G3i: Explain the Frank-Starling mechanism and its relationship to excitation-contraction coupling

Frank-Starling Mechanism

  • Sarcomere = the basic unit of striated muscle
  • Normal sarcomere length = 1.8µm
  • ↑sarcomere length = ↑force generated
  • ↑preL/EDV = ↑SV
  • This happens up to a point → 2.2µm, where any further ↑sarcomere length = detrimental to force generated
Frank-Starling Mechanism

This is an intrinsic property of heart that allows it to rapidly adapt to ∆ volumes of venous return

Excitation-Contraction Coupling

  • ECC = an electrical impulse linked to a mechanical response (contraction)
  • Mechanism of the ECC:
    • AP
    • Membrane depol
    • L type Ca2+ channel release Ca2+
    • Sensed by RYANODINE REC
    • Mass Ca2+ release from SR
    • Ca2+ binds TnC
    • Conformation ∆ Troponin-Tropomyosin complex moves away from Actin
    • Myosin head binds to Actin → forms cross-bridge
    • ATP hydrolysis powers cross-bridge cycling*
    • Shortens sarcomere length (contraction happening)
    • Until Ca2+ deplete OR ATP deplete
    • SERCA pump on SR (powered by ATP) → causes Ca2+ to return to cell*
    • Ca2+ from TnC
    • Conform ∆ → Troponin-Tropomyosin inhibition continued

*ATP for both contraction & relaxation

How F – S Causes ↑ECC

  • ↑sarcomere length = ↑efficiency of E-C-C (up to a point 2.2µm)
  • By:
    1. ↑overlap of Actin/Myosin = ↑cross-bridging
    2. ↑sensitivity of myofilaments to Ca2+
    3. ↑affinity of Tn to Ca2+
    • All these allow MAX FoC when E-C-C initiated