Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs

Question 171: Two electrodes are placed 4.5 cm apart. It takes 1.5 ms for current to propagate along the nerve from one electrode to the other. What is the velocity of nerve conduction?

A. 60 m/s
B. 30 m/s (Correct Answer)
C. 45 m/s
D. 80 m/s

Explanation: ### Explanation **1. Understanding the Calculation (Why B is Correct)** Nerve conduction velocity (NCV) is defined as the speed at which an electrochemical impulse propagates down a neural pathway. It is calculated using the basic physics formula for velocity: $$\text{Velocity} = \frac{\text{Distance}}{\text{Time}}$$ * **Step 1 (Unit Conversion):** To get the answer in meters per second (m/s), convert the given values to SI units. * Distance = $4.5\text{ cm} = 0.045\text{ meters}$ * Time = $1.5\text{ ms} = 0.0015\text{ seconds}$ * **Step 2 (Calculation):** $$\text{Velocity} = \frac{0.045\text{ m}}{0.0015\text{ s}} = \frac{45}{1.5} = \mathbf{30\text{ m/s}}$$ **2. Analysis of Incorrect Options** * **Option A (60 m/s):** This would be the result if the time taken was 0.75 ms. While 60 m/s is a typical velocity for large myelinated A-alpha fibers, it does not fit the provided data. * **Option C (45 m/s):** This is a distractor likely chosen because the distance provided is 4.5 cm. It represents a calculation error where units or time were not properly factored. * **Option D (80 m/s):** This represents the upper limit of conduction in the fastest human nerve fibers (A-alpha), but mathematically incorrect for this specific scenario. **3. Clinical Pearls for NEET-PG** * **Fiber Type & Speed:** Conduction velocity is directly proportional to **fiber diameter** and the presence of **myelin**. * **A-alpha fibers:** Fastest (70–120 m/s), responsible for proprioception and somatic motor. * **C fibers:** Slowest (<2 m/s), unmyelinated, responsible for slow pain and temperature. * **Clinical Correlation:** NCV studies are used to differentiate between **demyelinating diseases** (where velocity significantly decreases, e.g., Guillain-Barré Syndrome) and **axonal degeneration** (where velocity may remain normal but the amplitude of the action potential decreases). * **Temperature:** A decrease in body temperature slows down nerve conduction velocity.

Question 172: Fine, irregular contraction of individual muscle fibers is called:

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

Explanation: ### Explanation **Correct Answer: B. Fibrillation** **Fibrillation** refers to the spontaneous, independent contraction of **individual muscle fibers**. These contractions occur due to denervation hypersensitivity, where the muscle fiber becomes overly sensitive to circulating acetylcholine after losing its nerve supply. * **Key Feature:** Because these are single-fiber contractions, they are **not visible** to the naked eye through the skin. They can only be detected via Electromyography (EMG). **Analysis of Incorrect Options:** * **A. Fasciculations:** These are spontaneous contractions of a **motor unit** (a group of muscle fibers supplied by one motor neuron). Unlike fibrillations, fasciculations are **visible** as flickers under the skin. They are common in Lower Motor Neuron (LMN) lesions like Amyotrophic Lateral Sclerosis (ALS). * **C. Tics:** These are coordinated, repetitive, stereotyped movements involving groups of muscles (e.g., eye blinking). They are often psychogenic or related to basal ganglia dysfunction, rather than individual fiber pathology. * **D. Spasm:** A broad term for sudden, involuntary, and often painful contractions of an **entire muscle** or group of muscles. **High-Yield Clinical Pearls for NEET-PG:** * **EMG Findings:** Fibrillations and positive sharp waves on EMG are hallmark signs of **active axonal degeneration** (denervation). * **LMN vs. UMN:** Both fibrillations and fasciculations are classic signs of **Lower Motor Neuron (LMN)** lesions. * **The "Visibility" Rule:** If you can see it, it’s a fasciculation; if you can only see it on an EMG, it’s a fibrillation. * **Denervation Hypersensitivity:** This is the physiological basis for fibrillation, where the entire sarcolemma develops acetylcholine receptors (upregulation) following the loss of the neuromuscular junction.

Question 173: The action of acetylcholine at the neuromuscular junction is terminated primarily by?

A. Diffusion into the surrounding extracellular fluid
B. Uptake into the nerve ending
C. Uptake into the muscle
D. Enzymatic breakdown by acetylcholinesterase (Correct Answer)

Explanation: ### Explanation **1. Why Option D is Correct:** The primary mechanism for terminating the action of Acetylcholine (ACh) at the neuromuscular junction (NMJ) is **rapid enzymatic hydrolysis**. The enzyme **Acetylcholinesterase (AChE)** is concentrated in the synaptic cleft, specifically within the basal lamina. It breaks down ACh into **Choline and Acetate**. This process is incredibly efficient (one of the fastest enzymatic reactions in the body), ensuring that the muscle fiber can be repolarized quickly to respond to subsequent nerve impulses. **2. Why Other Options are Incorrect:** * **Option A (Diffusion):** While a small amount of ACh may diffuse away from the cleft, it is a minor contributor compared to the rapid enzymatic destruction. * **Option B (Uptake into nerve ending):** Unlike other neurotransmitters (like Norepinephrine or Serotonin), **ACh itself is not reuptaken**. Only the byproduct **Choline** is transported back into the presynaptic terminal via a Na⁺-choline symporter to synthesize new ACh. * **Option C (Uptake into muscle):** Muscle cells do not possess transport mechanisms to "uptake" intact ACh molecules. **3. NEET-PG High-Yield Clinical Pearls:** * **Myasthenia Gravis:** Caused by antibodies against post-synaptic ACh receptors. It is treated with **AChE inhibitors** (e.g., Neostigmine, Pyridostigmine) to increase the concentration and duration of ACh in the cleft. * **Organophosphate Poisoning:** These compounds irreversibly inhibit AChE, leading to a "cholinergic crisis" (SLUDGE syndrome) due to persistent ACh action. * **Pseudocholinesterase (Butyrylcholinesterase):** Found in the plasma (not the NMJ). It is responsible for the metabolism of drugs like **Succinylcholine**. Deficiency leads to prolonged apnea after anesthesia. * **Hemicholinium:** A drug that blocks the reuptake of Choline into the nerve terminal, depleting ACh stores.

Question 174: What is the nerve impulse that initiates muscle contraction?

A. It causes the opening of calcium channels, leading to an increase in calcium ion concentration within the sarcomere. (Correct Answer)
B. It causes both the plasma membrane and the T-tubules to undergo hyperpolarization.
C. It inhibits sodium entry into the sarcomere.
D. It is inhibited by the binding of acetylcholine to receptors in the sarcoplasmic reticulum.

Explanation: ### Explanation **1. Why Option A is Correct: Excitation-Contraction (E-C) Coupling** The nerve impulse (action potential) reaches the neuromuscular junction, triggering the release of Acetylcholine (ACh). ACh binds to nicotinic receptors on the motor endplate, causing depolarization that spreads along the sarcolemma and into the **T-tubules**. This depolarization activates voltage-gated L-type calcium channels (**DHP receptors**), which are mechanically linked to **Ryanodine receptors (RyR1)** on the sarcoplasmic reticulum (SR). This triggers the release of $Ca^{2+}$ into the sarcoplasm (sarcomere). The increase in cytosolic $Ca^{2+}$ allows it to bind to **Troponin C**, shifting tropomyosin and exposing actin-binding sites for myosin, thus initiating contraction. **2. Why the Other Options are Incorrect:** * **Option B:** The nerve impulse causes **depolarization** (making the membrane potential more positive), not hyperpolarization. Hyperpolarization would inhibit muscle contraction. * **Option C:** The impulse actually **promotes sodium entry** through nicotinic ACh-gated channels and voltage-gated $Na^+$ channels to propagate the action potential. * **Option D:** ACh receptors (nACHR) are located on the **sarcolemma (motor endplate)**, not the sarcoplasmic reticulum. Furthermore, ACh binding *initiates* the impulse rather than inhibiting it. **3. NEET-PG High-Yield Pearls:** * **DHP Receptor:** Acts as a voltage sensor in the T-tubule. * **Ryanodine Receptor (RyR1):** The calcium release channel in the SR. * **Malignant Hyperthermia:** Caused by a mutation in the *RYR1* gene, leading to excessive $Ca^{2+}$ release upon exposure to succinylcholine or volatile anesthetics. * **SERCA Pump:** Responsible for muscle relaxation by sequestering $Ca^{2+}$ back into the SR. * **Calsequestrin:** A protein within the SR that binds $Ca^{2+}$, allowing high-capacity storage.

Question 175: Which of the following statements about changes in articular cartilage with aging is NOT true?

A. Total proteoglycan content is decreased
B. Synthesis of proteoglycans is decreased
C. Enzymatic degradation of proteoglycans is increased (Correct Answer)
D. Total water content of cartilage is decreased

Explanation: ### Explanation The aging process of articular cartilage involves complex biochemical alterations in the extracellular matrix (ECM), primarily affecting proteoglycans and hydration. **Why Option C is the Correct Answer (The "False" Statement):** In normal aging (senescence), the **enzymatic degradation of proteoglycans does not increase**. Instead, the primary issue is a **decline in the synthetic capacity** of chondrocytes and the formation of smaller, less uniform proteoglycan aggregates. Increased enzymatic degradation (via matrix metalloproteinases or ADAMTS) is a hallmark of **Osteoarthritis (pathological change)**, not physiological aging. **Analysis of Other Options:** * **A & B (Proteoglycan Content/Synthesis):** With age, chondrocytes become less responsive to growth factors (like IGF-1). This leads to a **decrease in the total proteoglycan content** and a significant **reduction in the synthesis** of glycosaminoglycans (GAGs). Specifically, the ratio of chondroitin sulfate to keratan sulfate shifts, and the size of aggrecan molecules decreases. * **D (Water Content):** Contrary to popular belief, while the cartilage may appear "swollen" in early osteoarthritis, in **normal physiological aging**, the **total water content of the cartilage decreases**. This is due to the loss of proteoglycans, which are responsible for the osmotic pressure that retains water in the matrix. **High-Yield NEET-PG Pearls:** * **Advanced Glycation End-products (AGEs):** Aging cartilage shows an accumulation of AGEs, which cross-link collagen fibers, making the cartilage stiffer and more brittle. * **Chondrocyte Changes:** Aging leads to chondrocyte **telomere shortening** and "senescence-associated secretory phenotype" (SASP). * **Water Content Rule:** Water content **decreases** in aging but **increases** in early Osteoarthritis (due to collagen network damage allowing the matrix to swell). * **Most common GAG change:** Decrease in Chondroitin Sulfate and increase in Keratan Sulfate.

Question 176: When energy is derived from creatine phosphate to cause muscle contraction, what is the first step in this transfer of energy?

A. The creatine phosphate transfers its energy to the cross bridges to cause them to become locked
B. The creatine phosphate causes the power stroke of the cross bridges
C. The creatine phosphate transfers its energy to the actin filament
D. The energy of the creatine phosphate is used to convert ADP to ATP (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer is Right:** The primary source of energy for muscle contraction is **Adenosine Triphosphate (ATP)**. However, the amount of ATP stored in the muscle is extremely limited (enough for only 1–2 seconds of contraction). To sustain activity, the muscle utilizes **Creatine Phosphate (Phosphocreatine)** as a rapid energy buffer. The first step in this process is a chemical reaction catalyzed by the enzyme **Creatine Kinase (CK)**. Creatine phosphate contains a high-energy phosphate bond. It transfers this phosphate group directly to **ADP (Adenosine Diphosphate)** to reconstitute **ATP**. This ATP then binds to the myosin head to provide the energy required for the cross-bridge cycle. Therefore, creatine phosphate does not act on the filaments directly; its sole immediate role is the "recharging" of ADP into ATP. **2. Why the Incorrect Options are Wrong:** * **Options A & B:** Creatine phosphate does not interact with cross-bridges. The "locking" (rigor complex) and the "power stroke" are mediated by the binding and hydrolysis of **ATP**, not creatine phosphate. * **Option C:** The actin filament is a structural protein. Energy is utilized by the **myosin head** (which has ATPase activity), not the actin filament itself. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Lohmann’s Reaction:** The reversible transfer of phosphate from creatine phosphate to ADP is known as the Lohmann’s reaction. * **Temporal Buffer:** Creatine phosphate is considered a "temporal energy buffer" because it maintains ATP levels during the initial 5–8 seconds of maximal muscle exertion. * **Creatine Kinase (CK):** In clinical practice, elevated serum levels of CK (specifically the CK-MM isoenzyme) are markers of muscle damage, such as in rhabdomyolysis or muscular dystrophy. * **Sequence of Energy Sources:** 1. Stored ATP $\rightarrow$ 2. Creatine Phosphate $\rightarrow$ 3. Anaerobic Glycolysis $\rightarrow$ 4. Aerobic Metabolism (Oxidative Phosphorylation).

Question 177: Actin's active site is covered by

A. Myosin
B. Tropomyosin (Correct Answer)
C. Troponin
D. Desmin

Explanation: **Explanation:** In a resting muscle fiber, the interaction between actin and myosin is prevented to allow for relaxation. The **active sites (myosin-binding sites)** on the actin filament are physically masked by **Tropomyosin**, a long, rod-shaped protein that wraps around the actin helix. 1. **Why Tropomyosin is correct:** Tropomyosin lies in the grooves of the actin filament. In the relaxed state, it covers the active sites, preventing the myosin heads from forming cross-bridges. For contraction to occur, Calcium binds to Troponin C, causing a conformational change that pulls Tropomyosin away from these sites, exposing them for myosin binding. 2. **Why other options are incorrect:** * **Myosin:** This is the thick filament that *binds* to the active site on actin during contraction; it does not cover it. * **Troponin:** This is a complex of three subunits (I, T, and C) attached to tropomyosin. While it *regulates* the position of tropomyosin, it is tropomyosin itself that physically covers the active site. * **Desmin:** This is an intermediate filament that helps maintain the structural integrity of the sarcomere by linking Z-discs; it plays no direct role in masking active sites. **High-Yield NEET-PG Pearls:** * **Troponin I:** Inhibits the actin-myosin interaction. * **Troponin T:** Tethers the troponin complex to Tropomyosin. * **Troponin C:** Binds to Calcium (4 binding sites). * **The "Power Stroke":** Occurs when ADP and Pi are released from the myosin head, causing it to tilt. * **Rigor Mortis:** Occurs due to the lack of ATP, which is required to *detach* the myosin head from the actin active site.

Question 178: Energy in muscles is stored as:

A. ATP
B. ADP
C. Phosphocreatine (Correct Answer)
D. None of the above

Explanation: **Explanation:** The primary form of energy **storage** in skeletal muscle is **Phosphocreatine (Creatine Phosphate)**. While ATP is the direct source of energy for muscle contraction, its concentration within the muscle cell is very low—sufficient only to sustain maximal contraction for about 1 to 2 seconds. To maintain activity, muscles store high-energy phosphate bonds in the form of Phosphocreatine, which is present at concentrations **5 to 6 times higher than ATP**. * **Why Phosphocreatine is correct:** It acts as a "buffer" or a reservoir of high-energy phosphate. When ATP is hydrolyzed to ADP during contraction, the enzyme **Creatine Kinase (CK)** rapidly transfers a phosphate group from Phosphocreatine back to ADP to reconstitute ATP. This system (the Phosphagen system) provides energy for short bursts of maximal effort (approx. 5–8 seconds). * **Why ATP is incorrect:** ATP is the immediate energy *currency*, not the storage form. Because ATP is a potent allosteric effector of many enzymes, storing it in high concentrations would disrupt cellular metabolism. * **Why ADP is incorrect:** ADP is a metabolic byproduct of energy utilization. High levels of ADP signal a low-energy state in the cell and trigger pathways like glycolysis to produce more ATP. **High-Yield Clinical Pearls for NEET-PG:** 1. **Lohmann’s Reaction:** The reversible transfer of phosphate between creatine and ATP catalyzed by Creatine Kinase. 2. **Creatinine:** A waste product formed by the non-enzymatic breakdown of phosphocreatine. Its excretion rate is relatively constant and proportional to total muscle mass. 3. **Order of Energy Source Utilization:** ATP (1-2s) → Phosphocreatine (5-8s) → Muscle Glycogen (Anaerobic glycolysis) → Oxidative phosphorylation.

Question 179: Active tension in a muscle depends upon which of the following factors?

A. Number of muscle fibers
B. Number of motor units recruited (Correct Answer)
C. Aerobic capacity of the muscle
D. Length of the muscle fiber

Explanation: ### Explanation **1. Why the Correct Answer is Right:** Active tension is the force generated by the contraction of the contractile elements (actin and myosin cross-bridges) of a muscle. According to the **Size Principle (Henneman's Principle)**, the total force or tension produced by a muscle is primarily regulated by **motor unit recruitment**. As the requirement for force increases, the CNS recruits more motor units. Since a motor unit consists of a single motor neuron and all the muscle fibers it innervates, increasing the number of active motor units directly increases the number of cross-bridges cycling, thereby increasing the active tension. **2. Why the Other Options are Incorrect:** * **Option A (Number of muscle fibers):** While the total number of fibers determines the *potential* maximum strength of a muscle (anatomical factor), it does not regulate the active tension generated during a specific functional contraction. * **Option C (Aerobic capacity):** This determines the **endurance** and resistance to fatigue of a muscle, not the immediate generation of active tension. * **Option D (Length of the muscle fiber):** This is a distractor. While the *initial* length of the fiber (Preload) affects the *total* tension (Frank-Starling law equivalent in muscle), the **active** tension specifically depends on the degree of actin-myosin overlap. However, in the context of physiological control of graded muscle contraction, recruitment is the primary regulatory mechanism. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Total Tension = Active Tension + Passive Tension.** Passive tension is due to the stretching of elastic elements (like titin and connective tissue). * **Henneman’s Size Principle:** Small, fatigue-resistant motor units (Type I) are recruited first, followed by larger, powerful units (Type II). * **Frequency Summation (Tetany):** Apart from recruitment, the force of contraction can also be increased by increasing the frequency of action potentials. * **Optimal Length ($L_0$):** Active tension is maximal when the muscle is at its resting length (approx. 2.0–2.2 $\mu$m sarcomere length), where actin-myosin overlap is maximal.

Question 180: Which of the following muscle fiber types is brown in color?

A. Type I
B. Type II A (Correct Answer)
C. Type II B
D. Type III

Explanation: **Explanation:** The classification of skeletal muscle fibers is based on their metabolic profile, contraction speed, and myoglobin content. **Type IIA fibers (Fast-twitch oxidative-glycolytic)** are known as **"Brown fibers"** or "Intermediate fibers." They occupy a middle ground between Type I and Type IIB. They contain a high concentration of myoglobin and mitochondria (similar to Type I) but also possess high glycolytic capacity. The combination of high myoglobin content and specific enzymatic activity gives them a distinct brownish appearance under certain staining conditions. **Analysis of Incorrect Options:** * **Option A: Type I (Slow-twitch):** These are known as **"Red fibers."** They have the highest myoglobin content and mitochondrial density, specialized for endurance and aerobic metabolism. * **Option C: Type IIB (Fast-twitch glycolytic):** These are known as **"White fibers."** They have low myoglobin and mitochondrial content, relying primarily on anaerobic glycolysis for short bursts of power. * **Option D: Type III:** This is a **distractor.** In standard mammalian skeletal muscle classification, fibers are categorized into Types I, IIA, IIB, and sometimes IID/X. Type III is not a recognized skeletal muscle fiber type in this context. **High-Yield NEET-PG Pearls:** * **Mnemonic for Type I:** **"One Slow Red Ox"** (Type **I**, **Slow**-twitch, **Red** color, **Ox**idative metabolism). * **Fatigability:** Type I is fatigue-resistant; Type IIA is relatively resistant; Type IIB fatigues rapidly. * **Myosin ATPase activity:** Low in Type I, High in Type II. * **Order of Recruitment (Henneman’s Size Principle):** Type I fibers are recruited first, followed by Type IIA, and finally Type IIB for maximal force.

Practice by Chapter

Resting Membrane Potential

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Action Potential Generation and Propagation

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Neuromuscular Junction

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Skeletal Muscle Contraction

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Smooth Muscle Physiology

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Cardiac Muscle Properties

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Muscle Metabolism and Fatigue

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Motor Unit Function

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Neurotransmitters and Receptors

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Electrophysiological Measurements

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