An action potential send by a motor neuron arriving at the neuromuscular junction. Then this causes the muscle sarcolemma depolarizing and sending more action potentials into sarcomeres that release calcium ions from the sacroplasmic retinaculum. This causes the actin filaments to allow the globular heads of the myosin filaments to bind to them (like walking up a ladder) and shorten the muscle fiber into contraction.
Muscle fiber generates tension through the action of actin and myosin cross-bridge cycling.
Because the whole muscle fiber must contract at the same time, the signal (action potential)
is conducted through the cell by transverse tubules (T tubules) which have the same properties as the sarcolemma.
Within each muscle fiber are hundreds of lengthwise subdivisions called myofibrils.
Myofibrils are made up of bundles of the protein filaments (myofilaments) that are responsible for muscle contraction.
The 2 types of myofilaments are: thin filaments: made of the protein actin, and thick filaments: made of the protein myosin.
Ion pumps concentrate calcium ions (Ca++) in the cisternae. The calcium ions are released into the contractile units of the muscle (sarcomeres) at the beginning of a muscle contraction.
Two transverse tubules encircle each sarcomere near the 2 zones of overlap. When calcium ions are released by the sarcoplasmic reticulum, thin and thick filaments interact.
The complex interactions of thick and thin filaments which cause muscle contraction are determined by the structures of their protein molecules.
Thin filaments contain 4 proteins:
1. F actin (2 twisted rows of globular G actin. Active sites on G actin strands bind to myosin.)
2. nebulin (holds F actin strands together)
3. tropomyosin (a double strand, prevents actin-myosin interaction)
4. troponin (a globular protein, binds tropomyosin to G actin, controlled by Ca++)
When a Ca++ ion binds to the receptor on a troponin molecule, the troponin-tropomyosin complex changes, exposing the active site of the F actin and initiating contraction.
Thick Filaments contain twisted myosin subunits. The tail binds to other myosin molecules. The free head, made of 2 globular protein subunits, reaches out to the nearest thin filament.
During a contraction, myosin heads interact with actin filaments to form cross-bridges. The myosin head pivots, producing motion.
Thick filaments contain titin strands that recoil after stretching.
Acetylcholinesterase immediately destroys acetylcholine, so the motor end-plate is no longer stimulated (i.e. it cannot cause continuous muscle contraction)
you
stimulation of the muscle by a nerve ending.
Acetylcholine release is necessary for skeletal muscle contraction, because it serves as the first step in the process, enabling the subsequent cross-bridge formation. A muscle's ability to contract depends on the formation of cross-bridges between myosin & actin filaments. A drug that blocks acetylcholine release would interfere with this cross-bridge formation and prevent muscle contraction
Latent Phase
stimulation of the muscle by a nerve ending.
The mechanism by which skeletal muscle tissue obtains ATP to fuel contractions is the sliding - filament hypothesis. Two filaments, actin and myosin, slide over one another during contraction.
summation
a wave like muscle contraction that move food down the esasphogs
· First- the type and number of muscle fibers · Second- the initial length of muscle at time of contraction · Third- the nature of the neural stimulation
Being multinucleated enables anything to synthesize more protein. Also we know that skeletal muscle fibres are much longer than that of any other muscle fibre, so it needs a huge amount of actin and myosin protein to bring about required contraction of a muscle, as actin and myosin crossbridge is required for muscle contraction. Thus it can be postulated that this boon of being multinucleated is essential for a skeletal muscle to posses adequate amounts of actin and myosin for muscle contraction. By-- faireena singh ( mbbs first year cmc)
Acetylcholine release is necessary for skeletal muscle contraction, because it serves as the first step in the process, enabling the subsequent cross-bridge formation. A muscle's ability to contract depends on the formation of cross-bridges between myosin & actin filaments. A drug that blocks acetylcholine release would interfere with this cross-bridge formation and prevent muscle contraction
The first event in expiration is the relaxation of the diaphragm muscle, which is the primary muscle responsible for breathing. As the diaphragm relaxes, it moves upward, decreasing the volume in the chest cavity and causing air to be expelled from the lungs.
i know that you need a nerve impulse the second i think is calcium and i don't know what the third is. Movement is initiated by muscles (forces) moving about levers (bones, etc humerus) about axes (our joints). In order for a muscle to contract a neural impulse in needed and in the abssence of a neural impulse calcium is reabsorbed into the; sarcoplasmic reticulum ( part of a single muscle fibre)