Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs

Question 101: Which nerve fiber type is most susceptible to hypoxia?

A. Aa
B. Ab
C. B (Correct Answer)
D. C

Explanation: The susceptibility of nerve fibers to different types of insults follows a specific order based on their physiological characteristics. This is a high-yield topic frequently tested via the **Gasser-Erlanger classification**. ### **Why Option C (Type B) is Correct** The sensitivity of nerve fibers to **Hypoxia** is determined by their metabolic rate and oxygen demand. The order of susceptibility to hypoxia is **B > A > C**. * **Type B fibers** (preganglionic autonomic fibers) are the most sensitive to oxygen deprivation. * Although Type A fibers are larger, Type B fibers have a high surface-area-to-volume ratio and specific metabolic requirements that make them the first to fail when blood supply is compromised. ### **Analysis of Incorrect Options** * **Option A & B (Type A fibers):** While Type A fibers (including Alpha and Beta) are the most sensitive to **Pressure** (Order: A > B > C), they are intermediate in their sensitivity to hypoxia. * **Option D (Type C fibers):** These are small, unmyelinated fibers. They are the **most resistant** to hypoxia and pressure but are the **most sensitive to Local Anesthetics** (Order: C > B > A). ### **High-Yield Clinical Pearls for NEET-PG** To remember the susceptibility patterns, use the following table: | Insult | Most Sensitive | Least Sensitive | | :--- | :--- | :--- | | **Hypoxia** | **Type B** | Type C | | **Pressure** | **Type A** | Type C | | **Local Anesthesia** | **Type C** | Type A | * **Type A-delta fibers:** Responsible for fast pain and temperature. * **Type C fibers:** Responsible for slow pain, postganglionic autonomics, and olfaction. * **Type B fibers:** Preganglionic autonomic fibers.

Question 102: What is the primary function of tropomyosin in muscle contraction?

A. To assist in the fusion of actin and myosin filaments.
B. To block the binding sites on actin, preventing myosin attachment. (Correct Answer)
C. To slide along the myosin filament during muscle contraction.
D. To trigger the release of calcium ions from the sarcoplasmic reticulum.

Explanation: **Explanation:** In skeletal muscle, the **Troponin-Tropomyosin complex** acts as the regulatory "switch" for contraction. Tropomyosin is a long, fibrous protein that winds around the grooves of the F-actin helix. In a resting state (low intracellular calcium), tropomyosin is positioned such that it **physically masks the active myosin-binding sites on the actin filament**. This prevents the myosin heads from forming cross-bridges, thereby maintaining the muscle in a relaxed state. **Analysis of Options:** * **Option B (Correct):** When calcium binds to Troponin C, it induces a conformational change that pulls tropomyosin away from the binding sites, allowing contraction to begin. Thus, its primary function is inhibition via blocking. * **Option A:** Fusion of filaments does not occur; they slide past each other (Sliding Filament Theory). * **Option C:** Tropomyosin is part of the **thin filament (actin)**, not the thick filament (myosin). It moves relative to actin, not along myosin. * **Option D:** The release of calcium is triggered by the depolarization of the T-tubules and activation of **Dihydropyridine (DHP) and Ryanodine (RyR) receptors**, not by tropomyosin. **High-Yield NEET-PG Pearls:** * **Troponin Complex Components:** **T** (binds to Tropomyosin), **I** (Inhibitory; binds to actin), and **C** (binds to Calcium). * **Rigor Mortis:** Occurs because the lack of ATP prevents the detachment of myosin from actin, not because of tropomyosin dysfunction. * **Calcium Source:** In skeletal muscle, calcium comes entirely from the sarcoplasmic reticulum; in cardiac muscle, it requires extracellular calcium entry (Calcium-Induced Calcium Release).

Question 103: Following repolarization, a neuron may become hyperpolarized. How does the membrane potential subsequently return to the resting membrane potential (RMP)?

A. Action of the Na+/K+-ATPase pump
B. Inward leakage of Na+ ions (Correct Answer)
C. Decrease in K+ ion efflux
D. None of the above mechanisms

Explanation: **Explanation:** The return of the membrane potential to the Resting Membrane Potential (RMP) after hyperpolarization is a passive process primarily driven by the **inward leakage of Na+ ions**. 1. **Why Option B is Correct:** During the undershoot (hyperpolarization), the membrane potential is closer to the equilibrium potential of K+ (-94 mV) than the RMP (-70 mV). At this stage, the membrane is highly permeable to K+ but also possesses **non-gated "leak" channels**. Because the electrochemical gradient for Na+ is very high (high concentration outside, negative charge inside), Na+ ions slowly leak into the cell. This influx of positive charge gradually depolarizes the membrane back to its steady-state RMP. 2. **Why Other Options are Incorrect:** * **Option A (Na+/K+-ATPase):** While this pump is essential for maintaining long-term concentration gradients, it is **electrogenic** (pumping 3 Na+ out for 2 K+ in). Its net effect is to make the interior *more* negative. Therefore, it helps maintain or establish RMP but is not the primary mechanism that "pulls" the potential up from a hyperpolarized state. * **Option C (Decrease in K+ efflux):** While the closing of voltage-gated K+ channels stops further hyperpolarization, it does not actively return the potential to RMP; it merely prevents it from getting more negative. **High-Yield NEET-PG Pearls:** * **RMP** is primarily determined by **K+ efflux** through leak channels (K+ permeability is 50–100x higher than Na+ at rest). * **Hyperpolarization** occurs because voltage-gated K+ channels are slow to close. * **The Goldmann-Hodgkin-Katz equation** is used to calculate RMP considering multiple ions, whereas the **Nernst equation** is for a single ion.

Question 104: End plate potential follows which law?

A. All or none law
B. Depolarization (Correct Answer)
C. Hyperpolarization
D. Propagation

Explanation: **Explanation:** The **End Plate Potential (EPP)** is a localized, non-propagated potential change that occurs at the motor end plate of the neuromuscular junction (NMJ). **1. Why Depolarization is Correct:** When an action potential reaches the motor nerve terminal, it triggers the release of Acetylcholine (ACh). ACh binds to nicotinic receptors (nAChR) on the motor end plate, opening ligand-gated cation channels. This leads to a massive influx of **Na⁺ ions** (and a smaller efflux of K⁺), causing the resting membrane potential to shift toward a more positive value. This process is, by definition, **Depolarization**. If the EPP reaches a certain threshold, it triggers a propagated action potential in the muscle fiber. **2. Why other options are incorrect:** * **All or none law:** Unlike an action potential, the EPP is a **graded potential**. Its magnitude depends on the amount of ACh released; it does not follow the all-or-none law. * **Hyperpolarization:** This involves the membrane potential becoming more negative. EPP is excitatory and always involves a shift toward positivity. * **Propagation:** EPP is a **local potential**. It does not travel down the muscle fiber; instead, it triggers an action potential which then propagates. **High-Yield Clinical Pearls for NEET-PG:** * **Miniature End Plate Potential (MEPP):** The smallest possible EPP caused by the spontaneous release of a single vesicle (quantum) of ACh. * **Myasthenia Gravis:** Antibodies against nAChR reduce the amplitude of the EPP, making it difficult to reach the threshold for muscle contraction. * **Lambert-Eaton Syndrome:** Antibodies against voltage-gated Ca²⁺ channels reduce ACh release, also resulting in a decreased EPP. * **Curare:** Competitively inhibits nAChR, decreasing the EPP amplitude and causing paralysis.

Question 105: Site where myosin head bind to actin in skeletal muscle are covered by which of the following?

A. Tropomyosin (Correct Answer)
B. Titin
C. Troponin
D. Tropomodulin

Explanation: ### Explanation **Correct Option: A (Tropomyosin)** In a resting skeletal muscle, the active sites on the **actin filament** (where myosin heads must bind to initiate contraction) are physically blocked by **Tropomyosin**. Tropomyosin is a long, rod-like protein that wraps around the F-actin helix. For contraction to occur, Calcium ions bind to Troponin C, causing a conformational change that pulls Tropomyosin away from the binding sites, allowing the "cross-bridge" formation. **Analysis of Incorrect Options:** * **B. Titin:** This is the largest known protein. It acts as a molecular spring, anchoring the thick (myosin) filaments to the Z-discs, providing elasticity and stabilizing the sarcomere. It does not cover binding sites. * **C. Troponin:** While Troponin is part of the regulatory complex, it is a globular protein consisting of three subunits (I, T, and C). Its role is to *move* the tropomyosin; it does not directly cover the actin binding sites itself. * **D. Tropomodulin:** This is an actin-capping protein found at the minus end of the actin filament. It regulates the length of the thin filaments by preventing the addition or loss of actin monomers. **High-Yield Clinical Pearls for NEET-PG:** * **The Regulatory Complex:** Comprises Tropomyosin and Troponin. * **Troponin Subunits:** * **Troponin T:** Binds to **T**ropomyosin. * **Troponin I:** **I**nhibits the actin-myosin interaction. * **Troponin C:** Binds **C**alcium (initiates the shift). * **Rigor Mortis:** Occurs because ATP is required to *detach* the myosin head from actin. Without ATP, the cross-bridge remains locked. * **Dystrophin:** A structural protein (mutated in Duchenne Muscular Dystrophy) that anchors the cytoskeleton of the muscle fiber to the surrounding extracellular matrix.

Question 106: What is true about generator potential?

A. Graded (Correct Answer)
B. All or none
C. Propagated
D. No summation

Explanation: ### Explanation **Generator Potential** (also known as Receptor Potential) is the non-propagated local electrical response produced in a sensory receptor by a stimulus. **1. Why "Graded" is Correct:** Generator potentials are **graded**, meaning the amplitude of the potential is directly proportional to the intensity of the stimulus. Unlike action potentials, which have a fixed amplitude, a stronger stimulus results in a larger generator potential. Once this potential reaches a specific threshold, it triggers an action potential in the sensory nerve fiber. **2. Why the Other Options are Incorrect:** * **B. All or none:** This law applies to **Action Potentials**, not generator potentials. Generator potentials do not have a threshold for initiation and can vary in size. * **C. Propagated:** Generator potentials are **non-propagated** (local) responses. They spread passively via electrotonic conduction and decay over distance. Only action potentials are propagated along the axon. * **D. No summation:** Generator potentials **can be summated** (both temporally and spatially). If multiple stimuli are applied, the potentials add up to reach the threshold required to fire an action potential. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Usually involves the opening of non-specific cation channels (Na+ influx). * **Refractory Period:** Generator potentials have **no refractory period**, allowing for the summation of signals. * **Example:** The **Pacinian Corpuscle** is the classic model used to study generator potentials. If the first node of Ranvier is blocked (e.g., by local anesthetics), the generator potential still occurs, but the action potential is abolished. * **Key Distinction:** Generator potential = Graded, Local, Summable; Action potential = All-or-none, Propagated, Refractory period present.

Question 107: Involuntary contraction of a single motor unit is known as?

A. Fibrillation
B. Fasciculation (Correct Answer)
C. Tics
D. Spasm

Explanation: ### Explanation **Correct Answer: B. Fasciculation** **Understanding the Concept:** A **fasciculation** is defined as the spontaneous, involuntary contraction of a **single motor unit** (an alpha motor neuron and all the muscle fibers it innervates). Because a whole motor unit is involved, the contraction is often strong enough to be visible as a "flicker" or "twitch" under the skin, but it is usually insufficient to move a joint. Clinically, fasciculations are a hallmark sign of **Lower Motor Neuron (LMN)** lesions, such as Amyotrophic Lateral Sclerosis (ALS) or poliomyelitis. **Analysis of Incorrect Options:** * **A. Fibrillation:** This is the spontaneous contraction of a **single muscle fiber** (not a motor unit). Fibrillations are **not visible** to the naked eye and can only be detected via Electromyography (EMG). They occur due to "denervation hypersensitivity" to acetylcholine. * **C. Tics:** These are coordinated, repetitive, stereotyped movements involving **groups of muscles**. They are usually of psychogenic or basal ganglia origin, rather than a single motor unit pathology. * **D. Spasm:** A broad term for a sudden, involuntary, and often painful contraction of a **whole muscle or muscle group**, typically associated with muscle fatigue, electrolyte imbalances, or upper motor neuron lesions (spasticity). **High-Yield NEET-PG Pearls:** * **Visible vs. Invisible:** Fasciculation = Visible; Fibrillation = Invisible (EMG only). * **LMN Signs:** Fasciculations, fibrillations, hypotonia, hyporeflexia, and muscle atrophy. * **Benign Fasciculations:** These can occur in healthy individuals due to excessive caffeine, stress, or fatigue (e.g., eyelid twitching). * **Denervation Hypersensitivity:** The physiological basis for fibrillations; when a nerve is cut, the muscle fiber increases its synthesis of ACh receptors across the entire sarcolemma.

Question 108: During muscle contraction, ATP is constantly maintained due to which enzyme?

A. Creatinine kinase (Correct Answer)
B. Sodium potassium ATPase
C. Myosin kinase
D. Phosphokinase

Explanation: **Explanation:** The primary source of immediate energy for muscle contraction is ATP. However, the concentration of ATP in skeletal muscle is only sufficient to sustain maximal contraction for 1–2 seconds. To maintain constant ATP levels during activity, the **Phosphagen System** (ATP-CP system) acts as the first-line energy buffer. **1. Why Creatine Kinase (CK) is correct:** Creatine Kinase (also known as Creatine Phosphokinase) catalyzes the reversible transfer of a high-energy phosphate group from **Phosphocreatine (CP)** to ADP, rapidly regenerating ATP: $$ADP + Phosphocreatine \xrightarrow{CK} ATP + Creatine$$ This reaction is the fastest way to replenish ATP during the initial seconds of exercise, ensuring that ATP levels do not drop significantly even when the rate of utilization is high. **2. Why other options are incorrect:** * **Sodium-Potassium ATPase:** This is a membrane pump responsible for maintaining resting membrane potential by pumping $Na^+$ out and $K^+$ into the cell. It *consumes* ATP rather than regenerating it. * **Myosin Kinase (MLCK):** This enzyme is crucial in **smooth muscle contraction**, where it phosphorylates the myosin light chain to initiate cross-bridge cycling. It does not maintain ATP levels. * **Phosphokinase:** This is a generic term for enzymes that catalyze phosphorylation. It is not a specific enzyme responsible for the immediate buffering of ATP in muscles. **High-Yield Clinical Pearls for NEET-PG:** * **Lohmann’s Reaction:** The specific name for the reversible reaction catalyzed by Creatine Kinase. * **CK-MB Isoenzyme:** Elevated in Myocardial Infarction (Heart). * **CK-MM Isoenzyme:** Elevated in Skeletal Muscle injury (e.g., Rhabdomyolysis, Duchenne Muscular Dystrophy). * **Order of Energy Sources:** 1. Preformed ATP $\rightarrow$ 2. Phosphocreatine $\rightarrow$ 3. Anaerobic Glycolysis $\rightarrow$ 4. Oxidative Phosphorylation.

Question 109: Which of the following muscle groups exhibits isometric contraction?

A. Extraocular muscles
B. Small muscles of the hand
C. Abdominal muscles
D. Antigravity muscles (Correct Answer)

Explanation: ### Explanation **Isometric contraction** occurs when muscle tension increases, but the muscle length remains constant and no external work is performed. This is in contrast to **isotonic contraction**, where the muscle length changes while tension remains constant to produce movement. #### Why Antigravity Muscles are Correct: Antigravity muscles (such as the gastrocnemius, quadriceps, and longissimus dorsi) are primarily responsible for maintaining an upright posture against the force of gravity. When standing still, these muscles undergo **isometric contraction** to stabilize joints and support the body's weight without shortening. They provide the necessary tension to prevent the body from collapsing, making them the classic physiological example of isometric activity. #### Why the Other Options are Incorrect: * **A. Extraocular muscles:** These muscles are responsible for the rapid, precise movement of the eyeballs (saccades and tracking). Their primary function is movement, which is a hallmark of **isotonic contraction**. * **B. Small muscles of the hand:** These are involved in fine motor skills, grasping, and manipulation of objects. These actions require the muscles to shorten to move the phalanges, representing **isotonic contraction**. * **C. Abdominal muscles:** While they can act as stabilizers, their primary roles in breathing, trunk flexion, and rotation involve significant changes in muscle length (**isotonic**). #### High-Yield NEET-PG Pearls: * **Work Done:** In isometric contraction, Work ($W = F \times d$) is **zero** because the distance ($d$) is zero. * **Energy Expenditure:** Even though no external work is done, energy is still consumed (released as heat) to maintain tension. * **Muscle Spindles:** Isometric contraction is crucial for the **Static Stretch Reflex**, which helps maintain muscle tone. * **Mixed Contractions:** Most real-world movements (like walking) are a combination of both; however, for exam purposes, "posture maintenance" is the keyword for isometric.

Question 110: All of the following statements regarding electromechanical coupling are true, EXCEPT:

A. In smooth muscle, Ca2+ ions bind to calmodulin.
B. Smooth muscle contraction is initiated by myosin light chain phosphorylation.
C. In cardiac muscle, Ca2+ ions bind to troponin.
D. The major source of Ca2+ ions for contraction of skeletal muscle is influx of Ca2+ ions from the extracellular space following voltage-dependent opening of L-type Ca2+ channels. (Correct Answer)

Explanation: ### Explanation The correct answer is **D** because it describes the mechanism of cardiac muscle, not skeletal muscle. **1. Why Option D is the Correct Answer (The False Statement):** In **skeletal muscle**, the major source of $Ca^{2+}$ is the **Sarcoplasmic Reticulum (SR)**, not the extracellular space. The process involves a **mechanical coupling** between the L-type $Ca^{2+}$ channels (Dihydropyridine receptors - DHPR) on the T-tubule and the Ryanodine receptors (RyR1) on the SR. When the T-tubule depolarizes, DHPR undergoes a conformational change that physically "plucks" the RyR1 open, releasing $Ca^{2+}$ from internal stores. Skeletal muscle can contract even in a $Ca^{2+}$-free extracellular medium. **2. Analysis of Other Options:** * **Option A & B (Smooth Muscle):** Smooth muscle lacks troponin. Instead, $Ca^{2+}$ binds to **Calmodulin**. This complex activates **Myosin Light Chain Kinase (MLCK)**, which phosphorylates the myosin light chain, allowing cross-bridge cycling. * **Option C (Cardiac Muscle):** Like skeletal muscle, cardiac muscle uses the troponin-tropomyosin complex. However, unlike skeletal muscle, it relies on **Calcium-Induced Calcium Release (CICR)**, where extracellular $Ca^{2+}$ influx through L-type channels is essential to trigger SR $Ca^{2+}$ release. **3. High-Yield Clinical Pearls for NEET-PG:** * **Ryanodine Receptor Isoforms:** RyR1 is found in skeletal muscle; RyR2 is found in cardiac muscle. * **Malignant Hyperthermia:** Caused by a mutation in the **RyR1 gene**, leading to excessive $Ca^{2+}$ release upon exposure to volatile anesthetics (e.g., Halothane). * **Phospholamban:** A protein in cardiac muscle that inhibits SERCA (the pump that sequester $Ca^{2+}$ back into the SR). Phosphorylation of phospholamban (via sympathetic stimulation) removes this inhibition, increasing the rate of relaxation (**lusitropy**).

Practice by Chapter

Resting Membrane Potential

Practice Questions

Action Potential Generation and Propagation

Practice Questions

Neuromuscular Junction

Practice Questions

Skeletal Muscle Contraction

Practice Questions

Smooth Muscle Physiology

Practice Questions

Cardiac Muscle Properties

Practice Questions

Muscle Metabolism and Fatigue

Practice Questions

Motor Unit Function

Practice Questions

Neurotransmitters and Receptors

Practice Questions

Electrophysiological Measurements

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free