G1iii: Describe the structure and functional significance of contractile elements of the heart
3 types of cardiac muscle
- Atrial — Like skeletal m. but contract longer
- Ventricular — Like skeletal m. but contract longer
- 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