Excitation–Contraction Coupling
Start with the big picture
An action potential spreads along the sarcolemma and into T-tubules, where depolarization changes the conformation of DHPR voltage sensors. In skeletal muscle, DHPRs mechanically open nearby RyR1 channels; in cardiac muscle, calcium entering through DHPRs triggers further release through RyR2. The rise in cytosolic calcium allows calcium to bind troponin C, shifting tropomyosin and exposing actin’s myosin-binding sites. Myosin cross-bridge cycling then generates force. Relaxation follows as ATP-powered SERCA returns calcium to the sarcoplasmic reticulum, with other calcium-removal mechanisms contributing as well. The broader topic connects these steps to force, sustained stimulation, clinical conditions, pharmacology, and coupling latency.
What you'll learn
- Trace the sequence from sarcolemma depolarization to calcium release and muscle contraction.
- Distinguish DHPR–RyR coupling in skeletal muscle from calcium-triggered release in cardiac muscle.
- Explain how calcium binding to troponin C enables cross-bridge cycling.
- Describe how SERCA and other calcium-removal mechanisms contribute to relaxation.
- Relate calcium handling to force generation, tetanus, and malignant hyperthermia.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
