Excitation-contraction coupling is the combination of the electrical and mechanical events in the muscle fibres and is related by the release of calcium from the sarcoplasmic reticulum. (Silverthorn, 2007)
In the skeletal muscle, action potential in the nerves is generated when the somatic motor neurons releases the neurotransmitter acetylcholine (ACh), at the neuromuscular junction. This initiates muscle action potential which is then transmitted to the t-tubules. Action potential in the t-tubules leads to the release of calcium in the sarcoplasmic reticulum triggering muscle contraction.
In the cardiac muscles, the initial depolarisation in sino-atrial node initiates the action potential in the muscles. This is then transmitted to T-Tubule which leads to calcium influx from extracellular space. This leads to the sarcoplasmic reticulum releasing calcium which causes the muscle contraction.
The skeletal muscles need ACh from the somatic motor neuron, in order for skeletal muscle action potential to initiate excitation- contraction coupling. In cardiac muscles, the action potential also initiates EC coupling, but it originates impulsively in the hearts pace maker cells and spreads via gap junctions. (Richard and Pocock, 2006)
The skeletal muscles and cardiac muscles differ mainly in mechanisms by which the depolarisation in the membrane leads to the release of Ca2+. In the skeletal muscle, the T-tubule membrane is coupled closely to the sarcoplasmic reticulum via the L-type calcium channel and the ryanodine receptor. However, in the cardiac muscle the Ca2+ enters via voltage-gated calcium channels which initiate a regenerative release, through activation of the Ca2+ sensitive ryanodine receptor and this initial entry triggers further release from the sarcoplasmic reticulum. (Rang and Dale, 2003)