Question

 1. What role does a play in the actual contraction of a muscle ber (skeletal and cardiac)?

 2. How do cardiac muscle and skeletal muscle differ in the role of Cain stimulation of muscle fibers? How does this difference affect the changes in membrane potential in cardiac muscle?

 3. Based on the information in questions 1 and 2 explain why cardiac muscle does not demonstrate tetanic muscle contractions 

Answer 1

1.Skeletal muscle:A signal comes and relaeases the neurotransittor at the neuromuscular junction(ACh), it binds to the receptor present on the muscle cell membrane.The signal travels deep into the muscle through thr T-tubules.Surrounding the T-tubule, there is sarcoplasmic reticulum present.It stores the Ca2+ ions.On the T-tubule thre are receptors called 'Dihydropuridine receptor' and on the surface of the sarcoplasmic reticulum there are 'Ryanidine receptor'.Both of these channels interact with each other resulting in the opening of the channels and allow Ca2+ ions flow out into the cell out of the sarcoplasmic reticulum. This inititaes the muscle contraction.The calcium binds to the troponin(a protein).The activated troponin causes the conformational change in the protein tropomyosin which wind around the actin filament and mask the myosin binding sites on the actin chain.This opens the myosin binding sites on the actin chain.The myosin head contains the ATP which hydrolyzes by the enzyme ATPase and the energy is released along with the ADP + inorganic phosphate being remaining on the myosin head.The myosin head binds to the actin and releases the inorganic phosphate .The actin is pulled by the myosin molecule with the myosin exchanging ADP with a new molecule of ATP.This causes the myosin head to relax from the actin molecule and the cycle is repeated to pull the actin filament upto I band to cause the muscle contraction.

Cardiac muscle:It is same as that of the skeletal muscle contraction with some exceptions.

• Autorhythmicity: Pacemaker cells of the SA nodespontaneously depolarize.
• Gap junctions allow cell-cell transmission.- This allows ions to flow from one cell to the other.The action potential in one cell triggers another action potential in its neighbour and the impulse propagates rapidly.
• Excitation-contarction coupling : links the action potential to myofibril contraction.Ca2+ from the Extracellular fluid and the sarcoplasmic reticulum promotes the myofibril contraction.
• Excitation-contraction coupling in the cardiac muscle relies on the Calcium induced calcium release.
• Contractility: The intrinsic ability of cardiac muscle cells to produce force at a given cell length.
• Cardiac glycosides raise ICF(Intracellular Calcium Concentration) calcium and increases the contractility.
• Action potential is generated by the pacemaker cells of SA node and is then transported by cell-cell gap junctions.The action potential reaches the sarcolemma to open the voltage gated Ca2+ L-type channels and Ca2+ ions are moved into the intracrllular fluid. Rest of all action is alike the Skeletal muscle.

2.Calcium induced Calcium release

The calcium induced calcium release(The more calcium comes through the Dihydropyridine receptor,The more calcium exits the Ryanidine Calcium Channel, Hence a ton of Ca2+ will be building up inside the sarcoplasmic reticulum) is the peculiarity of the cardiac muscle when compared to the skeletal muscle.When the muscle cells depolarize, the sarcoplasmic reticulum releases the Ca2+, this release slows down the repolarization process making a platau of membrane potential 9membrane potential do not repolarize as quickly; at a certain point, Ca2+ are pumped back to sarcoplasic reticulum and repolarization of cardiac muscle cell occurs) .In cardiac muscle, influx of Ca2+ ions sustains the depolarization period so that it lasts longer.In skeletal muscle the duration of action potential is about 2-5 ms, where in cardiac muscle it ranges from 200-400 ms.

3.The calcium is constantly pumped back into the sarcoplasmic reticlum, the depolarization remains for more period.In case of muscle tetany due to hypocalcemia irregular repeated twitches of muscles occur by high frequency of depolarization in a short time.In cardiac  muscle, since the time of depolarization is more as compared to the skeletal  muscles, these spasm won't occur.