lec 13 practice 2

A skeletal muscle attaches to the periosteum through a wide, flat sheet of connective tissue. Which attachment is involved?

Aponeurosis, a broad flattened tendon.

A tendon sheath loses its lubricating synovial fluid. What happens when the tendon moves?

Friction increases because the tendon cannot glide as easily.

Inflammation develops in the synovial sheath surrounding a wrist tendon. Which condition fits this injury?

Tenosynovitis.

A superficial connective tissue layer beneath the skin is severely damaged. Which temperature-related function is reduced?

Insulation that reduces the rate of heat loss.

Damage to deep fascia lets neighboring muscles shift without their usual support. Which function was disrupted?

Holding muscles together while allowing free movement.

A surgeon removes the connective tissue wrapping an entire skeletal muscle. Which layer was removed?

Epimysium.

Damage to a muscle fascicle's covering also affects its larger blood vessels and stretch receptors. Which covering is injured?

Perimysium.

A defect in the connective tissue around each individual myofiber interferes with nearby capillaries. Which layer is affected?

Endomysium.

Embryonic muscle cells cannot fuse normally. Which characteristic of mature skeletal myofibers would be disrupted?

Their multinucleated organization.

An action potential travels along the surface of a myofiber but cannot enter its T-tubules. What is the likely effect?

Excitation cannot reach the interior rapidly and simultaneously.

A dye restricted to extracellular fluid enters the transverse tubules of a muscle fiber. Why is this expected?

T-tubule lumens are continuous with extracellular space.

A muscle fiber receives an electrical signal, but its sarcoplasmic reticulum cannot release Ca2+. What is impaired?

Activation of muscle contraction.

The enlarged sarcoplasmic reticulum sacs beside a T-tubule are damaged. Which function is directly threatened?

Local release of stored Ca2+ during excitation.

A section of a sarcomere has only thin filaments and no thick filaments. Which band is it?

I band.

A microscopic region at the center of an A band contains thick filaments without thin filaments. Which region is visible?

H zone.

A researcher identifies the full span occupied by thick myosin filaments, including overlapping actin. Which band is measured?

A band.

The protein structure connecting adjacent thick filaments at the center of the H zone is damaged. Which line is affected?

M line.

A defect prevents thin actin filaments from anchoring at the boundary of their sarcomere. Which structure is damaged?

Z disc.

During contraction, the Z discs move closer but neither type of filament changes length. What explains the shortening?

Thick and thin filaments slide past one another.

A contracting sarcomere becomes shorter without changing its thick filament length. What happens to the A band?

Its width remains constant.

A muscle sarcomere contracts as thin filaments slide farther inward. What happens to its I band?

It narrows.

Actin slides farther into the central region of a contracting sarcomere. What happens to the H zone?

It narrows as thick-thin overlap increases.

A myosin head cannot attach to its binding site on actin. Which interaction fails?

Formation of an actin-myosin cross-bridge.

The ATPase activity of myosin heads is impaired. Which energy-releasing reaction is reduced?

Hydrolysis of ATP.

Globular actin units cannot join into longer strands. Which form of actin fails to assemble?

F-actin.

In a relaxed muscle fiber, myosin heads cannot reach actin's binding sites despite intact thick filaments. What blocks the sites?

Tropomyosin.

Ca2+ is released but cannot bind troponin. Why do myosin-binding sites remain inaccessible?

Troponin cannot shift tropomyosin away from actin.

The elastic protein that helps anchor myosin to the Z disc is defective. Which protein is involved?

Titin.

The structural protein wrapping around thin filaments is lost. Which actin-related function becomes weaker?

Anchoring of thin filaments to the Z disc.

A muscle defect disconnects actin filaments from the sarcolemma. Which structural protein is most likely affected?

Dystrophin.

After strenuous exercise, delayed soreness is associated with damage to the structures that mark sarcomere boundaries. Which structures?

Z discs.

A motor neuron is damaged before its axon branches toward its muscle fibers. Which fibers lose their shared neural input?

All fibers belonging to that motor unit.

A motor neuron fires normally. How do the skeletal muscle fibers it innervates respond as a group?

They are stimulated together as one motor unit.

A muscle must make extremely precise adjustments to vocal cord position. Which motor-unit organization best supports this?

Small motor units with few fibers per motor neuron.

A muscle is specialized for hard physical work rather than fine vocal control. What motor-unit arrangement is expected?

Larger motor units supplying many muscle fibers.

A motor nerve impulse reaches the axon terminal, but presynaptic Ca2+ channels are blocked. What process fails?

Acetylcholine release by synaptic-vesicle exocytosis.

Presynaptic Ca2+ enters an axon terminal normally. Which membrane event does that entry trigger?

Fusion of synaptic vesicles with the terminal membrane.

A drug prevents synaptic vesicles from fusing with the axon terminal membrane. What directly decreases?

Acetylcholine release into the synaptic cleft.

Acetylcholine is released, but its receptors at the motor end plate are blocked. Which local electrical response is impaired?

End-plate potential (EPP).

The nicotinic receptor opens normally at the motor end plate. Which ion movement primarily causes depolarization?

Na+ entry into the muscle fiber.

ACh receptors allow Na+ inward and K+ outward at the same time. Why does the end plate become less negative?

The inward Na+ effect predominates.

The inward electrochemical driving force for Na+ at the motor end plate becomes weaker. What happens to the EPP?

The depolarizing end-plate potential becomes smaller.

The motor end plate produces an EPP, but adjacent voltage-gated Na+ channels are blocked. What cannot form normally?

A propagating muscle action potential.

A local end-plate depolarization reaches nearby excitable sarcolemma. Which channels open to start an action potential?

Voltage-gated Na+ channels.

Voltage-gated Na+ channels open in the muscle sarcolemma. What ion movement drives the rising action potential?

Na+ influx.

Voltage-gated K+ channels fail to open after the muscle action potential peaks. Which process is delayed?

Repolarization.

K+ leaves the muscle fiber through voltage-gated channels after depolarization. What happens to membrane potential?

It returns toward the negative resting potential.

A muscle shows a local EPP but no signal spreading along the sarcolemma. Which distinction explains the observation?

An EPP is local; an action potential propagates.

An electrical wave spreads along the sarcolemma but fails to enter the cell deeply. Which membrane extensions may be defective?

Transverse tubules (T-tubules).

A drug prevents Ca2+ release from the muscle sarcoplasmic reticulum but leaves nerve signaling intact. Which downstream event fails?

Calcium-dependent exposure of myosin-binding sites on actin.

After ACh activates the motor end plate, its voltage changes from -90 mV to -60 mV. What kind of signal occurred?

A local end-plate potential (EPP), produced mainly by inward Na+ movement.

An EPP forms at the motor end plate, but adjacent sarcolemma never reaches about -55 mV. What fails to occur?

A propagating muscle action potential because threshold was not reached.

Depolarization reaches about -55 mV in the muscle sarcolemma. What electrical event follows?

Voltage-gated Na+ channels open, driving an action potential toward +30 mV.

Only one ACh-binding site on a nicotinic receptor is occupied. What happens to the receptor channel?

It does not open normally; both ACh-binding sites must be occupied.

A second stimulus reaches a muscle fiber just after its voltage-gated Na+ channels became inactivated. Why is another action potential prevented?

The inactivated Na+ channels cannot reopen until they recover from inactivation.

A muscle membrane repolarizes, but the Na+ channel inactivation gates cannot reset. What is the likely consequence?

The membrane cannot generate another normal Na+-dependent action potential.

Presynaptic Ca2+ entry and ACh release occur normally, but Ca2+ remains trapped in the muscle SR. What step fails?

Troponin cannot receive the released Ca2+ needed to expose myosin-binding sites on actin.

The muscle SR contains Ca2+, but Ca2+ entry into the motor neuron terminal is blocked. Why can the muscle remain unexcited?

The nerve terminal cannot release ACh, so the muscle end plate is not activated.