Muscle Metabolism and Fatigue Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Muscle Metabolism and Fatigue. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Muscle Metabolism and Fatigue Indian Medical PG Question 1: Which of the following statements is NOT true regarding red muscle fibers?
- A. Decreased glycolytic enzymes
- B. Used for aerobic activity
- C. Increased blood flow
- D. Increased muscle fiber length (Correct Answer)
Muscle Metabolism and Fatigue Explanation: ***Increased muscle fiber length***
- The length of muscle fibers is generally determined by the muscle's anatomical structure and function, not by whether they are red or white fibers.
- While red muscle fibers (slow-twitch) are optimized for **endurance** and **sustained contractions**, this optimization does not involve an inherent increase in the length of individual muscle fibers.
*Decreased glycolytic enzymes*
- Red muscle fibers, also known as slow-oxidative fibers, primarily rely on **aerobic metabolism** for ATP production.
- They have a lower content of glycolytic enzymes compared to white muscle fibers, which are specialized for **anaerobic glycolysis**.
*Increased blood flow*
- Red muscle fibers have a rich capillary supply, leading to **increased blood flow**, which is essential for delivering oxygen and nutrients for sustained aerobic activity.
- This extensive vascularization contributes to their characteristic red appearance and their ability to resist fatigue.
*Used for aerobic activity*
- Red muscle fibers are well-suited for prolonged, low-intensity activities due to their high concentration of **mitochondria**, myoglobin, and oxidative enzymes.
- They are primarily responsible for maintaining posture and performing **endurance activities** such as long-distance running.
Muscle Metabolism and Fatigue Indian Medical PG Question 2: What are the products of the isocitrate to α-ketoglutarate conversion in the TCA cycle?
- A. GTP, CO2
- B. NADPH, H2O
- C. FADH2, ATP
- D. NADH, CO2 (Correct Answer)
Muscle Metabolism and Fatigue Explanation: ***NADH, CO2***
- The conversion of **isocitrate to α-ketoglutarate** is an oxidative decarboxylation step catalyzed by **isocitrate dehydrogenase**.
- This reaction produces **NADH** (from NAD+) and **carbon dioxide (CO2)**, as a carbon atom is lost.
*GTP, CO2*
- **GTP** is produced during the conversion of **succinyl-CoA to succinate** in a substrate-level phosphorylation step, not during the isocitrate to α-ketoglutarate conversion.
- While CO2 is produced in the latter, GTP is not.
*NADPH, H2O*
- **NADPH** is primarily generated in the **pentose phosphate pathway** and is used for reductive biosynthesis, not directly produced in the TCA cycle.
- **H2O** is consumed or produced in other steps of the TCA cycle but not as a direct product of this specific reaction.
*FADH2, ATP*
- **FADH2** is produced during the conversion of **succinate to fumarate** by succinate dehydrogenase.
- **ATP** (or GTP which can be converted to ATP) is produced in the succinyl-CoA to succinate step, not at the isocitrate dehydrogenase step.
Muscle Metabolism and Fatigue Indian Medical PG Question 3: Which of the following processes primarily utilizes lactate produced anaerobically?
- A. Cori cycle (Correct Answer)
- B. Gluconeogenesis
- C. TCA cycle
- D. Glycolysis
Muscle Metabolism and Fatigue Explanation: ***Cori cycle***
- The **Cori cycle** (lactic acid cycle) involves the transport of **lactate** produced during anaerobic metabolism in muscles to the liver.
- In the **liver**, this lactate is then converted back to **glucose** via gluconeogenesis, which can be returned to the muscles.
*Gluconeogenesis*
- **Gluconeogenesis** is the synthesis of glucose from non-carbohydrate precursors, one of which is lactate.
- While it uses lactate, it is only one component of the broader **Cori cycle**, which describes the inter-organ cooperation.
*Glycolysis*
- **Glycolysis** is the metabolic pathway that breaks down glucose into pyruvate, which can then be converted to lactate under anaerobic conditions.
- This process *produces* lactate but does not *utilize* it, acting upstream of lactate production.
*TCA cycle*
- The **TCA cycle** (Krebs cycle) is a central part of aerobic respiration that oxidizes acetyl-CoA to produce ATP, NADH, and FADH2.
- It does not directly utilize lactate; instead, lactate is typically converted to pyruvate before potentially entering the TCA cycle under aerobic conditions.
Muscle Metabolism and Fatigue Indian Medical PG Question 4: In severe exercise, decrease in pH is due to:
- A. Respiratory acidosis
- B. H+ retention
- C. HCO3 excretion
- D. Lactic acidosis (Correct Answer)
Muscle Metabolism and Fatigue Explanation: ***Lactic acidosis***
- During **severe exercise**, particularly anaerobic activity, muscles produce **lactic acid** secondary to **anaerobic glycolysis**.
- **Lactic acid** dissociates into **lactate** and **hydrogen ions (H+)**, leading to an increase in H+ concentration and a decrease in pH.
*Respiratory acidosis*
- **Respiratory acidosis** results from **hypoventilation**, leading to CO2 retention and an increase in carbonic acid, which lowers pH.
- During severe exercise, individuals typically **hyperventilate** to increase oxygen intake and expel CO2, thus preventing respiratory acidosis.
*H+ retention*
- **H+ retention** would imply that the body is failing to excrete hydrogen ions. While an accumulation of H+ ions does occur, it's primarily due to their overproduction (e.g., from lactic acid) rather than a simple failure of excretion mechanisms at the systemic level during exercise.
- The mechanism is direct production, not just failure to excrete.
*HCO3 excretion*
- **Bicarbonate (HCO3-)** is a crucial buffer in the blood that helps maintain pH. Its excretion would reduce buffering capacity.
- However, in cases of metabolic acidosis (like lactic acidosis), the body tries to **conserve** HCO3- or uses it to buffer excess H+ ions, rather than excrete it, until its stores are depleted.
Muscle Metabolism and Fatigue Indian Medical PG Question 5: In the context of muscle physiology, which structure is described as a threadlike component that extends along the length of a muscle fiber?
- A. Sarcomere
- B. Sarcolemma
- C. Myofibril (Correct Answer)
- D. Myofilament
Muscle Metabolism and Fatigue Explanation: ***Myofibril***
- A **myofibril** is a cylindrical organelle that runs longitudinally inside a muscle fiber and contains **contractile proteins**.
- Myofibrils are composed of repeating units called **sarcomeres**, which are the fundamental units of muscle contraction.
*Sarcomere*
- A **sarcomere** is the basic contractile unit of a muscle fiber, extending from one Z-disc to the next.
- While it is a key component for muscle contraction, it is a **segment within a myofibril**, not the threadlike component that extends the entire length of the fiber.
*Sarcolemma*
- The **sarcolemma** is the cell membrane of a muscle fiber, responsible for transmitting nerve impulses to the muscle cell.
- It encloses the muscle fiber but is not an internal, threadlike contractile component.
*Myofilament*
- **Myofilaments** are the individual protein filaments (actin and myosin) that make up a sarcomere within a myofibril.
- They are the **smallest contractile elements**, but they are not the threadlike structure that extends along the entire muscle fiber.
Muscle Metabolism and Fatigue Indian Medical PG Question 6: The most significant immediate result of lowered serum calcium is
- A. Decalcification of bones
- B. Decalcification of teeth
- C. Weakened heart action
- D. Hyperirritability of nerves and muscles (Correct Answer)
Muscle Metabolism and Fatigue Explanation: ***Hyperirritability of nerves and muscles***
- Lowered serum calcium (hypocalcemia) decreases the threshold potential of excitable cells, leading to **increased neuronal and muscular excitability**.
- This can manifest as **tetany**, muscle cramps, paresthesias, and in severe cases, seizures.
*Decalcification of bones*
- **Chronic hypocalcemia** can lead to secondary hyperparathyroidism, which may eventually cause bone decalcification.
- This is a **long-term effect**, not an immediate significant result of acutely lowered serum calcium.
*Decalcification of teeth*
- Tooth decalcification is primarily associated with **fluoride deficiency**, poor oral hygiene, or acidic erosion, not directly with acute systemic hypocalcemia.
- The calcium in teeth is **highly stable** and less readily mobilized than bone calcium in response to acute serum calcium changes.
*Weakened heart action*
- While severe **hypocalcemia can impair myocardial contractility** and lead to a weakened heart action, it is often preceded or accompanied by significant neuromuscular symptoms.
- **Hyperkalemia** is more classically associated with immediate life-threatening cardiac dysfunction, while hypocalcemia primarily affects nerve and muscle excitability first.
Muscle Metabolism and Fatigue Indian Medical PG Question 7: Protein connecting Z-lines to M-lines is:
- A. Kinin
- B. Desmin
- C. Titin (Correct Answer)
- D. Actin
Muscle Metabolism and Fatigue Explanation: ***Titin***
- **Titin** is a giant protein that extends from the **Z-disc to the M-line** in the sarcomere, acting as a molecular spring.
- It maintains the **structural integrity** of the sarcomere and provides passive elasticity to muscles.
*Kinin*
- **Kinin** is a protein involved in **inflammation and blood pressure regulation**, not a structural component of muscle sarcomeres.
- Examples include **bradykinin**, which mediates pain and vasodilation.
*Desmin*
- **Desmin** is an **intermediate filament protein** that forms a scaffold around the Z-discs, linking myofibrils together.
- While it connects myofibrils, it does not directly span between the Z-line and M-line within a single sarcomere.
*Actin*
- **Actin** is a primary component of **thin filaments** in the sarcomere and participates in muscle contraction, but it does not connect the Z-line to the M-line.
- Thin filaments are anchored at the **Z-disc** but only extend partway into the A-band.
Muscle Metabolism and Fatigue Indian Medical PG Question 8: Most common nerve used for nerve conduction study in H reflex -
- A. Median nerve
- B. Tibial nerve (Correct Answer)
- C. Peroneal nerve
- D. Ulnar nerve
Muscle Metabolism and Fatigue Explanation: ***Tibial nerve***
- The **tibial nerve** is the most commonly used nerve for H-reflex studies because it reliably activates the **soleus muscle's Ia afferents**, which are crucial for generating a strong and measurable H-reflex.
- The H-reflex of the **tibial nerve** is the most robust and easily elicitable, making it a standard for assessing **monosynaptic reflex arcs** and **S1 radiculopathy**.
*Median nerve*
- While the **median nerve** can elicit an H-reflex, it is less common and harder to obtain consistently compared to the tibial nerve due to its smaller Ia afferent input to distal muscles.
- H-reflexes in the upper limbs, including those of the median nerve, are generally smaller and more difficult to interpret clinically.
*Peroneal nerve*
- The **peroneal nerve** is primarily a motor nerve to the anterior and lateral compartments of the leg; it does not produce a significant or clinically useful H-reflex.
- An H-reflex is typically an electromyographic response to stimulation of **Ia afferent fibers**, and the peroneal nerve lacks the prominent Ia afferent pool necessary for a robust reflex.
*Ulnar nerve*
- Similar to the median nerve, the **ulnar nerve** can produce an H-reflex, but it is typically small and less reliable than the tibial nerve due to fewer Ia afferent fibers involved in a monosynaptic arc compared to the soleus.
- Its clinical utility for H-reflex studies is limited due to the difficulty in eliciting a consistent and large response.
Muscle Metabolism and Fatigue Indian Medical PG Question 9: Inverse stretch reflex is mediated :
- A. Unmyelinated C fibres
- B. Dorsal Column
- C. Muscle spindle
- D. Golgi tendon organ (Correct Answer)
Muscle Metabolism and Fatigue Explanation: ***Golgi tendon***
- The **Golgi tendon organ (GTO)** is a **proprioceptor** located at the junction of muscle fibers and tendons, sensitive to changes in muscle tension.
- When muscle tension becomes excessive, the GTO is activated, inhibiting the alpha motor neurons innervating that muscle, leading to muscle relaxation, which is the **inverse stretch reflex**.
*Unmyelinated C fibres*
- These fibers are primarily involved in transmitting **slow, dull pain** and **temperature sensations**, but not proprioceptive reflexes.
- Their conduction velocity is much slower than that required for rapid protective reflexes.
*Dorsal Column*
- The dorsal column-medial lemniscus pathway is responsible for transmitting **fine touch, vibration, and proprioception** to the brain, but it is an ascending sensory pathway and does not directly mediate spinal reflexes.
- This pathway is involved in conscious perception, not the direct arc of a reflex.
*Muscle spindle*
- The **muscle spindle** is responsible for the **stretch reflex** (myotatic reflex), which causes muscle contraction in response to stretch.
- It detects changes in **muscle length and rate of change of length**, which is distinct from the inverse stretch reflex mediated by the GTO.
Muscle Metabolism and Fatigue Indian Medical PG Question 10: What is the primary site of action of tetanospasmin in the nervous system?
- A. Presynaptic terminals of the spinal cord (Correct Answer)
- B. Postsynaptic terminals of the spinal cord
- C. Neuromuscular junction
- D. Muscle fibers
Muscle Metabolism and Fatigue Explanation: ***Presynaptic terminals of the spinal cord***
- **Tetanospasmin** is transported via **retrograde axonal transport** to the central nervous system, specifically targeting the **presynaptic terminals** of inhibitory interneurons in the spinal cord.
- It interferes with the release of **inhibitory neurotransmitters** like **GABA** and **glycine**, leading to uncontrolled muscle spasms.
*Postsynaptic terminals of the spinal cord*
- This is incorrect because tetanospasmin acts by preventing the release of inhibitory neurotransmitters from the **presynaptic terminal**, rather than directly affecting the postsynaptic receptor.
- While the absence of inhibition is perceived at the postsynaptic terminal, the direct mechanism of action is presynaptic.
*Neuromuscular junction*
- This is incorrect because **tetanospasmin** does not primarily act at the neuromuscular junction; that is the site of action for toxins like **botulinum toxin**.
- Tetanospasmin is transported to the central nervous system to exert its effects.
*Muscle fibers*
- This is incorrect as **tetanospasmin** does not act directly on muscle fibers.
- Its action is on the **nervous system**, leading to altered neuronal signaling that indirectly affects muscle contraction.
More Muscle Metabolism and Fatigue Indian Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
oka