amplitude rises, then median frequency drops, and force may decrease even with maintained effort.•Some students may see irregular firing patterns late in fatigue because of motor unit dropout.</p> <hd id="AN0192623345-26">Take-Home Points for Students</hd> <p>•Recruitment is reflected by number and amplitude of active motor units.•Fatigue is reflected by frequency slowing, amplitude changes, and force decline.•Observing these EMG patterns helps students connect physiology (fiber type, recruitment, fatigue) with real-time data.</p> <hd id="AN0192623345-27">Key Practical Laboratory Tips</hd> <p>•Emphasize gradual ramp contractions to clearly demonstrate motor unit (MU) recruitment.•Provide visual and verbal feedback to ensure consistent participant effort.•Repeat recordings if EMG traces show unusual patterns, to rule out technical errors.•Compare recordings from upper versus lower limbs to illustrate physiological differences in fatigue and recruitment patterns.</p> <hd id="AN0192623345-28">Technical Essentials</hd> <p>1) Place electrodes correctly and ensure low impedance.2) Standardize settings (10–500 Hz bandpass, 50/60 Hz notch).3) Maintain consistent participant effort and rest intervals.4) Warm muscles and ensure relaxation before recording.5) Interpret amplitude, frequency, and force together.6) Normalize data to individual MVC for comparison.7) Always rule out technical causes before clinical interpretation.Note: Most EMG errors result from poor electrode technique, inconsistent effort, or misreading amplitude/frequency changes. Careful setup, standardized procedures, and contextual interpretation ensure reliable data and effective teaching.See appendix for common pitfalls.</p> <hd id="AN0192623345-29">Discussion of Results—Recruitment and Fatigue Lesson</hd> <p></p> <hd id="AN0192623345-30">1. Motor unit recruitment observations.</hd> <p>•Light voluntary contraction: EMG shows small-amplitude (∼0.5–1 mV), low-frequency motor unit action potentials (MUAPs), reflecting recruitment of slow, fatigue-resistant fibers.•Moderate contraction: Increased MU recruitment, with amplitude rising (∼1–3 mV) and a developing interference pattern. Intermediate fibers are activated.•Maximal contraction: Dense interference pattern with high-amplitude (∼4–10 mV), near-continuous activity. All MUs, including fast, fatigable, are recruited.</p> <hd id="AN0192623345-31">Interpretation.</hd> <p>•Confirms Henneman's size principle: MUs are recruited from small to large as contraction strength increases (Fig. 3).•Students observe sequential recruitment patterns, reinforcing understanding of MU physiology.</p> <hd id="AN0192623345-32">Topics to discuss.</hd> <p></p> <hd id="AN0192623345-33">motor unit recruitment.</hd> <p>MU recruitment is the process by which the nervous system activates MUs to produce muscle contraction. It is defined as "the progressive activation of additional MUs with increasing voluntary muscle contraction strength" ([<reflink idref="bib28" id="ref30">28</reflink>]). The central nervous system (CNS) enhances muscle force through spatial recruitment (activating more MUs) and temporal recruitment (increasing MU firing frequency). At lower contraction strengths, spatial recruitment predominates, with additional MUs activated. As most MUs are recruited, increased firing frequency (from ∼8–50 pulses/s to 100–200 pulses/s in maximal efforts) becomes the primary mechanism for boosting force.</p> <hd id="AN0192623345-34">order of recruitment.</hd> <p>MUs are generally recruited in order of size, starting with small, low-tension MUs and progressing to larger, high-tension MUs as force demand increases. This results in a coordinated increase in muscle strength ([<reflink idref="bib29" id="ref31">29</reflink>], [<reflink idref="bib30" id="ref32">30</reflink>]). The Henneman size principle governs this systematic recruitment of increasingly larger MUs ([<reflink idref="bib30" id="ref33">30</reflink>]). Exceptions occur in specific tasks because of variations in muscle mechanical function, sensory feedback, or central control ([<reflink idref="bib31" id="ref34">31</reflink>]). After nerve injury, the relationship between motoneuron size and muscle fiber innervation is disrupted, but size-dependent axonal branching eventually restores size-ordered MU organization ([<reflink idref="bib32" id="ref35">32</reflink>], [<reflink idref="bib33" id="ref36">33</reflink>]).</p> <hd id="AN0192623345-35">2. Muscle fatigue observations.</hd> <p></p> <hd id="AN0192623345-36">During sustained contraction (∼50% MVC).</hd> <p>•EMG amplitude initially rises (∼2–6 mV) as additional MUs are recruited to maintain force.•Median frequency of the EMG power spectrum decreases (∼80–100 Hz to 50–70 Hz), reflecting slowed muscle fiber conduction velocity.•Force output may plateau or decline (10–20% drop by 30–60 s) despite high EMG amplitude.</p> <hd id="AN0192623345-37">Late contraction/near exhaustion.</hd> <p>•Some MUs may cease firing, leading to irregular patterns.•EMG amplitude may decline slightly (∼1–2 mV); interference pattern becomes less dense.</p> <hd id="AN0192623345-38">Physiological explanation.</hd> <p>Muscle fatigue is the decline in a muscle's ability to generate force during prolonged or intense activity.•Peripheral fatigue: Slowed conduction velocity due to metabolite accumulation [e.g., lactate, H<sups>+</sups>, inorganic phosphate (Pi), potassium efflux] and ATP depletion impairs cross-bridge cycling.•Central fatigue: Reduced corticospinal excitability decreases neural drive, lowering MU firing rates (∼20–50 Hz to 10–20 Hz).•Compensatory recruitment: Additional MUs are recruited to delay force decline, increasing EMG amplitude initially. EMG illustrates fatigue through shifts to lower frequencies and amplitude changes, providing students with a visual representation of how prolonged exercise impacts muscle performance at a physiological level.</p> <hd id="AN0192623345-39">3. Interpretation and patterns.</hd> <p>Table 4 outlines how EMG features evolve from light to maximal and sustained muscle contractions, illustrating the relationship between MU recruitment, firing behavior, and fatigue development.</p> <p>Table 4. Sequential recruitment and fatigue: EMG phase characteristics</p> <p> <ephtml> <table><thead><tr><th>Phase</th><th>EMG Feature</th><th>Physiological Significance</th></tr></thead><tbody><tr><td><p>Light contraction (∼20% MVC)</p></td><td><p>Small amplitude (∼0.5–1 mV), high median frequency (∼80–100 Hz), sparse interference pattern</p></td><td><p>Recruitment of small, fatigue-resistant MUs; low firing frequency (∼8–20 pulses/s)</p></td></tr><tr><td><p>Moderate contraction (∼40%–60% MVC)</p></td><td><p>Increased amplitude (∼1–3 mV), moderate interference pattern, stable median frequency (∼80–100 Hz)</p></td><td><p>Recruitment of additional progressively larger MUs; increased firing frequency (∼20–50 pulses/s)</p></td></tr><tr><td><p>Maximal contraction (∼100% MVC)</p></td><td><p>High amplitude (∼4–10 mV), dense interference pattern, slightly reduced median frequency (∼70–90 Hz)</p></td><td><p>Recruitment of all MUs, maximal firing frequency (∼50–200 pulses/s)</p></td></tr><tr><td><p>Sustained contraction (0–30 s, ∼50% MVC)</p></td><td><p>Rising amplitude (∼2–6 mV), decreasing median frequency (∼70–90 Hz), full interference pattern</p></td><td><p>Compensatory recruitment of larger MUs to maintain force; early peripheral fatigue (lactate, H+, potassium efflux) slows conduction velocity.</p></td></tr><tr><td><p>Near exhaustion (30–60 s, ∼50% MVC)</p></td><td><p>Amplitude plateaus or decreases (∼2–4 mV), low median frequency (∼50–70 Hz), irregular interference pattern</p></td><td><p>Reduced MU synchronization or cessation due to peripheral fatigue (ATP depletion, Pi accumulation) and central fatigue (reduced corticospinal excitability); force declines ∼10–20%</p></td></tr></tbody></table> </ephtml> </p> <p>EMG, electromyography; MU, motor unit; MVC, maximal voluntary contraction.</p> <hd id="AN0192623345-40">4. Variability and considerations.</hd> <p>•Upper vs. lower limb: Lower limb muscles (e.g., quadriceps) often fatigue more slowly because of a higher proportion of type I fibers compared to upper limb muscles (e.g., forearm flexors).•Interindividual differences: Variations in muscle fiber composition, fitness level, and motivation affect fatigue onset and EMG patterns.•Temperature effects: Cold muscles (∼25°C) slow conduction velocity, delaying recruitment and altering EMG amplitude.•Technical considerations: Poor electrode placement, baseline noise, or inconsistent participant effort can distort EMG signals, mimicking fatigue or pathological patterns.</p> <hd id="AN0192623345-41">Conclusions</hd> <p>•Recruitment follows the size principle: Small, slow MUs are activated first, followed by larger, fast MUs as force increases.•EMG reflects recruitment and fatigue: Increasing amplitude and interference patterns indicate progressive MU recruitment, decreasing median frequency and irregular firing signal fatigue.•Fatigue is multifactorial: Peripheral mechanisms (slowed conduction, metabolite accumulation) and central mechanisms (reduced neural drive) contribute to force decline.•Educational takeaway: Observing EMG during graded and sustained contractions enables students to visualize MU recruitment and fatigue principles, highlighting the interplay between MU activation, fiber type, and fatigue mechanisms.</p> <hd id="AN0192623345-42">Key Teaching Points for Students</hd> <p>•EMG amplitude and frequency changes differentiate recruitment patterns from fatigue effects.•Force output may decline despite high EMG amplitude, distinguishing neural drive from muscle fiber performance.•Understanding these patterns is foundational for clinical EMG interpretation and applications in sports/exercise physiology.</p> <hd id="AN0192623345-43">LESSON PLAN 2: ABNORMAL EMG SIGNALS AND THEIR NEURO-MUSCULAR ORIGINS</hd> <p>(Format: Lecture + Practical + Case-Based Discussion)</p> <hd id="AN0192623345-44">Learning Objectives</hd> <p>By the end of this session, students should be able to:1) Describe the features of normal EMG signals during rest and contraction.2) Identify common abnormal EMG patterns associated with neuropathy, myopathy, and neuromuscular junction disorders.3) Explain the physiological basis of these abnormalities.4) Interpret EMG traces and link them to potential clinical conditions.</p> <hd id="AN0192623345-45">Lesson Structure</hd> <p></p> <hd id="AN0192623345-46">1. Introduction and motivation (10 min).</hd> <p>•Begin with a clinical scenario: "A patient presents with progressive muscle weakness. How can EMG distinguish whether the problem lies in the nerve, muscle, or neuromuscular junction?"•Introduce EMG as a diagnostic tool for neuromuscular disorders.•Display a side-by-side image of normal vs. abnormal EMG traces to spark curiosity.</p> <hd id="AN0192623345-47">2. Normal EMG practical demonstration (20 min).</hd> <p>Activity: Students record EMG from forearm muscles (grip or finger flexors) (see details below and in appendix).•At rest: baseline noise, minimal activity.•Light contraction: discrete motor unit action potentials.•Stronger contraction: increased recruitment, interference pattern, higher amplitude.Discussion prompt: "What happens as contraction strength increases? What does this tell us about motor unit recruitment?"</p> <hd id="AN0192623345-48">3. Mini-lecture: abnormal EMG patterns (20 min).</hd> <p>Use slides or prerecorded traces (video/diagram) to illustrate abnormal EMG patterns. Below are summarized some of the main features (in an EMG recording) of neuropathy, myopathy and neuromuscular junction disorders.•Neuropathy (nerve damage):At rest: fibrillations, positive sharp waves.During contraction: reduced recruitment, large-amplitude potentials (reinnervation).•Myopathy (muscle disease):Small, short-duration potentials.Early recruitment (many small units activated quickly).•Neuromuscular junction disorder:Normal at first, but fatigability or jitter with repetitive stimulation.Tip: Show side-by-side normal classroom EMG trace versus clinical abnormal traces.</p> <hd id="AN0192623345-49">4. Guided discussion and case-based learning (25 min).</hd> <p>Divide students into small groups. Provide EMG case sheets with example traces and minimal clinical information.Case examples (see more in appendix):1) Patient with peripheral nerve injury → Trace shows fibrillations, reduced recruitment.2) Patient with muscular dystrophy → Trace shows low-amplitude, short-duration potentials.3) Patient with myasthenia gravis → Trace shows decrement with repetitive stimulation.Task: For each case, students answer:•What abnormalities are seen?•Is the origin nerve, muscle, or neuromuscular junction?•What mechanism explains it?</p> <hd id="AN0192623345-50">5. Wrap-up and synthesis (15 min).</hd> <p>•Recapitulate differences between normal vs. abnormal EMG.•Reinforce differences between neuropathy (large units, reduced recruitment), myopathy (small units, early recruitment), and neuromuscular junction disorders.End with a clinical pearl: "EMG doesn't just measure muscle activity, it localizes the problem in the neuromuscular system."</p> <hd id="AN0192623345-51">Materials Needed</hd> <p>•EMG recording setup (Biopac MP36 acquisition system).•Electrodes and conductive gel.•Computer with data acquisition software (LabChart software).•Prerecorded abnormal EMG traces (images or videos from textbooks/teaching databases).•Case handouts with EMG examples.</p> <hd id="AN0192623345-52">Expected Results</hd> <p></p> <hd id="AN0192623345-53">1. Normal EMG (baseline for comparison).</hd> <p>Table 5 describes how EMG features change with increasing contraction intensity, reflecting the orderly recruitment of motor units according to the Henneman size principle.</p> <p>Table 5. Progressive motor unit recruitment reflected in normal EMG activity</p> <p> <ephtml> <table><thead><tr><th>Feature</th><th>Expected Pattern</th><th>Explanation</th></tr></thead><tbody><tr><td><p>At rest</p></td><td><p>Flat baseline; minimal noise (∼0.1–0.5 mV)</p></td><td><p>No spontaneous MU activity; muscle relaxed</p></td></tr><tr><td><p>Light voluntary contraction (∼20% MVC)</p></td><td><p>Discrete, small-amplitude MUAPs (∼0.5–1 mV); high median frequency (∼80–100 Hz)</p></td><td><p>Recruitment of small, slow MUs; low firing frequency (∼8–20 pulses/s)</p></td></tr><tr><td><p>Moderate contraction (∼40–60% MVC)</p></td><td><p>Increased MUAPs (∼1–3 mV); moderate interference pattern; stable median frequency (∼80–100 Hz)</p></td><td><p>Recruitment of progressively larger MUs; increased firing frequency (∼20–50 pulses/s)</p></td></tr><tr><td><p>Maximal contraction (∼100% MVC)</p></td><td><p>Dense interference pattern; high amplitude (∼4–10 mV); slightly reduced median frequency (∼70–90 Hz)</p></td><td><p>Full recruitment of MUs; maximal firing frequency (∼50–200 pulses/s)</p></td></tr></tbody></table> </ephtml> </p> <p>EMG, electromyography; MU, motor unit; MUAP, motor unit action potential; MVC, maximal voluntary contraction.</p> <hd id="AN0192623345-54">2. Neuropathic (nerve) abnormalities.</hd> <p>Table 6 outlines how EMG signals change in muscles affected by denervation and subsequent reinnervation, helping students distinguish normal recruitment from pathological patterns.</p> <p>Table 6. Electromyographic indicators of motor neuron damage and recovery</p> <p> <ephtml> <table><thead><tr><th>Feature</th><th>Expected EMG Pattern</th><th>Explanation</th></tr></thead><tbody><tr><td><p>At rest</p></td><td><p>Fibrillation potentials, positive sharp waves (∼0.1–1 mV)</p></td><td><p>Spontaneous muscle fiber depolarization due to denervation</p></td></tr><tr><td><p>During voluntary contraction</p></td><td><p>Reduced recruitment; large-amplitude (∼2–5 mV), long-duration (∼10–20 ms) MUAPs</p></td><td><p>Collateral reinnervation via axonal sprouting; fewer but larger MUs recruited</p></td></tr><tr><td><p>Key teaching point</p></td><td><p>Early recruitment absent; increased amplitude for remaining MUs</p></td><td><p>Indicates motor neuron loss and compensatory reinnervation.</p></td></tr></tbody></table> </ephtml> </p> <p>EMG, electromyography; MU, motor unit; MUAP, motor unit action potential.</p> <hd id="AN0192623345-55">3. Myopathic (muscle) abnormalities.</hd> <p>Table 7 summarizes how EMG findings in myopathic conditions differ from normal muscle activity. At rest EMG is typically normal, but during voluntary contraction MUAPs are smaller and shorter because of fiber loss. Early recruitment of motor units is a hallmark sign, helping distinguish myopathies from neurogenic disorders.</p> <p>Table 7. Typical EMG findings in myopathic disorders</p> <p> <ephtml> <table><thead><tr><th>Feature</th><th>Expected EMG Pattern</th><th>Explanation</th></tr></thead><tbody><tr><td><p>At rest</p></td><td><p>Usually normal; minimal spontaneous activity (∼0.1–0.5 mV)</p></td><td><p>Muscle fibers intact but fewer per motor unit</p></td></tr><tr><td><p>During voluntary contraction</p></td><td><p>Early recruitment; small-amplitude (∼0.2–1 mV), short-duration (∼2–5 ms) MUAPs; less dense interference pattern</p></td><td><p>Reduced number of fibers per motor unit; low force per contraction</p></td></tr><tr><td><p>Key teaching point</p></td><td><p>Early recruitment of small MUAPs: muscle cannot generate enough force with fewer fibers.</p></td><td><p>Characteristic of myopathies (e.g., muscular dystrophy)</p></td></tr></tbody></table> </ephtml> </p> <p>EMG, electromyography; MUAP, motor unit action potential.</p> <hd id="AN0192623345-56">4. Neuromuscular junction disorders.</hd> <p>Table 8 outlines EMG findings typical of neuromuscular junction disorders. Resting EMG is normal, but with sustained or repetitive activity the amplitude of MUAPs declines because of transmission failure. This amplitude decrement is a key diagnostic feature distinguishing these disorders from myopathies or neuropathies.</p> <p>Table 8. Typical EMG findings in neuromuscular junction disorders</p> <p> <ephtml> <table><thead><tr><th>Feature</th><th>Expected EMG Pattern</th><th>Explanation</th></tr></thead><tbody><tr><td><p>At rest</p></td><td><p>Usually normal (∼0.1–0.5 mV)</p></td><td><p>No denervation; muscle fibers intact</p></td></tr><tr><td><p>During sustained/repetitive contraction (3–5 Hz)</p></td><td><p>Normal initial MUAPs (∼1–3 mV); progressive amplitude decrement (∼10–20%) or increased jitter (∼50–100 µs)</p></td><td><p>Impaired acetylcholine release or receptor function (e.g., myasthenia gravis) causes transmission failure.</p></td></tr><tr><td><p>Key teaching point</p></td><td><p>Amplitude decrement or jitter with repetitive stimulation distinguishes junction disorders.</p></td><td><p>Differentiates from nerve or muscle pathology.</p></td></tr></tbody></table> </ephtml> </p> <p>EMG, electromyography; MUAP, motor unit action potential.</p> <hd id="AN0192623345-57">5. Expected variability and summary.</hd> <p>•Amplitude and duration vary by muscle size and fiber type.•Firing patterns may appear irregular in early reinnervation or in mild neuropathies.•Spontaneous activity may be subtle and require careful observation of baseline.Table 9 compares EMG findings across four conditions: normal, neuropathy, myopathy, and neuromuscular junction disorder.</p> <p>Table 9. EMG findings across neuromuscular conditions</p> <p> <ephtml> <table><thead><tr><th>Condition</th><th>Rest EMG</th><th>Voluntary Contraction</th><th>Motor Unit Action Potential Characteristics</th><th>Recruitment</th></tr></thead><tbody><tr><td><p>Normal</p></td><td><p>Flat (∼0.1–0.5 mV)</p></td><td><p>Small (∼0.5–1 mV) to dense interference with effort</p></td><td><p>Normal amplitude (∼1–3 mV), duration (∼5–10 ms)</p></td><td><p>Sequential, Henneman's size principle</p></td></tr><tr><td><p>Neuropathy</p></td><td><p>Fibrillations, positive sharp waves (∼0.1–1 mV)</p></td><td><p>Reduced recruitment</p></td><td><p>Large-amplitude (∼2–5 mV), long-duration (∼10–20 ms) MUAPs</p></td><td><p>Reduced small MUs; increased large MU recruitment</p></td></tr><tr><td><p>Myopathy</p></td><td><p>Usually normal (∼0.1–0.5 mV)</p></td><td><p>Early recruitment; less dense interference</p></td><td><p>Small-amplitude (∼0.2–1 mV), short-duration (∼2–5 ms) MUAPs</p></td><td><p>Many small MUs activated early</p></td></tr><tr><td><p>Neuromuscular junction disorder</p></td><td><p>Usually normal (∼0.1–0.5 mV)</p></td><td><p>Progressive amplitude decrement (∼10–20%)</p></td><td><p>Normal amplitude/duration initially (∼1–3 mV, 5–10 ms); increased jitter (∼50–100 µs) with fatigue</p></td><td><p>Normal initially; fails with repetitive stimulation</p></td></tr></tbody></table> </ephtml> </p> <p>EMG, electromyography; MU, motor unit; MUAP, motor unit action potential.</p> <hd id="AN0192623345-58">Take-Home Points for Students</hd> <p>1) Compare baseline vs. voluntary contraction to identify abnormal patterns.2) Distinguish neuropathy vs. myopathy vs. neuromuscular junction disorder based on spontaneous activity, amplitude/duration, and recruitment pattern.3) Observe how EMG reflects the underlying physiological or pathological mechanism.</p> <hd id="AN0192623345-59">Teaching Tips for Avoiding Pitfalls</hd> <p>Here are some tips to ensure better global outcomes:•Demonstrate both normal and abnormal EMG side by side so students can see real differences.•Highlight typical sources of error before students start recording.•Encourage students to repeat questionable traces rather than recording once.•Use case-based discussion: "If this trace looks abnormal, what technical vs. pathological factors could explain it?"Integrating this into your lesson plan ensures that students understand both physiology and the limitations of EMG, which reduces misinterpretation and builds critical thinking. See appendix for common pitfalls.</p> <hd id="AN0192623345-60">Discussion of Results</hd> <p></p> <hd id="AN0192623345-61">1. Normal EMG observations.</hd> <p>•At rest: flat baseline, no spontaneous activity.•During voluntary contraction: progressive recruitment of motor units (small → large), increasing amplitude, and eventual interference pattern at maximal effort.</p> <hd id="AN0192623345-62">Interpretation.</hd> <p>•Demonstrates the size principle of motor unit recruitment.•Provides baseline patterns to compare with abnormal traces.</p> <hd id="AN0192623345-63">2. Neuropathic (motor neuron/nerve) abnormalities.</hd> <p></p> <hd id="AN0192623345-64">Main findings obtained from case examples.</hd> <p>•Fibrillation potentials and positive sharp waves at rest.•Reduced number of recruited motor units during voluntary contraction.•Remaining motor units show large amplitude, long-duration potentials.</p> <hd id="AN0192623345-65">Physiological explanation.</hd> <p>•Denervation of muscle fibers leads to spontaneous activity at rest.•Surviving motor neurons reinnervate orphaned fibers → larger motor units.•Reduced recruitment reflects loss of small motor units.</p> <hd id="AN0192623345-66">Clinical relevance.</hd> <p>•Typical of peripheral neuropathies (e.g., radiculopathy, ALS early stages).</p> <hd id="AN0192623345-67">3. Myopathic (muscle) abnormalities.</hd> <p></p> <hd id="AN0192623345-68">Main findings obtained from case examples.</hd> <p>•Usually normal baseline at rest.•Early recruitment during voluntary contraction.•Motor units are small amplitude, short duration, with less dense interference pattern.</p> <hd id="AN0192623345-69">Physiological explanation.</hd> <p>•Loss of muscle fibers per motor unit → Each unit contributes less force.•Early recruitment compensates for reduced force production.</p> <hd id="AN0192623345-70">Clinical relevance.</hd> <p>•Seen in muscular dystrophies, inflammatory myopathies.•EMG shows characteristic small, early-recruited units despite normal firing pattern.</p> <hd id="AN0192623345-71">4. Neuromuscular junction disorders.</hd> <p></p> <hd id="AN0192623345-72">Main findings obtained from case examples.</hd> <p>•Baseline at rest usually normal.•Initial MUAPs normal, but progressive amplitude decrement or jitter during sustained/repetitive contraction.</p> <hd id="AN0192623345-73">Physiological explanation.</hd> <p>•Failure of neuromuscular transmission due to reduced acetylcholine release or receptor dysfunction.</p> <hd id="AN0192623345-74">Clinical relevance.</hd> <p>•Myasthenia gravis and Lambert–Eaton syndrome.•EMG allows distinction from nerve or muscle pathology.</p> <hd id="AN0192623345-75">5. Comparison across conditions.</hd> <p>Table 10 summarizes key EMG differences among normal muscle, neuropathy, myopathy, and neuromuscular junction disorders. Neuropathy shows reduced recruitment and large potentials from reinnervation; myopathy displays early recruitment with small potentials; neuromuscular junction disorders (e.g., myasthenia gravis) show normal initial responses with amplitude decrement upon repetition.</p> <p>Table 10. Comparison of EMG findings in normal, neuropathic, myopathic, and neuromuscular junction disorders</p> <p> <ephtml> <table><thead><tr><th>Feature</th><th>Normal</th><th>Neuropathy</th><th>Myopathy</th><th>Neuromuscular Junction Disorder</th></tr></thead><tbody><tr><td><p>Rest EMG</p></td><td><p>Flat</p></td><td><p>Fibrillations</p></td><td><p>Normal</p></td><td><p>Normal</p></td></tr><tr><td><p>Voluntary contraction</p></td><td><p>Sequential recruitment</p></td><td><p>Reduced recruitment, large potentials</p></td><td><p>Early recruitment, small potentials</p></td><td><p>Normal initially; amplitude drops with repetition</p></td></tr><tr><td><p>Recruitment</p></td><td><p>Small → large</p></td><td><p>Loss of small units</p></td><td><p>Many small units early</p></td><td><p>Normal → failure over time</p></td></tr><tr><td><p>CMAP amplitude</p></td><td><p>Normal</p></td><td><p>May be increased for surviving units.</p></td><td><p>Reduced</p></td><td><p>Normal initially, decreases</p></td></tr></tbody></table> </ephtml> </p> <p>CMAP, compound muscle action potential; EMG, electromyography.</p> <hd id="AN0192623345-76">Assessment Ideas</hd> <p>•In-class quiz: Show a trace → ask students to identify if it is nerve, muscle, or neuromuscular junction.•Short written assignment: "Explain why EMG in myopathy shows early recruitment of motor units."•Practical exam question: Interpret a provided EMG pattern.</p> <hd id="AN0192623345-77">Conclusions</hd> <p>•EMG reveals underlying neuromuscular physiology:The pattern of MUAPs, recruitment, and spontaneous activity provides direct insight into nerve, muscle, or neuromuscular junction function.•Different pathologies produce characteristic EMG signatures:Neuropathy: fibrillations, reduced recruitment, large motor units.Myopathy: early recruitment, small motor units.Neuromuscular junction disorders: normal at rest, decrement with sustained activity.•EMG interpretation requires context:Always combine EMG with clinical history, examination, and other investigations.Spontaneous activity or amplitude changes alone are not sufficient to diagnose pathology.•Educational value for students:Comparing normal versus abnormal EMG helps students understand the link between physiology and pathology.Reinforces principles of motor unit recruitment, size, and adaptation to injury.</p> <hd id="AN0192623345-78">Key Take-Home Messages</hd> <p>•EMG is a functional window into the neuromuscular system.•Understanding patterns allows differentiation between nerve, muscle, and neuromuscular junction disorders.•Careful measurement and interpretation are essential to avoid misdiagnosis.</p> <hd id="AN0192623345-79">LESSON PLAN 3: NERVE CONDUCTION STUDIES AND CMAP ANALYSIS</hd> <p>(Format: Lecture + Practical + Discussion)</p> <hd id="AN0192623345-80">Learning Objectives</hd> <p>By the end of this session, students should be able to:1) Record a compound muscle action potential (CMAP) using surface EMG.2) Identify distal and proximal latencies from EMG traces.3) Calculate nerve conduction velocity (NCV) from latency and distance measurements.4) Describe how NCV changes with age, temperature, and pathology.5) Interpret CMAP findings in physiological and pathological contexts.</p> <hd id="AN0192623345-81">Lesson Structure</hd> <p></p> <hd id="AN0192623345-82">1. Introduction and motivation (10 min)</hd> <p>•Begin with a clinical scenario: "A patient presents with weak reflexes. How can EMG and nerve conduction studies (NCSs) assess motor neuron-to-muscle signal integrity?"•Introduce EMG and NCS as tools to measure nerve-to-muscle signal timing, yielding latencies and velocities.</p> <hd id="AN0192623345-83">2. Mini-lecture: principles (10 min).</hd> <p>•EMG and NCS are complementary: EMG measures muscle electrical activity, whereas NCS evaluates nerve signal speed and strength.•CMAP: summed electrical response of muscle fibers following motor nerve stimulation.</p> <hd id="AN0192623345-84">Definitions.</hd> <p>•Distal latency: time from distal stimulation (e.g., wrist) to muscle response onset.•Proximal latency: time from proximal stimulation (e.g., elbow) to muscle response onset.•Conduction velocity formula: <ephtml> <math overflow="scroll" display="inline" xmlns="http://www.w3.org/1998/Math/MathML"><mrow><mtext>NCV</mtext><mo>=</mo><mfrac><mrow><mtext>distance (proximal </mtext><mo>−</mo><mspace width="0.25em" /><mtext>distal)</mtext></mrow><mrow><mtext>proximal latency </mtext><mo>−</mo><mspace width="0.25em" /><mtext>distal latency</mtext></mrow></mfrac></mrow></math> </ephtml></p> <hd id="AN0192623345-85">3. Practical demonstration: recording CMAP (25 min).</hd> <p></p> <hd id="AN0192623345-86">Setup (upper limb example).</hd> <p>•Stimulate median nerve at wrist and elbow (Fig. 4).•Record from abductor pollicis brevis (APB).</p> <p></p> <p>DIAGRAM: Figure 4. Top: diagram of the forearm showing the median nerve, with examples of elbow and wrist stimulation sites. Motor and sensory stimulation sites in the hand are also depicted, along with the placement of the ground electrode. Compound muscle action potentials (CMAPs) obtained from elbow and wrist stimulations display different latencies: proximal latency (L2) and distal latency (L1). Bottom: typical CMAPs recorded from the abductor pollicis brevis with 2 stimulation points along the median nerve. Note the waveform similarity in morphology and amplitude at both wrist (left CMAP) and elbow (right CMAP) stimulation. The upward deflection from baseline indicates a well-positioned recording electrode over the muscle endplate site, where the action potential is generated. The distal latency (3.5 ms) and proximal latency (7.5 ms) are derived from the CMAPs. The distance between the 2 stimulation points on the student's forearm (220 mm) allows for the calculation of the median nerve conduction velocity (NCV = 55 m/s).</p> <hd id="AN0192623345-87">Procedure.</hd> <p>•Deliver distal stimulus; measure latency to CMAP onset.•Deliver proximal stimulus; measure latency.•Measure distance between stimulation sites.•Students calculate NCV.Discussion prompt: "Why measure both distal and proximal latencies?"</p> <hd id="AN0192623345-88">4. Comparison example: lower limb recording (10 min).</hd> <p>•Demonstrate CMAP recording from peroneal nerve to extensor digitorum brevis (EDB).•Students compare latency and NCV differences between upper and lower limbs, noting limb length effects.</p> <hd id="AN0192623345-89">5. Factors affecting conduction velocity (20 min).</hd> <p></p> <hd id="AN0192623345-90">Physiological factors.</hd> <p>•Axon diameter: Larger axons conduct faster because of lower resistance.•Myelination: Myelinated fibers conduct faster (∼50–65 m/s) than unmyelinated fibers (∼1–5 m/s).•Age: NCV is slower in infants and elderly because of incomplete myelination and degradation, respectively.•Limb length: Longer nerves increase absolute latency; NCV normalizes for distance.</p> <hd id="AN0192623345-91">Metabolic and lifestyle factors.</hd> <p>•Hydration: Dehydration impairs ion channel function, slightly reducing NCV.•Sleep deprivation: Increases nerve excitability, potentially altering latency.•Electrolyte levels: Deficiencies (e.g., potassium, calcium) disrupt nerve transmission.</p> <hd id="AN0192623345-92">Physiological state and health conditions.</hd> <p>•Muscle fatigue: temporary NCV reduction due to metabolite accumulation (e.g., lactate, H<sups>+</sups>).•Blood circulation: Poor circulation or cold limbs slows NCV.•Pathologies:•Demyelination (e.g., Guillain–Barré, multiple sclerosis): marked NCV slowing (<35 m/s), conduction block.•Axonal loss: reduced CMAP amplitude, near-normal NCV.•Entrapment neuropathies (e.g., carpal tunnel): focal slowing (e.g., distal latency >4.2 ms for median nerve).</p> <hd id="AN0192623345-93">External influences.</hd> <p>•Temperature: Cooling (∼25°C) slows NCV, increasing latency; warming enhances NCV.•Nerve compression: Prolonged pressure (e.g., wrist flexion) impairs NCV.•Stimulation intensity: Submaximal stimulation reduces CMAP amplitude, affecting latency measurements.Interactive element: Show normal versus abnormal CMAP traces; ask students to interpret differences.</p> <hd id="AN0192623345-94">6. Case-based interpretation (10 min).</hd> <p>Provide sample conduction data (latencies, distances, CMAP amplitudes).Case examples:1) Normal conduction velocity.2) Slowed NCV, preserved amplitude (demyelination).3) Reduced amplitude, near-normal NCV (axonal loss).4) Focal slowing at distal site (entrapment neuropathy).Task: Students calculate NCV and interpret findings.</p> <hd id="AN0192623345-95">7. Wrap-up and synthesis (5 min).</hd> <p></p> <hd id="AN0192623345-96">Recap.</hd> <p>•EMG records CMAP; NCS measures latencies and NCV.•NCV depends on latency difference and distance.•Physiological (age, temperature) and pathological (demyelination, axonal loss) factors alter results.Clinical pearl: "Slowed NCV suggests demyelination; reduced CMAP amplitude suggests axonal loss."</p> <hd id="AN0192623345-97">Clinical relevance.</hd> <p>NCV diagnoses peripheral neuropathy, nerve trauma, or compression and monitors disease progression or treatment efficacy.</p> <hd id="AN0192623345-98">Materials Needed</hd> <p>•EMG/NCV recording device (e.g., BIOPAC, PowerLab).•Surface electrodes and conductive gel.•Computer with data acquisition software.•Measuring tape for limb distance measurements.•Sample EMG/NCV traces for case interpretation.•Excel for data analysis.</p> <hd id="AN0192623345-99">Assessment Ideas</hd> <p>•Calculation task: Provide distal/proximal latencies and distances; students calculate NCV.•Short-answer question: "How does cooling affect CMAP latency and why?"•Interpretation exercise: Students classify traces as normal, demyelinating, or axonal.</p> <hd id="AN0192623345-100">Expected Results</hd> <p>1) Upper limb example—median nerve to abductor pollicis brevis•Distal latency (wrist to APB, ∼3.5 ms): ∼3.0–4.0 ms.•Proximal latency (elbow to APB, ∼7.5 ms): ∼7.0–8.0 ms.•Distance (wrist to elbow, ∼250 mm): ∼200–250 mm.•Conduction velocity: <ephtml> <math overflow="scroll" display="inline" xmlns="http://www.w3.org/1998/Math/MathML"><mrow><mfrac><mrow><mn>250</mn><mspace width="0.25em" /><mtext>mm</mtext></mrow><mrow><mrow><mo>(</mo><mrow><mn>7.5</mn><mo>−</mo><mn>3.5</mn></mrow><mo>)</mo></mrow><mtext>ms</mtext></mrow></mfrac><mo>≈</mo><mn>62.5</mn><mspace width="0.25em" /><mtext>m/s</mtext></mrow></math> </ephtml> ; normal range: ∼50–65 m/s.•CMAP amplitude (wrist stimulation): ∼5–10 mV (normal range).2) Lower limb example—peroneal nerve to extensor digitorum brevis•Distal latency (ankle to EDB, 5 ms): ∼4.0–6.0 ms.•Proximal latency (knee to EDB, 13 ms): ∼12–14 ms.•Distance (ankle to fibular head, 380 mm): ∼350–400 mm.•Conduction velocity: <ephtml> <math overflow="scroll" display="inline" xmlns="http://www.w3.org/1998/Math/MathML"><mrow><mfrac><mrow><mn>380</mn><mspace width="0.25em" /><mtext>mm</mtext></mrow><mrow><mrow><mo>(</mo><mrow><mn>13</mn><mo>−</mo><mn>5</mn></mrow><mo>)</mo></mrow><mtext>ms</mtext></mrow></mfrac><mo>≈</mo><mn>47.5</mn><mspace width="0.25em" /><mtext>m/s</mtext></mrow></math> </ephtml> ; normal range: ∼40–55 m/s.•CMAP amplitude (ankle stimulation): ∼2–6 mV (smaller than hand muscles).3) General normative ranges (healthy adults, 20–40 yr)•Upper limb motor conduction velocity: 50–65 m/s.•Lower limb motor conduction velocity: 40–55 m/s.•Distal latency: upper limb (∼3.0–4.0 ms); lower limb (∼4.0–6.0 ms).•CMAP amplitude: hand muscles (∼5–10 mV); foot muscles (∼2–6 mV).4) Expected effects of different factors•Age and temperature (see discussion below).•Pathological changes:•Demyelination (e.g., Guillain–Barré): NCV < 35 m/s, prolonged distal latency (>4.5 ms), possible conduction block.•Axonal loss: normal/mildly reduced velocity but CMAP amplitude reduced.•Entrapment neuropathy (e.g., carpal tunnel): focal slowing in distal latency of median nerve (>4.2 ms to APB).5) Sample data table for student lab reportsTable 11 provides normal reference values for motor nerve conduction studies (NCSs). The median nerve to APB shows faster NCV (∼60–62 m/s) and higher CMAP amplitude (∼5–10 mV), reflecting efficient upper limb conduction. The peroneal nerve to EDB shows slightly slower NCV (∼47–50 m/s) and lower amplitude (∼2–6 mV), consistent with longer conduction distances and lower fiber density in lower limb muscles. Students can record EMG/CMAP, measure latencies, calculate NCV, and compare findings to these ranges. Significant deviations highlight technical errors, physiological variability, or pathology.</p> <p>Table 11. Normal motor nerve conduction study values for median and peroneal nerves</p> <p> <ephtml> <table><thead><tr><th>Site/Muscle</th><th>Distance, mm</th><th>Distal Latency, ms</th><th>Proximal Latency, ms</th><th>Velocity, m/s</th><th>CMAP Amplitude, mV</th></tr></thead><tbody><tr><td><p>Median nerve → APB</p></td><td><p>200–250 (wrist to elbow)</p></td><td><p>3.0–4.0</p></td><td><p>7.0–8.0</p></td><td><p>60–62</p></td><td><p>5–10</p></td></tr><tr><td><p>Peroneal nerve → EDB</p></td><td><p>350–400 (ankle to fibular head)</p></td><td><p>4.0–6.0</p></td><td><p>12.0–14.0</p></td><td><p>47–50</p></td><td><p>2–6</p></td></tr></tbody></table> </ephtml> </p> <p>APB, abductor pollicis brevis; CMAP, compound muscle action potential; EDB, extensor digitorum brevis.</p> <hd id="AN0192623345-101">EMG/CMAP Lab Troubleshooting Worksheet</hd> <p>Assist students in identifying and correcting common errors in CMAP recording, latency measurement, and NCV calculation. See appendix for common pitfalls in NCS.</p> <hd id="AN0192623345-102">Troubleshooting checklist (stepwise).</hd> <p>Several physiological and environmental factors influence NCS results. Maintaining optimal limb temperature, muscle relaxation, and patient comfort, while accounting for age, ensures accurate measurements.1) Verify electrode placement and contact quality.2) Ensure stimulus intensity is supramaximal (CMAP amplitude no longer increases).3) Measure distance along the correct anatomical nerve path.4) Keep muscle relaxed (baseline noise should be ≤1 mV).5) Warm limb if temperature <32°C.6) Compare results with expected values (see discussion below).</p> <hd id="AN0192623345-103">Notes for Students</hd> <p>1) Record both distal and proximal latencies for accurate NCV.2) Interpret latency, amplitude, and velocity together.3) Investigate deviations (technical, physiological, or pathological).4) Document all observations and corrective steps.</p> <hd id="AN0192623345-104">Discussion of Results—Nerve Conduction Lesson</hd> <p></p> <hd id="AN0192623345-105">1. Basic observations.</hd> <p></p> <hd id="AN0192623345-106">CMAP recording.</hd> <p>•Distal stimulation produces a clear CMAP with measurable latency.•Proximal stimulation yields a longer latency, enabling NCV calculation.</p> <hd id="AN0192623345-107">Expected velocities.</hd> <p>•Upper limb (median nerve): ∼50–65 m/s.•Lower limb (peroneal/tibial nerve): ∼40–55 m/s.</p> <hd id="AN0192623345-108">CMAP amplitude.</hd> <p>Reflects the number of activated fibers; higher in hand muscles (∼5–10 mV) than foot muscles (∼2–6 mV).</p> <hd id="AN0192623345-109">Interpretation.</hd> <p>•Latency and NCV quantify motor nerve function.•Distal vs. proximal comparison identifies segmental conduction issues or focal slowing.</p> <hd id="AN0192623345-110">2. Influence of temperature.</hd> <p></p> <hd id="AN0192623345-111">Cooling (∼25°C).</hd> <p>Increases distal and proximal latencies (∼0.1–0.2 ms per °C below 32°C) and decreases NCV (∼1.5–2.5 m/s per °C).</p> <hd id="AN0192623345-112">Warming.</hd> <p>Decreases latency and increases NCV.</p> <hd id="AN0192623345-113">Physiological basis.</hd> <p>Temperature affects ion channel kinetics and myelin conduction efficiency; cooling slows Na<sups>+</sups>/K<sups>+</sups> channel opening, reducing action potential propagation speed.</p> <hd id="AN0192623345-114">Practical implication.</hd> <p>Maintain consistent limb temperature (∼32°C); temperature variations explain interlimb differences and are relevant in conditions like Raynaud's disease or hypothermia.</p> <hd id="AN0192623345-115">3. Influence of age.</hd> <p>•Infants and children: slower NCV (∼20–30 m/s in neonates, ∼30–40 m/s in children) due to incomplete myelination.•Adults (20–40 yr): peak NCV (∼50–65 m/s).•Elderly (>60 yr): mild slowing (∼40–50 m/s, 10%–20% reduction) due to age-related demyelination or axonal loss.</p> <hd id="AN0192623345-116">Interpretation.</hd> <p>Compare measured NCV to age-appropriate norms to distinguish physiological from pathological slowing.</p> <hd id="AN0192623345-117">4. Other influencing factors.</hd> <p>Table 12 outlines factors affecting latency and NCV in NCS.</p> <p>Table 12. Factors influencing latency and nerve conduction velocity in EMG/NCV studies</p> <p> <ephtml> <table><thead><tr><th>Factor</th><th>Effect on Latency/NCV</th><th>Explanation</th></tr></thead><tbody><tr><td><p>Limb length</p></td><td><p>Longer limbs → longer latencies</p></td><td><p>Longer nerve distance increases latency; NCV calculation normalizes for distance.</p></td></tr><tr><td><p>Electrode placement</p></td><td><p>Improper placement → inaccurate distance measurement or latency recording</p></td><td><p>Always measure along nerve course; place electrodes over target muscles.</p></td></tr><tr><td><p>Pathologies</p></td><td><p>Demyelination slows NCV; axonal loss reduces amplitude.</p></td><td><p>Clinical interpretation of EMG/NCV relies on both latency and amplitude.</p></td></tr><tr><td><p>Fatigue/repeated stimulation</p></td><td><p>Minimal effect in short tests; amplitude reduction in prolonged tests</p></td><td><p>Fatigue or repetitive stimulation may reduce amplitude because of neuromuscular junction effects.</p></td></tr></tbody></table> </ephtml> </p> <p>EMG, electromyography.</p> <hd id="AN0192623345-118">Typical Observations in Lab</hd> <p>•Median nerve (APB): distal latency ∼3.0–4.0 ms; proximal latency ∼7.0–8.0 ms; distance ∼200–250 mm; NCV ∼60–62 m/s; amplitude ∼5–10 mV.•Peroneal nerve (EDB): distal latency ∼4.0–6.0 ms; proximal latency ∼12.0–14.0 ms; distance ∼350–400 mm; NCV ∼47–50 m/s; amplitude ∼2–6 mV.•Key patterns:•Normal latency/NCV: intact myelination.•Reduced amplitude, normal NCV: axonal loss.•Slowed NCV: demyelination.</p> <hd id="AN0192623345-119">Conclusions</hd> <p>NCS provide quantitative insights into peripheral nerve function, with CMAP latency and NCV reflecting myelinated motor fiber integrity.Practical and clinical takeaway: Accurate NCV requires proper electrode placement, consistent limb temperature, and precise distance measurement. Interpretation integrates age, temperature, and pathology.</p> <hd id="AN0192623345-120">Key Teaching Points for Students</hd> <p>•NCV is calculated from latency difference over distance, not absolute latency.•Consider physiological factors before attributing changes to pathology.•EMG and NCS together provide a comprehensive assessment of neuromuscular function.</p> <hd id="AN0192623345-121">CONCLUSIONS</hd> <p>These lessons equip students with the foundational skills needed for neurophysiological testing and provide them with practical tools for analyzing muscle and nerve health in various contexts. Overall, students will gain hands-on experience in measuring sEMG in muscles and determining nerve conduction velocity and appreciate the importance of nerve conduction studies in diagnosing neurological diseases.In summary, these lesson plans aim to use EMG as a tool to illustrate the nerve-muscle interaction. Indeed, EMG offers a real-time, objective way to assess how nerves communicate with muscles, making it an invaluable tool for understanding the physiology of normal and abnormal nerve-muscle interactions. This is particularly important for diagnosing and distinguishing between neuropathies, where nerve damage disrupts muscle activation, and myopathies, where the muscles themselves are compromised ([<reflink idref="bib5" id="ref37">5</reflink>], [<reflink idref="bib18" id="ref38">18</reflink>]). Through this detailed examination, EMG helps clinicians tailor treatments to the specific nature of the neuromuscular dysfunction.</p> <hd id="AN0192623345-122">DATA AVAILABILITY</hd> <p>Data will be made available on request to the corresponding author.</p> <hd id="AN0192623345-123">GRANTS</hd> <p>This work was supported by the Fundação para a Ciência e Tecnologia, Portugal (Reference number: 2022.04526.PTDC).</p> <hd id="AN0192623345-124">DISCLOSURES</hd> <p>No conflicts of interest, financial or otherwise, are declared by the author.</p> <hd id="AN0192623345-125">AUTHOR CONTRIBUTIONS</hd> <p>C.M.S. conceived and designed research; performed experiments; analyzed data; interpreted results of experiments; prepared figures; drafted manuscript; edited and revised manuscript; approved final version of manuscript.</p> <hd id="AN0192623345-126">APPENDIX</hd> <p></p> <hd id="AN0192623345-127">I. Surface EMG Setup: Step-by-Step Guide for Recording Muscle Activity</hd> <p></p> <hd id="AN0192623345-128">1. Materials needed.</hd> <p>•EMG device: a device to record and display EMG signals (PowerLab 26T or Biopac System MP36 systems) (Chart or LabChart software).•Surface electrodes: typically, self-adhesive silver/silver chloride electrodes (2–4 for the muscle and 1 ground electrode).•Conductive gel (optional): Some electrodes require conductive gel to improve signal quality.•Alcohol wipes or skin cleaner: to clean the skin and reduce impedance.•Cables/leads: connect electrodes to the EMG device•Computer/display monitor: for visualizing EMG signals in real time.</p> <hd id="AN0192623345-129">2. Preparing the skin.</hd> <p>1) Identify the muscle group: Choose the target muscle(s). For example:2) Biceps brachii (upper arm): responsible for flexing the elbow.3) Forearm muscles (e.g., flexor carpi radialis): responsible for wrist flexion.4) Clean the skin: Use alcohol wipes to clean the area where the electrodes will be placed. This step reduces skin impedance by removing oils and dirt, ensuring better signal quality.</p> <hd id="AN0192623345-130">3. Electrode placement.</hd> <p>Surface electrodes should be placed correctly to capture the best muscle signals. For this:</p> <p>A. Bipolar electrode configuration:</p> <p>This setup uses two active electrodes placed over the muscle and one ground electrode.</p> <p>B. Placement for biceps brachii:1) <emph>Active electrode 1</emph> (positive):</p> <p>Place the first electrode over the midpoint of the biceps brachii. This is typically halfway between the shoulder and the elbow on the anterior side of the upper arm.1) <emph>Active electrode 2</emph> (negative):</p> <p>Place the second electrode 2 cm apart from the first electrode, aligned parallel to the muscle fibers. The placement should be along the longitudinal axis of the muscle to capture the muscle's electrical activity.1) Ground electrode:</p> <p>Place the ground electrode on a bony prominence away from the muscle being recorded, such as the olecranon (the bony part of the elbow) or acromion (shoulder bone).</p> <p>C. Placement for forearm muscles:1) <emph>Active electrode 1</emph> (positive):</p> <p>Place the first electrode on the belly of the forearm flexor muscle, typically ∼1/3rd of the way down from the elbow to the wrist, aligned with the muscle fibers.1) <emph>Active electrode 2</emph> (negative):</p> <p>Place the second electrode ∼2 cm distal from the first, also along the muscle fibers.1) Ground electrode:</p> <p>As above, place the ground electrode on a bony prominence, such as the ulnar styloid (wrist bone) or lateral epicondyle of the humerus (outer elbow).</p> <hd id="AN0192623345-131">4. Connecting to the EMG device.</hd> <p>1) Attach the cables/leads: Connect the electrode leads to the input ports of the EMG device. Ensure the polarity is correct, with one lead connected to each active electrode and one to the ground electrode.2) Check signal quality: Verify that the electrodes are securely attached to the skin and check the device for any signs of poor contact (such as high baseline noise). If necessary, reclean the skin or adjust the electrode position.</p> <hd id="AN0192623345-132">5. Calibration and baseline recording.</hd> <p>1) Relaxed position: Have the student rest their arm in a relaxed position (e.g., arm resting on a table) to record a baseline EMG with no muscle contraction. This ensures that there is minimal noise and a clear starting point for recording muscle activity.2) Muscle activation: Ask the student to contract the target muscle, such as flexing the elbow to activate the biceps brachii or flexing the wrist for the forearm muscles. Record the active EMG signal during the contraction.</p> <hd id="AN0192623345-133">6. Visualizing EMG signals.</hd> <p>Monitor the output: The EMG device will display the MUAPs generated by muscle contraction. The signal should show low amplitude during rest and high amplitude during active muscle contraction.</p> <p>Analyzing the signal:•Amplitude: Indicates the strength of muscle activation.•Frequency: Corresponds to the rate of MU firing.</p> <hd id="AN0192623345-134">7. Example of real-time task.</hd> <p>Once the setup is complete, you can conduct tasks to visualize muscle activity:•For biceps brachii: Ask the student to perform an isometric contraction by holding a dumbbell or pushing against a surface. The EMG will show continuous muscle activity during the contraction.•For forearm flexors: Have the student grip a ball or hand dynamometer, and the EMG will record the electrical signals associated with the muscle movements.</p> <p>Diagram description (for visual representation):•Electrodes: Two active electrodes are positioned on the muscle belly, aligned along the muscle fibers.•Ground electrode: Positioned on a bony landmark, away from the muscle of interest.•Cables/leads: Connect the electrodes to the EMG device.•EMG device: Displays the EMG signals on a computer or monitor, showing muscle activation patterns during contraction and rest.</p> <p>This surface EMG setup provides a clear and effective way to visualize and study muscle activation patterns in real time.</p> <hd id="AN0192623345-135">II. Interpretation of EMG Signals</hd> <p>Waveform patterns: Explain the significance of different waveforms—spontaneous activity, polyphasic potentials, fasciculations, etc.</p> <p>Highlight how muscle fiber size, recruitment, and MU density affect the EMG trace.</p> <p>Clinical relevance: Show examples of abnormal iEMG signals seen in neuropathies, myopathies, and radiculopathies. Discuss how these patterns help in diagnosing conditions.</p> <hd id="AN0192623345-136">Understanding the neuromuscular junction.</hd> <p>The neuromuscular junction is the site where a motor neuron communicates with a muscle fiber. When a nerve impulse reaches the junction, it triggers the release of neurotransmitters (acetylcholine) that cause the muscle to contract.</p> <p>EMG captures the electrical activity that results from nerve signals activating the muscle. By examining the pattern and timing of these signals, EMG shows how effectively the motor neurons are communicating with muscle fibers. For instance, a smooth, coordinated signal indicates healthy neuromuscular communication, whereas irregular or diminished signals may suggest an issue at the neuromuscular junction (e.g., in conditions like myasthenia gravis).</p> <hd id="AN0192623345-137">EMG differentiating between neuropathies and myopathies.</hd> <p>•Neuropathies: Disorders where there is damage to the peripheral nerves, affecting the nerve's ability to send signals to muscles. Common examples include diabetic neuropathy and carpal tunnel syndrome.•Myopathies: Diseases that affect muscle fibers directly, such as muscular dystrophy or polymyositis.</p> <hd id="AN0192623345-138">EMG findings in neuropathies.</hd> <p>•Delayed or absent muscle activation: EMG reveals abnormal or reduced muscle responses due to impaired nerve signal transmission.•Fibrillation potentials and positive sharp waves: These spontaneous discharges are hallmarks of nerve damage and denervation. They indicate that the muscle is not receiving adequate input from the nerve.•Reduced recruitment patterns: Neuropathies often result in fewer MUs being activated, which can be seen as smaller or fewer action potentials on the EMG recording.</p> <p>Example: In a case of peripheral neuropathy, EMG may show prolonged distal motor latencies and reduced conduction velocities. This demonstrates that the nerve signals are delayed, and the muscles receive less frequent and weaker input, leading to muscle weakness or paralysis.</p> <hd id="AN0192623345-139">EMG findings in myopathies.</hd> <p>•Small, low-amplitude MU potentials: EMG recordings show that the muscles display lower electrical activity, but the nerve signals are normal. This is because the problem lies within the muscle itself, not the nerve.•Early recruitment: In myopathies, muscles tend to activate smaller MUs early on in response to even small efforts, leading to rapid recruitment seen on EMG, but the force output remains weak because of intrinsic muscle pathology.</p> <p>Example: In conditions like muscular dystrophy, the muscle fibers are damaged or degenerated, so the EMG will show reduced muscle fiber recruitment despite normal nerve input. This helps to confirm that the issue lies with the muscle, rather than the nerve.</p> <hd id="AN0192623345-140">III. Common Pitfalls in EMG and NCV Recordings and Analysis</hd> <p>Accurate EMG and NCV recordings and interpretation require attention to electrode placement, participant preparation, equipment settings, and proper data analysis. Errors in these areas can obscure true muscle activity or lead to several misinterpretations. #TA1 and #TA2 summarize key pitfalls, their causes, and best practices to avoid them.</p> <hd id="AN0192623345-141">IV. Case-Based Problems</hd> <p>EMG plays a critical role in differentiating between various neuromuscular disorders ([<reflink idref="bib5" id="ref39">5</reflink>]). Through careful analysis of motor and sensory conduction studies and EMG findings, physicians can pinpoint the exact location and nature of nerve or muscle dysfunction, enabling accurate diagnosis and appropriate treatment.</p> <hd id="AN0192623345-142">Case 1: Differentiating carpal tunnel syndrome from cervical radiculopathy.</hd> <p>Background: A 45-yr-old woman presented with numbness, tingling, and weakness in her right hand. She reported worsening symptoms over 6 mo, especially at night. Initial physical examination suggested two possible diagnoses: carpal tunnel syndrome or cervical radiculopathy (C6–C7).</p> <p>EMG/NCS Findings:1) NCS:•Median nerve: prolonged distal motor and sensory latencies across the wrist, with a reduced conduction velocity.•Ulnar nerve: normal conduction velocity.2) EMG:•Abductor pollicis brevis (innervated by the median nerve): increased insertional activity and fibrillation potentials, suggesting denervation.•Cervical paraspinal muscles (C6–C7 innervation): no abnormal spontaneous activity, ruling out radiculopathy.</p> <p>Diagnosis: The EMG findings pointed to carpal tunnel syndrome, as the abnormalities were restricted to the median nerve. The absence of abnormalities in the cervical paraspinal muscles helped exclude cervical radiculopathy. The patient underwent carpal tunnel release surgery, with significant improvement in symptoms.</p> <hd id="AN0192623345-143">Case 2: Amyotrophic lateral sclerosis vs. peripheral neuropathy.</hd> <p>Background: A 52-yr-old man presented with progressive muscle weakness and atrophy in both hands and lower extremities, associated with fasciculations. There was no sensory loss. His clinical picture raised concerns about amyotrophic lateral sclerosis (ALS) or severe peripheral neuropathy.</p> <p>EMG/NCS Findings:1) NCS:•Sensory nerve conduction studies were normal.•Motor nerve conduction studies showed reduced amplitudes but normal conduction velocities.2) EMG:•Widespread fibrillation potentials and positive sharp waves in multiple regions (including the thoracic paraspinals, cervical spine, and distal limb muscles).•Fasciculations were seen in multiple muscle groups.•Chronic MU remodeling with large, polyphasic MUs in both the upper and lower limbs.</p> <p>Diagnosis: The iEMG findings of widespread denervation and reinnervation, combined with the absence of sensory nerve involvement, supported a diagnosis of ALS rather than peripheral neuropathy. This diagnosis was confirmed by clinical progression, and the patient was referred to a neurologist specializing in motor neuron diseases.</p> <hd id="AN0192623345-144">Case 3: Myasthenia gravis vs. Lambert–Eaton myasthenic syndrome.</hd> <p>Background: A 35-yr-old man presented with fluctuating muscle weakness, primarily affecting the ocular and facial muscles. He also reported mild limb weakness, raising suspicion of myasthenia gravis or Lambert–Eaton myasthenic syndrome (LEMS).</p> <p>EMG/NCS Findings:1) NCS:•Repetitive nerve stimulation at slow frequencies showed a significant decrement in the compound muscle action potential (CMAP) amplitude.•High-frequency repetitive stimulation resulted in no facilitation, arguing against LEMS.2) EMG:•No evidence of denervation in the resting muscle.•A consistent decremental response in MUs upon repetitive stimulation, suggestive of a neuromuscular junction disorder.</p> <p>Diagnosis: The EMG findings, particularly the decremental response on repetitive stimulation, confirmed myasthenia gravis. LEMS was ruled out because of the absence of facilitation on high-frequency stimulation. The patient was treated with pyridostigmine and responded well.</p> <p>Table A1. Common EMG pitfalls and best practices</p> <p> <ephtml> <table><thead><tr><th>Category/Problem</th><th>Explanation</th><th>How to Avoid/Correct</th></tr></thead><tbody><tr><td>Electrode misplacement</td><td>Electrodes placed away from the muscle belly reduce amplitude (⁓50–70%) and distort MUAPs.</td><td>Place electrodes over the muscle belly (per SENIAM); use bony site for reference electrode.</td></tr><tr><td>Poor skin contact/high impedance</td><td>Causes baseline noise (⁓0.5–1 mV) and waveform distortion.</td><td>Clean skin with alcohol, apply conductive gel, secure electrodes firmly.</td></tr><tr><td>Electrical artifact</td><td>Stimulus artifact mistaken for MUAP or onset.</td><td>Identify artifact; measure CMAP onset from first true deflection.</td></tr><tr><td>Improper filter or gain settings</td><td>Incorrect bandwidth (too narrow/wide) or gain distorts EMG amplitude and pattern.</td><td>Use bandpass 10–500 Hz; notch 50/60 Hz; adjust gain (1,000–5,000) to avoid clipping.</td></tr><tr><td>Muscle contraction at rest</td><td>Residual tension elevates baseline and masks fibrillations.</td><td>Ensure full relaxation; support limb with padding or sling.</td></tr><tr><td>Inconsistent or low voluntary effort</td><td>Variable effort mimics fatigue or pathology (reduced CMAP 30–50%).</td><td>Use visual feedback (dynamometer), provide clear instructions, and allow practice trials.</td></tr><tr><td>Low muscle temperature</td><td>Cold muscles (⁓25°C) slow conduction and prolong latency.</td><td>Warm limb if needed; maintain lab at 22–25°C.</td></tr><tr><td>Participant fatigue/low motivation</td><td>Prior exertion or poor effort reduces amplitude and MU recruitment.</td><td>Allow 2- to 5-min rest between trials; encourage motivation and consistent effort.</td></tr><tr><td>Interindividual variability</td><td>Differences in fiber type, training, or muscle size alter EMG amplitude.</td><td>Focus on relative patterns; normalize to individual MVC.</td></tr><tr><td>Misinterpreting early recruitment as fatigue</td><td>Normal small MU recruitment misread as fatigue-related amplitude drop.</td><td>Teach Henneman's size principle; compare to typical low-to-high MU recruitment curves.</td></tr><tr><td>Misinterpreting amplitude changes</td><td>Increased amplitude (2–6 mV) may reflect added recruitment, not fatigue.</td><td>Analyze amplitude and median frequency together; correlate with force output.</td></tr><tr><td>Overlooking frequency changes</td><td>Fatigue reduces MU firing frequency (⁓50 → 20 Hz); amplitude alone misses this.</td><td>Use spectral analysis (FFT) to track frequency and amplitude trends.</td></tr><tr><td>Misattributing fatigue mechanisms</td><td>Central fatigue mistaken for peripheral.</td><td>Discuss central vs. peripheral fatigue; compare EMG and force decline patterns.</td></tr><tr><td>Misinterpreting low amplitude as pathology</td><td>Small amplitude (⁓0.2–1 mV) may reflect small muscles or few fibers.</td><td>Correlate with firing pattern, latency, and clinical data; normalize to MVC.</td></tr><tr><td>Over-/underinterpreting spontaneous activity</td><td>Minor fibrillations (⁓0.1–0.5 mV) may appear in healthy subjects.</td><td>Use normative data; interpret in clinical context.</td></tr><tr><td>Misclassifying MUAP type</td><td>Fast/slow or short/long MUAPs misidentified (⁓2–20 ms).</td><td>Measure amplitude and duration precisely; consider reinnervation effects.</td></tr><tr><td>Ignoring technical artifacts</td><td>Artifacts (⁓0.5–1 mV) misread as abnormal activity.</td><td>Repeat recordings; verify electrode and equipment setup.</td></tr></tbody></table> </ephtml> </p> <p>3 CMAP, compound muscle action potential; EMG, electromyography; FFT, fast Fourier transform; MU, motor unit; MUAP, motor unit action potential; MVC, maximal voluntary contraction.</p> <p>Table A2. Common pitfalls in nerve conduction studies</p> <p> <ephtml> <table><thead><tr><th>Problem</th><th>Possible Cause</th><th>Suggested Action</th></tr></thead><tbody><tr><td>Weak or absent CMAP</td><td>Recording electrode too far from muscle belly</td><td>Reposition electrode over muscle belly (per SENIAM guidelines).</td></tr><tr><td>Distorted CMAP waveform</td><td>Reference electrode misplaced</td><td>Place reference on an electrically neutral site (e.g., bony prominence).</td></tr><tr><td>Noisy baseline</td><td>High impedance or poor skin contact</td><td>Clean skin with alcohol, apply conductive gel, ensure firm contact, use 10–500 Hz band-pass filter.</td></tr><tr><td>Reduced CMAP amplitude (⁓50–70% normal)</td><td>Submaximal stimulus</td><td>Increase stimulus intensity until amplitude plateaus (supramaximal, 0.1–0.2 ms).</td></tr><tr><td>Mixed response</td><td>Costimulation of adjacent nerves</td><td>Adjust electrode placement; reduce stimulus intensity.</td></tr><tr><td>Unclear latency onset</td><td>Stimulus artifact overlaps CMAP</td><td>Use 10–500 Hz filter; adjust stimulus duration (0.1–0.2 ms).</td></tr><tr><td>Conduction velocity too high (>70 m/s)</td><td>Distance measured too short</td><td>Measure along true anatomical path (e.g., wrist to elbow).</td></tr><tr><td>Conduction velocity too low (<40 m/s)</td><td>Distance too long or latency from peak</td><td>Verify distance; measure onset latency.</td></tr><tr><td>Mistaking stimulus artifact for CMAP onset</td><td>Artifact misidentified as CMAP</td><td>Identify first true deflection from baseline.</td></tr><tr><td>Using CMAP peak instead of onset</td><td>Incorrect latency measurement</td><td>Measure from stimulus to CMAP onset, not peak.</td></tr><tr><td>Confusing amplitude drop with conduction slowing</td><td>Misinterpretation</td><td>Remember: velocity depends on latency difference; amplitude reflects fiber recruitment.</td></tr></tbody></table> </ephtml> </p> <p>4 CMAP, compound muscle action potential.</p> <ref id="AN0192623345-145"> <title> REFERENCES </title> <blist> <bibl id="bib1" idref="ref1" type="bt">1</bibl> <bibtext> Shun K. 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  Data: Integrating Electromyography into the Physiology Curriculum
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  Data: <searchLink fieldCode="AR" term="%22Cristina+M%2E+Sena%22">Cristina M. Sena</searchLink> (ORCID <externalLink term="https://orcid.org/0000-0002-0889-2977">0000-0002-0889-2977</externalLink>)
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  Data: <searchLink fieldCode="SO" term="%22Advances+in+Physiology+Education%22"><i>Advances in Physiology Education</i></searchLink>. 2026 50(1):261-279.
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  Data: American Physiological Society. 9650 Rockville Pike, Bethesda, MD 20814-3991. Tel: 301-634-7164; Fax: 301-634-7241; e-mail: webmaster@the-aps.org; Web site: https://www.physiology.org/journal/advances
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  Data: 19
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  Data: 2026
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  Data: Journal Articles<br />Reports - Descriptive
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  Data: <searchLink fieldCode="DE" term="%22Physiology%22">Physiology</searchLink><br /><searchLink fieldCode="DE" term="%22Curriculum+Development%22">Curriculum Development</searchLink><br /><searchLink fieldCode="DE" term="%22Human+Body%22">Human Body</searchLink><br /><searchLink fieldCode="DE" term="%22Teaching+Methods%22">Teaching Methods</searchLink><br /><searchLink fieldCode="DE" term="%22Learning+Activities%22">Learning Activities</searchLink><br /><searchLink fieldCode="DE" term="%22Motor+Reactions%22">Motor Reactions</searchLink><br /><searchLink fieldCode="DE" term="%22Muscular+Strength%22">Muscular Strength</searchLink><br /><searchLink fieldCode="DE" term="%22Clinical+Diagnosis%22">Clinical Diagnosis</searchLink><br /><searchLink fieldCode="DE" term="%22Neurological+Impairments%22">Neurological Impairments</searchLink><br /><searchLink fieldCode="DE" term="%22Lesson+Plans%22">Lesson Plans</searchLink><br /><searchLink fieldCode="DE" term="%22Fatigue+%28Biology%29%22">Fatigue (Biology)</searchLink><br /><searchLink fieldCode="DE" term="%22College+Students%22">College Students</searchLink><br /><searchLink fieldCode="DE" term="%22Science+Instruction%22">Science Instruction</searchLink>
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  Data: 10.1152/advan.00237.2024
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  Data: 1043-4046<br />1522-1229
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  Data: Muscle physiology is included in the core curriculum in the biomedical, health, and exercise science fields. It is always challenging to understand the dynamic nature of motor unit (MU) functioning, neuromuscular activity, or muscle contractions. Different teaching instruments can be used during a didactic lecture to make it more engaging for the students, including the use of electromyography (EMG) and dynamometry techniques. EMG serves as a clinical and educational tool to evaluate skeletal muscle activity, enhancing the understanding of muscle physiology. This activity aims to describe several sessions where EMG is used as a tool to teach muscle physiology. EMG demonstrates muscle activation and MU recruitment, bridging theory and practice in physiology education. Surface EMG measures electrical activity in muscles, providing real-time data during rest, contraction, and fatigue. At rest, muscles exhibit minimal electrical activity. During contraction, increasing MU recruitment raises the amplitude and frequency of EMG signals. Fatigue is shown by altered patterns, reflecting declining muscle force and changes in MU activation. These principles highlight Henneman's size principle, where smaller motor units are activated first, followed by larger, stronger ones as contraction strength increases. Clinically, EMG distinguishes between neuropathies and myopathies. Neuropathies show delayed or reduced MU activation, spontaneous discharges, and impaired nerve-muscle communication. Myopathies display low-amplitude signals and rapid MU recruitment due to intrinsic muscle weakness. EMG also tracks denervation and reinnervation, revealing fibrillations or polyphasic MU potentials during nerve recovery. Integrating EMG with nerve conduction studies enhances diagnostics, clarifying whether issues stem from nerve or muscle pathology.
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      – SubjectFull: Muscular Strength
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