Contraction in skeletal muscle

Structural differences between Striated and Smooth muscle

 * Smooth muscle fibers do not have their myofibrils arranged in strict patterns as in striated muscle, thus no distinct striation is observed in smooth muscle cells under the microscopical examination.
 * In smooth muscle, the sarcomeres are attached on structures called densed bodies playing the same role as Z disks in the striated muscle. They provide an anchoring site for the sarcomeres in order to induce mechanical work when the fibrils contract.
 * Smooth muscle cells contain a single rod-like nucleus located in the center of the cell, whereas striated muscle cells are polynucleated and their nuclei are located on the periphery.
 * Smooth muscle cells have a fusiform shape introducing a very distinct pattern of cell arrangement, whereas striated muscle cells have a rather rod-like shape.
 * The resting membrane potential of a smooth muscle fiber is about -40 mV whereas in the striated muscle is about -90 mV.

Functional differences between Striated and Smooth muscle

 * The smooth muscle contraction is much slower than in the striated muscle primarily due to the presence of G protein coupled ligand receptors instead of ion channel coupled ligand gated receptors present in striated muscle. Also, after activation of the receptors there is a long process in order to elicit an action potential, involving second messengers and activation of enzymes.
 * Smooth muscle thin actin filaments lack troponin protein.
 * In both striated and smooth muscle, contraction entirely depends on Ca2+ intracellular concentration but through different pathways. In striated muscle Ca2+ exposes actin binding sites promoting cross bridge formation between myosin and actin filaments, whereas in smooth muscle Ca2+ will activate kinases that will eventually induce conformational changes of the myosin heads in order to form cross bridges.
 * Smooth muscle cell overall contraction squeezes the cell from every direction since the myofibrils are not arranged on the longitudinal axis of the cell. In striated muscle cell the overall contraction compresses mainly the two end towards the center of the cell minimizing the total length

Skeletal muscle contraction

 * An action potential travels through the axon terminal and eventually reaches the synaptic terminal
 * The depolarization of the synaptic terminal from the action potential induces opening of the Ca2+ voltage gated channels
 * Opening of these channels allows flux of Ca2+ ions inside the neuron
 * Increase of the intracellular Ca2+ concentration introduces conformational changes of the microtubular component of the neuronal synaptic terminal cytoskeleton
 * These cytoskeletal changes lead the exocytotic process concerning the synaptic vesicles containing acetylcholine (ACh) neurotransmitter
 * Through exocytosis secretion of ACh occurs that diffuses from the synaptic terminal membrane towards the motor end plate membrane
 * As soon as the neurotransmitter reaches the plasma membrane of the skeletal musce fiber, it binds with ligand gated ion channel coupled receptors specific for ACh. These receptors are called nicotinic receptors and are sensitive to nicotine besides ACh
 * As soon as the neurotransmitter-receptors complex occurs it activates an integral protein coupled with the nicotinic receptor, undergoing conformational changes
 * These conformational changes allow the opening of the channel which in turn cause the flux of Na+ ions inside the muscle fiber
 * Accumulation of Na+ within the cell commence the depolarization of the membrane giving rise to the end plate potential that keeps rising towards an action potential threshold
 * The action potential spreads throughout the membrane of the fiber and especially within the T tubules of the muscle fiber deep inside the fiber
 * The thorough spreading of depolarization promotes activation of the Ca2+ voltage gated channels located on the plasma membrane and in the T tubules
 * Opening of the Ca2+ channels cause influx of Ca2+ ions inside the cell increases the intracellular calcium concentration which in turn open Ca2+ voltage gated channels of the sarcoplasmic reticuli near the T tubules allowing even greater increase of intracellular Ca2+
 * The Ca2+ that accumulates after a skeletal muscle cell depolarization is the reason for the initiation and the maintenance of the contraction of the sarcomere, thus increasing the Ca2+ inside the cell, will also increase the contractile force produced by the fibers.
 * The free Ca2+ binds with the troponin C protein component of the thin actin filaments introducing the active calcium-troponin complex
 * This binding causes the conformational change of the troponin C
 * The conformational change of the troponin C induces the alteration of the conformation of the tropomyosin protein component of the thin actin filaments
 * These changes, all together, promote the exposure of the actin binding sites in order to provide anchoring of the myosin filament heads in order to induce interaction between the thick and thin filaments and elicit contraction
 * Myosin binds to the newly uncovered binding sites on the thin filament. The release of ADP and phosphate are tightly coupled to the power stroke. This will pull the Z bands towards each other, thus shortening the sarcomere and the I band.
 * ATP binds myosin, allowing it to release actin and be in the weak binding state
 * The myosin then hydrolyzes the ATP and uses the energy to move into the "cocked back" conformation.