Nerve and Muscle Physiology Practice Questions

Q: Which of the following channelopathies is associated with a calcium channel disorder of muscles?

Hypokalemic periodic paralysis. **Explanation:** **Hypokalemic Periodic Paralysis (HypoPP)** is the correct answer because it is primarily caused by mutations in the **CACNA1S gene**, which encodes the alpha-1 subunit of the **L-type voltage-gated calcium channel** (dihydropyridine receptor) in skeletal muscle [1]. This defect leads to muscle inexcitability and episodic flaccid paralysis, typically triggered by high carbohydrate meals or strenuous exercise which lower serum potassium levels [1]. **Analysis of Incorrect Options:** * **Episodic Ataxia Type 1 (EA1):** This is a potassium channelopathy involving the **KCNA1 gene** (Kv1.1 voltage-gated K+ channel). It presents with brief episodes of ataxia and myokymia. * **Hyperkalemic Periodic Paralysis (HyperPP):** This is a sodium channelopathy caused by mutations in the **SCN4A gene** [1]. It is characterized by attacks of weakness triggered by fasting or potassium intake. * **Spinocerebellar Ataxia Type 1 (SCA1):** This is not a primary channelopathy; it is a **trinucleotide repeat (CAG) disorder** resulting in polyglutamine expansion, leading to progressive cerebellar degeneration. **High-Yield NEET-PG Pearls:** * **HypoPP Type 1:** Calcium channel (CACNA1S) - Most common. * **HypoPP Type 2:** Sodium channel (SCN4A) - Less common [1]. * **Lambert-Eaton Myasthenic Syndrome (LEMS):** Associated with P/Q-type calcium channel antibodies (Presynaptic) [2]. * **Treatment Tip:** Acetazolamide is used for prophylaxis in both HypoPP and HyperPP, but acute attacks of HypoPP are managed with potassium replacement.

Q: Which muscle fiber type has a high glycogen content?

White fibers. **Explanation:** The classification of muscle fibers is based on their metabolic profile and contraction speed. **White fibers (Type IIb/IIx)** are designed for short bursts of high-intensity activity (anaerobic power). Because they have fewer mitochondria and less myoglobin, they rely primarily on **anaerobic glycolysis** for ATP production. To support this rapid energy demand, they store significantly **high amounts of glycogen** and have high glycolytic enzyme activity. **Analysis of Options:** * **White fibers (Correct):** These are "Fast-twitch" fibers. They have high glycogen content, high myosin ATPase activity, and fatigue rapidly. * **Red fibers / Type 1 fibers (Incorrect):** These are "Slow-twitch" fibers. They are rich in myoglobin and mitochondria, relying on aerobic oxidative phosphorylation. They have high triglyceride (fat) stores rather than high glycogen stores and are resistant to fatigue. * **Tonic fibers (Incorrect):** These are specialized fibers (like those in extraocular muscles) that do not follow the "all-or-none" law and have multiple nerve endings. They are not characterized by high glycogen content. **High-Yield NEET-PG Pearls:** 1. **Myoglobin Content:** Type 1 (Red) = High; Type 2 (White) = Low. 2. **Mitochondria/Capillaries:** Type 1 = High (for oxygen utilization); Type 2 = Low. 3. **ATPase Activity:** Type 2 fibers have high myosin ATPase activity, leading to faster contraction. 4. **Fatigability:** Type 1 is fatigue-resistant (postural muscles); Type 2 is easily fatigued (sprinter's muscles). 5. **Intermediate Fibers:** Type IIa fibers are "Fast-Oxidative Glycolytic," sharing characteristics of both types.

Q: Which of the following contains the site of attachment for calcium ions that initiates muscle contraction?

Troponin C. **Explanation:** Muscle contraction is initiated by the **Excitation-Contraction (E-C) coupling** process, where an increase in intracellular calcium ions ($Ca^{2+}$) acts as the primary trigger. **1. Why Troponin C is Correct:** The troponin complex is a regulatory protein associated with the actin (thin) filament. It consists of three subunits, each with a specific function. **Troponin C (TnC)** is the specific subunit that contains four binding sites for calcium. When $Ca^{2+}$ binds to Troponin C, it induces a conformational change in the entire troponin-tropomyosin complex. This shift moves tropomyosin away from the active sites on the actin filament, allowing the myosin heads to bind and initiate the cross-bridge cycle. **2. Analysis of Incorrect Options:** * **Troponin I (TnI):** The "I" stands for **Inhibitory**. It binds to actin and inhibits the interaction between actin and myosin by physically blocking the binding site. * **Troponin T (TnT):** The "T" stands for **Tropomyosin**. Its primary role is to anchor the troponin complex to the tropomyosin molecule. * **Myosin:** This is the thick filament. While it has binding sites for ATP and Actin, it does not have the primary regulatory binding site for calcium to initiate contraction. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cardiac Biomarkers:** Troponin I and T are highly specific markers for myocardial infarction (MI). Troponin C is not used clinically because it is identical in both skeletal and cardiac muscle. * **The "Power Stroke":** This occurs when ADP and inorganic phosphate are released from the myosin head, not when calcium binds. * **Relaxation:** Muscle relaxation occurs when $Ca^{2+}$ is pumped back into the Sarcoplasmic Reticulum via the **SERCA pump** (an active process requiring ATP).

Q: Which of the following steps is NOT involved in muscle contraction following a nerve impulse?

Dopamine release at the NMJ. **Explanation:** The process of muscle contraction, known as **Excitation-Contraction Coupling**, relies on a specific sequence of electrochemical events. **Why Option B is Correct:** The neurotransmitter responsible for signal transmission at the Neuromuscular Junction (NMJ) is **Acetylcholine (ACh)**, not dopamine. When an action potential reaches the motor nerve terminal, voltage-gated calcium channels open, leading to the exocytosis of ACh into the synaptic cleft. Dopamine is a neurotransmitter primarily involved in the Central Nervous System (e.g., basal ganglia) and does not play a role in peripheral skeletal muscle contraction. **Why Other Options are Incorrect:** * **Option A:** An action potential must cross the NMJ via ACh binding to nicotinic receptors to initiate depolarization of the sarcolemma. * **Option C:** Depolarization travels down **T-tubules**, activating DHP receptors, which triggers the **Ryanodine receptors** to release stored Calcium from the **Sarcoplasmic Reticulum (SR)**. * **Option D:** Once released, Calcium binds to **Troponin C**, causing a conformational change in Tropomyosin. This exposes the active sites on actin, allowing the "attractive forces" (cross-bridge formation) between actin and myosin to occur. **High-Yield Clinical Pearls for NEET-PG:** * **Lambert-Eaton Syndrome:** Antibodies against *pre-synaptic* voltage-gated calcium channels. * **Myasthenia Gravis:** Antibodies against *post-synaptic* NMJ nicotinic ACh receptors. * **Malignant Hyperthermia:** Caused by a mutation in the **Ryanodine receptor (RYR1)**, leading to excessive calcium release. * **Rigor Mortis:** Occurs because ATP is required for the *detachment* of myosin from actin; without ATP, the cross-bridge remains locked.

Q: Rigor mortis results after death is due to which of the following?

Failure of ATP supply. **Explanation:** Rigor mortis is the post-mortem stiffening of muscles caused by the depletion of **Adenosine Triphosphate (ATP)**. **Why Option B is Correct:** In a living muscle, ATP is required for two critical steps in the cross-bridge cycle: 1. **Dissociation:** ATP binding to the myosin head is essential to break the bond between actin and myosin. 2. **Relaxation:** ATP powers the SERCA pump (Sarcoplasmic Endoplasmic Reticulum Calcium ATPase) to pump calcium back into the sarcoplasmic reticulum. After death, cellular respiration ceases, leading to a **failure of ATP supply**. Without ATP, the myosin heads remain permanently attached to actin filaments in a "latched" state, and calcium remains in the cytosol, maintaining a state of rigid contraction. **Why Other Options are Incorrect:** * **Option A:** Acetylcholine (ACh) is responsible for initiating depolarization at the neuromuscular junction. While ACh release stops after death, it is the lack of ATP for detachment, not the absence of ACh diffusion, that causes the physical rigidity. * **Option C:** This is a distractor. While calcium bridges (troponin-tropomyosin interactions) remain active because calcium cannot be sequestered, the fundamental "failure" is the lack of the energy molecule (ATP) required to break the actin-myosin cross-bridge. **High-Yield Clinical Pearls for NEET-PG:** * **Sequence:** Rigor mortis typically starts in the small muscles (eyelids, jaw) and follows a **proximal-to-distal** (Nysten’s Law) progression. * **Timeline:** It usually begins 2–3 hours after death, peaks at 12 hours, and disappears after 36–48 hours due to **autolysis** (proteolytic enzyme action). * **Temperature:** High ambient temperatures accelerate the onset of rigor mortis.

Question 1

What is meant by resting muscle length?

Accepted Answer

The length of the muscle fiber at the onset of contraction, which is required to attain maximum active tension.

Answer

The length of actin and myosin filaments before contraction.

Answer

Approximately 4 micrometers.

Answer

The length at which the muscle has minimal tension.

Question 2

Which of the following channelopathies is associated with a calcium channel disorder of muscles?

Accepted Answer

Hypokalemic periodic paralysis

Answer

Episodic ataxia type 1

Answer

Hyperkalemic periodic paralysis

Answer

Spinocerebellar ataxia type 1

Question 3

Which muscle fiber type has a high glycogen content?

Accepted Answer

White fibers

Answer

Red fibers

Answer

Type 1 fibers

Answer

Tonic fibers

Question 4

Presynaptic facilitation is caused by?

Accepted Answer

Prolonged opening of calcium channels

Answer

Prolonged opening of chloride channels

Answer

Prolonged opening of sodium channels

Answer

Prolonged closure of potassium channels

Question 5

All of the following functions are associated with myelination except?

Accepted Answer

Decreases the release of neurotransmitter from the nerve endings

Answer

Decreases energy expenditure

Answer

Increases speed of conduction

Answer

Provides protective covering for the axon

Question 6

Which of the following contains the site of attachment for calcium ions that initiates muscle contraction?

Accepted Answer

Troponin C

Answer

Troponin I

Answer

Troponin T

Answer

Myosin

Question 7

Which of the following steps is NOT involved in muscle contraction following a nerve impulse?

Accepted Answer

Dopamine release at the NMJ

Answer

Action potential across the neuromuscular junction (NMJ)

Answer

Release of calcium from the sarcoplasmic reticulum

Answer

Calcium initiates attractive forces between actin and myosin filaments

Question 8

What is the chronaxie minimum?

Accepted Answer

Myelinated nerve

Answer

Mixed nerves

Answer

Unmyelinated nerve

Answer

Sensory nerves

Question 9

Rigor mortis results after death is due to which of the following?

Accepted Answer

Failure of ATP supply

Answer

Failure of acetylcholine to diffuse

Answer

Failure of breakdown of calcium bridges

Answer

None of the above

Question 10

Determine the chronaxie and rheobase from the provided graph.

Accepted Answer

Chronaxie 0.2 msec; rheobase 0.3V

Answer

Chronaxie 0.3V; rheobase 0.2 msec

Answer

Chronaxie 0.3V; rheobase 0.6V

Answer

Chronaxie 0.2 msec; rheobase 0.6V

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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