Muscular Tissue Practice Quiz (44 questions)

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The three muscular tissue types are skeletal, cardiac, and smooth muscle. The alternatives incorrectly substitute connective, nervous, or epithelial tissue or omit one of the three types.

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All muscle types share excitability, conductivity, contractility, extensibility, and elasticity. Striation and voluntary control are not shared properties of every muscle type.

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Skeletal muscle is striated, usually attached to bones, and usually subject to conscious control. Cardiac and smooth muscle are involuntary, while smooth muscle is not striated.

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Endomysium surrounds an individual muscle fiber. Perimysium surrounds a fascicle, epimysium surrounds the entire muscle, and a tendon attaches muscle to bone matrix.

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Perimysium surrounds a fascicle, which is a bundle of muscle fibers. Endomysium wraps an individual fiber, epimysium surrounds the whole muscle, and the sarcolemma is a muscle fiber's plasma membrane.

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Epimysium surrounds an entire muscle and separates it from neighboring muscles. Perimysium and endomysium surround fascicles and individual fibers, respectively; a tendon attaches muscle to bone.

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A muscle contains fascicles, each made of muscle fibers; fibers contain myofibrils composed of myofilaments, and sarcomeres are contractile units within myofibrils. The incorrect sequences reverse or misplace levels of this hierarchy.

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Thick filaments are made of myosin molecules whose heads project outward, leaving a head-free bare zone in the middle. The alternatives misplace the bare zone, attribute it to actin, or put heads in the central region.

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Thin filaments contain two intertwined strands of fibrous actin, and globular actin subunits have active sites that bind myosin heads. Myosin forms thick filaments, while calcium binds troponin rather than actin's active sites.

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Calcium binding changes troponin's shape, moving tropomyosin away from actin's active sites and permitting contraction. The alternatives confuse which protein binds calcium or reverse the movement that exposes the sites.

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A sarcomere is the segment of a myofibril from one Z disc to the next and is the functional contractile unit of a muscle fiber. The alternatives use different boundaries or refer to a much larger structure.

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A motor unit comprises one nerve fiber and every muscle fiber it innervates. A muscle fiber is one target cell, a neuromuscular junction is a synapse, and a whole muscle contains many motor units.

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The neuromuscular junction is the synapse between a nerve fiber and a skeletal muscle fiber. A motor unit is a nerve fiber plus its innervated fibers, the sarcolemma is the muscle-cell membrane, and an interneuronal synapse connects neurons.

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The junction includes an axon terminal with acetylcholine vesicles, a synaptic cleft between the terminal and sarcolemma, and a Schwann cell that envelops and isolates it. The distractors relocate the vesicles or cleft, or assign neurotransmitter release to the Schwann cell.

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A nerve impulse triggers acetylcholine release into the cleft, where it binds receptors on the sarcolemma's junctional folds; acetylcholinesterase in the basal lamina breaks it down. The alternatives reverse this order, misplace receptors, or assign acetylcholine release to the enzyme.

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The resting membrane potential of a skeletal muscle cell is about −90 mV and is maintained by the sodium–potassium pump. A positive voltage confuses resting polarity, while acetylcholinesterase and acetylcholine receptors do not maintain the resting potential.

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Sodium entering the cell makes the interior more positive and depolarizes the membrane; potassium leaving then makes it negative again and repolarizes it. The distractors swap the ions or their directions.

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An action potential is the rapid voltage shift of depolarization followed by repolarization in a stimulated excitable cell. Resting membrane potential is a maintained state, an impulse describes propagation, and depolarization is only one phase.

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Spastic paralysis involves sustained muscle contraction, whereas flaccid paralysis is limp muscle that cannot contract. Denervation atrophy is muscle shrinkage after loss of nerve connection, and resting membrane potential is an electrical state.

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The four phases proceed through excitation, excitation–contraction coupling, contraction, and relaxation. The distractors reorder the coupling or contraction phases, or substitute electrical events for the four named phases.

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The length–tension relationship describes how muscle tension depends on its length before stimulation. Muscle tone is partial contraction, excitation–contraction coupling links stimulation to contraction, and rigor mortis is postmortem stiffening.

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Over-shortening weakens contraction because thick filaments butt against Z discs, while overstretching leaves too little filament overlap for many cross-bridges. The distractors swap these distinct causes or incorrectly apply one cause to both conditions.

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A stimulus below threshold does not generate a muscle-fiber action potential and therefore produces no contraction. A weak twitch reflects a mistaken partial-threshold idea, a sustained contraction confuses a twitch with repeated stimulation, and motor-unit recruitment concerns increasing stimulus strength above threshold.

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Recruitment, or multiple motor unit summation, increases contraction strength by bringing more motor units into action as stimulus strength rises. Temporal summation increases tension through more frequent stimuli, isotonic contraction describes a length change, and threshold concerns activation of a muscle fiber.

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An isometric contraction develops internal tension without changing muscle length. Isotonic contractions involve a length change while tension remains constant; concentric and eccentric identify shortening and lengthening, respectively.

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An eccentric contraction occurs when a muscle lengthens while maintaining tension. Concentric contraction involves shortening under tension, isometric contraction involves no length change, and the distractor about falling tension misstates the defining condition.

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Anaerobic fermentation can produce ATP without oxygen, but yields little ATP and produces lactate; aerobic respiration requires oxygen, yields far more ATP, and does not generate lactate. The alternatives reverse oxygen needs, assign lactate to the wrong pathway, or misstate their relative ATP yields.

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The phosphagen system, combining ATP and creatine phosphate, supplies nearly all energy for short bursts and supports about six seconds of sprinting. The glycogen–lactate system supports longer maximum efforts, aerobic respiration requires oxygen delivery, and myokinase is an enzyme rather than the overall system.

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Anaerobic glycolysis yields a net of two ATP per glucose and converts glucose to lactate. The much larger yield belongs to aerobic respiration, creatine phosphate is associated with the phosphagen system, and omission of lactate contradicts the pathway’s stated product.

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Muscle fatigue is progressive weakness resulting from prolonged muscle use. Atrophy refers to reduced muscle size, anaerobic threshold concerns detectable lactate in blood, and conditioning describes adaptation rather than worsening weakness.

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Slow oxidative type I fibers resist fatigue through aerobic ATP production, whereas fast glycolytic type II fibers support quick, powerful responses using glycolysis and anaerobic fermentation. The incorrect pairings reverse these roles or assign both types the same primary energy strategy.

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Muscular strength depends in part on the size of active motor units and multiple motor unit summation, so a larger active unit and activation of more units can increase tension. The alternatives ignore these contributors, confuse recruitment with temporal summation, or make resting length the sole condition.

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Cardiac myocytes are involuntary and receive autonomic rather than somatic motor innervation; somatic motor input is characteristic of skeletal muscle, while the other choices mistake autonomic control for absent or sensory innervation.

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Cardiac muscle contracts rhythmically, resists fatigue, and coordinates cells within each chamber so they contract in unison long enough to expel blood. Isolated or brief twitches misstate this coordinated, sustained function, and cardiac muscle is fatigue-resistant.

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Intercalated discs contain gap junctions that electrically connect neighboring cardiomyocytes and mechanical junctions that prevent them from pulling apart. Reversing those functions or substituting intracellular structures confuses cell-to-cell junctions with other cell components.

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A built-in pacemaker generates electrical waves that allow cardiac muscle to contract rhythmically without nervous stimulation. Autonomic input can modify cardiac activity, but it is not required to generate the basic rhythm; the other choices misattribute rhythm generation to skeletal innervation or mechanical attachments.

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Smooth muscle myocytes are fusiform, have one central nucleus, and contain thick and thin filaments that are not aligned into sarcomeres. The alternatives import skeletal-muscle traits or incorrectly place smooth-muscle filaments into sarcomeres.

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Multiunit smooth muscle has nerve branches that synapse with individual myocytes, and its motor units contract independently. Single-unit smooth muscle instead electrically couples cells through gap junctions so many contract together; the remaining choices are different muscle types.

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Smooth muscle can undergo mitosis and hyperplasia, regenerates well after injury, and contracts more slowly than skeletal or cardiac muscle while sustaining contraction without fatigue. The alternatives misstate its regeneration, contraction speed, or fatigue resistance.

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Smooth muscle can respond to stretch as well as autonomic activity, hormones, gases, pH, temperature, and autorhythmicity. The other choices are also regulatory inputs, but they do not describe the stated mechanical stimulus.

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Calcium binds calmodulin, which activates myosin light-chain kinase to phosphorylate a regulatory protein on myosin; myosin ATPase then hydrolyzes ATP to enable filament sliding. Troponin is the skeletal-muscle confusion, while the other choices reverse or misassign steps in the sequence.

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Smooth muscle can contract powerfully from half to twice its resting length because it lacks Z discs and sarcomeres, and myosin heads extend along the thick filaments. Z discs can obstruct shortening, while sarcomere organization and end-limited myosin heads do not match the mechanisms described.

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Muscular dystrophy refers to hereditary diseases in which skeletal muscles degenerate and weaken, with fat and fibrous scar tissue replacing muscle. The autoimmune-receptor distractor describes myasthenia gravis; the fatigue and inflammation distractors mischaracterize the tissue changes.

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In myasthenia gravis, antibodies attack neuromuscular junctions and cluster acetylcholine receptors, reducing muscle-fiber sensitivity to acetylcholine. Cholinesterase inhibitors prolong acetylcholine activity, while the other distractors concern hereditary muscle degeneration or defective dystrophin.