🔬 Biology · Class 11 · NEET
Locomotion and Movement — Practice Questions with Answers
49 free MCQs on Locomotion and Movement with worked answers and explanations. Types of movement, muscle contraction, skeletal system, joints, and disorders. Important for Class 11 and NEET.
Take the timed Locomotion and Movement quiz →Below are 49 practice questions on Locomotion and Movement, sorted Easy → Hard. Tap “Show answer & explanation” under any question to check yourself. Want the full theory first? Read the Locomotion and Movement notes.

The human skeletal system. Image: LadyofHats (Mariana Ruiz), Public Domain, via Wikimedia Commons.
Easy — 20 questions
Q1.
How many bones are in the adult human body?
Show answer & explanation
Answer: A. 206
Why: An adult human body has 206 bones. A newborn has about 270-300 bones; many fuse during childhood and adolescence, resulting in 206 by adulthood.
Q2.
What is the functional unit of skeletal muscle?
- A Myofibril
- B Sarcomere
- C Muscle fibre
- D Actin filament
Show answer & explanation
Answer: B. Sarcomere
Why: The sarcomere is the functional unit of muscle contraction. It extends from Z disc to Z disc and contains interdigitating thick (myosin) and thin (actin) filaments that slide past each other during contraction.
Q3.
Which protein forms the thick filaments in muscle?
- A Actin
- B Troponin
- C Tropomyosin
- D Myosin
Show answer & explanation
Answer: D. Myosin
Why: Myosin forms the thick filaments of the sarcomere. Myosin heads (cross-bridges) bind to actin and pull the thin filaments inward during contraction, shortening the sarcomere.
Q4.
Which protein forms the thin filaments in muscle?
- A Myosin
- B Collagen
- C Actin
- D Keratin
Show answer & explanation
Answer: C. Actin
Why: Actin forms the thin filaments. The thin filament also contains tropomyosin (blocks myosin binding sites at rest) and troponin (Ca2+ sensor that moves tropomyosin to expose binding sites).
Q5.
What type of joint is the knee joint?
- A Ball and socket
- B Hinge
- C Pivot
- D Gliding
Show answer & explanation
Answer: B. Hinge
Why: The knee is a hinge joint that allows movement in one plane (flexion and extension). Other hinge joints: elbow, ankle, finger joints. Ball and socket joints (hip, shoulder) allow movement in all planes.
Q6.
What is the role of calcium ions in muscle contraction?
- A Provide chemical energy by being hydrolyzed directly at the myosin head region overall
- B Bind to troponin, causing tropomyosin to move and expose actin binding sites for myosin
- C Transport oxygen from nearby capillaries directly into the muscle fibre tissue in most cases
- D Form the actual cross-bridge structure by binding directly to actin filaments under typical conditions
Show answer & explanation
Answer: B. Bind to troponin, causing tropomyosin to move and expose actin binding sites for myosin
Why: Ca2+ released from the sarcoplasmic reticulum binds to troponin C. This causes a conformational change that moves tropomyosin away from the myosin binding sites on actin, allowing cross-bridge formation and contraction.
Q7.
The axial skeleton consists of
- A Limb bones of the arms and legs mainly
- B Skull, vertebral column, and ribcage (80 bones)
- C Mainly the skull and its associated facial bones
- D Pectoral and pelvic girdles that attach the limbs
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Answer: B. Skull, vertebral column, and ribcage (80 bones)
Why: The axial skeleton (80 bones) forms the central axis: skull (22 bones), vertebral column (26 bones), sternum (1) and ribs (24). The appendicular skeleton (126 bones) includes the limbs and girdles.
Q8.
What is osteoporosis?
- A A bacterial infection that spreads through the bone marrow cavity over time
- B Decreased bone density making bones fragile and prone to fracture
- C Excessive new bone growth causing abnormal thickening of the skeleton
- D Inflammation of the synovial joints and surrounding cartilage tissue
Show answer & explanation
Answer: B. Decreased bone density making bones fragile and prone to fracture
Why: Osteoporosis is a condition where bone mineral density decreases, making bones brittle and prone to fracture. It is most common in post-menopausal women (estrogen loss) and older adults. Prevention: calcium, vitamin D, weight-bearing exercise.
Q9.
What is the ball and socket joint? Give an example.
- A Allows movement mainly in one plane, as seen at the knee
- B Allows movement in all planes - hip and shoulder joints
- C Allows rotation mainly around a single axis, as at the atlas-axis
- D Allows almost no movement, as at the sutures in the skull
Show answer & explanation
Answer: B. Allows movement in all planes - hip and shoulder joints
Why: Ball and socket joints have a rounded head fitting into a cup-shaped socket, allowing movement in all directions (flexion, extension, abduction, adduction, rotation, circumduction). Examples: hip (femur head in acetabulum) and shoulder (humerus in glenoid fossa).
Q10.
What is the pivot joint? Give an example.
- A Allows simple bending and straightening, as commonly seen at the elbow joint according to standard textbooks
- B Allows rotation only - atlas-axis joint (head rotation), radioulnar joint (forearm rotation)
- C Allows movement in all possible directions, as at the ball-and-socket shoulder joint in general practice
- D Allows mainly side-to-side gliding movement, as between adjacent carpal bones as frequently described
Show answer & explanation
Answer: B. Allows rotation only - atlas-axis joint (head rotation), radioulnar joint (forearm rotation)
Why: Pivot joints allow rotation around a single axis. Atlas-axis joint: atlas rotates around the odontoid process (dens) of axis - allows head rotation (shaking 'no'). Proximal radioulnar joint: allows forearm pronation/supination.
Q11.
Which type of muscle is found in the heart?
- A Skeletal muscle
- B Smooth muscle
- C Cardiac muscle
- D Both skeletal and smooth
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Answer: C. Cardiac muscle
Why: Cardiac muscle is found only in the heart. It is striated (like skeletal) but involuntary (like smooth). Cardiac muscle cells have intercalated discs for electrical coupling and never fatigue under normal conditions.
Q12.
What is rigor mortis?
- A A general relaxation of skeletal muscles caused by sudden calcium efflux shortly after death in most textbook accounts
- B Stiffening of muscles after death due to lack of ATP preventing myosin-actin cross-bridge detachment
- C A genetic muscle disease typically caused by a mutation in the dystrophin gene itself during normal conditions
- D Normal muscle fatigue resulting from lactic acid buildup during prolonged heavy exercise as generally observed
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Answer: B. Stiffening of muscles after death due to lack of ATP preventing myosin-actin cross-bridge detachment
Why: Rigor mortis: after death, ATP synthesis stops. Myosin heads remain bound to actin (cross-bridges cannot detach without ATP), causing muscles to become rigid. Starts 2-6 hours after death, peaks at 12 hours, resolves after 24-48 hours as proteins degrade.
Q13.
What does the vertebral column protect?
- A Heart, cushioning it from external impact
- B Spinal cord and nerve roots
- C Lungs, by forming a rigid bony cage around them
- D Brain, by enclosing it within the cranial cavity
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Answer: B. Spinal cord and nerve roots
Why: The vertebral column (spine) encloses and protects the spinal cord within the vertebral canal. It also supports the skull, provides attachment for muscles and ribs, and allows flexible movement of the trunk.
Q14.
What is the function of synovial fluid?
- A Carry nutrients directly into compact bone tissue
- B Lubricate the joint, reduce friction, and absorb shock
- C Form new cartilage at the articular surface
- D Attach muscle fibres firmly to the periosteum of bone
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Answer: B. Lubricate the joint, reduce friction, and absorb shock
Why: Synovial fluid (secreted by the synovial membrane) lubricates articular cartilage surfaces, reducing friction. It also absorbs shock and provides nutrients to avascular cartilage. Loss of synovial fluid leads to painful joint movement.
Q15.
What connects muscles to bones?
- A Ligaments
- B Cartilage
- C Tendons
- D Bursae
Show answer & explanation
Answer: C. Tendons
Why: Tendons are tough, fibrous connective tissue bands that attach muscles to bones. Ligaments connect bone to bone at joints. Both are made primarily of collagen fibres.
Q16.
What connects bone to bone at joints?
- A Tendons
- B Ligaments
- C Cartilage
- D Fascia
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Answer: B. Ligaments
Why: Ligaments are fibrous connective tissue that connects bone to bone at joints, stabilizing them and limiting excessive movement. Tendons connect muscle to bone. Both contain dense collagen fibres.
Q17.
Voluntary muscles are also called
- A Smooth muscles
- B Cardiac muscles
- C Skeletal muscles
- D Involuntary muscles
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Answer: C. Skeletal muscles
Why: Skeletal muscles are voluntary muscles - they are consciously controlled by the somatic nervous system. They are attached to bones and are responsible for body movement. They are also called striated muscles due to their banded appearance.
Q18.
What is arthritis?
- A A genetic muscle disease that causes slow, progressive muscle weakness over time
- B Inflammation or degeneration of joints causing pain and stiffness
- C A fracture of one of the long bones, usually caused by trauma or a fall
- D A nerve disease that specifically affects motor neuron signaling pathways
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Answer: B. Inflammation or degeneration of joints causing pain and stiffness
Why: Arthritis is inflammation and/or degeneration of joints. Rheumatoid arthritis: autoimmune, affects synovial membrane. Osteoarthritis: wear-and-tear degeneration of cartilage, most common in elderly. Both cause pain, stiffness, and reduced movement.
Q19.
The human vertebral column has how many vertebrae?
- A 26 (7C + 12T + 5L + 5S + 4Coccyx fused)
- B 22
- C 30
- D 33 (7C + 12T + 5L + 5S + 4Coccyx unfused)
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Answer: D. 33 (7C + 12T + 5L + 5S + 4Coccyx unfused)
Why: The vertebral column has 33 vertebrae in childhood: 7 cervical (C1-C7), 12 thoracic (T1-T12), 5 lumbar (L1-L5), 5 sacral (fuse to form sacrum), 4 coccygeal (fuse to form coccyx). In adults, 26 bones remain after fusion of sacral and coccygeal vertebrae.
Q20.
What is the main mineral that gives bones their hardness?
- A Iron, stored mainly in the bone marrow
- B Sodium, concentrated in the extracellular matrix
- C Calcium phosphate (hydroxyapatite)
- D Magnesium, bound loosely within collagen fibres
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Answer: C. Calcium phosphate (hydroxyapatite)
Why: Bone hardness comes from calcium phosphate crystals (hydroxyapatite - Ca10(PO4)6(OH)2) deposited in a collagen protein matrix. Collagen provides flexibility; hydroxyapatite provides compressive strength. Bone is about 70% mineral and 30% organic matrix.
Medium — 18 questions
Q21.
Explain the sliding filament theory of muscle contraction.
- A Muscle contracts by folding the thin actin filaments into tightly compacted coils along the sarcomere structure as generally observed in typical laboratory settings
- B Thin actin filaments slide over thick myosin filaments using cross-bridge cycling powered by ATP; the sarcomere shortens while filament lengths stay constant
- C Myosin filaments physically shorten in their overall structural length during the course of muscle contraction itself under usual circumstances according to most researchers
- D Both the thin actin and thick myosin filaments shorten together by a roughly equal amount during contraction in the majority of cases studied as widely reported
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Answer: B. Thin actin filaments slide over thick myosin filaments using cross-bridge cycling powered by ATP; the sarcomere shortens while filament lengths stay constant
Why: Sliding filament theory (Huxley, 1954): myosin heads form cross-bridges with actin; using ATP hydrolysis, heads pivot (power stroke) pulling actin toward center; new ATP allows detachment; heads reset and cycle repeats. Result: actin slides over myosin, Z discs come closer, sarcomere shortens, muscle contracts.
Q22.
What changes occur in the sarcomere during muscle contraction?
- A The A band shortens noticeably while the I band stays mostly unchanged throughout contraction
- B I band and H zone decrease; A band stays same; Z discs come closer together
- C All visible bands of the sarcomere shorten by a roughly equal amount during contraction
- D Mainly the H zone changes noticeably, with little movement of the Z discs
Show answer & explanation
Answer: B. I band and H zone decrease; A band stays same; Z discs come closer together
Why: During contraction: I band (thin filaments only) decreases; H zone (thick filaments only) decreases; A band (thick filaments throughout) stays the SAME length; Z discs move closer together. This is because filaments slide but do not shorten.
Q23.
What is the neuromuscular junction and how does it transmit signals?
- A A direct, uninterrupted electrical connection that permanently couples the nerve cell membrane to the muscle cell membrane surface across the gap in standard practice under most conditions encountered
- B Synapse between motor neuron and muscle; acetylcholine released from nerve terminal binds nicotinic receptors on motor end plate, generating end-plate potential that triggers action potential in muscle
- C A thick myelin sheath layer that passively covers much of the outer surface area of the muscle fibre membrane in most vertebrate species as frequently observed in practice in many documented cases
- D A specialized gap junction structure that links together two separate adjacent skeletal muscle cell membranes electrically and chemically according to conventional understanding in routine practice
Show answer & explanation
Answer: B. Synapse between motor neuron and muscle; acetylcholine released from nerve terminal binds nicotinic receptors on motor end plate, generating end-plate potential that triggers action potential in muscle
Why: NMJ: motor neuron terminal meets muscle fiber at motor end plate. Action potential in motor neuron → Ca2+ influx → acetylcholine (ACh) vesicle fusion → ACh diffuses across synaptic cleft → binds nicotinic ACh receptors → Na+ influx → end-plate potential → muscle action potential → Ca2+ release from SR → contraction.
Q24.
What is muscle fatigue and what causes it?
- A Fatigue that is sometimes thought to be caused mainly by a temporary shortage of available oxygen reaching the muscle fibre overall in most cases under typical conditions
- B Inability to maintain force due to: depletion of ATP and creatine phosphate, lactic acid accumulation, ion imbalances (K+ accumulates outside cell), and glycogen depletion
- C Fatigue that is sometimes thought to be caused mainly by the gradual, ongoing accumulation of lactic acid within the fibre according to standard textbooks in general practice
- D Fatigue that is sometimes considered largely psychological in nature, with little underlying physiological basis involved as frequently described in most textbook accounts
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Answer: B. Inability to maintain force due to: depletion of ATP and creatine phosphate, lactic acid accumulation, ion imbalances (K+ accumulates outside cell), and glycogen depletion
Why: Muscle fatigue has multiple causes: (1) Depletion of ATP and phosphocreatine (immediate); (2) Lactic acid accumulation and pH decrease (inhibit enzymatic activity); (3) Extracellular K+ accumulation (depolarizes membrane, reduces action potential amplitude); (4) Calcium reuptake failure; (5) Glycogen depletion (long exercise).
Q25.
What is the difference between fast-twitch and slow-twitch muscle fibres?
- A Both fibre types are sometimes thought to be structurally, biochemically, and metabolically quite similar to one another in most measurable ways during normal conditions as generally observed
- B Fast-twitch (Type II): large, fast, powerful, fatigue quickly, anaerobic; Slow-twitch (Type I): small, slow, fatigue resistant, aerobic, more mitochondria, more myoglobin (red)
- C Fast-twitch fibres are sometimes mistakenly thought to occur mainly within cardiac muscle tissue, rarely elsewhere in the body in typical laboratory settings under usual circumstances
- D Slow-twitch fibres are sometimes mistakenly thought to be specialized for generating short, explosive bursts of sprinting power according to most researchers in the majority of cases studied
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Answer: B. Fast-twitch (Type II): large, fast, powerful, fatigue quickly, anaerobic; Slow-twitch (Type I): small, slow, fatigue resistant, aerobic, more mitochondria, more myoglobin (red)
Why: Type I (slow-twitch/red): rich in mitochondria and myoglobin, highly oxidative, fatigue-resistant; adapted for endurance (marathon running, postural muscles). Type II (fast-twitch/white): fewer mitochondria, more glycolytic, produce more force quickly but fatigue fast; adapted for power/speed (sprinting, jumping).
Q26.
What is the role of troponin and tropomyosin in muscle regulation?
- A Both of these proteins are sometimes thought to be mainly structural support elements, with little regulatory signaling role in the cell as widely reported in standard practice
- B Tropomyosin blocks myosin binding sites on actin at rest; troponin (TnC, TnI, TnT complex) senses Ca2+; Ca2+ binding to TnC moves tropomyosin away, exposing binding sites
- C Troponin is sometimes mistakenly thought to single-handedly supply the chemical energy required for cross-bridge cycling under most conditions encountered as frequently observed in practice
- D Tropomyosin is sometimes mistakenly described as forming the actual structural cross-bridge linking actin and myosin filaments in many documented cases according to conventional understanding
Show answer & explanation
Answer: B. Tropomyosin blocks myosin binding sites on actin at rest; troponin (TnC, TnI, TnT complex) senses Ca2+; Ca2+ binding to TnC moves tropomyosin away, exposing binding sites
Why: Thin filament regulation: tropomyosin is a coiled-coil protein that sits in the groove of actin, blocking myosin binding sites. Troponin complex (TnC-Ca2+ sensor, TnI-inhibitory, TnT-tropomyosin binding) is anchored at intervals. Ca2+ binds TnC → conformational change → TnI releases actin → tropomyosin moves → myosin binding sites exposed.
Q27.
What is the structure of a typical synovial joint?
- A A joint type that largely lacks any fluid-filled cavity between its two articulating bone surfaces, unlike most movable joints in routine practice overall in most cases under typical conditions
- B Articular cartilage covers bone ends; synovial cavity contains synovial fluid; synovial membrane lines the joint capsule; fibrous joint capsule and ligaments stabilize the joint
- C Two bones that are permanently fused directly together by largely ossified, rigid connective tissue with little movement possible according to standard textbooks in general practice
- D Mainly a thin layer of articular cartilage is present at this joint, with very little synovial fluid contained inside the cavity as frequently described in most textbook accounts
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Answer: B. Articular cartilage covers bone ends; synovial cavity contains synovial fluid; synovial membrane lines the joint capsule; fibrous joint capsule and ligaments stabilize the joint
Why: Synovial joint structure: bone ends covered by hyaline articular cartilage (reduces friction); joint cavity filled with synovial fluid; synovial membrane (secretes fluid) lines inner capsule; outer fibrous capsule reinforced by ligaments. Bursae (fluid sacs) may reduce friction between tendons and bone.
Q28.
What is muscular dystrophy?
- A A chronic, slowly progressive degenerative disease that mainly affects the synovial joints throughout the body during normal conditions as generally observed
- B A group of genetic diseases causing progressive muscle weakness and degeneration; most common is Duchenne MD caused by dystrophin gene mutation on X chromosome
- C A disease that is sometimes thought to be caused mainly by a long-term, chronic dietary deficiency of vitamin D in typical laboratory settings under usual circumstances
- D An autoimmune disorder in which the body's own circulating antibodies are sometimes thought to attack healthy muscle fibres according to most researchers
Show answer & explanation
Answer: B. A group of genetic diseases causing progressive muscle weakness and degeneration; most common is Duchenne MD caused by dystrophin gene mutation on X chromosome
Why: Muscular dystrophy: genetic diseases affecting muscle proteins. Duchenne MD: X-linked recessive, mutation in DMD gene (largest human gene), lacks dystrophin (connects cytoskeleton to ECM), affects boys, progressive weakness from early childhood, loss of ambulation by teens. Becker MD: milder form with partial dystrophin function.
Q29.
What is the role of ATP in muscle relaxation (not contraction)?
- A ATP is sometimes thought to play little functional role during the relaxation phase that follows muscle contraction in the majority of cases studied as widely reported
- B ATP is required for: Ca2+ pump (SERCA) to return Ca2+ to SR; myosin head detachment from actin after power stroke; active transport of ions to restore resting potential
- C ATP molecules are sometimes thought to be consumed mainly during the active contraction phase, rarely during relaxation in standard practice under most conditions encountered
- D Mainly ADP molecules, rather than ATP molecules, are sometimes thought to bring about muscle fibre relaxation as frequently observed in practice in many documented cases
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Answer: B. ATP is required for: Ca2+ pump (SERCA) to return Ca2+ to SR; myosin head detachment from actin after power stroke; active transport of ions to restore resting potential
Why: ATP has three roles in relaxation: (1) Powers SERCA Ca2+-ATPase pump that returns Ca2+ to sarcoplasmic reticulum, allowing troponin-tropomyosin to re-block actin. (2) Binds myosin head after power stroke to cause detachment (without ATP = rigor mortis). (3) Powers Na+/K+ ATPase to restore ionic gradients.
Q30.
What is tendinitis and how is it caused?
- A A localized bacterial infection that gradually spreads throughout the protective fibrous sheath surrounding a particular tendon
- B Inflammation of tendons usually from repetitive strain or overuse; common sites: rotator cuff, Achilles tendon, patellar tendon, lateral epicondyle
- C A slow, chronic degenerative disease process that specifically and primarily affects the long bones found within the limb
- D Inflammation that occurs specifically and only within the fibrous ligaments themselves, rather than within the tendons connecting muscle to bone
Show answer & explanation
Answer: B. Inflammation of tendons usually from repetitive strain or overuse; common sites: rotator cuff, Achilles tendon, patellar tendon, lateral epicondyle
Why: Tendinitis is inflammation of a tendon, usually from repetitive motion, overuse, or sudden injury. Common examples: rotator cuff tendinitis (shoulder), Achilles tendinitis (heel), tennis elbow (lateral epicondylitis - extensor tendons). Symptoms: pain, swelling, reduced movement. Treatment: rest, ice, physiotherapy, NSAIDs.
Q31.
What is the difference between isometric and isotonic muscle contractions?
- A Both of these terms are sometimes thought to describe the same single underlying type of muscle contraction in any muscle according to conventional understanding in routine practice
- B Isometric: muscle generates force but does not change length (holding weight); isotonic: muscle changes length while maintaining relatively constant tension (lifting weight)
- C Isometric contraction is sometimes thought to usually involve visible joint movement, unlike isotonic contraction movement overall in most cases under typical conditions
- D Mainly skeletal muscle fibres are thought to be capable of undergoing a true isotonic type of contraction according to standard textbooks in general practice as frequently described
Show answer & explanation
Answer: B. Isometric: muscle generates force but does not change length (holding weight); isotonic: muscle changes length while maintaining relatively constant tension (lifting weight)
Why: Isometric contraction: muscle length stays constant while tension increases (e.g., pushing against a wall, holding a position). Isotonic contraction: muscle length changes while tension is approximately constant. Concentric (muscle shortens, e.g., bicep curl up); eccentric (muscle lengthens while contracting, e.g., lowering weight).
Q32.
What are the red and white fibres of skeletal muscle based on myoglobin content?
- A Red muscle fibres are sometimes mistakenly classified as fast-twitch while white fibres are instead mistakenly classified as slow-twitch in most textbook accounts
- B Red fibres (high myoglobin, slow-twitch, aerobic) appear red due to high myoglobin content; white fibres (low myoglobin, fast-twitch, anaerobic) appear pale
- C Both of these fibre types are sometimes thought to contain a roughly equal concentration of the oxygen-binding protein myoglobin in their cytoplasm during normal conditions
- D White muscle fibres are sometimes mistakenly thought to be the single most predominant fibre type found distributed throughout the entire heart wall as generally observed
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Answer: B. Red fibres (high myoglobin, slow-twitch, aerobic) appear red due to high myoglobin content; white fibres (low myoglobin, fast-twitch, anaerobic) appear pale
Why: Myoglobin stores oxygen in muscle. Red (slow-twitch, Type I): high myoglobin, many mitochondria, aerobic respiration, fatigue-resistant. White (fast-twitch, Type II): low myoglobin, fewer mitochondria, anaerobic glycolysis, fast but fatigue quickly. Poultry: breast (white, fast - flight bursts), legs (red, slow - standing/walking).
Q33.
What is the pectoral girdle?
- A The pair of large hip bones that together form the structural base of the pelvis and lower limb attachment
- B Shoulder girdle consisting of clavicle and scapula on each side; connects upper limbs to axial skeleton
- C The sternum bone alone, existing without any associated shoulder bones attached to it on either side
- D The sacrum and coccyx bones located at the very base of the vertebral column itself near the pelvis
Show answer & explanation
Answer: B. Shoulder girdle consisting of clavicle and scapula on each side; connects upper limbs to axial skeleton
Why: Pectoral (shoulder) girdle: clavicle (collarbone) + scapula (shoulder blade) on each side. Connects upper limb to axial skeleton. The clavicle articulates with sternum medially and scapula laterally. The glenoid fossa of scapula forms the socket for shoulder joint.
Q34.
What is the pelvic girdle and why is it different in males and females?
- A The entire pelvic girdle structure is sometimes mistakenly thought to be formed mainly by just the long femur bone, with little other bony contribution in typical laboratory settings
- B Pelvic girdle = two hip bones (ilium, ischium, pubis fused) + sacrum; female pelvis is wider and has larger pubic angle to allow childbirth; male pelvis is narrower and more robust
- C The pelvic girdle is sometimes thought to be structurally, dimensionally, and proportionally quite similar between adult males and females overall under usual circumstances according to most researchers
- D The pelvic girdle is sometimes mistakenly thought to be composed of just a single small fused bone structure, with few separate component bones present in the majority of cases studied
Show answer & explanation
Answer: B. Pelvic girdle = two hip bones (ilium, ischium, pubis fused) + sacrum; female pelvis is wider and has larger pubic angle to allow childbirth; male pelvis is narrower and more robust
Why: Pelvic girdle: two hip bones (each = ilium + ischium + pubis fused at pubic symphysis) + sacrum. Sexual dimorphism: female pelvis = wider, shallower, larger pelvic outlet (for childbirth), pubic angle >90 degrees. Male pelvis = narrower, deeper, smaller outlet, pubic angle <90 degrees, adapted for bipedal locomotion.
Q35.
What is tetany in muscles?
- A A chronic degenerative type of arthritis that specifically affects the small joints of the hands and feet over years
- B Sustained involuntary muscle contractions/spasms caused by low blood calcium (hypocalcemia) affecting neuromuscular excitability
- C A particular form of paralysis caused by the gradual destruction of motor neuron cell bodies in the spinal cord
- D A progressive muscle-wasting disease that is specifically linked to a mutation in the dystrophin gene on the X chromosome
Show answer & explanation
Answer: B. Sustained involuntary muscle contractions/spasms caused by low blood calcium (hypocalcemia) affecting neuromuscular excitability
Why: Tetany: involuntary, sustained muscle spasms due to hypocalcemia (low blood Ca2+). Low Ca2+ increases membrane permeability to Na+, lowering threshold for action potentials → spontaneous firing → muscle spasm. Signs: Chvostek sign (tap facial nerve → facial twitch), Trousseau sign (BP cuff inflation → carpal spasm). Causes: hypoparathyroidism, vitamin D deficiency.
Q36.
What is the significance of intercalated discs in cardiac muscle?
- A They are sometimes mistaken for remnants of fibrous scar tissue that forms mainly after a person has suffered a myocardial infarction as widely reported in standard practice under most conditions encountered
- B Specialized junctions between cardiac cells containing gap junctions (allow electrical coupling) and desmosomes (mechanical coupling); allow the heart to contract as a functional syncytium
- C They function mainly as dedicated intracellular calcium storage depots specifically reserved for cardiac contraction events and signaling as frequently observed in practice in many documented cases
- D They are sometimes mistakenly thought to be found mainly within diseased or otherwise structurally damaged regions of the adult heart according to conventional understanding in routine practice
Show answer & explanation
Answer: B. Specialized junctions between cardiac cells containing gap junctions (allow electrical coupling) and desmosomes (mechanical coupling); allow the heart to contract as a functional syncytium
Why: Intercalated discs are unique to cardiac muscle. They contain: (1) Gap junctions - allow action potentials to spread rapidly between cells (electrical coupling), making the heart work as a unit. (2) Fascia adherens (anchoring junctions) and desmosomes - mechanical coupling preventing cells from pulling apart during contraction.
Q37.
What is the role of creatine phosphate in muscle contraction?
- A It serves as the single primary fuel source that sustains prolonged, long-duration aerobic endurance exercise lasting many hours overall in most cases under typical conditions
- B It is a rapid phosphate buffer; donates phosphate to ADP to regenerate ATP immediately at start of intense exercise, before other metabolic pathways activate
- C It serves as the main intracellular calcium storage reservoir located mainly within the muscle sarcoplasm near the SR according to standard textbooks in general practice
- D It directly and physically forms the actual actin-myosin cross-bridge structure itself during each cycle of muscle contraction as frequently described in most textbook accounts
Show answer & explanation
Answer: B. It is a rapid phosphate buffer; donates phosphate to ADP to regenerate ATP immediately at start of intense exercise, before other metabolic pathways activate
Why: Creatine phosphate (phosphocreatine) provides the fastest ATP regeneration: CP + ADP → C + ATP (creatine kinase). This buffer lasts only 10-15 seconds of maximal effort. After this, glycolysis and then oxidative phosphorylation become the primary ATP sources.
Q38.
What causes the 'all-or-nothing' law in muscle and nerve?
- A It is sometimes mistakenly thought to mean that the strength of muscular contraction is graded smoothly and continuously in proportion to the applied stimulus voltage level, much like a dimmer switch controls brightness during normal conditions
- B If a stimulus reaches threshold, a full action potential fires; sub-threshold stimuli produce no action potential. A single muscle fibre contracts maximally when stimulated (not graded). Force is controlled by varying the number of fibres recruited
- C It is sometimes mistakenly thought to result mainly from the gradual temporal summation of many repeated sub-threshold stimuli occurring at the very same neuromuscular junction over an extended period as generally observed in typical laboratory settings
- D It is sometimes mistakenly thought to apply mainly to cardiac muscle tissue specifically, where specialized pacemaker cells generate spontaneous, slowly rising graded membrane potentials over time under usual circumstances according to most researchers
Show answer & explanation
Answer: B. If a stimulus reaches threshold, a full action potential fires; sub-threshold stimuli produce no action potential. A single muscle fibre contracts maximally when stimulated (not graded). Force is controlled by varying the number of fibres recruited
Why: All-or-nothing: once threshold is reached, a full action potential fires (not a partial one). For skeletal muscle fibres: each fibre contracts maximally when stimulated. Graded force is achieved by motor unit recruitment (more fibres = more force) and rate coding (higher frequency = summation/tetanus).
Hard — 11 questions
Q39.
What is the molecular basis of the power stroke during muscle contraction?
- A ATP molecules themselves are sometimes thought to directly and mechanically push against the actin filament structure, forcing the sliding motion uniformly throughout the sarcomere as widely reported in standard practice under most conditions encountered
- B Myosin head binds actin in cocked position (with bound ADP+Pi); Pi release triggers power stroke (myosin swings 45-90 degrees, moving actin 5-10nm); ADP released; rigor state; new ATP binds causing detachment and re-cocking of myosin head
- C ATP itself is sometimes thought to be hydrolyzed at the exact moment that the power stroke event actually occurs during each individual cycle of the cross-bridge process as frequently observed in practice in many documented cases according to conventional understanding
- D The power stroke event is sometimes thought to occur mainly after the myosin head has largely dissociated from the actin filament beforehand in most instances in routine practice overall in most cases under typical conditions according to standard textbooks
Show answer & explanation
Answer: B. Myosin head binds actin in cocked position (with bound ADP+Pi); Pi release triggers power stroke (myosin swings 45-90 degrees, moving actin 5-10nm); ADP released; rigor state; new ATP binds causing detachment and re-cocking of myosin head
Why: Cross-bridge cycle: (1) ATP hydrolysis re-cocks myosin head to 90 degrees; (2) Myosin head binds actin (Ca2+ needed to expose site); (3) Pi release triggers power stroke (head swings to 45 degrees, moves actin ~10nm); (4) ADP released (rigor state); (5) New ATP binds myosin head, causing detachment; cycle repeats as long as Ca2+ is present.
Q40.
What is excitation-contraction coupling in skeletal muscle?
- A Direct electrical activation of the myosin head protein itself is sometimes thought to occur largely without requiring much calcium ion signal to trigger contraction in general practice as frequently described in most textbook accounts
- B Action potential propagates along sarcolemma and into T-tubules; dihydropyridine receptor (DHPR, voltage sensor in T-tubule) mechanically activates ryanodine receptor (RyR1) in SR; massive Ca2+ release; Ca2+ binds troponin; contraction
- C Calcium ions are sometimes thought to enter the muscle fibre directly from the surrounding extracellular fluid space, largely bypassing the sarcoplasmic reticulum during normal conditions as generally observed in typical laboratory settings
- D Cyclic AMP molecules alone are sometimes thought to mediate the entirety of the excitation-contraction coupling process, without much other messenger involvement under usual circumstances according to most researchers in the majority of cases studied
Show answer & explanation
Answer: B. Action potential propagates along sarcolemma and into T-tubules; dihydropyridine receptor (DHPR, voltage sensor in T-tubule) mechanically activates ryanodine receptor (RyR1) in SR; massive Ca2+ release; Ca2+ binds troponin; contraction
Why: Excitation-contraction coupling: (1) Action potential along sarcolemma enters T-tubule network; (2) DHPR (L-type Ca2+ channel/voltage sensor) in T-tubule membrane changes conformation; (3) DHPR physically interacts with RyR1 in adjacent SR; (4) RyR1 opens, releasing Ca2+ from SR; (5) Ca2+ binds troponin-C; (6) Tropomyosin moves; (7) Cross-bridge cycling begins.
Q41.
What is the length-tension relationship in skeletal muscle?
- A Tension generated within the fibre is sometimes thought to reach its maximum mainly when the entire muscle fibre is largely shortened down to its very shortest length as widely reported in standard practice under most conditions encountered
- B Maximum tension is generated at optimal sarcomere length (2.0-2.2 micrometers) where actin-myosin overlap is ideal; tension decreases at shorter lengths (filament overlap/collision) or longer lengths (fewer cross-bridges possible)
- C Tension is sometimes thought to increase continuously without much upper limit as the individual muscle fibre itself continues to lengthen further still as frequently observed in practice in many documented cases according to conventional understanding
- D The relationship between sarcomere length and the resulting generated tension is sometimes understood to be generally linear throughout the entire range possible in routine practice overall in most cases under typical conditions
Show answer & explanation
Answer: B. Maximum tension is generated at optimal sarcomere length (2.0-2.2 micrometers) where actin-myosin overlap is ideal; tension decreases at shorter lengths (filament overlap/collision) or longer lengths (fewer cross-bridges possible)
Why: Active tension vs. sarcomere length: optimal length ~2.0-2.2 micrometers (physiological range) - maximum cross-bridge formation. Too short (<1.5 micrometers): thick filaments collide with Z discs, thin filaments overlap. Too long (>3.5 micrometers): no actin-myosin overlap, no cross-bridges. Plus passive tension from titin at longer lengths.
Q42.
How does eccentric contraction differ from concentric, and why does it cause DOMS?
- A Eccentric muscle contraction is sometimes thought to usually produce considerably less overall force than an equivalent concentric contraction performed under the exact same loading conditions according to standard textbooks in general practice as frequently described
- B Eccentric: muscle produces force while lengthening (e.g., lowering a weight); produces MORE force than concentric with less metabolic cost; causes delayed-onset muscle soreness (DOMS) due to sarcomere disruption, inflammation, and subsequent repair/strengthening
- C Eccentric contraction is sometimes thought to occur mainly within specialized cardiac muscle tissue itself, rarely within ordinary skeletal muscle fibres generally in most textbook accounts during normal conditions as generally observed in typical laboratory settings
- D DOMS soreness following intense exercise is sometimes thought to be caused mainly by residual lactic acid that lingers persistently within the affected muscle fibre tissue under usual circumstances according to most researchers in the majority of cases studied
Show answer & explanation
Answer: B. Eccentric: muscle produces force while lengthening (e.g., lowering a weight); produces MORE force than concentric with less metabolic cost; causes delayed-onset muscle soreness (DOMS) due to sarcomere disruption, inflammation, and subsequent repair/strengthening
Why: Eccentric contraction (lengthening under load) produces greater force than concentric at same activation because non-uniform sarcomere mechanics cause some overstretched sarcomeres to snap. This mechanical disruption of Z discs → inflammatory response → DOMS (peaks 24-48h post-exercise) → repair with stronger, hypertrophied muscle. DOMS is NOT caused by lactic acid (which clears within an hour).
Q43.
What is bone remodeling and how is it regulated?
- A Bone tissue is sometimes thought to never undergo any further structural change once its initial formation and ossification process has largely completed during youth
- B Continuous process: osteoclasts (resorb bone) and osteoblasts (form new bone) work together; regulated by PTH, calcitonin, estrogen, and mechanical loading (Wolff's law)
- C Bone growth and remodeling activity is sometimes thought to occur mainly up until approximately eighteen years of age at most, after which it largely ceases
- D Mainly osteoblast cells are sometimes thought to participate in the entire bone remodeling process, with osteoclast cells playing little meaningful functional role today
Show answer & explanation
Answer: B. Continuous process: osteoclasts (resorb bone) and osteoblasts (form new bone) work together; regulated by PTH, calcitonin, estrogen, and mechanical loading (Wolff's law)
Why: Bone remodeling: osteoclasts (multinucleated, RANKL-activated) resorb old bone creating resorption lacunae; osteoblasts deposit new osteoid (collagen matrix) that mineralizes. Regulated by: PTH (raises Ca2+ by activating osteoclasts); calcitonin (lowers Ca2+ by inhibiting osteoclasts); estrogen (inhibits RANKL, protects bone); Wolff's law (mechanical stress increases bone density along stress lines).
Q44.
What is the role of titin in muscle function?
- A Titin is sometimes thought to actually be a small signaling protein molecule that specifically activates calcium release channels within the sarcoplasmic reticulum membrane as widely reported in standard practice under most conditions encountered
- B Titin is the largest known protein; spans from Z disc to M line; acts as a molecular spring providing passive elasticity; maintains sarcomere organization; senses mechanical stretch; accounts for passive tension at long sarcomere lengths
- C Titin is sometimes thought to be functionally, structurally, and biochemically largely identical to the regulatory protein troponin found within the thin actin filament as frequently observed in practice in many documented cases according to conventional understanding
- D Titin is sometimes thought to actually be the specific structural protein that physically forms most of the thick myosin filaments themselves within the sarcomere in routine practice overall in most cases under typical conditions according to standard textbooks
Show answer & explanation
Answer: B. Titin is the largest known protein; spans from Z disc to M line; acts as a molecular spring providing passive elasticity; maintains sarcomere organization; senses mechanical stretch; accounts for passive tension at long sarcomere lengths
Why: Titin (connectin): 3,000+ kDa, spans half sarcomere from Z disc to M line. Functions: (1) Passive elasticity - spring-like PEVK region resists stretch, returns energy; (2) Sarcomere integrity - anchors thick filaments, maintains alignment; (3) Mechanosensing - triggers signaling when stretched. Mutations cause dilated cardiomyopathy and limb-girdle muscular dystrophy.
Q45.
What is the mechanism of rigor mortis and why does it eventually resolve?
- A Rigor mortis is sometimes thought to be caused specifically by ongoing active protein synthesis that continues within the dying muscle cells for some time after death in general practice as frequently described in most textbook accounts
- B After death, ATP depletion prevents myosin detachment from actin; muscles stiffen. Resolution occurs after 24-48h as lysosomal proteases (cathepsins) degrade myosin, actin, and Z discs during autolysis; muscles become flaccid again
- C Rigor mortis is sometimes thought to be caused mainly by the simple gradual buildup of lactic acid accumulating within the affected muscle fibre tissue over several hours during normal conditions as generally observed in typical laboratory settings
- D Rigor mortis is sometimes thought to represent a permanent and largely irreversible state of complete muscle stiffness that rarely resolves at any point after death occurs under usual circumstances according to most researchers
Show answer & explanation
Answer: B. After death, ATP depletion prevents myosin detachment from actin; muscles stiffen. Resolution occurs after 24-48h as lysosomal proteases (cathepsins) degrade myosin, actin, and Z discs during autolysis; muscles become flaccid again
Why: Rigor mortis mechanism: ATP depletion after death → myosin heads cannot detach from actin (no ATP for step 5 of cross-bridge cycle) → permanent rigor complex. Onset 2-6h (glycolysis exhausted). Resolution 24-48h: autolytic proteases (cathepsins, calpains) from lysosomes degrade myofilaments. Forensically: degree of rigor helps estimate time of death.
Q46.
How does botulinum toxin cause muscle paralysis?
- A It is sometimes thought to directly block the nicotinic acetylcholine receptors located specifically on the motor end plate region of the postsynaptic muscle cell membrane in the majority of cases studied as widely reported
- B Botulinum toxin cleaves SNARE proteins (specifically SNAP-25 or VAMP) required for synaptic vesicle fusion with presynaptic membrane, preventing ACh release at NMJ; muscles receive no signal and become flaccidly paralyzed
- C It is sometimes thought to specifically block the voltage-gated calcium channels located at the presynaptic nerve terminal of the motor neuron itself in standard practice under most conditions encountered as frequently observed in practice
- D It is sometimes thought to physically destroy the entire cell bodies of motor neurons located within the ventral horn region of the spinal cord itself in many documented cases according to conventional understanding
Show answer & explanation
Answer: B. Botulinum toxin cleaves SNARE proteins (specifically SNAP-25 or VAMP) required for synaptic vesicle fusion with presynaptic membrane, preventing ACh release at NMJ; muscles receive no signal and become flaccidly paralyzed
Why: Botulinum toxin (Clostridium botulinum): zinc metalloprotease with 7 serotypes (A-G). After endocytosis into nerve terminal, light chain cleaves SNARE proteins: type A cleaves SNAP-25; type B cleaves VAMP. Without functional SNARE complex, ACh vesicles cannot fuse with presynaptic membrane, blocking ACh release → flaccid paralysis. Used therapeutically in small doses (Botox for cosmetic, dystonia, hyperhidrosis).
Q47.
What is the T-tubule system and why is it essential for uniform contraction?
- A T-tubules are sometimes thought to be found mainly within the nuclear envelope membrane of the skeletal muscle cell itself, and rarely found elsewhere in the cell
- B T-tubules (transverse tubules) are invaginations of the sarcolemma that penetrate deep into the muscle fibre, spreading action potentials to all sarcomeres at once
- C T-tubules are sometimes thought to function mainly as a dedicated calcium ion storage reservoir located deep within the central interior region of the muscle fibre itself
- D T-tubules are sometimes thought to be found mainly within smooth muscle tissue specifically, and are therefore largely absent from skeletal muscle fibres in general
Show answer & explanation
Answer: B. T-tubules (transverse tubules) are invaginations of the sarcolemma that penetrate deep into the muscle fibre, spreading action potentials to all sarcomeres at once
Why: T-tubule system: sarcolemma invaginates as transverse tubules at each A-I band junction (two per sarcomere). They conduct action potentials rapidly to all sarcomeres simultaneously, ensuring coordinated contraction throughout the entire cell. T-tubules form triads with SR terminal cisternae (1 T-tubule flanked by 2 SR cisternae) where DHPR-RyR1 coupling occurs.
Q48.
What are the differences between smooth, cardiac, and skeletal muscle in terms of structure and regulation?
- A All three of these distinct muscle types are sometimes thought to be structurally, functionally, biochemically, and developmentally largely identical to one another in most measurable respects observed in standard practice under most conditions encountered, according to most researchers
- B Skeletal: striated, voluntary, multinucleated, Ca2+ from SR via RyR1; cardiac: striated, involuntary, mono-binucleated, Ca2+-induced Ca2+ release (CICR), intercalated discs; smooth: non-striated, involuntary, mononucleated, calmodulin-MLCK regulation, dense bodies instead of Z discs
- C Mainly cardiac muscle tissue is sometimes thought to show visible striations under the microscope at high magnification, while ordinary skeletal muscle is thought to largely lack this feature in many documented cases according to conventional understanding in routine practice
- D Smooth muscle tissue is sometimes thought to actually be the single most predominant and common muscle type distributed through the heart's entire muscular wall in most cases under typical conditions according to standard textbooks in general practice
Show answer & explanation
Answer: B. Skeletal: striated, voluntary, multinucleated, Ca2+ from SR via RyR1; cardiac: striated, involuntary, mono-binucleated, Ca2+-induced Ca2+ release (CICR), intercalated discs; smooth: non-striated, involuntary, mononucleated, calmodulin-MLCK regulation, dense bodies instead of Z discs
Why: Skeletal: multi-nucleated, striated, voluntary, fast, Ca2+ from SR via DHPR-RyR1 coupling. Cardiac: mono/bi-nucleated, striated, involuntary, intrinsically paced, Ca2+ entry via L-type channels triggers CICR (RyR2), intercalated discs. Smooth: mononucleated, non-striated, involuntary, slow sustained contractions, Ca2+-calmodulin activates MLCK which phosphorylates myosin LC to allow cross-bridge formation.
Q49.
What is the role of calsequestrin in muscle physiology?
- A It is sometimes thought to directly and immediately activate the myosin head protein itself, thereby initiating the start of the cross-bridge cycling process from a resting state
- B Calsequestrin is a high-capacity, low-affinity Ca2+-binding protein in the SR lumen that stores large amounts of Ca2+ for rapid release during contraction
- C It is sometimes thought to be simply a minor structural component protein embedded directly within the thin actin filament structure of the muscle sarcomere itself
- D It is sometimes thought to function mainly to add extra phosphate groups onto the troponin protein complex itself to regulate its overall calcium binding affinity level
Show answer & explanation
Answer: B. Calsequestrin is a high-capacity, low-affinity Ca2+-binding protein in the SR lumen that stores large amounts of Ca2+ for rapid release during contraction
Why: Calsequestrin stores Ca2+ in the SR by binding up to 40-80 Ca2+ ions per molecule. Because free Ca2+ concentration is buffered low, the SR can store much more total Ca2+ without the osmotic consequences of free Ca2+. Associated with ryanodine receptor complex (via junctin, triadin) and modulates RyR gating. Mutations cause catecholaminergic polymorphic ventricular tachycardia (CPVT).