Excitation-Contraction Coupling in Cardiac Muscle

What is excitation–contraction coupling in cardiac muscle?

The process by which an electrical action potential triggers a mechanical contraction in cardiac muscle via calcium entry, calcium-induced calcium release from the sarcoplasmic reticulum, and activation of the contractile apparatus.

What ion is central to excitation–contraction coupling in cardiac muscle?

Calcium ions (Ca2+), which link electrical depolarisation to mechanical force generation.

What is the role of the cardiac action potential in excitation–contraction coupling?

The action potential depolarises the sarcolemma and T-tubules, opening L-type Ca2+ channels and initiating calcium entry that triggers calcium-induced calcium release.

Where are L-type Ca2+ channels located in cardiomyocytes?

In the sarcolemma and T-tubule membranes of cardiac muscle cells.

What phase of the cardiac action potential activates L-type Ca2+ channels?

The early plateau phase of the action potential.

What is the approximate extracellular Ca2+ concentration compared to intracellular Ca2+?

Extracellular Ca2+ concentration is ~2 mM, while resting intracellular Ca2+ is very low and rises transiently during contraction.

Why is Ca2+ entry through L-type channels considered small but crucial?

The Ca2+ influx is small in quantity but essential because it triggers a much larger Ca2+ release from the sarcoplasmic reticulum.

What is calcium-induced calcium release (CICR)?

A process where Ca2+ entering the cell through L-type Ca2+ channels activates ryanodine receptors on the sarcoplasmic reticulum, causing a large release of stored Ca2+.

Which channel mediates Ca2+ release from the sarcoplasmic reticulum in cardiac muscle?

Ryanodine receptor (RyR) Ca2+ release channels.

What is the state of SR Ca2+ release channels during diastole?

They are closed because cytoplasmic Ca2+ concentration is low.

How quickly does intracellular Ca2+ rise after SR release?

Cytoplasmic Ca2+ rises to a high level within approximately 10 milliseconds.

What is the approximate peak cytosolic Ca2+ concentration during contraction?

Approximately 0.2–1 µM during Ca2+ transients, with local peaks reaching ~2 µM.

What is the effect of increased cytosolic Ca2+ on the sarcomere?

Ca2+ diffuses into the sarcomere and binds to troponin C, initiating cross-bridge cycling and tension development.

Which protein does Ca2+ bind to in order to activate contraction?

Troponin C.

What is the role of tropomyosin in resting cardiac muscle?

Tropomyosin blocks the myosin-binding sites on actin, preventing cross-bridge formation.

How does Ca2+ binding to troponin C enable contraction?

It displaces tropomyosin from actin binding sites, allowing myosin heads to bind to actin.

Describe the power stroke of the myosin head

The myosin head changes angle, pulling the actin filament toward the Z-line in a rowing motion.

What happens to Ca2+ during relaxation of cardiac muscle?

Ca2+ is removed from the cytoplasm by reuptake into the sarcoplasmic reticulum and extrusion from the cell.

Which transporter pumps Ca2+ back into the sarcoplasmic reticulum?

The sarcoplasmic reticulum Ca2+ ATPase (SERCA).

What percentage of Ca2+ is returned to the SR during relaxation?

Approximately 80–90% of the released Ca2+.

Which transporter is primarily responsible for Ca2+ extrusion from the cell?

The sarcolemmal Na+/Ca2+ exchanger (NCX).

What percentage of Ca2+ is extruded via sarcolemmal transporters?

Approximately 10–20% of the released Ca2+.

How does the Na+/Ca2+ exchanger work?

It exchanges 3 Na+ ions into the cell for 1 Ca2+ ion out of the cell, using the Na+ electrochemical gradient.

What role does the sarcolemmal Ca2+ ATPase play?

It contributes a small amount to Ca2+ extrusion from the cell during relaxation.

Why is the cardiac cell refractory for a long period?

Because the action potential has a prolonged plateau phase lasting 200–400 ms.

What is the functional consequence of the long refractory period in cardiac muscle?

It prevents tetanic contractions and ensures the heart relaxes between beats.

How long does active contraction last in cardiac muscle?

Approximately 200–250 ms.

Why is cardiac contraction normally limited to a single twitch?

The cell remains refractory during most of the contraction, preventing re-excitation before relaxation occurs.

How does the plateau phase influence contraction strength?

The duration and magnitude of Ca2+ influx during the plateau determine the amount of Ca2+ stored in the SR and released during contraction.

What effect does increased plateau current have on contraction force?

It increases intracellular Ca2+ availability, leading to a more forceful contraction.

Which neurotransmitter enhances plateau Ca2+ current and contraction strength?

Noradrenaline.

How does intracellular Ca2+ relate temporally to contraction?

The Ca2+ transient rises shortly after depolarisation and precedes the development of mechanical tension.

What is the key difference between skeletal and cardiac muscle action potentials?

Cardiac muscle has a prolonged plateau phase, whereas skeletal muscle action potentials are brief.

What is the main source of Ca2+ for contraction in skeletal muscle?

The sarcoplasmic reticulum, with minimal dependence on extracellular Ca2+.

What is the main source of Ca2+ for contraction in cardiac muscle?

Both extracellular Ca2+ entry and sarcoplasmic reticulum release.

Why does skeletal muscle allow tetanic contractions but cardiac muscle does not?

Skeletal muscle has a short refractory period, whereas cardiac muscle has a long refractory period due to the plateau phase.

How does contraction timing differ between skeletal and cardiac muscle?

In skeletal muscle, contraction outlasts the action potential; in cardiac muscle, contraction overlaps with the prolonged action potential.