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Excitation-contraction coupling
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Definition: a process in which an initiating stimulus (e.g., AP, chemical stimulus) triggers an increase in intracellular Ca2+ and subsequent myofilament shortening, resulting in muscular contraction

Types
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Electromechanical coupling
Pharmacomechanical coupling

Description
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The mechanism by which the intracellular Ca2+ concentration increases differs for each muscle type.
Skeletal muscle: stimulus → opening of dihydropyridine receptors and ryanodine receptors → Ca2+ release from the SR
Smooth muscle: stimulus → Ca2+ influx from the extracellular space into the muscle cell
Cardiac muscle: stimulus → Ca2+ influx from the extracellular space into the muscle cell → Ca2+ release from the SR

At resting position, actin and myosin are unable to interact because they are inhibited by regulatory proteins. An initiating stimulus is needed to enable interaction between the myofilaments.

Mechanism: stimulus (AP) from efferent neuron → presynaptic voltage-gated Ca2+ channels open → ACh is released into the synaptic gap → ACh binds to postsynaptic ACh receptors → muscle cell depolarization that diffuses across the sarcolemma and into T-tubules → opening of voltage-sensitive dihydropyridine receptors (DHPR) in the T tubules and the mechanically coupled ryanodine receptors (RYR) in the SR → SR releases Ca2+ into the sarcoplasm → increased intracellular Ca2+

Steps of the contraction cycle (crossbridge cycling)
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Crossbridge formation: released intracellular Ca2+ binds to troponin C and causes a conformational change → tropomyosin moves away from the myosin binding site of the actin filament → myosin head binds actin at a 90° angle, forming a crossbridge
Powerstroke of the myosin head: myosin head releases phosphate (Pi)→ myosin head tilts by 45°, pulling myosin along actin → muscle shortens (contracts) → ADP is released
Loosening of the crossbridge: new ATP binds to myosin head → myosin head detaches from the actin filament → myosin returns to its original position
Reorientation of the myosin head: hydrolysis of ATP to ADP and Pi (both remain on the myosin head) → myosin head alters its conformation (changes to a “cocked state”) → myosin returns to its original position (ready to bind to actin again)
Replication of the cycle
If the Ca2+ concentration in the muscle cell remains elevated, a new cycle begins with crossbridge formation

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