Nerve and Muscle Physiology Practice Questions

Q: Fine, irregular contraction of individual muscle fibers is called:

Fibrillation. ### 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.

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

Enzymatic breakdown by acetylcholinesterase. ### 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.

Q: Actin's active site is covered by

Tropomyosin. **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.

Q: Energy in muscles is stored as:

Phosphocreatine. **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.

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

Type II A. **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.

Question 1

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?

Accepted Answer

30 m/s

Answer

60 m/s

Answer

45 m/s

Answer

80 m/s

Question 2

Fine, irregular contraction of individual muscle fibers is called:

Accepted Answer

Fibrillation

Answer

Fasciculations

Answer

Tics

Answer

Spasm

Question 3

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

Accepted Answer

Enzymatic breakdown by acetylcholinesterase

Answer

Diffusion into the surrounding extracellular fluid

Answer

Uptake into the nerve ending

Answer

Uptake into the muscle

Question 4

What is the nerve impulse that initiates muscle contraction?

Accepted Answer

It causes the opening of calcium channels, leading to an increase in calcium ion concentration within the sarcomere.

Answer

It causes both the plasma membrane and the T-tubules to undergo hyperpolarization.

Answer

It inhibits sodium entry into the sarcomere.

Answer

It is inhibited by the binding of acetylcholine to receptors in the sarcoplasmic reticulum.

Question 5

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

Accepted Answer

Enzymatic degradation of proteoglycans is increased

Answer

Total proteoglycan content is decreased

Answer

Synthesis of proteoglycans is decreased

Answer

Total water content of cartilage is decreased

Question 6

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

Accepted Answer

The energy of the creatine phosphate is used to convert ADP to ATP

Answer

The creatine phosphate transfers its energy to the cross bridges to cause them to become locked

Answer

The creatine phosphate causes the power stroke of the cross bridges

Answer

The creatine phosphate transfers its energy to the actin filament

Question 7

Actin's active site is covered by

Accepted Answer

Tropomyosin

Answer

Myosin

Answer

Troponin

Answer

Desmin

Question 8

Energy in muscles is stored as:

Accepted Answer

Phosphocreatine

Answer

ATP

Answer

ADP

Answer

None of the above

Question 9

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

Accepted Answer

Number of motor units recruited

Answer

Number of muscle fibers

Answer

Aerobic capacity of the muscle

Answer

Length of the muscle fiber

Question 10

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

Accepted Answer

Type II A

Answer

Type I

Answer

Type II B

Answer

Type III

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?