Sliding filament theory :
• During muscle contraction, thin filaments show sliding inward towards the H-zone.
• Sarcomere shortens, without changing the length of thin and thick myofilaments.
• The cross bridge of the thick myofilaments connects with the portions of actin of the thin myofilaments. These cross bridge move on the surface of the thin myofilaments resulting to sliding of thin and thick myofilaments over each other.
• A muscle fibre maintains a resting potential under resting conditions just like a nerve fibre as soon as nerve impulses reach the terminal end of the axon, small sacs called synaptic vesicles to fuse with the axon membrane and release a chemical transmitter, acetylcholine.
• Acetylcholine diffuses across the synaptic cleft and binds to the receptor sites of the motor and plate.
• As soon as depolarization of the motor end plate reaches and plate reaches a certain level, it creates an action potential. After this, an enzyme cholinesterase present along with the receptor sites for acetylcholine breaks down acetylcholine into acetate and choline.
• The area of contact between a nerve and muscle fibre is called motor end plate or muscular junction.
• Calcium plays a key regulatory role in muscle contraction. These ions bind to troponin causing a change in its shape and position. This, in turn, alters and the position of tropomyosin. This shift exposes the active sites on the F-actin and myosin cross-bridges are then able to bind these active sites.
• The head of each myosin molecule contains an enzyme myosin ATPase. In the presence of myosin ATPase, calcium ions and Magnesium ions, ATP breaks down into ADP and inorganic phosphate and some amount of energy.
• Energy from ATP causes energized myosin, cross bridges to bind to actin. The energized cross bridge move causing thin myofilaments to slide along the thick myofilaments.