Cardiac Muscle: Structure, Function, and Physiology

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Cardiac Muscle

Structure and Cellular Organization

Cardiac muscle is a specialized form of muscle tissue found only in the heart. It is composed of cardiac myocytes, which are shorter, branched cells typically containing a single nucleus. These cells are interconnected by intercalated disks, which facilitate both mechanical and electrical coupling.

Cardiac myocytes: Short, branched, usually single-nucleated cells.
Intercalated disks: Specialized junctions containing desmosomes (mechanical linkage) and gap junctions (electrical linkage).
Striations: Cardiac muscle is striated, with sarcomeres containing thick (myosin) and thin (actin) filaments.
Mitochondria: Abundant, occupying about one-third of cell volume, supporting oxidative metabolism.
T-tubules: Larger and less abundant than in skeletal muscle.
Sarcoplasmic reticulum: Smaller, requiring extracellular Ca2+ entry for contraction.

Histology and diagram of cardiac muscle showing intercalated disks, branching, striations, and nuclei Diagram of intercalated disk structure and connections in cardiac muscle Electron micrograph of cardiac muscle showing intercalated disks

Autorhythmic and Contractile Cells

The heart contains two main types of myocardial cells: contractile cells (responsible for contraction) and autorhythmic cells (pacemaker cells, ~1% of total). Autorhythmic cells generate action potentials spontaneously, initiating the heartbeat.

Autorhythmic cells: Located primarily in the sinoatrial (SA) node, have unstable resting membrane potentials (~-60 mV).
Contractile cells: Make up the majority of cardiac muscle, responsible for force generation.
HCN channels: Hyperpolarization-activated cyclic nucleotide-gated channels ("funny current") open at -60 mV, allowing Na+ influx and gradual depolarization.
T-type Ca2+ channels: Open just before threshold, further depolarizing the cell.
L-type Ca2+ channels: Open at threshold, causing the action potential spike.
K+ channels: Open to repolarize the cell.

Electrical conduction in myocardial cells: action potentials spread from autorhythmic to contractile cells The conducting system of the heart: SA node, AV node, bundle branches, Purkinje fibers

Action Potentials in Cardiac Muscle

Cardiac muscle action potentials differ between autorhythmic and contractile cells.

Autorhythmic cells: Unstable resting potential, gradual depolarization via HCN channels, T-type and L-type Ca2+ channels, repolarization via K+ channels.
Contractile cells: Rapid depolarization via Na+ channels, brief repolarization, sustained plateau via L-type Ca2+ channels, final repolarization via K+ channels.
Plateau phase: Prolonged depolarization prevents summation and tetanus, ensuring rhythmic contractions.

Graph of ion channel states during cardiac action potential Graph of ion channel states with color-coded channel activity Action potential of a cardiac contractile cell with phases and channel activity Comparison of action potentials and muscle tension in skeletal vs cardiac muscle

Excitation-Contraction Coupling

Cardiac muscle contraction is triggered by Ca2+ influx through L-type Ca2+ channels, which is not mechanically coupled to ryanodine receptors (RyR) as in skeletal muscle. Instead, Ca2+ entry induces further Ca2+ release from the sarcoplasmic reticulum (SR) via RyR, a process known as "Ca2+-induced Ca2+ release."

L-type Ca2+ channels: Allow extracellular Ca2+ entry.
RyR: Ryanodine receptors on SR release additional Ca2+.
Cross-bridge cycling: Ca2+ binds to troponin, removing inhibition and allowing actin-myosin interaction.

EC coupling in cardiac muscle: Ca2+ entry, RyR activation, contraction Ca2+ induces Ca2+ release through RyR Actin-myosin interaction: relaxed and contracted states Tight binding in the rigor state: myosin-actin interaction ATP binds to myosin, releasing actin Myosin hydrolyzes ATP, rotates to cocked position

Relaxation and Regulation

Relaxation occurs primarily via reuptake of Ca2+ into the SR, though removal to the extracellular space is also important. The SERCA pump (SR Ca2+-ATPase) is regulated by phospholamban (PLN); phosphorylation of PLN enhances Ca2+ uptake, increasing relaxation rates and contractility.

SERCA pump: Main mechanism for Ca2+ reuptake.
Phospholamban (PLN): Inhibits SERCA when dephosphorylated; phosphorylation removes inhibition.
Neuronal input: The autonomic nervous system modulates heart rate and contractility.
Sympathetic stimulation: Increases heart rate, conduction, contractility via phosphorylation of Ca2+ channels, RyR, SERCA, and myosin ATPase.
Parasympathetic stimulation: Decreases heart rate and conduction.

Force Generation and Length-Tension Relationship

Cardiac muscle is capable of graded single twitch contractions. The force of contraction is regulated by intracellular Ca2+ concentration and the length-tension relationship.

Graded contractions: Increased Ca2+ activates more troponin complexes, increasing cross-bridge formation.
Length-tension relationship: Slightly stretched sarcomeres generate greater force due to increased Ca2+ sensitivity and entry.

Feature	Skeletal Muscle	Cardiac Muscle
Action Potential Duration	Short	Long (plateau phase)
Summation/Tetanus	Possible	Prevented by long refractory period
Ca2+ Source	SR only	Extracellular + SR
Regulation	Neuronal	Autorhythmic + neuronal modulation

Length-tension relationship in cardiac muscle

Summary Table: Cardiac Muscle Physiology

Aspect	Cardiac Muscle
Cell Type	Cardiac myocytes (contractile), autorhythmic cells
Intercalated Disks	Desmosomes (mechanical), gap junctions (electrical)
Action Potential	Long duration, plateau phase
Ca2+ Handling	Ca2+-induced Ca2+ release
Regulation	Autonomic nervous system, phospholamban
Force Generation	Graded contractions, length-tension relationship

Additional info: Academic context was added to clarify the mechanisms of excitation-contraction coupling, action potential phases, and regulatory pathways in cardiac muscle.