G1i: Describe the structure and functional significance of contractile elements of the heart

3 types of cardiac muscle

  1. Atrial — Like skeletal m. but contract longer
  2. Ventricular — Like skeletal m. but contract longer
  3. Conduction → few contractile fibres; they exhibit automatic rhythmic electrical D/C in the form of AP which controls rhythmical beating of the heart

Consist of:

  • Sarcomeres → with actin & myosin filaments
    • The functional unit of cardiac muscle
  • Intercalated discs → cell membranes that separate muscle cells but join the ends of myocytes together
    • Fusion of the cell membrane via IC discs allows fast communication between myocytes
    • Enables rapid propagation of AP
  • Gap Junction → a low resistance pathway within an intercalated disc
    • Cell connection which lets adjacent cytoplasm communication & ions pass v. quickly
  • T-tubules → extension of cell membrane that penetrates cell
    • Bigger & wider cf. T-tubule of skeletal m., which allows greater Ca2+ influx
    • AP passes over cardiac myocyte PM
    • Causes SR to release Ca2+
    • Extra Ca2+ enters myocyte via T-tubule
    • Mass Ca2+ release allows non-bridge formation & contraction
    • SR of cardiac myocyte less developed skeletal m. → requires extra Ca2+ from T-tubule to generate an appropriate muscle contraction

Strength of contraction ∝ [Ca2+ ECF]

  • Syncytium
    • Cardiac m. performs as a unit of atrial & ventricular syncytium
    • When suprathreshold stimulus applied → AP → depolarisation → contraction of entire syncytium
    • Atrial & ventricular syncytium separated by fibrous tissue, which prevents conduction from atrial → ventricular syncytium directly
    • AV bundle conducts the message ∴allows the atria to contract before ventricles

Cardiac muscle has high energy requirements

  • Contracts repetitively
  • Aerobic metabolism only
  • Requires constant O2 supply
  • Very rich in mitochondria
  • Very rich capillary network ~ 1 cap / fibre → minimal diffusion distance for substrates & waste

Function

Excitation – contraction coupling = the mechanism by which an AP causes myofibrils of muscle to contract

• K+

  • Responsible for RMP
  • EC K+ = ↑RMP = ↓excitability of cell by inactivating Na+ channel
  • ↑↑↑EC K+ = loss excitability = cardiac arrest

• Na+

  • Responsible for AP generation
  • Influences excitability

• Ca2+

  • Responsible for contraction

Mechanism of Contraction

  • Cross Bridge Recycling is the molecular mechanism of muscle contraction
  • Ca2+ enters myocyte from ECF during Plateau phase via T-tubules

→ triggers Ca2+ release from IC SR stores (essential)

→ cytosolic Ca2+ initiates contraction

  • Ca2+ binds Tn C on Actin Filaments
  • This displaces TROPOMYOSIN which is blocking the myosin binding sites
  • Exposure of Myosin Binding Sites
  • ATP hydrolysis on Myosin head
  • Release of Pi → myosin binds to myosin binding site
  • Actin + myosin filaments slide past each other

→ k.a. SLIDING FILAMENT MECHANISM

Mechanism of Relaxation

  • Ca2+ influx ceases at end systole

→ Ca2+ is pumped out via 3 Na+ in/ Ca2+ out exchanger

→ Ca2+ is taken up by SR

→ Tropomyosin covers the Myosin Binding Sites of Actin filaments