Chapter #9 Part 2

Where does the skeletal muscle action potential occur?

In the sarcolemma (cell membrane) of the skeletal muscle cell.

What neuromuscular structure initiates the muscle action potential?

Events at the neuromuscular (nerve–muscle) junction.

How does the action potential spread within the muscle fiber?

It travels in all directions along the sarcolemma & down T-tubules to triads in the cell interior.

What directly triggers skeletal muscle contraction?

A rise in intracellular Ca²⁺.

What is the source of the Ca²⁺ that triggers contraction?

Release from the terminal cisternae of the sarcoplasmic reticulum (part of the triad).

Define excitation–contraction coupling.

The linking of the sarcolemmal action potential to thin filament movement (sarcomere contraction).

What two events are “coupled” in E–C coupling?

1. The membrane action potential

2. The contraction mechanism of the sarcomere.

List the three main parts of the NMJ.

1. Axon terminal

2. Synaptic cleft

3. Junctional folds of the (muscle cell membrane).

What do synaptic vesicles in the axon terminal contain?

Acetylcholine (ACh).

What is the function of junctional folds?

Increase membrane surface area to hold many ACh receptor proteins.

Where is the motor neuron AP generated & where does it go?

Generated in the spinal cord; travels down the axon to the axon terminal at the NMJ.

Which channels open when the AP reaches the axon terminal & what enters?

Voltage-gated Ca²⁺ channels; Ca²⁺ enters from extracellular fluid.

What does Ca²⁺ entry into the axon terminal cause?

Synaptic vesicle fusion & ACh release into the synaptic cleft.

What happens after ACh is released?

ACh diffuses across the cleft & binds ACh receptors in junctional folds.

What type of channel is the ACh receptor & which ions pass?

Chemically gated cation channel; allows Na⁺& K⁺ (more Na⁺ in than K⁺ out).

What is the end plate potential (EPP)?

Local depolarization under the axon ending due to ACh receptor activation.

What channels populate the sarcolemma outside the NMJ?

Voltage-gated Na⁺ channels & voltage-gated K⁺ channels.

What is “threshold” in this context?

The critical membrane potential change that opens voltage-gated Na⁺ & K⁺ channels.

What is the sequence of voltage-gated channel activity during the AP?

-Rapid opening of Na⁺ channels →

-Na⁺ influx (depolarization);

-Then Na⁺ channels close while slower

-K⁺ channels open → K⁺ efflux (repolarization).

How does the AP propagate along the sarcolemma?

Depolarization at one patch opens Na⁺ channels in the next patch, spreading the wave.

Which voltage-gated channels are in the motor neuron axon?

Voltage-gated Na⁺ & K⁺ channels.

Which channels are in the axon terminal membrane?

Voltage-gated Ca²⁺ channels.

Where are ACh receptor channels located?

Junctional folds of the sarcolemma.

Which voltage-gated channels are in the sarcolemma outside the NMJ?

-Voltage-gated Na⁺ & voltage-gated K⁺ channels

-(Also along T-tubule membranes).

What is the source of Na⁺ during excitation?

High extracellular Na⁺ enters the muscle cell.

What is the source & movement of K⁺ during repolarization?

High intracellular K⁺ exits the cell.

Where are the Ca²⁺ channels that release Ca²⁺ for contraction?

In terminal cisternae membranes of the triad (release Ca²⁺ into sarcoplasm).

What is the role of axon terminal Ca²⁺ channels?

Allow Ca²⁺ entry to trigger ACh release.

What prevents cross-bridge formation in relaxed muscle?

Tropomyosin blocks actin’s myosin-binding sites.

Where is Ca²⁺ located in resting muscle?

Stored in terminal cisternae of the SR.

Are motor neurons firing APs in relaxed muscle?

No.

What is the state of the myosin head before binding actin?

“Primed” with ADP + Pi after ATP hydrolysis (by myosin ATPase).

What exposes actin binding sites?

-Ca²⁺ binds troponin →

-Troponin changes shape →

-Moves tropomyosin.

What happens when myosin binds actin?

It performs the power stroke (pivot), releasing ADP + Pi.

What causes myosin to detach from actin?

Binding of a new ATP to myosin.

How is myosin re-cocked?

ATP hydrolysis to ADP + Pi re-primes the head.

Define a motor unit.

One motor neuron & all the muscle fibers it innervates.

Name the three phases of a muscle twitch.

1. Latent period

2. Contraction phase

3. Relaxation phase.

What occurs in the latent period?

-Cross-bridges begin cycling;

-Tension has not developed yet.

What occurs in the contraction phase?

-Active cross-bridge cycling;

-Tension increases.

What occurs in the relaxation phase?

-Ca²⁺ is returned to the SR;

-Fewer cross-bridges;

-Tension falls.

Define muscle tension.

The force exerted by contracting muscle on an object.

What is an isometric contraction?

Tension develops but the load does not move.

What is an isotonic contraction?

Tension develops & the load moves.

Differentiate concentric vs eccentric isotonic contractions.

Concentric: Muscle shortens;

Eccentric: Muscle lengthens.

How does the nervous system grade muscle force?

By changing AP frequency & by recruitment (strength of stimulation).

Define wave summation.

Increased force due to higher stimulation frequency, with incomplete relaxation between stimuli.

Why does wave summation increase force?

-Ca²⁺ doesn’t fully return to SR →

-Higher sarcoplasmic Ca²⁺ →

-More cross-bridges.

Name the three ATP sources in skeletal muscle.

1. Direct phosphorylation

2. Anaerobic respiration

3. Aerobic respiration.

Describe direct phosphorylation.

-Creatine phosphate donates Pi to ADP → ATP + creatine;

-Creatine is re-phosphorylated later.

What are the phases of aerobic respiration?

-Glycolysis,

-Krebs cycle,

-Electron transport chain/oxidative phosphorylation.

What happens when O₂ is limited?

-Only glycolysis occurs;

-Pyruvic acid → lactic acid + small ATP yield (cytoplasm).

What happens when O₂ is sufficient?

-Pyruvate enters mitochondria; Krebs cycle

-Makes CO₂, NADH, FADH₂ →

-ETC creates H⁺ gradient → ATP synthase makes ATP.

Define muscle fatigue.

Physiological inability to contract.

List contributors to fatigue

-Ionic imbalances;

-Pi accumulation (from CP/ATP use);

-Lactic acid buildup;

-Altered E–C coupling.

What is excess post-exercise oxygen consumption (EPOC) used for?

-Replenish myoglobin O₂;

-Convert lactic acid → pyruvic acid;

-Restore glycogen;

-Resynthesize CP & ATP.

What ultimately determines force of muscle contraction?

# of cross-bridges formed.

What factors increase cross-bridge formation (force)?

-More fibers recruited;

-Larger fiber size;

-Higher stimulation frequency;

-Optimal length–tension.

On what two criteria are fiber types functionally classified?

1. Speed of contraction (fast/slow)

2. ATP pathway (oxidative/glycolytic).

Name the three major functional fiber types.

1. Slow oxidative 

2. Fast oxidative

3. Fast glycolytic.

Key features of slow oxidative fibers?

• High myoglobin

• Many mitochondria/capillaries;

• Endurance.

Key features of fast oxidative fibers?

• High myoglobin

• Many mitochondria/capillaries;

• Faster contraction,

• Relatively fatigue-resistant.

Key features of fast glycolytic fibers?

• Low myoglobin

• Fewer mitochondria/capillaries

• High glycogen; powerful,

• Fatigue quickly.

Is smooth muscle voluntary or involuntary, & how many nuclei per cell?

Involuntary; one nucleus per cell.

What connective tissue sheaths are present in smooth muscle?

Thin endomysium only (no perimysium or epimysium).

Where is smooth muscle located?

Walls of blood vessels & hollow organs (e.g., digestive tract).

Typical smooth muscle organization in organs?

Two sheets: Circular & Longitudinal.

What is the autonomic input pattern in smooth muscle?

Varicosities (swellings) release neurotransmitters diffusely.

Describe smooth muscle SR & filament organization.

-Minimal SR;

-No regular myofilament pattern;

-No striations,

-No sarcomeres.

What are caveolae & their role?

Membrane invaginations rich in Ca²⁺ channels that allow Ca²⁺ influx.

Do thin filaments in smooth muscle have troponin?

No; they lack troponin.

What Ca²⁺-binding protein is used in smooth muscle?

Calmodulin.

What structure transmits force to the outside in smooth muscle?

Intermediate filament–dense body network

(dense bodies anchor thin filaments & attach to membrane/endomysium).

How are smooth muscle cells electrically coupled?

Gap junctions (→ slow, synchronized contractions in unitary smooth muscle).

What is the final trigger for smooth muscle contraction?

Rise in intracellular Ca²⁺.

What provides energy for sliding filaments in smooth muscle?

ATP.

Outline the Ca²⁺-dependent activation pathway in smooth muscle.

-Ca²⁺ binds calmodulin →

-Activates myosin light chain kinase (MLCK) →

-Phosphorylates myosin → activates cross-bridge cycling.

How does smooth muscle relaxation occur?

-Decrease in intracellular Ca²⁺

-(SR reuptake + extrusion outside cell) → reduced MLCK activity →

-Dephosphorylation of myosin.

Which neurotransmitters can act on smooth muscle?

Acetylcholine or norepinephrine

(depending on tissue/receptors).

Name non-neuronal stimuli that can activate smooth muscle.

-Hormones;

-Excess CO₂;

-Histamine;

-Low pH;

-Lack of O₂.

What is unitary (single-unit) smooth muscle?

Sheets with gap junctions, synchronized activity.

What is multi-unit smooth muscle?

Discrete fibers forming motor-unit-like groups; graded responses by recruitment; can respond to specific hormones.

How do sarcolemma APs reach the SR?

Via T-tubules connected to the sarcolemma, conducting APs to triads.

What happens at the triad during excitation?

Voltage changes open Ca²⁺-release channels in terminal cisternae

→ Ca²⁺ floods the sarcoplasm.

Is the end plate potential the muscle AP?

No; the EPP is a local depolarization at the NMJ that, if reaching threshold, triggers a propagated muscle AP via voltage-gated channels.

Which channels generate the propagated muscle AP?

Voltage-gated Na⁺ (depolarization) & K⁺ (repolarization) channels across the sarcolemma (& along T-tubules).