Student-PDF-PSL300-Muscle-1and2

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p.2

Name the three types of muscle.

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p.2

Skeletal muscle, Smooth muscle, Cardiac muscle.

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p.2

Name the three types of muscle.

Skeletal muscle, Smooth muscle, Cardiac muscle.

p.39
40

Explain how ATP is involved in crossbridge detachment.

ATP binds to myosin causing it to release actin; hydrolysis of ATP re-cocks the head for the next cycle. [pages 39–40]

p.12

What determines the smoothness and precision of movement at the muscle level?

The number and timing of activated motor units (recruitment and firing patterns).

p.12

Why do muscle fibers of a motor unit contract together and why is recruitment important?

Because one motor neuron innervates all fibers in the unit; recruitment of more/smaller motor units adjusts force and precision—small units first for fine control.

p.12

What is a motor unit?

A motor unit is one motor neuron and all the muscle fibers it innervates; all fibers in a motor unit contract together.

p.4

Where does chemical signaling between a motor neuron and a skeletal muscle occur?

At the neuromuscular junction (NMJ), the synapse between a motor neuron's axon terminal and a muscle fiber.

p.4
10

List two structural specializations of skeletal muscle that support rapid contraction.

Well-developed sarcoplasmic reticulum (SR) and T-tubule system (invaginations of sarcolemma).

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28

Describe the organization of a skeletal muscle from largest to smallest structure.

Muscle → fascicles → muscle fibers → myofibrils → sarcomeres (thin and thick filaments).

p.27

Which filament is thin and which is thick in a sarcomere?

Thin filament = actin; Thick filament = myosin.

p.32

What role does troponin play when Ca2+ is absent?

Troponin holds tropomyosin over myosin-binding sites on actin, preventing crossbridge formation and causing muscle relaxation.

p.33

Explain what happens when Ca2+ binds to troponin.

Troponin moves, shifting tropomyosin off myosin-binding sites on actin, allowing crossbridge formation and contraction.

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37

Describe the power stroke in the crossbridge cycle.

The myosin head pivots, pulling the thin filament toward the center of the sarcomere; ADP is released at the end of the power stroke.

p.38

What causes rigor mortis at the molecular level?

Tight binding of myosin to actin in the absence of ATP, locking crossbridges in place (rigor state).

p.20
21

Give the sequence of events at the NMJ from action potential arrival to muscle AP.

  1. AP arrives at terminal bouton → 2) Voltage-gated Ca2+ channels open → 3) Ca2+ entry triggers ACh release → 4) ACh binds nicotinic receptors on motor end plate → 5) Cation channels open (Na+ in, K+ out) → 6) Depolarization → 7) Muscle AP generated. [pages 20–21]
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24
25

Name three types of toxins that affect the NMJ and give one example each.

Nicotinic receptor blockers (e.g., curare), Exocytosis blockers (e.g., Botox), ACh-esterase inhibitors (e.g., nerve gases, pesticides). [pages 22–25]

p.14
15

Compare slow-twitch oxidative and fast-twitch glycolytic fibers: contraction speed, mitochondria, fatigue.

Slow-twitch oxidative: slow contraction, many mitochondria, fatigue-resistant. Fast-twitch glycolytic: fast contraction, few mitochondria, rapidly fatigues. [pages 14–15]

p.16

Which motor neuron size innervates slow oxidative vs fast glycolytic fibers, and which is more easily excited?

Small-diameter motor neurons innervate slow oxidative fibers and are more easily excited; large-diameter neurons innervate fast glycolytic fibers.

p.28
29

What structural features define a sarcomere?

Z-disks at ends, overlapping actin (thin) and myosin (thick) filaments, A band, I band, H zone, and M line. Sarcomere shortens during contraction. [pages 28–29]

p.30

Name two binding sites on the myosin head.

Actin-binding site and ATP-binding site.

p.37
40
41

Outline the main steps of the crossbridge cycle (brief).

Rigor (tight binding) → ATP binds myosin (release) → Myosin hydrolyzes ATP (cocked) → Weak binding to actin → Power stroke (release of ADP, Pi) → Tight binding. [pages 37–41]

p.44

What channels mediate Ca2+ release from the SR during excitation–contraction coupling?

Conformational change in DHP (L-type) channels in T-tubules opens RyR (ryanodine receptor) Ca2+ release channels in the sarcoplasmic reticulum.

p.46

How is cytosolic Ca2+ removed to terminate contraction?

Ca2+ ATPase in the sarcoplasmic reticulum pumps Ca2+ from the cytosol back into the SR.

p.47

Define a muscle twitch and name its three phases.

A muscle twitch is a single contraction–relaxation cycle. Phases: latent period, period of contraction, period of relaxation.

p.48
50

What occurs during the latent period of a twitch?

Excitation–contraction coupling occurs (AP propagation, Ca2+ release) before tension rises. [pages 48–50]

p.48
49

During the contraction phase of a twitch, what is happening intracellularly?

Intracellular Ca2+ is high and crossbridge cycling is occurring, producing tension. [pages 48–49]

p.20
21

What is the role of acetylcholinesterase (AChE) at the NMJ?

AChE breaks down ACh in the synaptic cleft, terminating the signal and preventing continuous activation. [page 20/21]

p.10
44

What is the function of the T-tubule system?

To rapidly conduct the muscle action potential into the interior of the fiber, triggering SR Ca2+ release.

p.23

Describe one clinical or pharmacological implication of blocking ACh receptors at the NMJ.

Blocking nicotinic receptors (e.g., curare) causes muscle paralysis because ACh cannot depolarize the motor end plate, preventing muscle APs.

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