Muscle Metabolism — MCQs
Episodic muscle weakness is seen in all of the following EXCEPT:
What are the products of the isocitrate to α-ketoglutarate conversion in the TCA cycle?
Muscle phosphorylase deficiency leads to which glycogen storage disorder?
Both the liver and muscle contain glycogen, yet, unlike the liver, muscle is not capable of contributing glucose to the circulation. What is the reason for this?
Glycogen storage disorder due to muscle phosphorylase deficiency is which type of disease?
Which of the following pathways is the major energy-providing pathway for fast-twitch muscle?
During a 100 m sprint which of the following is used by the muscle for meeting energy demands?
Postmortem caloricity may be seen in all the following causes of death, except:
What is the earliest sign of malignant hyperthermia?
What is the sequence of rigor mortis in the human body?
Muscle Metabolism Indian Medical PG Practice Questions and MCQs
Question 1: Episodic muscle weakness is seen in all of the following EXCEPT:
- A. Eaton-Lambert syndrome
- B. Hyperglycemia (Correct Answer)
- C. Hypercalcemia
- D. Hypokalemia
Explanation: ***Hyperglycemia*** - While chronic and severe hyperglycemia can lead to **neuropathies** and muscle wasting over time, it typically does not cause acute, episodic muscle weakness. - Acute muscle weakness in diabetes is more commonly due to **hypoglycemia** or severe electrolyte imbalances, not hyperglycemia itself. *Eaton-Lambert syndrome* - This **presynaptic disorder** of neuromuscular transmission is characterized by episodic and progressive proximal muscle weakness, which often improves with repetitive muscle contraction [3]. - It is frequently associated with **small cell lung cancer** [2]. *Hypercalcemia* - High levels of calcium can interfere with neuromuscular excitability, leading to **proximal muscle weakness**, fatigue, and lethargy, which can be episodic. - This is due to the impact of calcium on **nerve and muscle cell membrane potential**. *Hypokalemia* - Low potassium levels can cause several neuromuscular symptoms, including **episodic muscle weakness**, cramps, and even paralysis [1]. - Potassium plays a crucial role in maintaining the **resting membrane potential** of muscle cells, and its depletion impairs muscle contraction.
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)
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.
Question 3: Muscle phosphorylase deficiency leads to which glycogen storage disorder?
- A. Hers disease
- B. Cori's disease
- C. Andersen disease
- D. McArdle's disease (Correct Answer)
Explanation: **McArdle's disease** - **McArdle's disease** (Glycogen Storage Disease Type V) is characterized by a deficiency of **muscle phosphorylase** (myophosphorylase). - This enzyme defect prevents the breakdown of glycogen in muscle cells, leading to symptoms like **exercise intolerance**, muscle pain, and cramping. *Hers disease* - **Hers disease** (Glycogen Storage Disease Type VI) is caused by a deficiency of **liver phosphorylase**. - Its primary manifestations are **hepatomegaly**, hypoglycemia, and sometimes hyperlipidemia, due to impaired glycogenolysis in the liver. *Cori's disease* - **Cori's disease** (Glycogen Storage Disease Type III) is caused by a deficiency of **glycogen debranching enzyme** (amylo-1,6-glucosidase). - This leads to abnormal glycogen structure accumulation in the liver, heart, and muscle, causing **hypoglycemia**, hepatomegaly, and myopathy. *Andersen disease* - **Andersen disease** (Glycogen Storage Disease Type IV) is caused by a deficiency of **glycogen branching enzyme** (amylo-α-1,4-α-1,6-transglucosidase). - This results in the formation of abnormally structured, long-chain glycogen, primarily affecting **liver** and sometimes heart, leading to cirrhosis and liver failure.
Question 4: Both the liver and muscle contain glycogen, yet, unlike the liver, muscle is not capable of contributing glucose to the circulation. What is the reason for this?
- A. Glycolytic activity consumes all of the glucose it generates, preventing release into circulation.
- B. Does not have the enzyme glucose-1-phosphatase.
- C. Does not have the enzyme glycogen phosphorylase.
- D. Does not have the enzyme glucose-6-phosphatase (Correct Answer)
Explanation: ***Does not have the enzyme glucose-6-phosphatase*** - **Glucose-6-phosphatase** is the enzyme responsible for dephosphorylating **glucose-6-phosphate** to glucose, allowing it to exit the cell and enter the bloodstream. - Since muscle cells lack this enzyme, the glucose-6-phosphate produced from glycogenolysis is trapped within the muscle cell and used for its own energy needs. *Glycolytic activity consumes all of the glucose it generates, preventing release into circulation.* - While muscle does utilize the glucose it generates for its own energy via glycolysis, the fundamental reason for trapping glucose within the cell is the absence of **glucose-6-phosphatase**, not just the consumption itself. - If **glucose-6-phosphatase** were present, the muscle could still release glucose even if some was used for glycolysis, especially under conditions of high glycogenolysis. *Does not have the enzyme glucose-1-phosphatase.* - **Glucose-1-phosphatase** is not a commonly recognized enzyme in glucose metabolism; the conversion between glucose-1-phosphate and glucose-6-phosphate is catalyzed by **phosphoglucomutase**. - Therefore, the absence of an enzyme with this specific name is not the reason muscle cannot release glucose into circulation. *Does not have the enzyme glycogen phosphorylase.* - Muscle tissue readily expresses **glycogen phosphorylase**, which is the enzyme responsible for breaking down glycogen into **glucose-1-phosphate** during glycogenolysis. - If muscle lacked **glycogen phosphorylase**, it would not be able to break down glycogen at all, which is contrary to its role as an energy reserve.
Question 5: Glycogen storage disorder due to muscle phosphorylase deficiency is which type of disease?
- A. Pompe's disease
- B. Andersen's disease
- C. Tarui's disease
- D. McArdle's disease (Correct Answer)
Explanation: ***McArdle's disease*** - This condition is also known as **Glycogen Storage Disease Type V**, which is specifically caused by a deficiency in **muscle phosphorylase** (myophosphorylase). - Patients typically present with exercise intolerance, muscle pain, and cramping due to the inability to break down muscle glycogen for energy. *Pompe's disease* - This is **Glycogen Storage Disease Type II**, caused by a deficiency in **acid alpha-glucosidase** (acid maltase). - It primarily affects the heart and skeletal muscles, leading to cardiomegaly and hypotonia, and is not a muscle phosphorylase deficiency. *Andersen's disease* - Also known as **Glycogen Storage Disease Type IV**, this results from a deficiency in **glycogen-branching enzyme**. - It leads to the accumulation of abnormal glycogen structures in the liver and muscles, causing liver cirrhosis and muscle weakness. *Tarui's disease* - This is **Glycogen Storage Disease Type VII**, caused by a deficiency in **phosphofructokinase-1 (PFK-1)**, an enzyme involved in glycolysis. - Like McArdle's, it presents with exercise intolerance and muscle pain, but the enzymatic defect is distinct from muscle phosphorylase.
Question 6: Which of the following pathways is the major energy-providing pathway for fast-twitch muscle?
- A. Glycolysis (Correct Answer)
- B. Utilisation of ketone bodies
- C. Amino acid breakdown
- D. β oxidation of fatty acids
Explanation: ***Glycolysis*** - **Fast-twitch muscle fibers** (Type II) are designed for rapid, powerful contractions over short periods and rely primarily on **anaerobic metabolism**. - **Glycolysis** is the major energy-providing pathway under these conditions, quickly converting **glucose** into ATP without the need for oxygen, leading to lactate production. *β oxidation of fatty acids* - This pathway is the primary energy source for **slow-twitch muscle fibers** (Type I) which are adapted for sustained activity and rely on **aerobic respiration**. - **Fatty acid oxidation** is slower and requires oxygen, making it less suitable for the rapid ATP demands of fast-twitch muscles. *Utilisation of ketone bodies* - **Ketone bodies** are typically used as an alternative fuel source by the **brain** and **muscle** during prolonged fasting or starvation, when glucose availability is low. - While muscles can utilize ketone bodies, they are not the primary or major energy source for fast-twitch muscle activity, especially during immediate, intense exertion. *Amino acid breakdown* - **Amino acid breakdown** (protein catabolism) is primarily used for energy during conditions of severe calorie restriction or prolonged exercise when other fuel sources are depleted, or for glucose synthesis via **gluconeogenesis**. - It is not a major or rapidly accessible energy source for the immediate, high-demand ATP requirements of fast-twitch muscle.
Question 7: During a 100 m sprint which of the following is used by the muscle for meeting energy demands?
- A. Phosphofructokinase
- B. Phosphocreatine (Correct Answer)
- C. Glucose 1 - phosphate
- D. Creatine phosphokinase
Explanation: ***Phosphocreatine*** - **Phosphocreatine (PCr)** is the primary energy source for a **100m sprint** (lasting 10-20 seconds). - The **ATP-PC (phosphagen) system** provides **immediate energy** by rapidly regenerating **ATP** from ADP through the transfer of a high-energy phosphate group. - This system is crucial for **short bursts of maximal intensity exercise** where energy demand exceeds the capacity of glycolysis and oxidative phosphorylation to respond quickly enough. - Phosphocreatine stores can fuel maximum effort for approximately **10-15 seconds**, making it ideal for sprint activities. *Phosphofructokinase* - **Phosphofructokinase (PFK)** is a key regulatory enzyme in **glycolysis**, not an energy substrate. - While PFK-catalyzed glycolysis contributes ATP during intense exercise, it cannot provide energy as rapidly as the phosphocreatine system. - Glycolysis becomes more prominent after the first 10-15 seconds of maximal effort. *Glucose 1-phosphate* - **Glucose 1-phosphate** is an intermediate in **glycogenolysis** (breakdown of glycogen to glucose-6-phosphate). - It is part of the pathway leading to glucose availability for glycolysis, but is not a **direct, immediate energy source** for muscle contraction. - Unlike phosphocreatine, it cannot directly regenerate ATP. *Creatine phosphokinase* - **Creatine phosphokinase (CPK)**, also known as **creatine kinase (CK)**, is the **enzyme** that catalyzes the reversible transfer of phosphate from phosphocreatine to ADP. - It facilitates the energy transfer reaction but is **not an energy substrate** itself. - The enzyme enables the phosphocreatine system to function, but the actual energy comes from phosphocreatine.
Question 8: Postmortem caloricity may be seen in all the following causes of death, except:
- A. Barbiturates poisoning (Correct Answer)
- B. Septicemia
- C. Strychnine poisoning
- D. Tetanus
Explanation: ***Barbiturates poisoning*** - **Barbiturate poisoning** is a **CNS depressant** that typically leads to **hypothermia**, not postmortem caloricity, due to central nervous system depression and reduced metabolic rate. - The body's temperature tends to fall faster than normal after death in such cases. - Barbiturates suppress the thermoregulatory center and decrease metabolic activity. *Septicemia* - **Septicemia** often causes **hyperpyrexia** (high fever) ante-mortem due to systemic inflammation and infection. - This elevated core temperature can persist for a short period after death, resulting in **postmortem caloricity**. - The inflammatory response generates significant heat that remains temporarily post-death. *Strychnine poisoning* - **Strychnine poisoning** leads to severe **convulsions** and muscle rigidity due to inhibition of inhibitory neurotransmitters. - Sustained periods of intense muscle activity generate excessive **heat** ante-mortem, which is retained postmortem, causing caloricity. - The violent convulsions and opisthotonus posture produce marked heat generation. *Tetanus* - **Tetanus** is characterized by muscle spasms and rigidity caused by the **tetanospasmin toxin** blocking inhibitory signals. - The prolonged and intense **muscle contractions** before death generate a large amount of heat, contributing to postmortem caloricity. - Similar mechanism to strychnine but caused by bacterial toxin rather than plant alkaloid.
Question 9: What is the earliest sign of malignant hyperthermia?
- A. Elevated end tidal carbon dioxide is an early sign (Correct Answer)
- B. Hyperkalemia and myoglobinuria
- C. Masseter muscle rigidity after succinylcholine
- D. Tachycardia and arrhythmias
Explanation: ***Elevated end tidal carbon dioxide is an early sign*** - An abrupt and unexplained **increase in end-tidal carbon dioxide (ETCO2)** is often the *first and most sensitive indicator* of malignant hyperthermia during anesthesia. - This rise reflects the excessive **CO2 production** due to uncontrolled muscle metabolism before a significant temperature increase is observed. *Dantrolene sodium is the drug of choice* - While **dantrolene sodium** is indeed the definitive treatment for malignant hyperthermia, it is *not an early sign* of the condition. - Administration of dantrolene is initiated *after* the signs and symptoms, such as elevated ETCO2, become apparent. *Isoflurane is an absolute contraindication* - **Volatile anesthetic agents** like **isoflurane** are known triggers for malignant hyperthermia in susceptible individuals. - Therefore, using isoflurane in a patient with a history of or susceptibility to MH is indeed contraindicated, but this statement describes a *trigger* or *preventative measure*, not an early sign. *Characterized by muscle rigidity, hyperthermia, and metabolic acidosis* - **Muscle rigidity**, **hyperthermia**, and **metabolic acidosis** are *later and more prominent signs* of malignant hyperthermia as the uncontrolled muscle contraction and metabolism progress. - They represent the more advanced stages of the syndrome and typically follow the initial rise in ETCO2.
Question 10: What is the sequence of rigor mortis in the human body?
- A. Centre to periphery
- B. Head to foot (Correct Answer)
- C. Foot to head
- D. Simultaneously
Explanation: ***Head to foot*** - Rigor mortis follows **Nysten's Law**, progressing in a **descending pattern** from head to feet. - Begins in smaller muscles with higher metabolic activity: **masseter (jaw), eyelids, and facial muscles** (2-4 hours post-mortem). - Then progresses to **neck → upper extremities → trunk → lower extremities** (completing over 12 hours). - This sequence relates to muscle size, ATP depletion rates, and surface area-to-volume ratios. *Centre to periphery* - This pattern does **not accurately describe** rigor mortis progression. - While smaller muscles are affected first, the progression follows a **craniocaudal (head-to-foot) direction**, not a radial center-to-periphery pattern. - The anatomical distribution is vertically sequential, not centrifugal. *Foot to head* - This is the **opposite of the established progression** described by Nysten's Law. - Lower extremity muscles develop rigor mortis **last**, not first. - This would contradict classic forensic pathology observations. *Simultaneously* - Rigor mortis is a **time-dependent sequential process**, not simultaneous. - Different muscle groups deplete ATP and accumulate calcium at **varying rates over several hours**. - The progressive nature (2-4 hours onset, 12 hours peak, 36-48 hours resolution) demonstrates it cannot be simultaneous.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free