Nerve and Muscle Physiology Practice Questions

Q: Which nerve fiber type is most susceptible to hypoxia?

B. 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.

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

Inward leakage of Na+ ions. **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.

Q: End plate potential follows which law?

Depolarization. **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.

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

Tropomyosin. ### 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.

Q: What is true about generator potential?

Graded. ### 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.

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

Fasciculation. ### 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.

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

Creatinine kinase. **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 1

Which nerve fiber type is most susceptible to hypoxia?

Accepted Answer

B

Answer

Aa

Answer

Ab

Answer

C

Question 2

What is the primary function of tropomyosin in muscle contraction?

Accepted Answer

To block the binding sites on actin, preventing myosin attachment.

Answer

To assist in the fusion of actin and myosin filaments.

Answer

To slide along the myosin filament during muscle contraction.

Answer

To trigger the release of calcium ions from the sarcoplasmic reticulum.

Question 3

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

Accepted Answer

Inward leakage of Na+ ions

Answer

Action of the Na+/K+-ATPase pump

Answer

Decrease in K+ ion efflux

Answer

None of the above mechanisms

Question 4

End plate potential follows which law?

Accepted Answer

Depolarization

Answer

All or none law

Answer

Hyperpolarization

Answer

Propagation

Question 5

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

Accepted Answer

Tropomyosin

Answer

Titin

Answer

Troponin

Answer

Tropomodulin

Question 6

What is true about generator potential?

Accepted Answer

Graded

Answer

All or none

Answer

Propagated

Answer

No summation

Question 7

Involuntary contraction of a single motor unit is known as?

Accepted Answer

Fasciculation

Answer

Fibrillation

Answer

Tics

Answer

Spasm

Question 8

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

Accepted Answer

Creatinine kinase

Answer

Sodium potassium ATPase

Answer

Myosin kinase

Answer

Phosphokinase

Question 9

Which of the following muscle groups exhibits isometric contraction?

Accepted Answer

Antigravity muscles

Answer

Extraocular muscles

Answer

Small muscles of the hand

Answer

Abdominal muscles

Question 10

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

Accepted Answer

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.

Answer

In smooth muscle, Ca2+ ions bind to calmodulin.

Answer

Smooth muscle contraction is initiated by myosin light chain phosphorylation.

Answer

In cardiac muscle, Ca2+ ions bind to troponin.

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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