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BIOM2011 > Muscle 2025 > Flashcards

Muscle 2025 Flashcards

(70 cards)

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1
Q

Q: What did Sidney Ringer discover in 1883?

A

A: That calcium in London tap water was essential for maintaining frog heart contractions, leading to the development of Ringer’s solution.

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2
Q

Q: What is the formula for cardiac output (CO)?

A

CO = Heart Rate × Stroke Volume
At rest:

HR = 70 bpm
SV = 70 mL/beat
CO ≈ 5 L/min
During exercise: up to 20–30 L/min

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3
Q

Q: What are the three main types of membrane transport proteins?

A

Ion channels: Voltage- or ligand-gated, selective, passive
Pumps: ATP-dependent, active transport
Exchangers: ATP-independent, use ion gradients

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4
Q

Q: What are examples of ion channels in the heart?

A

Ca²⁺ channels: L-type, T-type
K⁺ channels: ≥15 types
Na⁺ channels: One major type

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5
Q

Q: What is the role of the S4 region in voltage-gated ion channels?

A

A: It contains charged amino acids that move in response to voltage changes, triggering channel opening.

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6
Q

Q: What are the three states of a voltage-gated ion channel?

A

Reprimed (ready to open)
Activated (open)
Inactivated (closed despite depolarization)

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7
Q

Q: What does the Na⁺/K⁺ pump do?

A

A: Maintains ion gradients by pumping 3 Na⁺ out and 2 K⁺ in, using ATP.

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8
Q

Q: How does the Ca²⁺ pump work?

A

A: Uses ATP to move Ca²⁺ against a steep gradient (from nM–µM to mM).

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9
Q

Q: How does the Na⁺/Ca²⁺ exchanger work?

A

A: Uses the Na⁺ gradient to move Ca²⁺ out of the cell without ATP.

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10
Q

Q: How is cardiac muscle similar to skeletal muscle?

A

Striated appearance
Contains actin, myosin, T-tubules, and sarcoplasmic reticulum
Follows length-tension relationship and crossbridge cycling

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11
Q

Q: What are intercalated discs?

A

Specialized structures containing desmosomes (mechanical connection) and gap junctions (electrical coupling), allowing cardiac cells to function as a functional syncytium.

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12
Q

Q: What are the two main types of cardiac cells?

A

Contractile cells (~99%): Perform mechanical work
Autorhythmic/conducting cells (~1%): Generate and conduct action potentials

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13
Q

Q: What is the Nernst equation used for?

A

A: Calculating the equilibrium potential for a single ion.

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14
Q

Q: What causes the rapid depolarization in ventricular cells?

A

A: Na⁺ channel activation

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15
Q

Q: What maintains the plateau phase?

A

A: Ca²⁺ influx through L-type Ca²⁺ channels

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16
Q

Q: What causes repolarization?

A

A: K⁺ efflux and inactivation of Ca²⁺ channels

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17
Q

Q: What is the absolute refractory period in ventricular muscle?

A

A: ~0.25–0.30 seconds

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18
Q

Q: Why is the refractory period important?

A

A: Prevents summation and tetanus, ensuring rhythmic contractions.

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19
Q

Q: What is the correct order of electrical conduction in the heart?

A

SA node
Internodal pathways
AV node
Bundle of His
Right and left bundle branches
Purkinje fibers

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20
Q

Q: What causes the pacemaker potential in SA node cells?

A

I_f current (slow Na⁺ influx)
T-type Ca²⁺ channels (transient)
L-type Ca²⁺ channels (long-lasting)

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21
Q

Q: How does the SA node differ from ventricular cells?

A

SA node has unstable resting potential and spontaneous depolarization
Ventricular cells have a stable resting potential and require external stimulation

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22
Q

Q: What ensures efficient pumping of the heart?

A

The electrical conduction system, which ensures:

Atrial excitation and contraction occur before ventricular events
Rapid transmission to ventricles
Coordinated ventricular excitation and contraction

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23
Q

Q: What is the sinoatrial (SA) node’s role?

A

A: It initiates the cardiac action potential, setting the pace for the heart.

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24
Q

Q: What does an ECG measure?

A

A: The electrical activity induced in body fluids by the cardiac impulse—not a direct recording of heart muscle activity.

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25
Q: What does the ECG reflect?
A: A composite of all action potentials generated at a given time.
26
Q: What are the phases of the cardiac cycle?
Systole: Contraction (blood ejection) Diastole: Relaxation (chamber filling)
27
Q: What is the duration of the cardiac cycle at 75 bpm?
0.8 seconds Ventricular systole: 0.3 s Ventricular diastole: 0.5 s
28
Q: How does the heart fill at high rates?
A: Diastole shortens significantly (e.g., from 500 ms to 125 ms), but rapid ventricular filling and atrial contraction help maintain output.
29
Q: What are the two branches of the autonomic nervous system that regulate heart rate?
Parasympathetic (vagus nerve) Sympathetic (noradrenaline)
30
Q: How does acetylcholine affect the SA node?
Increases K⁺ permeability → hyperpolarization Slows Ca²⁺ channel opening → slower depolarization Result: Decreased heart rate
31
Q: What are the effects of vagus nerve stimulation?
SA node: Slows pacemaker activity AV node: Increases AV delay Atria: Weakened contraction Ventricles: Slightly weakened contraction
32
Q: How does noradrenaline affect the SA node?
Decreases K⁺ permeability → faster depolarization Increases Ca²⁺ influx → faster rise to threshold Result: Increased heart rate
33
Q: What are the effects of sympathetic stimulation?
SA node: Increases pacemaker activity AV node: Shortens AV delay Atria & ventricles: Stronger contraction Ventricular conduction: Increased excitability and speed
34
Q: Why is calcium (Ca²⁺) used as a signaling molecule?
It has two positive charges, giving it high affinity for negatively charged proteins. It acts as a second messenger in processes like excitability, exocytosis, motility, apoptosis, and transcription.
35
Q: What is unique about calcium signaling in skeletal muscle?
A: It is highly specialized and rapid, with Ca²⁺ transients lasting ~5 ms (vs. ~1–2 min in smooth muscle).
36
Q: What is the functional unit of striated muscle?
A: The sarcomere, composed of actin and myosin filaments.
37
Q: What is the structural hierarchy of skeletal muscle?
Muscle → Muscle fibers → Myofibrils → Sarcomeres
38
Q: Where is calcium stored and buffered in muscle cells?
Extracellular fluid: ~2 mM Cytoplasm (resting): ~0.0001 mM Sarcoplasmic reticulum (SR): ~1 mM Bound to proteins: Troponin C, Parvalbumin, Calsequestrin
39
Q: What is the role of calsequestrin?
A: It binds large amounts of Ca²⁺ in the SR, acting as a major intracellular Ca²⁺ buffer.
40
Q: What is the apparent dissociation constant (K_D)?
A: The [Ca²⁺] at which 50% of a protein’s binding sites are saturated with Ca²⁺.
41
Q: What happens when Ca²⁺ binds to proteins like troponin C?
A: It causes conformational and functional changes, enabling muscle contraction.
42
Q: What are the six steps of EC coupling in skeletal muscle?
Action potential propagates along the sarcolemma Voltage sensor (VS) in T-tubule is activated VS mechanically activates the SR Ca²⁺ release channel (ryanodine receptor) Ca²⁺ is released from SR into cytoplasm (↑100× in ms) Ca²⁺ binds to contractile proteins → filament sliding → force generation Ca²⁺ is pumped back into SR → relaxation
43
Q: Is the voltage sensor a G-protein or second messenger system?
A: No, it directly activates the SR Ca²⁺ release channel mechanically.
44
Q: How is Ca²⁺ removed from the cytoplasm after contraction?
A: By Ca²⁺-ATPase pumps in the SR membrane, which actively transport Ca²⁺ back into the SR.
45
Q: How do T-tubules and SR differ between skeletal and cardiac muscle?
Cardiac T-tubules: Larger (~200 nm), located at Z-lines Skeletal T-tubules: Smaller (~30 nm), located at A–I junction Cardiac SR: More sparse Cardiac forms dyads, skeletal forms triads
46
Q: What are the two types of Ca²⁺-dependent inactivation?
Cytoplasmic Ca²⁺-dependent inactivation: Regulates release based on cytosolic Ca²⁺ Lumenal Ca²⁺-dependent inactivation: Regulates release based on SR Ca²⁺ content
47
Q: What is CICR in cardiac muscle?
A: Ca²⁺ influx through DHPR triggers RyR to release more Ca²⁺ from the SR.
48
Q: What maintains Ca²⁺ balance in cardiac cells?
Ca²⁺ entry: DHPR, RyR Ca²⁺ exit: SR Ca²⁺-ATPase, surface Ca²⁺-ATPase, Na⁺/Ca²⁺ exchanger (NCX)
49
Q: What happens to Ca²⁺ balance during fast heart rates?
↑ Influx, ↓ time for efflux → ↑ SR Ca²⁺ → stronger contraction
50
Q: What is the effect of β-adrenergic stimulation (e.g., isoproterenol)?
↑ DHPR Ca²⁺ influx ↑ SR Ca²⁺ pump efficiency → ↑ SR Ca²⁺ → stronger contraction
51
Q: How does cardiac muscle stiffness compare to skeletal muscle?
A: Cardiac muscle is stiffer.
52
Q: What is Starling’s Law?
A: ↑ Diastolic volume → ↑ Systolic contraction → ↑ Blood ejection (intrinsic regulation)
53
Q: How do the durations of cardiac AP and contraction compare?
A: They are similar in duration, preventing tetanus.
54
Q: What is an inotrope?
A: A substance that alters the force of muscle contraction.
55
Q: Give examples of negative inotropic agents.
Beta blockers Diltiazem Verapamil (all reduce Ca²⁺ entry)
56
Q: Give examples of positive inotropic agents.
Digitalis (inhibits Na⁺/K⁺ ATPase) Catecholamines (e.g., epinephrine, norepinephrine) Isoproterenol (β-adrenergic agonist)
57
Q: How does sympathetic stimulation affect cardiac contractility?
Activates β-adrenergic receptors ↑ cAMP → activates PKA PKA enhances DHPR, SR Ca²⁺ pump, and pacemaker channels
58
Q: How does parasympathetic stimulation affect the heart?
Via ACh → activates KACh channels ↓ cAMP → ↓ contractility and pacemaker activity
59
At the action potential threshold, what occurs
At threshold, Ca²⁺ influx occurs
60
Q: What is the major difference between EC coupling in skeletal and cardiac muscle?
A. Activation of the ryanodine receptor by mechanical coupling (skeletal) vs. Ca²⁺-induced Ca²⁺ release (cardiac)
61
Q: What happens when Decreased sympathetic tone
slow heart rate occurs
62
Q: Why are SA node and ventricular APs different?
SA node: Slow depolarization due to I_f (Na⁺), Ca²⁺ influx at threshold, no stable resting potential Ventricular cells: Rapid Na⁺-driven depolarization, long Ca²⁺-driven plateau, stable resting potential Function: SA node sets rhythm; ventricular AP prevents tetanus
63
Q: What are the key steps in skeletal muscle EC coupling?
AP propagates along sarcolemma Activates voltage sensor (DHPR) in T-tubule Mechanical activation of RyR on SR Ca²⁺ released into cytoplasm Ca²⁺ binds troponin → contraction Ca²⁺ pumped back into SR → relaxation
64
Q: What determines blood flow through systemic circulation?
Pressure gradient (ΔP) Resistance (R) Flow = ΔP / R Influenced by vessel diameter, length, and blood viscosity
65
Q: Why are mouse ventricular APs shorter than human APs?
Faster repolarization Shorter plateau phase Enhanced K⁺ channel activity Allows higher heart rates (e.g., 6 Hz in mice vs. 3 Hz in humans)
66
Q: Why is the intracellular AP amplitude much greater than the ECG QRS wave?
Intracellular AP measures voltage across a single cell membrane ECG measures summed extracellular potentials across the body surface Signal attenuation and spatial averaging reduce ECG amplitude
67
Q: Why is Ca²⁺ valency important?
High charge density Strong binding to proteins (e.g., troponin, calmodulin) Enables precise signaling and rapid conformational changes
68
Q: What happens if extracellular Na⁺ is replaced with K⁺?
Membrane depolarizes Na⁺ influx is blocked → no AP Muscle becomes inexcitable → flaccid paralysis
69
Q: What specialization allows rapid EC coupling in muscle?
Triad structure: T-tubule + 2 terminal cisternae of SR Close proximity of DHPR and RyR enables fast Ca²⁺ release
70
Q: How does increased Ca²⁺ load enhance cardiac output?
More Ca²⁺ in SR → greater release during AP Stronger contraction (positive inotropy) Enhanced by higher pacing and diastolic volume (Starling’s law)

BIOM2011 (19 decks)

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