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Questions and Answers
Which component of the sarcomere defines its boundaries?
Which component of the sarcomere defines its boundaries?
What is the primary role of tropomyosin in the relaxed state of a cardiac muscle?
What is the primary role of tropomyosin in the relaxed state of a cardiac muscle?
Which part of the cardiac myosin molecule contains ATPase activity?
Which part of the cardiac myosin molecule contains ATPase activity?
What is the direct effect of calcium ions binding to troponin during cardiac muscle contraction?
What is the direct effect of calcium ions binding to troponin during cardiac muscle contraction?
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Which regulatory protein complex directly inhibits actin-myosin interaction in the absence of calcium?
Which regulatory protein complex directly inhibits actin-myosin interaction in the absence of calcium?
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Which of the following accurately describes the role of the dihydropyridine (DHP) receptors in cardiac muscle excitation-contraction coupling?
Which of the following accurately describes the role of the dihydropyridine (DHP) receptors in cardiac muscle excitation-contraction coupling?
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What is the primary mechanism by which cardiac muscle contraction is graded based on calcium concentration?
What is the primary mechanism by which cardiac muscle contraction is graded based on calcium concentration?
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Which of the following directly causes cross-bridge formation in cardiac muscle?
Which of the following directly causes cross-bridge formation in cardiac muscle?
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What is the significance of 'length-dependent activation' in cardiac muscle physiology?
What is the significance of 'length-dependent activation' in cardiac muscle physiology?
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According to the sliding filament theory, what event directly leads to sarcomere shortening during cardiac muscle contraction?
According to the sliding filament theory, what event directly leads to sarcomere shortening during cardiac muscle contraction?
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Which of the following is a consequence of increasing muscle preload?
Which of the following is a consequence of increasing muscle preload?
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What effect does increasing afterload have on the isometric contraction phase?
What effect does increasing afterload have on the isometric contraction phase?
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At maximal shortening velocity, what is the state of the afterload?
At maximal shortening velocity, what is the state of the afterload?
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According to the force-velocity relationship, what happens to shortening velocity when afterload increases?
According to the force-velocity relationship, what happens to shortening velocity when afterload increases?
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What does an increase in preload do to the force-velocity curve?
What does an increase in preload do to the force-velocity curve?
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Which of the following best describes the effect of increased inotropy on the length-tension relationship?
Which of the following best describes the effect of increased inotropy on the length-tension relationship?
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How does increased preload affect the ability of the muscle to maintain shortening velocity under increasing afterloads?
How does increased preload affect the ability of the muscle to maintain shortening velocity under increasing afterloads?
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What is the effect of increased inotropy on isometric force generation at a given preload?
What is the effect of increased inotropy on isometric force generation at a given preload?
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Which of the following best describes the effect of increased afterload on muscle shortening?
Which of the following best describes the effect of increased afterload on muscle shortening?
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What variable distinguishes inotropy from preload in terms of their influence on muscle contraction?
What variable distinguishes inotropy from preload in terms of their influence on muscle contraction?
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Flashcards
Action Potential Sequence
Action Potential Sequence
The process where action potentials move across the sarcolemma and into T-tubules, leading to calcium entry.
Calcium Triggering
Calcium Triggering
Dihydropyridine receptors open to allow Ca++ entry, triggering muscle contraction.
Troponin C Function
Troponin C Function
Ca++ binds to troponin C, changing its shape to expose actin's binding sites.
Length-Tension Relationship
Length-Tension Relationship
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Isotonic Contraction & Sarcomere Length
Isotonic Contraction & Sarcomere Length
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Myofibrils
Myofibrils
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Sarcomere
Sarcomere
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Excitation-Contraction Coupling
Excitation-Contraction Coupling
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Thick Filaments
Thick Filaments
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Troponin
Troponin
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Preload
Preload
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Effect of Increased Preload
Effect of Increased Preload
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Afterload
Afterload
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Increased Afterload Effects
Increased Afterload Effects
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Force-Velocity Relationship
Force-Velocity Relationship
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F-V Curve Shift
F-V Curve Shift
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Effects of Increased Afterload
Effects of Increased Afterload
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Inotropy
Inotropy
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Inotropy Effects on L-T Relationship
Inotropy Effects on L-T Relationship
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Decreased Inotropy Effects
Decreased Inotropy Effects
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Study Notes
Cardiac Excitation-Contraction Coupling and Muscle Mechanics
- Learning Objectives:
- Define myofibrils, myofilaments, sarcomere, thick and thin filaments.
- Describe cardiac muscle's cellular components and excitation-contraction coupling sequence. Explain critical regulatory sites.
- Compare and contrast excitation-coupling mechanisms in cardiac and skeletal muscle.
- Define preload, afterload, and inotropy.
- Contrast isometric and isotonic contractions, including how they relate to preload, afterload, and inotropy. Include tension and length changes over time, the length-tension relationship, and the force-velocity relationship.
- Summarize how autonomic nerves, hormones, heart rate, and hypoxia affect inotropy.
Cardiac Cell Structure
- Cardiac myocytes are relatively short (~100μm), branching cells, connected by intercalated discs.
- Myocytes consist of myofibrils, which contain bundled myofilaments.
- Sarcomeres are the contractile units, containing contractile and regulatory proteins, spanning between Z-lines. Sarcomere length is 1.6– 2.2 μm.
Excitation-Contraction Coupling
- Action potentials travel through sarcolemma and T-tubules. Membrane depolarization opens dihydropyridine (DHP) receptors (L-type Ca2+ channels), leading to intracellular Ca2+ entry. This triggers calcium release from the sarcoplasmic reticulum (SR).
- Ryanodine receptors (RyR) on the SR open in response to the Ca2+ influx, releasing more Ca2+ into the cytoplasm. Cytoplasmic Ca2+ concentration rises from ~10-7 to ~10-5 M.
- Ca2+ binds to troponin C (TN-C), causing conformational changes in the troponin complex, shifting tropomyosin (TM) to expose the myosin-binding sites on actin.
- Myosin heads bind to actin, leading to cross-bridge formation and movement, requiring ATP hydrolysis. This shortens the sarcomere length.
- Ca2+ is re-sequestered by the SR via the SERCA pump.
- Ca2+ unbinds from TN-C, myosin releases from actin (requiring ATP). This allows sarcomere to return to its resting length.
Contractile Proteins
- Thin Filaments (Actin):
- Globular proteins in a repeating helical structure, with myosin binding sites.
- Tropomyosin:
- Rod-shaped proteins, associated with seven actin molecules, obstructing myosin binding sites in a relaxed state.
- Thick Filaments (Myosin):
- Composed of a long tail region, with several myosin molecules bundled together.
- Each myosin molecule has two heads, containing myosin ATPase, actin binding sites.
Regulatory Proteins (Troponin)
- TN-I: Inhibits myosin binding to actin in the absence of calcium.
- TN-T: Binds to tropomyosin.
- TN-C: Binds to calcium.
Distinguishing Characteristics of Cardiac Muscle EC-Coupling
- Cell-to-cell depolarization via gap junctions creates action potentials in adjacent cells.
- Nerves do not activate cardiac muscle contraction directly.
- Contractile forces are graded, depending on the amount of Ca2+ bound to TN-C (~3 Ca2+/TN-C).
- Autonomic nerves through β- and muscarinic receptors regulate contractile force and relaxation.
- Autonomic nerves regulate Ca2+ release and reuptake by the SR.
Sliding Filament Theory of Contraction
- Ca2+ release triggers cross-bridge formation between actin and myosin.
- Cycles of cross-bridge attachment and detachment cause the thin filaments to slide inward, shortening the sarcomere.
- Ca2+ uptake by the SR causes cross-bridge detachment and relaxation.
Time-Course of Cardiac EC-Coupling
- A graphic illustration of action potentials, Ca2+, and active tension levels over time in cardiac muscle.
Mechanical Properties of Cardiac Muscle
- Preload: The resting length of cardiac fibers (initial sarcomere length) before contraction, affecting active tension generation.
- Length-Tension Relationship: The graphical relationship between sarcomere length and active tension. The optimal length for maximal force generation is near peak sarcomere length (e.g., 2.2µm).
Afterload
- The force a muscle fiber must generate to overcome load and shorten. An increase in afterload decreases shortening velocity and increases duration of isometric contraction phase.
Force-Velocity Relationship
- Relationship between the force generated and the velocity of shortening. Increased afterload reduces shortening velocity.
- Maximal shortening velocity (Vmax) occurs at zero afterload.
Inotropy
- Changes in cardiac muscle contraction independent of changes in sarcomere length.
- Affects the ability of muscle to generate maximum contraction.
- Factors influencing inotropy include sympathetic nerve activity, hormones, heart rate, and cellular hypoxia.
Regulation of Inotropy
- Autonomic Nerves:
- Sympathetic nerve activation (β-adrenoceptors) increases inotropy.
- Parasympathetic nerve activity (muscarinic type 2 receptors) decreases inotropy.
- Hormones: Circulating catecholamines increase inotropy.
- Heart Rate: Increased heart rate (Bowditch effect) increases inotropy.
- Cellular Hypoxia: Cellular hypoxia depresses inotropy.
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Description
Test your knowledge on cardiac muscle physiology with this quiz focusing on critical components such as the sarcomere, regulatory proteins, and excitation-contraction coupling mechanisms. Explore how these factors contribute to heart function and muscle contraction dynamics.
