Nerve and Muscle Physiology Practice Questions

Q: Which of the following changes occur in bone growth?

Increased osteocalcin. ### Explanation **Correct Answer: D. Increased osteocalcin** **Why it is correct:** Bone growth and remodeling are driven by the activity of **osteoblasts** (bone-forming cells). **Osteocalcin** (also known as Bone Gamma-Carboxyglutamic Acid Protein) is a non-collagenous protein hormone synthesized exclusively by osteoblasts. It plays a crucial role in bone mineralization and calcium ion binding. Because its synthesis is specific to osteoblasts, serum levels of osteocalcin are considered a highly specific **biochemical marker of bone formation** and turnover. During periods of active bone growth, osteoblast activity increases, leading to elevated osteocalcin levels. **Why the other options are incorrect:** * **A. Increased acid phosphatase:** Tartrate-resistant acid phosphatase (TRAP) is a marker of **osteoclast** activity (bone resorption), not bone growth. * **B. Increased urinary calcium:** High urinary calcium (hypercalciuria) is typically a sign of bone resorption or impaired renal reabsorption, often seen in conditions like hyperparathyroidism or immobilization, rather than healthy bone growth. * **C. Increased bone nucleotidase:** While 5'-nucleotidase is a marker for liver/biliary disease, it is not a specific or standard marker for bone growth or mineralization. **NEET-PG High-Yield Pearls:** * **Markers of Bone Formation:** Osteocalcin, Bone-specific Alkaline Phosphatase (ALP), and Procollagen type 1 N-terminal propeptide (P1NP). * **Markers of Bone Resorption:** Urinary hydroxyproline, Pyridinoline cross-links, and Serum TRAP. * **Vitamin K Dependency:** Osteocalcin requires Vitamin K for carboxylation to become functional; thus, Vitamin K deficiency can impair bone mineralization. * **Metabolic Link:** Osteocalcin also acts as a hormone that increases insulin secretion and sensitivity, linking bone metabolism to energy homeostasis.

Q: What is the resting membrane potential of a muscle fiber?

-90mV. The Resting Membrane Potential (RMP) is the electrical potential difference across the cell membrane when the cell is at rest. In skeletal muscle fibers, the RMP is typically **-90 mV**. ### Why -90 mV is Correct The RMP is primarily determined by the equilibrium potential of Potassium ($K^+$). According to the Nernst equation, the equilibrium potential for $K^+$ is approximately -94 mV. Because the resting muscle membrane is highly permeable to $K^+$ (via leak channels) and relatively impermeable to $Na^+$, the RMP sits very close to the $K^+$ equilibrium potential. The slight difference (-90 mV vs -94 mV) is due to a minor influx of $Na^+$ and the electrogenic contribution of the $Na^+-K^+$ ATPase pump. ### Analysis of Incorrect Options * **-70 mV (Option B):** This is the typical RMP for **large neurons**. Neurons have a slightly higher RMP than muscle fibers, making them more excitable. * **-60 mV (Option A):** This is closer to the RMP of **smooth muscle cells** (ranging from -50 to -60 mV) or the threshold potential for firing an action potential in many excitable tissues. * **-80 mV (Option C):** While some cardiac cells or specific fibers may show this value, -90 mV is the standard physiological value cited for skeletal muscle and ventricular myocytes. ### High-Yield NEET-PG Pearls * **Skeletal Muscle vs. Nerve:** Muscle fibers have a more negative RMP (-90 mV) compared to nerves (-70 mV). * **Ionic Basis:** $K^+$ efflux is the most important factor in establishing RMP. * **Maintenance:** The $Na^+-K^+$ ATPase pump maintains the concentration gradients but only contributes about -4 to -5 mV directly to the RMP. * **Clinical Correlation:** Hypokalemia hyperpolarizes the membrane (makes it more negative), making it harder to trigger an action potential, leading to muscle weakness.

Q: A cross-sectional view of a skeletal muscle fiber through the H-zone would show the presence of what?

Myosin only. To understand the cross-sectional anatomy of a sarcomere, one must visualize the arrangement of myofilaments within its specific zones. ### **Explanation of the Correct Answer** The **H-zone** (Hensen’s zone) is the central region of the **A-band**. During muscle relaxation, the thin filaments (actin) do not extend all the way to the center of the sarcomere. Therefore, the H-zone contains **only thick filaments (myosin)**. In a cross-section through this specific area, you would see the hexagonal arrangement of myosin filaments without any overlapping actin. ### **Why Other Options are Incorrect** * **A. Actin and myosin:** This combination is found in the **outer regions of the A-band** (the overlap zone). This is the site where cross-bridges form. * **B. Titin and myosin:** While titin anchors myosin to the Z-discs, it is generally not the primary focus of cross-sectional identification in standard physiological models of the H-zone. * **C. Actin and titin:** This combination (along with other proteins like nebulin) is characteristic of the **I-band**, which contains only thin filaments and no myosin. ### **High-Yield NEET-PG Pearls** * **M-line:** Located in the dead center of the H-zone; it contains proteins (like myomesin) that hold the thick filaments together. * **Sarcomere Dynamics:** During muscle contraction (Sliding Filament Theory), the **H-zone and I-band shorten**, while the **A-band remains constant** in length. * **Pseudo-H Zone:** A narrow region in the center of the H-zone that lacks myosin heads (the "bare zone"). * **Ratio:** In the overlap zone of mammalian skeletal muscle, each thick filament is surrounded by **6 thin filaments**.

Q: What is the main component of the thin filament?

Actin. **Explanation:** The sarcomere, the functional unit of skeletal muscle, is composed of thick and thin filaments. The **thin filament** is primarily composed of three proteins: **Actin**, Tropomyosin, and the Troponin complex. **1. Why Actin is Correct:** Actin is the backbone of the thin filament. It exists as globular monomers (**G-actin**) that polymerize to form two long, helical strands known as **F-actin** (filamentous actin). Each G-actin molecule possesses a specific binding site for myosin heads, which is essential for cross-bridge formation and muscle contraction. **2. Analysis of Incorrect Options:** * **B. Myosin:** This is the primary component of the **thick filament**. It is a large protein with a "head" (possessing ATPase activity) and a "tail." * **C. Tropomyosin:** While it is a component of the thin filament, it is a regulatory protein, not the "main" structural component. It wraps around the actin helix to cover the myosin-binding sites during rest. * **D. Dystrophin:** This is a cytoskeletal protein that anchors the entire myofibril to the sarcolemma (cell membrane). It is not part of the thin filament itself. **High-Yield NEET-PG Pearls:** * **Troponin Complex:** Consists of **Troponin T** (binds to tropomyosin), **Troponin I** (inhibits actin-myosin binding), and **Troponin C** (binds to Calcium). * **Clinical Correlation:** Mutations in the **Dystrophin** gene lead to Duchenne and Becker Muscular Dystrophies. * **The Sliding Filament Theory:** During contraction, neither the thick nor thin filaments shorten; instead, they slide past each other, shortening the H-zone and I-band, while the **A-band remains constant** in length.

Q: In preload, which of the following can be seen?

Isotonic contraction with shortening of muscle fibers. ### Explanation In muscle physiology, **Preload** refers to the load applied to a muscle *before* it begins to contract. This load stretches the muscle to a certain resting length, determining the initial overlap between actin and myosin filaments. **Why Option B is Correct:** When a muscle is subjected to preload, it is stretched to a specific length. Upon stimulation, if the muscle develops enough tension to overcome this load, it undergoes **isotonic contraction**. In an isotonic contraction, the tension remains constant while the **muscle fibers shorten** to perform work (moving the load). Therefore, preload is fundamentally associated with the length-tension relationship and subsequent shortening during contraction. **Analysis of Incorrect Options:** * **Option A:** Isotonic contraction, by definition, involves a change in muscle length. A contraction "without shortening" cannot be isotonic if the muscle is performing work. * **Option C:** **Isometric contraction** occurs when the muscle develops tension without changing its length (e.g., pushing against a fixed wall). While preload determines the starting point for isometric tension, the hallmark of the *action* following preload in a standard experimental setup is the ability to shorten. * **Option D:** This is a physiological contradiction. Isometric means "same length"; therefore, shortening cannot occur during an isometric contraction. **High-Yield NEET-PG Pearls:** * **Preload vs. Afterload:** Preload sets the **resting length** (related to the Frank-Starling Law in the heart), while Afterload is the resistance the muscle must contract *against*. * **Isotonic vs. Isometric:** Remember: **Iso-metric** = Same Length (No work done, $W=0$); **Iso-tonic** = Same Tension (Work is done). * **Optimal Length ($L_0$):** The length at which the muscle develops maximum active tension. Preload helps the muscle reach this $L_0$.

Q: The hyperpolarization phase of the action potential is due to?

Prolonged opening of voltage-gated K+ channels. ### Explanation The hyperpolarization phase (also known as the **undershoot**) occurs because voltage-gated potassium ($K^+$) channels are slow to close. **1. Why Option B is Correct:** During the repolarization phase, voltage-gated $K^+$ channels open to allow $K^+$ to exit the cell. Unlike sodium channels, which have a rapid inactivation gate, $K^+$ channels close slowly. This **prolonged conductance** allows $K^+$ efflux to continue even after the membrane potential has reached the resting level (-70 mV). The potential moves closer to the **equilibrium potential of Potassium (-94 mV)**, resulting in a temporary state where the interior of the cell is more negative than at rest. **2. Why the Other Options are Incorrect:** * **Option A & D:** Chloride ($Cl^-$) channels do not play a primary role in the generation of a standard neuronal action potential. While $Cl^-$ influx can cause inhibitory postsynaptic potentials (IPSPs), it is not the mechanism behind the action potential's hyperpolarization phase. * **Option C:** The closure of $Na^+$ channels (specifically the inactivation of the 'h' gate) is responsible for the initiation of **repolarization**, not hyperpolarization. --- ### NEET-PG High-Yield Pearls * **Equilibrium Potentials (Nernst Equation):** $Na^+$ is +60 mV, $K^+$ is -94 mV. The membrane potential always moves toward the equilibrium potential of the ion to which it is most permeable. * **After-hyperpolarization:** This phase is responsible for the **Relative Refractory Period**, as a stronger-than-normal stimulus is required to reach the threshold from a more negative starting point. * **Tetrodotoxin (TTX):** A high-yield toxin (from Pufferfish) that blocks voltage-gated $Na^+$ channels, preventing the depolarization phase. * **Tetraethylammonium (TEA):** Blocks voltage-gated $K^+$ channels, specifically abolishing the hyperpolarization phase.

Q: What is the contribution of noncontractile muscle elements to total tension?

E. In skeletal muscle physiology, the **Total Tension** produced by a muscle is the sum of its **Active Tension** (generated by cross-bridge cycling) and **Passive Tension** (generated by noncontractile elastic elements). ### Explanation of the Correct Answer The correct answer is **E**. In a standard length-tension relationship graph: * **Passive Tension (Curve E):** This represents the tension developed by stretching the muscle's noncontractile components (such as the sarcolemma, connective tissue sheaths like endomysium/perimysium, and the protein **titin**) without any electrical stimulation. As the muscle is stretched beyond its resting length, this tension increases exponentially. * **Total Tension:** This is the sum of active and passive tension. At longer muscle lengths, the contribution of noncontractile elements (Curve E) becomes the dominant factor in total tension. ### Explanation of Incorrect Options * **Option A (Active Tension):** This curve typically shows a bell shape, peaking at the optimal resting length ($L_0$) where actin-myosin overlap is maximal, and decreasing as the muscle is overstretched. * **Option B & D:** These usually represent intermediate points or specific components of the active tension curve (like the descending limb) rather than the standalone contribution of elastic elements. * **Option C:** Often represents the "Total Tension" curve itself, which is the resultant of adding the active and passive components. ### High-Yield NEET-PG Pearls * **Titin:** The primary protein responsible for passive tension and for keeping thick filaments centered in the sarcomere. * **Frank-Starling Law:** In cardiac muscle, the passive tension curve is much steeper than in skeletal muscle, preventing overstretch and ensuring efficient pumping. * **Optimal Length ($L_0$):** The length at which active tension is maximal (approx. 2.0–2.2 μm per sarcomere).

Question 1

The force of muscle contraction can be increased by all of the following mechanisms except:

Accepted Answer

Increasing the amplitude of action potentials in the motor neurons

Answer

Increasing the frequency of activation of motor units

Answer

Increasing the number of motor units activated

Answer

Recruiting larger motor units

Question 2

Which of the following changes occur in bone growth?

Accepted Answer

Increased osteocalcin

Answer

Increased acid phosphatase

Answer

Increased urinary calcium

Answer

Increased bone nucleotidase

Question 3

What is the resting membrane potential of a muscle fiber?

Accepted Answer

-90mV

Answer

-60mV

Answer

-70mV

Answer

-80mV

Question 4

Muscle weakness may be a feature of all of the following EXCEPT:

Accepted Answer

Physostigmine therapy

Answer

Progressive degeneration of muscle fibres

Answer

Magnesium deficiency

Answer

Myasthenia gravis

Question 5

All of the following are true about excitation-contraction coupling EXCEPT:

Accepted Answer

Calcium binds to troponin to initiate muscle contraction.

Answer

Acetylcholine is released at the nerve terminal.

Answer

Calcium is pumped back into the sarcoplasmic reticulum during relaxation.

Answer

Calcium is released from the sarcoplasmic reticulum during contraction.

Question 6

A cross-sectional view of a skeletal muscle fiber through the H-zone would show the presence of what?

Accepted Answer

Myosin only

Answer

Actin and myosin

Answer

Titin and myosin

Answer

Actin and titin

Question 7

What is the main component of the thin filament?

Accepted Answer

Actin

Answer

Myosin

Answer

Tropomyosin

Answer

Dystrophin

Question 8

In preload, which of the following can be seen?

Accepted Answer

Isotonic contraction with shortening of muscle fibers

Answer

Isotonic contraction without shortening of muscle fibers

Answer

Isometric contraction without shortening of muscle fibers

Answer

Isometric contraction with shortening of muscle fibers

Question 9

The hyperpolarization phase of the action potential is due to?

Accepted Answer

Prolonged opening of voltage-gated K+ channels

Answer

Opening of voltage-gated Cl- channels

Answer

Closure of resting Na+ channels

Answer

Closure of Cl- channels

Question 10

What is the contribution of noncontractile muscle elements to total tension?

Accepted Answer

E

Answer

A

Answer

C

Answer

B

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?