Muscle Contraction and Types

• Muscle contraction facilitates movement and circulation.
• Cardiac, skeletal, and smooth muscles each have unique structure-function characteristics.

Muscle Structure

• Skeletal muscle is attached to the skeleton and is under voluntary control.
• Skeletal muscle fibers are large, striated, multinucleated, and range from 20-100μm in diameter and up to 12cm in length are unbranched, and each fiber is innervated by a motor neuron.
• A motor unit consists of multiple muscle fibers innervated by a single motor neuron.
• Cardiac muscle forms the walls of the heart, undergoing spontaneous and involuntary contraction.
• Cardiac muscle cells are brick-shaped, striated, ranging from 10-20μm in diameter and 100μm in length forming a branched syncytium
• Contraction is initiated through conduction, originating in the sino-atrial (SA) node, not through motor nerves.
• Smooth muscle lines blood vessels and organs, contracting involuntarily, often slowly, and sustained.
• Smooth muscle cells are spindle-shaped, non-striated, approximately 5μm in diameter and 200μm in length, with actin and myosin arrangements that are unstructured.
• Striated muscle distinct features include Z line, T-tubule, sarcomere, H-band, M-line, A-band (thick filaments, containing myosin), and I-band (thin filaments).
• Sarcomere contains thick (myosin) and thin (actin) filaments and is the basic unit of striated muscle contraction.
• Z line marks the sarcomere boundaries, where thin filaments anchor.
• A band marks entire length of thick filaments where myosin is present.
• I band contains only thin filaments, appearing lighter in color.

Membrane Potential and Action Potentials

• Neuronal action potential is short in duration (APD) and has a long relative refractory period for input integration.
• Ventricular muscle action potential if triggered by excitation across the heart.
• Wave originates in the sino-atrial (SA) node.
• Cardiac action potential characterized by a very long refractory period lasting 200-400ms.
• Lengthened action potential, protects against re-entrant arrhythmias and prevents tetany.
• Skeletal muscle action potential exhibits a short APD and a short refractory period that allows tetany, its triggered by activation of a motor neuron
• Excitation in skeletal muscle initiates at the neuromuscular junction.
• Smooth muscle exhibits action potentials and graded depolarization.
• Smooth muscle resting potential ranges from -20 to -70mV, being more depolarized.
• Duration of smooth muscle action potential can be long, exceeding 5 seconds.
• Smooth muscle action potentials are driven by time-dependent channels, including voltage-gated and ligand-gated types.
• In smooth muscle constrictors cause depolarization, dilators cause hyperpolarization.
• These actions are driven by time-independent channels, like voltage-gated and ligand-gated channels.
• Slow waves of depolarization can trigger these action potentials within smooth muscle.
• Strongest contractions in smooth muscle are linked to bursts of action potentials.

Role of Calcium

• Calcium is essential for contraction in cardiac, skeletal, and smooth muscle.
• Method of calcium elevation differs among muscle types.
• Locke and Rosenheim discovered role of calcium in heart function, converting electrical excitation to mechanical contraction.
• Action potential triggers intracellular calcium transient and contraction for all muscle types.

Calcium and Excitation-Contraction Coupling (ECC)

• Calcium causes the myofilaments to slide past each other.
• ECC is the process linking muscle excitation to contraction.

Cardiac Muscle

• L-type calcium channels play a role in cardiac muscle ECC.
• Calcium-induced calcium release is a signature feature. Relaxation involves the sodium/calcium exchanger, sarco(endo)plasmic reticulum calcium ATPase (SERCA), and phospholamban (PLB).

Skeletal Muscle

• Voltage-induced calcium release characterizes skeletal muscle ECC.
• Relaxation is similar to cardiac muscle, with all calcium returning to the sarcoplasmic reticulum (SR).

Smooth Muscle

• Voltage and ligand gated channels and membrane potential are key to calcium entry in smooth muscles.
• Calcium then enters the cytosol through gated channels from the sarcoplasmic reticulum stores.
• Smooth muscle contraction is triggered by receptors and messenger pathways.
• Calcium binds to calmodulin, activating MLCK, which phosphorylates myosin light chains, leading to contraction and cell contraction.
• Sarcomere shortens as myosin filaments slide past actin filaments.
• Calcium binds to troponin C, pulling tropomyosin out of the actin groove.
• ATP is needed so the myosin head binds to actin to slide past.

Tension

• Skeletal muscle motor units operate on an 'all or nothing' principle, recruiting more units to apply more tension.
• Cardiac muscle tension is regulated by calcium levels.
• Myofilament calcium sensitivity also affects cardiac muscle contraction.

Factors Influencing Contraction Strength

• The magnitude of the calcium transient directly affects contraction strength.
• Myofilament calcium sensitivity can be altered by factors such as temperature, pH, and the presence of drugs.
• In cardiac muscle, more calcium leads to more cross-bridges and increased tension, showing a graded response.
• Skeletal muscle follows the 'all or nothing' principle, where more motor units recruited results in greater tension.

Clinical Significance

• Disruptions in ECC lead to muscular disorders.
• Duchenne Muscular Dystrophy (DMD) affects dystrophin, leading to skeletal muscle degeneration.
• Cardiac arrhythmias may result from abnormal ECC processes.
• Hypertension can arise from dysregulated smooth muscle contraction in blood vessels.