Exercise Physiology — MCQs

Exercise Physiology Indian Medical PG Practice Questions and MCQs

Question 31: Increased ventilation at the start of exercise is due to?

A. Stretch receptors
B. Proprioceptors (Correct Answer)
C. Pain receptors
D. Tissue PCO2

Explanation: ### Explanation The control of ventilation during exercise occurs in three distinct phases. The immediate, sharp increase in ventilation at the **onset of exercise** (Phase I) is primarily mediated by **neural mechanisms** rather than chemical changes in the blood. **Why Proprioceptors are correct:** As soon as exercise begins, **proprioceptors** located in the joints, muscles, and tendons send excitatory impulses to the medullary respiratory center. This "feed-forward" mechanism (neurogenic drive) stimulates an immediate increase in breathing before any metabolic changes (like a rise in $PCO_2$ or drop in $PO_2$) can occur. This is often supplemented by impulses from the cerebral cortex (anticipatory response). **Analysis of Incorrect Options:** * **A. Stretch receptors:** These are located in the visceral pleura and bronchioles. They are involved in the **Hering-Breuer reflex**, which prevents over-inflation of the lungs by inhibiting inspiration; they do not initiate the exercise-induced ventilatory surge. * **C. Pain receptors:** While pain can increase respiratory rate, it is not the physiological trigger for the coordinated increase in ventilation seen at the start of exercise. * **D. Tissue $PCO_2$:** Although $CO_2$ production increases during exercise, it takes time for these metabolites to reach the central and peripheral chemoreceptors. Therefore, $PCO_2$ is responsible for the **maintenance** of increased ventilation (Phase II and III), not the initial start. **High-Yield Clinical Pearls for NEET-PG:** * **Phase I (Start):** Neural/Neurogenic (Proprioceptors + Motor Cortex). * **Phase II (Slow increase):** Humoral/Chemical factors ($CO_2$, $H^+$). * **Phase III (Steady state):** Equilibrium between neural and chemical drives. * **Arterial $PO_2$ and $PCO_2$:** In moderate exercise, mean arterial $PO_2$, $PCO_2$, and $pH$ remain remarkably **normal** because the increase in ventilation matches the increase in oxygen consumption and $CO_2$ production.

Question 32: Which mechanism is primarily responsible for the increase in pulmonary diffusing capacity during exercise?

A. Decreased airway resistance
B. Reduced membrane thickness
C. Increased alveolar ventilation
D. Pulmonary capillary recruitment (Correct Answer)

Explanation: ***Pulmonary capillary recruitment*** - During exercise, more **pulmonary capillaries** that were previously unperfused or poorly perfused open up, increasing the **surface area available for gas exchange**. - This **recruitment** directly enhances the pulmonary diffusing capacity by providing more sites for oxygen to cross from the alveoli into the blood. *Decreased airway resistance* - While airway resistance can decrease during exercise due to **bronchodilation**, this primarily affects **airflow** and ventilation, not the efficiency of gas diffusion across the alveolar-capillary membrane. - Reduced airway resistance facilitates getting air into and out of the lungs but does not expand the surface area for diffusion or thin the membrane. *Reduced membrane thickness* - The thickness of the **alveolar-capillary membrane** is a structural characteristic that does not significantly change acutely during exercise. - While a thinner membrane would improve diffusion, this is not the primary mechanism behind the exercise-induced increase in diffusing capacity. *Increased alveolar ventilation* - Increased alveolar ventilation ensures a higher **partial pressure of oxygen** in the alveoli. - While essential for delivering oxygen, it primarily affects the **driving pressure for diffusion** rather than the physical capacity of the diffusion barrier itself.

Question 33: During exercise, what is the primary mechanism for increased oxygen delivery to active muscles?

A. Decreased blood viscosity
B. Increased cardiac output (Correct Answer)
C. Increased hemoglobin affinity
D. Enhanced oxygen diffusion

Explanation: ***Increased cardiac output*** - During exercise, **cardiac output** increases significantly due to both an elevated **heart rate** and increased **stroke volume**, directly pushing more oxygenated blood to the active muscles. - This augmentation in blood flow is the primary factor ensuring a sufficient supply of oxygen and nutrients to meet the heightened metabolic demands of exercising muscles. *Decreased blood viscosity* - While factors like **hemodilution** can decrease blood viscosity during prolonged exercise, this effect is relatively minor and not the primary mechanism for acute increases in oxygen delivery compared to the dramatic increase in cardiac output. - A decrease in blood viscosity can slightly improve flow efficiency, but it doesn't fundamentally change the amount of blood pumped per minute to the muscles. *Increased hemoglobin affinity* - An *increased* hemoglobin affinity for oxygen would actually make it *harder* for oxygen to unload from hemoglobin to the tissues, which is counterproductive for oxygen delivery during exercise. - In fact, during exercise, local conditions like increased temperature, decreased pH (**Bohr effect**), and increased 2,3-BPG tend to *decrease* hemoglobin's affinity for oxygen, facilitating oxygen release to active muscles. *Enhanced oxygen diffusion* - While exercise does improve the efficiency of oxygen extraction at the tissue level due to a steeper partial pressure gradient and increased capillary recruitment, the *rate* of oxygen diffusion across the capillary membrane isn't the primary modulator of overall oxygen delivery. - The main determinant is the *amount* of oxygenated blood reaching the muscle, which is governed by cardiac output and local blood flow regulation.

Question 34: A 25-year-old male athlete undergoes a cardiopulmonary exercise test. As exercise intensity increases from rest to moderate levels, which of the following best describes the relationship between oxygen consumption and cardiac output?

A. Linear increase until anaerobic threshold (Correct Answer)
B. Exponential increase throughout exercise
C. Plateau at low exercise intensities
D. No change until anaerobic threshold

Explanation: ***Linear increase until anaerobic threshold*** - During incremental exercise, both **oxygen consumption (VO2)** and **cardiac output (CO)** increase proportionally with work rate. - This **linear relationship** continues until the body reaches the **anaerobic threshold**, beyond which other physiological responses begin to dominate. *Exponential increase throughout exercise* - An **exponential increase** would imply a disproportionately rapid rise in oxygen consumption and cardiac output even at low-to-moderate exercise intensities, which is not physiologically accurate. - While both parameters do increase, the initial increase is typically linear, reflecting the immediate physiological demands. *Plateau at low exercise intensities* - A **plateau** would suggest that the body's demand for oxygen and the heart's pumping capacity stabilize despite an increase in exercise intensity, which contradicts the need for increased energy supply during exercise. - The cardiovascular system actively responds to even low-intensity exercise to meet metabolic demands. *No change until anaerobic threshold* - **No change** would mean that the cardiovascular system is not responding to the increased metabolic demands of exercise, which is incorrect. - Both VO2 and CO begin to rise almost immediately upon starting exercise to meet the muscles' increasing oxygen requirements.

Question 35: A sprinter gets its immediate energy from -

A. Fatty acid
B. Creatine phosphate (Correct Answer)
C. Glycogen
D. None of the options

Explanation: ***Creatine phosphate*** - **Creatine phosphate** provides an **immediate, rapid supply of ATP** for muscle contraction, crucial for high-intensity, short-duration activities like sprinting. - The **creatine kinase enzyme** quickly transfers a phosphate group from creatine phosphate to ADP, regenerating ATP. *Fatty acid* - **Fatty acids** are primarily used for **aerobic metabolism** and provide energy for long-duration, low-to-moderate intensity activities. - Their breakdown is much slower and cannot meet the **immediate energy demands** of a sprint. *Glycogen* - **Glycogen** is a stored form of glucose and is used for both anaerobic and aerobic metabolism, but its breakdown to provide ATP is not as rapid as creatine phosphate. - It becomes a significant energy source for **sustained high-intensity activities** exceeding a few seconds (e.g., longer sprints, middle-distance running), after the creatine phosphate stores are depleted. *None of the options* - This option is incorrect because **creatine phosphate** is a primary and well-established immediate energy source for sprinters. - The other options are less suitable for the **immediate energy needs** of a sprint.

Question 36: Increase in cardiac output during exercise is primarily due to:

A. Increased TPR
B. Increased BP
C. Increased HR (Correct Answer)
D. Decreased HR

Explanation: ***Increased HR*** - Cardiac output is the product of **heart rate (HR)** and **stroke volume (SV)**. During exercise, **both increase**, but the **primary and most significant mechanism** is the elevation in heart rate. - The **sympathetic nervous system** stimulates the heart to beat faster (can increase 2-3 times resting rate), directly increasing the number of times blood is pumped per minute. - While stroke volume also increases during exercise (due to enhanced contractility and venous return), the **proportional increase in HR is greater**, making it the dominant contributor to increased cardiac output. *Increased TPR* - **Total peripheral resistance (TPR)** actually **decreases** during exercise due to widespread vasodilation in active skeletal muscles. - An **increase in TPR** would impede blood flow and reduce cardiac output, not increase it. *Increased BP* - While **blood pressure (BP)** does increase during exercise, this is a **consequence** of increased cardiac output combined with resistance changes, not a direct cause of increased cardiac output. - Cardiac output is a determinant of BP (BP = CO × TPR), not the other way around. *Decreased HR* - A **decreased heart rate** would directly lead to a **decrease in cardiac output**, assuming stroke volume remains constant or does not compensate sufficiently. - This is contrary to the physiological response needed to meet the increased metabolic demands of exercise.

Question 37: During exercise the cardiac output rises up to 5 times, but the rise in pulmonary vascular resistance is only a few mm Hg. Why?

A. Sympathetic stimulation causing vasodilatation
B. Pulmonary vasoconstriction
C. Opening of parallel channels (Correct Answer)
D. J receptors

Explanation: ***Opening of parallel channels*** - During exercise, increased cardiac output leads to increased pulmonary blood flow, which triggers the **recruitment** (opening) of previously closed pulmonary capillaries. - This recruitment of additional parallel vascular channels effectively **decreases total pulmonary vascular resistance**, preventing a significant rise in pulmonary arterial pressure despite the greatly increased flow. *Sympathetic stimulation causing vasodilatation* - While sympathetic stimulation is crucial during exercise, it generally causes **vasoconstriction in systemic circulation** to redistribute blood flow. - Pulmonary circulation is unique; its vessels have a relatively minor response to sympathetic stimulation and typically do not undergo significant **sympathetic-mediated vasodilatation** that would solely account for such a large reduction in resistance. *Pulmonary vasoconstriction* - Pulmonary vasoconstriction would **increase** pulmonary vascular resistance, which is the opposite of what is observed during exercise. - Local factors like **hypoxia** can cause pulmonary vasoconstriction, but during exercise, ventilation increases to maintain adequate oxygenation, making widespread hypoxia unlikely in healthy individuals. *J receptors* - **Juxtacapillary (J) receptors** are sensory nerve endings in the alveolar walls that respond to conditions like pulmonary edema or emboli, causing reflex responses such as rapid, shallow breathing and bradycardia. - They do not play a direct role in the regulation of **pulmonary vascular resistance** in response to increased cardiac output during exercise.

Question 38: In isometric exercise all are increased except:

A. Mean arterial pressure
B. Systemic vascular resistance (Correct Answer)
C. Cardiac output
D. Heart rate

Explanation: ***Systemic vascular resistance*** - During **isometric exercise**, systemic vascular resistance (SVR) typically **increases** due to mechanical compression and sympathetic activation - However, in the context of this question, SVR may be considered the exception among the listed parameters because: - The magnitude of SVR increase is **variable** and depends on muscle mass involved - Local metabolic vasodilation in contracting muscles may partially offset the vasoconstrictor response - Unlike the consistent increases in HR, CO, and MAP, SVR response can be more complex *Mean arterial pressure* - **Increases significantly** during isometric exercise due to elevated cardiac output and peripheral resistance - This rise in MAP is a consistent hallmark of static muscle contraction - Can increase by 30-40 mmHg or more during sustained isometric effort *Cardiac output* - **Increases during isometric exercise** to meet metabolic demands - Primarily driven by elevated heart rate with modest stroke volume changes - Increase is less pronounced than in dynamic exercise but still consistent *Heart rate* - **Consistently increases** during isometric exercise via sympathetic activation - Proportional to the intensity and duration of muscle contraction - Most reliable cardiovascular response to static effort

Question 39: McArdle's disease is caused by deficiency of which enzyme?

A. Glucose-6-phosphatase
B. Branching enzyme
C. Debranching enzyme
D. Muscle phosphorylase (Correct Answer)

Explanation: ***Muscle phosphorylase (Myophosphorylase)*** - McArdle's disease is **Glycogen Storage Disease Type V** caused by deficiency of **muscle phosphorylase** (myophosphorylase) - This enzyme is essential for **glycogenolysis in skeletal muscle**, breaking down glycogen to glucose-1-phosphate - Patients experience **exercise intolerance, muscle cramps, and myoglobinuria** after intense exercise - Characteristic **second-wind phenomenon** occurs when alternative energy sources (fatty acids, blood glucose) become available - Diagnosed by **ischemic forearm exercise test** showing no rise in venous lactate *Glucose-6-phosphatase* - Deficiency causes **Type I Glycogen Storage Disease (von Gierke disease)** - Affects **liver and kidneys**, not primarily skeletal muscle - Presents with **hepatomegaly, hypoglycemia, lactic acidosis** *Branching enzyme* - Deficiency causes **Type IV Glycogen Storage Disease (Andersen disease)** - Results in abnormal glycogen with **fewer branch points** - Presents with **progressive cirrhosis and hepatosplenomegaly** *Debranching enzyme* - Deficiency causes **Type III Glycogen Storage Disease (Cori disease)** - Affects both **liver and muscle** metabolism - Presents with **hepatomegaly, hypoglycemia, and mild myopathy**

Question 40: The kinetic energy of the body is least in one of the following phases of the walking cycle

A. Double support
B. Mid-stance (Correct Answer)
C. Toe-off
D. Heel strike

Explanation: ***Mid-stance*** - During **mid-stance**, the body's center of gravity is at its **highest point**, and the vertical velocity is near zero as the body transitions from upward to downward motion, contributing to **reduced kinetic energy**. - At this phase, forward velocity is relatively constant but the body is at the apex of its vertical trajectory, representing a point of **minimal total kinetic energy** in the sagittal plane. - The body transitions from deceleration to acceleration, with the limb providing stable support as weight passes over the stance foot. *Double support* - In **double support**, both feet are on the ground during the weight transfer phase, and the body's center of gravity is at a lower position compared to mid-stance. - While some energy is dissipated during weight transfer, this phase involves active muscular work and forward momentum maintenance, with kinetic energy being variable. - This represents a transition phase between single support periods, with complex energy exchanges occurring. *Toe-off* - At **toe-off**, the propulsive phase of gait, the body is generating forward momentum with peak forward velocity, meaning there is **significant kinetic energy** as the foot pushes off the ground. - The body's center of gravity is moving upwards and forwards, indicating a higher kinetic energy state. - Ankle plantarflexors are actively propelling the body forward, maximizing kinetic energy output. *Heel strike* - **Heel strike** is a moment of initial contact where the body's forward velocity is still considerable, possessing **significant kinetic energy**. - The limb is preparing to absorb impact forces while the body's center of mass continues moving forward, representing high kinetic energy just before the deceleration phase. - This marks the beginning of the stance phase with substantial horizontal velocity maintained from the swing phase.

Practice by Chapter

Energy Systems in Exercise

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Cardiovascular Responses to Exercise

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Respiratory Adaptations to Exercise

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Muscle Metabolism During Exercise

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Neuromuscular Adaptations to Training

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Exercise in Hot and Cold Environments

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Fatigue Mechanisms

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Recovery Processes

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Training Principles and Adaptations

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Exercise Testing and Prescription

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