Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs

Question 271: In muscle cells, resting membrane potential is equal to the isoelectric potential of which ion?

A. Na+
B. Cl-
C. K+ (Correct Answer)
D. Mg++

Explanation: **Explanation:** The Resting Membrane Potential (RMP) of a skeletal muscle cell is typically around **-90 mV**. This value is determined by the permeability of the cell membrane to specific ions and their respective concentration gradients. **Why K+ is correct:** According to the **Nernst Equation**, the equilibrium potential (isoelectric potential) for Potassium (**K+**) is approximately **-94 mV**. In a resting state, the muscle cell membrane is highly permeable to K+ due to the presence of "leak channels," while it remains relatively impermeable to other ions like Na+. Because K+ is the most permeable ion, it exerts the greatest influence on the RMP, pulling the membrane potential very close to its own equilibrium potential (-94 mV vs -90 mV). **Why other options are incorrect:** * **Na+ (Sodium):** The equilibrium potential for Na+ is approximately **+60 mV**. If the RMP were equal to Na+, the cell would be in a state of permanent depolarization. * **Cl- (Chloride):** While Cl- has an equilibrium potential close to the RMP in some cells (-70 to -80 mV), it is not the primary determinant of RMP in muscle cells; K+ conductance is the dominant factor. * **Mg++ (Magnesium):** Magnesium is primarily an intracellular divalent cation that acts as a cofactor for enzymatic reactions (like ATP-Mg complexes) but does not significantly contribute to the setting of the RMP. **High-Yield Clinical Pearls for NEET-PG:** * **Goldman-Hodgkin-Katz (GHK) Equation:** Unlike the Nernst equation (which looks at one ion), the GHK equation calculates RMP by considering the permeability of all ions (Na+, K+, and Cl-). * **Na+-K+ ATPase:** This pump maintains the concentration gradient (3 Na+ out/2 K+ in) but only contributes about -5 to -10 mV directly to the RMP (electrogenic effect). * **Hyperkalemia:** An increase in extracellular K+ decreases the concentration gradient, making the RMP less negative (closer to threshold), which increases excitability initially but eventually leads to inactivation of Na+ channels.

Question 272: After the application of one stimulus, the time period during which a second, stronger stimulus can evoke an impulse is called?

A. Absolute refractory period
B. Relative refractory period (Correct Answer)
C. Latent period
D. Local response

Explanation: ### Explanation **Correct Answer: B. Relative Refractory Period** The **Relative Refractory Period (RRP)** is the interval following the Absolute Refractory Period during which a second action potential can be generated, but only if the stimulus is **stronger than the initial threshold stimulus**. * **Mechanism:** During this phase, voltage-gated $Na^+$ channels have begun to recover from their inactivated state (transitioning back to the closed/resting state), and $K^+$ channels are wide open (causing hyperpolarization). Because the membrane is further from the threshold and some $Na^+$ channels are still inactive, a suprathreshold stimulus is required to trigger a response. **Why other options are incorrect:** * **A. Absolute Refractory Period (ARP):** This is the period from the start of the upstroke until roughly one-third of repolarization. During this time, **no stimulus**, regardless of strength, can excite the nerve because $Na^+$ channels are either already open or in an inactivated state. * **C. Latent Period:** This is the time delay between the application of a stimulus and the first measurable response (e.g., the time between nerve stimulation and muscle contraction). * **D. Local Response:** This refers to a non-propagated, graded potential (sub-threshold) that does not obey the "All-or-None" law. **High-Yield NEET-PG Pearls:** * **ARP** determines the **maximum frequency** of impulse discharge in a neuron. * The ARP corresponds to the period from the firing level until repolarization is about **one-third complete**. * In **cardiac muscle**, the refractory period is significantly longer than in skeletal muscle, which prevents **tetanization** of the heart. * **Accommodation:** If a nerve is subjected to a slowly increasing constant current, the threshold rises; this is due to the inactivation of $Na^+$ channels during the slow depolarization.

Question 273: A 17-year-old soccer player suffered a fracture to the left tibia. After his lower leg has been in a cast for 8 weeks, he found that the left gastrocnemius muscle is significantly smaller in circumference than it was before the fracture. What is the most likely explanation?

A. Decrease in the number of individual muscle fibers in the muscle.
B. Decrease in blood flow to the muscle caused by constriction from the cast.
C. Temporary reduction in actin and myosin protein synthesis. (Correct Answer)
D. Progressive denervation.

Explanation: ### Explanation The clinical scenario describes **Disuse Atrophy**. When a muscle is immobilized (e.g., in a cast), it is not subjected to regular mechanical stress or contraction, leading to a decrease in muscle mass. **1. Why Option C is Correct:** Muscle mass is maintained by a delicate balance between protein synthesis and protein degradation. In disuse atrophy, there is a **downregulation of protein synthesis** (specifically contractile proteins like **actin and myosin**) and an upregulation of the **Ubiquitin-proteasome pathway**, which increases protein degradation. This results in a decrease in the diameter of individual muscle fibers (decreased myofibrils), leading to a reduction in the overall muscle circumference. **2. Why the Other Options are Incorrect:** * **Option A:** Atrophy involves a decrease in the **size/diameter** of existing muscle fibers, not a decrease in the *number* of fibers (hypoplasia). The number of fibers remains relatively constant. * **Option B:** While a cast could theoretically cause ischemia if too tight (Compartment Syndrome), chronic reduction in blood flow would cause necrosis or Volkmann’s ischemic contracture, not simple disuse atrophy. * **Option D:** Denervation atrophy occurs when the nerve supply is severed (e.g., trauma to the peroneal nerve). In this case, the atrophy is due to immobilization (disuse), not a loss of nerve continuity. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Disuse atrophy primarily affects **Type I (Slow-twitch) fibers** more rapidly than Type II fibers. * **Molecular Marker:** **MuRF-1** (Muscle Ring Finger-1) is a muscle-specific ubiquitin ligase often upregulated during atrophy. * **Hypertrophy vs. Hyperplasia:** Muscle growth (hypertrophy) in adults occurs by increasing the number of actin/myosin filaments and sarcoplasm within a fiber, not by creating new cells. * **Reversibility:** Unlike denervation atrophy (which can become permanent with fibrosis), disuse atrophy is generally reversible with physical therapy and weight-bearing exercises.

Question 274: The length of a muscle at which tension is maximum is called:

A. Active length
B. Resting length
C. Optimal length (Correct Answer)
D. Maximal length

Explanation: ### Explanation The correct answer is **Optimal length ($L_0$)**. **1. Why Optimal Length is Correct:** In muscle physiology, the **Length-Tension Relationship** dictates that the force a muscle can generate depends on the degree of overlap between actin and myosin filaments. At the **Optimal Length ($L_0$)**, there is a maximum number of cross-bridge formations between actin and myosin. * If the muscle is too short, filaments overlap and interfere with each other. * If the muscle is too stretched, fewer cross-bridges can form. Therefore, the **Total Tension** (the sum of active and passive tension) reaches its peak when the muscle is at this specific length, which in humans is usually close to the normal resting length of the muscle in the body. **2. Why Other Options are Incorrect:** * **Active length:** This is not a standard physiological term. "Active tension" refers to the force generated by the contractile elements, but the length itself is not called active length. * **Resting length:** While the optimal length often coincides with the resting length in vivo, they are not synonymous. Resting length refers to the length of the muscle when it is not contracted and attached to bones, whereas optimal length is a functional definition based on maximum tension. * **Maximal length:** This refers to the muscle being stretched to its limit. At maximal length, active tension drops to zero because actin and myosin filaments no longer overlap. **3. NEET-PG High-Yield Pearls:** * **Starling’s Law of the Heart** is a clinical application of this concept: increased stretching of cardiac muscle (within physiological limits) leads to increased force of contraction. * **Passive Tension:** This is the tension developed by stretching the non-contractile components (like collagen and titin) without electrical stimulation. It increases exponentially as the muscle is stretched beyond its resting length. * **Titin:** The protein responsible for the passive elasticity of muscles.

Question 275: After an injury to an axon, the subsequent degeneration of all axonal fibres distal to the injury, with all fibres proximal to the injury remaining unaffected, is known as which type of degeneration?

A. Retrograde degeneration.
B. Wallerian degeneration. (Correct Answer)
C. Transneuronal degeneration.
D. None of the above.

Explanation: **Explanation:** **Wallerian Degeneration (Orthograde Degeneration)** refers to the pathological changes that occur in the **distal segment** of an axon following a traumatic injury or transection. Since the distal portion is separated from the neuronal cell body (the metabolic center), it loses its supply of essential proteins and nutrients. This leads to the disintegration of the axon and the breakdown of the myelin sheath, which are subsequently cleared by macrophages and Schwann cells. **Analysis of Incorrect Options:** * **Retrograde Degeneration:** This refers to pathological changes occurring **proximal** to the site of injury (towards the cell body). It involves the breakdown of the axon up to the first node of Ranvier and characteristic changes in the cell body known as *chromatolysis* (swelling of the cell body and displacement of the nucleus). * **Transneuronal Degeneration:** This occurs when the death of one neuron leads to the degeneration of another neuron with which it synapses. It can be anterograde (affecting the postsynaptic neuron) or retrograde (affecting the presynaptic neuron). **High-Yield NEET-PG Pearls:** * **Chromatolysis:** The hallmark of retrograde degeneration in the cell body; involves the disappearance of Nissl granules (RER). * **Regeneration:** In the Peripheral Nervous System (PNS), Schwann cells form **Bungner bands**, which act as physical guides for regenerating axonal sprouts. * **Rate of Growth:** Regenerating nerve fibers typically grow at a rate of **1–4 mm/day**. * **Blood-Brain Barrier:** Wallerian degeneration is slower in the CNS compared to the PNS because oligodendrocytes do not provide the same growth-promoting environment as Schwann cells.

Question 276: Which of the following statements regarding skeletal and cardiac muscle is false?

A. Both require calcium for excitation-contraction coupling.
B. The excitation-contraction coupling of skeletal muscle is independent of extracellular calcium.
C. Both have graded contractions. (Correct Answer)
D. A plateau phase is seen in the action potential of cardiac muscle.

Explanation: ### Explanation The correct answer is **C**, as the statement "Both have graded contractions" is false. **1. Why Option C is False (The Correct Answer):** Skeletal muscle fibers follow the **"All-or-None Law"** at the cellular level. However, the muscle as a whole can produce graded contractions through motor unit recruitment and frequency summation. In contrast, **cardiac muscle** functions as a **functional syncytium** due to gap junctions in intercalated discs. When one cell is excited, the entire myocardium contracts as a single unit. Therefore, cardiac muscle cannot recruit additional motor units; it follows the all-or-none law for the entire organ, making "graded contractions" (in the sense of recruitment) impossible for the heart. **2. Analysis of Incorrect Options:** * **Option A:** Both muscles require calcium to bind to **Troponin C**, which moves tropomyosin and allows actin-myosin cross-bridge formation. * **Option B:** In skeletal muscle, the Dihydropyridine (DHP) receptor acts as a voltage sensor physically coupled to the Ryanodine receptor (RyR1). It triggers calcium release from the Sarcoplasmic Reticulum (SR) without needing extracellular calcium influx. Thus, it is independent of extracellular $Ca^{2+}$. * **Option D:** Cardiac muscle has a prolonged **Plateau Phase (Phase 2)** caused by the opening of L-type $Ca^{2+}$ channels, which prevents tetany and allows for adequate ventricular filling. **High-Yield NEET-PG Pearls:** * **Trigger for $Ca^{2+}$ release:** In skeletal muscle, it is **Voltage-gated** (electromechanical coupling). In cardiac muscle, it is **Calcium-Induced Calcium Release (CICR)** via RyR2. * **Refractory Period:** Cardiac muscle has a very long absolute refractory period (250ms), making it **impossible to tetanize**, unlike skeletal muscle. * **Source of $Ca^{2+}$:** Skeletal muscle relies 100% on the SR; Cardiac muscle relies on both the SR and extracellular fluid (ECF).

Question 277: Which of the following decreases in length during the contraction of a skeletal muscle fiber?

A. A band of the sarcomere
B. I band of the sarcomere (Correct Answer)
C. Thick filaments
D. Thin filaments

Explanation: ### Explanation The mechanism of skeletal muscle contraction is best explained by the **Sliding Filament Theory**. According to this theory, muscle contraction occurs when thin (actin) filaments slide over thick (myosin) filaments, pulling the Z-lines closer together. #### Why the Correct Answer is Right: * **I band (Isotropic band):** This region contains only thin filaments. During contraction, as the thin filaments slide toward the center of the sarcomere (H-zone), the distance between the thick filaments of adjacent sarcomeres decreases. Consequently, the **I band shortens** and may even disappear during maximal contraction. * **H zone:** Although not an option here, it is important to note that the H zone (containing only thick filaments) also decreases in length or disappears. #### Why the Other Options are Wrong: * **A band (Anisotropic band):** This represents the entire length of the thick filaments. Since the filaments themselves do not shrink or fold but merely slide, the **A band remains constant** in length. * **Thick and Thin Filaments:** The individual protein filaments (myosin and actin) **do not change their physical length**. Their appearance of "shortening" the sarcomere is due to an increase in their degree of overlap, not a change in their actual dimensions. #### High-Yield Clinical Pearls for NEET-PG: * **Sarcomere:** Defined as the distance between two **Z-lines**; it is the functional unit of contraction and shortens during muscle activity. * **Mnemonic:** During contraction, **"HI"** (H-zone and I-band) **shortens**, while the **A-band** stays the **Same**. * **Titans:** The protein **Titin** acts as a molecular spring, connecting the Z-line to the M-line, providing passive elasticity to the muscle. * **Calcium Binding:** Contraction is initiated when $Ca^{2+}$ binds to **Troponin C**, leading to the displacement of tropomyosin and exposing the myosin-binding sites on actin.

Question 278: An action potential is produced by which of the following ionic movements?

A. Sodium influx (Correct Answer)
B. Sodium efflux
C. Potassium influx
D. Potassium efflux

Explanation: ### Explanation The generation of an action potential is a fundamental process in excitable tissues (nerve and muscle). It is primarily driven by the sequential opening and closing of voltage-gated ion channels. **1. Why Sodium Influx is Correct:** The **depolarization phase** (the initiation of the action potential) is caused by the rapid opening of **voltage-gated sodium (Na⁺) channels**. Since the concentration of Na⁺ is significantly higher in the extracellular fluid (ECF) than in the intracellular fluid (ICF), and the resting membrane is negatively charged, Na⁺ rushes **into** the cell (influx) down both its chemical and electrical gradients. This influx makes the interior of the cell positive, triggering the action potential once the threshold is reached. **2. Why the Other Options are Incorrect:** * **Sodium efflux:** This would involve moving Na⁺ out of the cell against its gradient, which requires active transport (Na⁺-K⁺ ATPase) and does not occur during the rapid depolarization phase. * **Potassium influx:** K⁺ concentration is higher inside the cell. Influx would only occur under extreme experimental conditions and is not a physiological part of the action potential. * **Potassium efflux:** This occurs during the **repolarization phase**. As K⁺ leaves the cell, the membrane potential returns toward its resting negative state. While essential for the cycle, it does not *produce* the initial action potential; it terminates it. ### High-Yield Clinical Pearls for NEET-PG: * **Tetrodotoxin (Pufferfish) & Saxitoxin:** Block voltage-gated Na⁺ channels, preventing action potential generation (leads to paralysis). * **Local Anesthetics (e.g., Lidocaine):** Work by blocking voltage-gated Na⁺ channels from the inside, preventing pain signal conduction. * **Hyperkalemia:** Increases resting membrane potential (making it less negative), initially making cells more excitable but eventually leading to inactivation of Na⁺ channels and cardiac arrest. * **All-or-None Law:** Once the threshold (usually -55mV) is reached, an action potential of constant magnitude is produced regardless of the stimulus strength.

Question 279: The 'all or none' law refers to which physiological phenomenon?

A. Action potential (Correct Answer)
B. Resting potential
C. Membrane potential
D. None of the above

Explanation: The **'All-or-None' Law** is a fundamental principle in neurophysiology stating that if a stimulus is strong enough to reach the **threshold potential** (typically -55mV), an action potential of maximal and constant amplitude is triggered. If the stimulus is sub-threshold, no action potential occurs at all. ### Why Action Potential is Correct: The action potential is an active, regenerative electrical event. Once the threshold is crossed, voltage-gated sodium channels open in a positive feedback loop (Hodgkin cycle). The resulting depolarization does not vary in size based on the strength of the stimulus; instead, a stronger stimulus increases the **frequency** of firing, not the **amplitude** of the individual spike. ### Why Other Options are Incorrect: * **Resting Membrane Potential (RMP):** This is a static state (typically -70mV in neurons) maintained by ion leak channels and the Na+/K+ ATPase pump. It is a baseline condition, not a triggered response that follows an all-or-none rule. * **Membrane Potential:** This is a general term for the voltage difference across a membrane. It includes **graded potentials** (like EPSPs or IPSPs), which do *not* follow the all-or-none law; their magnitude is proportional to the stimulus intensity and they decay over distance. ### NEET-PG High-Yield Pearls: * **Applicability:** The All-or-None law applies to **individual nerve fibers** and **individual muscle fibers**. It does **not** apply to a whole nerve trunk or a whole skeletal muscle, which show "graded" responses due to the recruitment of multiple motor units. * **Exception:** Cardiac muscle as a whole (syncytium) follows the All-or-None law because of gap junctions. * **Key Distinction:** Action potentials are **non-decremental** (do not lose strength over distance), whereas graded potentials are **decremental**.

Question 280: Magnitude of action potential is determined by:

A. Na+ (Correct Answer)
B. Mg++
C. K++
D. Ca++

Explanation: **Explanation:** The magnitude (amplitude) of an action potential is primarily determined by the **extracellular concentration of Sodium (Na+)**. 1. **Why Na+ is correct:** According to the **Hodgkin-Huxley model**, the rising phase of an action potential is caused by a rapid influx of Na+ ions through voltage-gated channels. The peak of the action potential tends to approach the **Equilibrium Potential of Sodium (ENa)**, which is approximately +60 mV. If the extracellular Na+ concentration decreases, the concentration gradient weakens, leading to a lower peak and reduced magnitude of the action potential. 2. **Why other options are incorrect:** * **K+ (Potassium):** While K+ is crucial for establishing the **Resting Membrane Potential (RMP)** and mediating repolarization, it does not determine the peak magnitude of the depolarization phase. * **Ca++ (Calcium):** Extracellular calcium levels primarily affect the **threshold** for firing an action potential. Low Ca++ (hypocalcemia) makes the nerve more excitable (tetany) by lowering the threshold, but it doesn't dictate the total magnitude. * **Mg++ (Magnesium):** Magnesium acts as a physiological calcium channel blocker and stabilizes membranes, but it is not the primary ion responsible for the action potential spike. **High-Yield NEET-PG Pearls:** * **Amplitude vs. Frequency:** Nerve signals use **Frequency Coding**. The magnitude (amplitude) of an action potential is constant for a given nerve fiber (All-or-None Law); only the frequency of firing changes with stimulus intensity. * **Hyponatremia:** Severe hyponatremia can decrease action potential amplitude, potentially leading to neurological symptoms. * **Tetrodotoxin (Pufferfish):** Blocks voltage-gated Na+ channels, completely abolishing the action potential magnitude.

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