Nerve and Muscle Physiology Practice Questions

Q: Group A nerve fibers are most susceptible to which of the following?

Pressure. The susceptibility of nerve fibers to different insults depends on their diameter and myelination. This concept is a high-yield topic based on the **Erlanger-Gasser classification**. ### **Explanation** **Group A nerve fibers** are the thickest, most heavily myelinated fibers. Because they have the largest diameter, they are physically more vulnerable to mechanical compression. When **pressure** is applied to a nerve trunk, these large-diameter fibers are the first to undergo mechanical deformation and ischemia of their vasa nervorum, leading to a rapid conduction block. ### **Analysis of Other Options** * **B. Hypoxia:** **Group B fibers** (preganglionic autonomic fibers) are the most susceptible to hypoxia. Group A fibers are intermediate, and Group C fibers are the most resistant. * **C. Local Anesthesia:** **Group C fibers** (small, unmyelinated pain fibers) are the most susceptible to local anesthetics. Because they lack myelin and have a small surface area, the anesthetic can easily penetrate and block the sodium channels. * **D. Temperature:** While extreme temperatures can affect nerve conduction, it is not the primary differentiating factor used in the Erlanger-Gasser susceptibility hierarchy. ### **High-Yield NEET-PG Pearls** To remember the order of susceptibility (from most to least sensitive), use the mnemonic **"PHL"**: 1. **P**ressure: **A** > B > C (Think: "A" is big and easily squashed) 2. **H**ypoxia: **B** > A > C 3. **L**ocal Anesthesia: **C** > B > A (Think: "C" is small and easily drugged) **Clinical Correlation:** "Saturday Night Palsy" (radial nerve compression) primarily affects Group A motor and sensory fibers first, causing motor weakness and loss of touch before affecting pain sensation.

Q: In tetany, hyperexcitability is due to which of the following mechanisms?

Low calcium levels cause increased sodium permeability.. **Mechanism of Hypocalcemic Tetany** The correct answer is **A: Low calcium levels cause increased sodium permeability.** **Explanation:** In the extracellular fluid (ECF), calcium ions ($Ca^{2+}$) play a critical role in stabilizing the resting membrane potential of excitable tissues (nerve and muscle). Calcium ions normally bind to the external surface of voltage-gated sodium channels, increasing the voltage threshold required to open them. When ECF calcium levels drop (**hypocalcemia**), there are fewer positive charges to "mask" the negative charges on the cell membrane. This reduces the threshold for excitation, making the sodium channels much easier to open. Consequently, sodium permeability increases even with slight stimuli, leading to spontaneous depolarization and repetitive firing of action potentials. This manifests clinically as involuntary muscle contractions (tetany). **Analysis of Incorrect Options:** * **B & C:** These options are incorrect because tetany is primarily a phenomenon of the **cell membrane threshold** and sodium influx, rather than a direct inhibition of potassium release or intracellular calcium sequestration. * **D:** While intracellular calcium is required for muscle contraction (excitation-contraction coupling), the *hyperexcitability* (the tendency to fire) is triggered by the **extracellular** calcium deficit affecting sodium channel gating. **High-Yield NEET-PG Pearls:** * **Trousseau’s Sign:** Carpopedal spasm induced by inflating a BP cuff above systolic pressure (more sensitive than Chvostek's). * **Chvostek’s Sign:** Twitching of facial muscles upon tapping the facial nerve. * **ECG Finding:** Hypocalcemia characteristically causes **prolonged QT interval**. * **Rule of Thumb:** "Hypocalcemia excites, Hypercalcemia excites (the heart) but depresses (the nerves)."

Q: Which statement is true regarding Type-2 muscle fibers?

Increased Isoenzyme ATPase activity. ### Explanation **Correct Answer: C. Increased Isoenzyme ATPase activity** Skeletal muscle fibers are classified into Type 1 (Slow-twitch) and Type 2 (Fast-twitch) based on their metabolic profile and contraction speed. The speed of muscle contraction is directly proportional to the **Myosin ATPase activity**. Type 2 fibers possess a specific isoenzyme of myosin ATPase that hydrolyzes ATP rapidly, allowing for fast cross-bridge cycling and quick, powerful contractions. **Analysis of Options:** * **Option A & B (Incorrect):** These describe **Type 1 (Slow Oxidative) fibers**. Type 1 fibers are rich in myoglobin (giving them a red color) and mitochondria to support aerobic metabolism for endurance. Type 2 fibers have low myoglobin content and appear pale/white. * **Option D (Incorrect):** Type 2 fibers (specifically Type 2b) have a **high glycolytic capacity**, not moderate. They rely on anaerobic glycolysis for rapid energy production, making them prone to early fatigue due to lactic acid accumulation. --- ### High-Yield Clinical Pearls for NEET-PG: * **Type 1 Fibers (Slow-twitch):** "One Slow Red Ox" (Type **1**, **Slow**-twitch, **Red** color, **Ox**idative metabolism). Found in postural muscles like the **Soleus**. * **Type 2 Fibers (Fast-twitch):** "Two Fast White Sugar" (Type **2**, **Fast**-twitch, **White** color, **Sugar**/Glycolytic metabolism). Found in muscles used for sprinting or weightlifting, such as the **Gastrocnemius**. * **Intermediate Fibers (Type 2a):** These are fast-twitch but have both oxidative and glycolytic capacities (Fast Oxidative Glycolytic). * **Order of Recruitment:** According to **Henneman’s Size Principle**, smaller Type 1 motor units are recruited first, followed by larger Type 2 units as force requirements increase.

Q: What structure facilitates the unidirectional flow of a nerve impulse?

Synapse. **Explanation:** The correct answer is **Synapse**. This phenomenon is known as the **Bell-Magendie Law** or the principle of **One-Way Conduction**. **Why Synapse is Correct:** In a chemical synapse, neurotransmitters are stored exclusively in the **presynaptic vesicles** and the specific receptors for these neurotransmitters are located on the **postsynaptic membrane**. Therefore, when an action potential reaches the axon terminal, the chemical messenger can only be released from the presynaptic side to act on the postsynaptic side. This structural asymmetry ensures that the nerve impulse travels in only one direction. **Why Other Options are Incorrect:** * **Axon:** While axons conduct impulses away from the cell body, they are theoretically capable of **bidirectional conduction** (orthodromic and antidromic) if stimulated experimentally in the middle of the fiber. * **Dendrites:** These are receptive structures that carry impulses toward the cell body. Like axons, they do not possess the "valve-like" mechanism of the synapse to enforce unidirectionality in a circuit. * **Node of Ranvier:** These are gaps in the myelin sheath that facilitate **Saltatory Conduction** (jumping of the impulse). Their primary function is to increase the velocity of nerve conduction, not to determine its direction. **High-Yield Clinical Pearls for NEET-PG:** * **Synaptic Delay:** The time required for neurotransmitter release and binding (approx. **0.5 msec**). It is the reason why reflex arcs with more synapses are slower. * **Synaptic Fatigue:** Repeated stimulation leads to the exhaustion of neurotransmitter stores in the presynaptic terminal, acting as a protective mechanism against excessive neuronal activity (e.g., terminating a seizure). * **Electrical Synapses:** Unlike chemical synapses, these occur via **gap junctions** and allow for faster, often bidirectional flow (found in cardiac muscle and some brain regions).

Q: The major cation directly involved in the interaction of actin and myosin in skeletal muscle is:

Ca++. **Explanation:** **1. Why Calcium (Ca++) is the Correct Answer:** In skeletal muscle, Calcium is the essential link between excitation and contraction (**Excitation-Contraction Coupling**). In a resting state, the binding sites on actin are covered by the **troponin-tropomyosin complex**. When an action potential reaches the muscle fiber, Ca++ is released from the **Sarcoplasmic Reticulum (SR)**. This Ca++ binds specifically to **Troponin C**, causing a conformational change that pulls tropomyosin away from the myosin-binding sites on the actin filament. This allows the myosin head to bind to actin, forming cross-bridges and initiating the power stroke. **2. Why Other Options are Incorrect:** * **Na+ (Sodium):** Primarily responsible for the **depolarization** phase of the action potential at the neuromuscular junction and along the sarcolemma, but it does not interact with contractile proteins. * **K+ (Potassium):** Responsible for the **repolarization** phase and maintaining the resting membrane potential. * **Mg++ (Magnesium):** Acts as a cofactor for ATPase activity and competes with Ca++ for binding sites. While it is necessary for ATP hydrolysis, it is not the "trigger" cation for actin-myosin interaction; in fact, low magnesium can lead to hyperexcitability (tetany). **3. Clinical Pearls & High-Yield Facts:** * **Calsequestrin:** The protein that buffers and stores Ca++ within the Sarcoplasmic Reticulum. * **Ryanodine Receptors (RyR1):** The calcium release channels in the SR. Mutations in these receptors lead to **Malignant Hyperthermia** (triggered by halothane/succinylcholine). * **SERCA Pump:** Responsible for the reuptake of Ca++ into the SR, which is required for muscle **relaxation**. * **Rigor Mortis:** Occurs due to the lack of ATP, which is needed to break the actin-myosin bond, not due to an excess of Calcium.

Q: All of the following are true about neurotrophins except?

They are always transported antegrade along the axon.. **Explanation** Neurotrophins are a family of proteins essential for the survival, development, and function of neurons. **Why Option D is the Correct Answer (The False Statement):** Neurotrophins are primarily characterized by **retrograde axonal transport**. They are typically secreted by target tissues, bind to receptors on the nerve terminals, and are internalized and transported "backward" (retrograde) along the axon to the cell body (soma) to influence gene expression and promote survival. While some antegrade transport occurs, saying they are "always" transported antegrade is physiologically incorrect. **Analysis of Other Options:** * **Option A:** Neurotrophins play a vital role in maintaining the structural and functional integrity of both presynaptic and postsynaptic neurons, preventing apoptosis. * **Option B:** There is high specificity between neurotrophins and **Trk (Tropomyosin receptor kinase)** receptors. **BDNF** (Brain-Derived Neurotrophic Factor) and Neurotrophin-4/5 bind to **TrkB**. (Note: NGF binds to TrkA; NT-3 binds to TrkC). * **Option C:** Nerve Growth Factor (NGF) is specifically known to support the growth and maintenance of cholinergic neurons in the basal forebrain, which are often affected in Alzheimer’s disease. **High-Yield NEET-PG Pearls:** * **Pro-neurotrophins:** All neurotrophins are synthesized as precursors (pro-forms) which promote apoptosis via the **p75 receptor**, while mature forms promote survival via **Trk receptors**. * **Retrograde Transport Motor:** Mediated by **Dynein**. * **Antegrade Transport Motor:** Mediated by **Kinesin**. * **BDNF Clinical Link:** Reduced levels of BDNF are associated with depression and neurodegenerative diseases; exercise is known to increase BDNF levels.

Q: What is the smooth muscle counterpart of troponin?

Calmodulin. ### Explanation In **skeletal and cardiac muscle**, contraction is regulated by the **troponin-tropomyosin complex**. When calcium enters the sarcoplasm, it binds to Troponin C, causing a conformational change that uncovers the actin-binding sites. However, **smooth muscle lacks troponin**. Instead, the regulatory protein is **Calmodulin**. When intracellular calcium levels rise, calcium binds to Calmodulin to form a **Calcium-Calmodulin complex**. This complex activates an enzyme called **Myosin Light Chain Kinase (MLCK)**, which phosphorylates the myosin head, allowing it to bind to actin and initiate contraction. **Analysis of Incorrect Options:** * **Nebulin:** A large protein in skeletal muscle that acts as a "molecular ruler," regulating the length of the thin (actin) filaments. * **Calsequestrin:** A calcium-binding protein located within the **Sarcoplasmic Reticulum (SR)**. It acts as a buffer, allowing large amounts of calcium to be stored at low free concentrations. * **Titin:** The largest known protein; it acts as a spring, connecting the Z-disk to the M-line in the sarcomere, providing passive elasticity to skeletal muscle. **High-Yield NEET-PG Pearls:** * **Contraction Mechanism:** Smooth muscle uses **thick-filament regulation** (via MLCK), whereas skeletal muscle uses **thin-filament regulation** (via Troponin). * **Relaxation:** In smooth muscle, relaxation requires **Myosin Light Chain Phosphatase (MLCP)** to dephosphorylate the myosin head. * **Latch-bridge Mechanism:** A unique feature of smooth muscle allowing it to maintain prolonged tension with minimal ATP consumption.

Question 1

Group A nerve fibers are most susceptible to which of the following?

Accepted Answer

Pressure

Answer

Hypoxia

Answer

Local anesthesia

Answer

Temperature

Question 2

In tetany, hyperexcitability is due to which of the following mechanisms?

Accepted Answer

Low calcium levels cause increased sodium permeability.

Answer

Prevent potassium release.

Answer

Prevent sodium and intracellular calcium release.

Answer

Increased intracellular calcium produces the generation of an action potential.

Question 3

Which statement is true regarding Type-2 muscle fibers?

Accepted Answer

Increased Isoenzyme ATPase activity

Answer

Increased myoglobin content

Answer

Slow oxidative and red in color

Answer

Moderate glycolytic capacity

Question 4

Which of the following statements is true regarding total heat production during muscle contraction?

Accepted Answer

Activation heat is produced when a muscle is contracting.

Answer

Initial heat is due to basal metabolic processes.

Answer

Relaxation heat is present in both isotonic and isometric contractions.

Answer

Recovery heat of muscle is greater than the initial heat.

Question 5

What structure facilitates the unidirectional flow of a nerve impulse?

Accepted Answer

Synapse

Answer

Axon

Answer

Dendrites

Answer

Node of Ranvier

Question 6

The major cation directly involved in the interaction of actin and myosin in skeletal muscle is:

Accepted Answer

Ca++

Answer

Na+

Answer

K+

Answer

Mg++

Question 7

What is the characteristic of the skeletal muscle action potential?

Accepted Answer

It spreads inward to all parts of the muscle via the T-tubule system.

Answer

It is not essential for contraction to occur.

Answer

It has a prolonged plateau phase.

Answer

It begins with an inward movement of K+ ion.

Question 8

All of the following are true about neurotrophins except?

Accepted Answer

They are always transported antegrade along the axon.

Answer

They help maintain the integrity of postsynaptic neurons.

Answer

TrkB receptor is associated with brain-derived neurotrophic factor.

Answer

They aid in the growth of cholinergic neurons in the basal forebrain.

Question 9

Which of the following events accompanies the rapid voluntary flexion of the arm?

Accepted Answer

An increase in the activity of the Ia afferent fibers from the triceps (the antagonist)

Answer

An increase in the activity of the Ia afferent fibers from the biceps (the agonist)

Answer

A decrease in the activity of the Ib afferent fibers from the biceps (the agonist)

Answer

A decrease in the activity of the Ib afferent fibers from the triceps (the antagonist)

Question 10

What is the smooth muscle counterpart of troponin?

Accepted Answer

Calmodulin

Answer

Nebulin

Answer

Calsequestrin

Answer

Titin

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?