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UWL BIO 312 - Muscle contraction

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Lecture 20Lecture Outline:1. Muscular contractiona. Anatomy of synapsesb. Physiology of contractionc. Pharmacology 2. Muscle Mechanicsa. Motor unitsb. Types of contractionMuscular Contraction:- Neuromuscular junction: where nerve cell axon synapses with skeletal muscleo Always excitatory, somatic muscles are always nicotinico Synapse in middle of muscle fiber for most uniform action potential throughout fiber- Sarcoplasmic reticulum: membranous sac surrounding every myofibril, stores Ca2+ when not stimulatedo Releases calcium during stimulationo Active re-uptake of calcium when relaxed- Transverse tubules: invaginations of sarcolemma that occur at regular intervals throughout sarcolemmao Rapidly conduct action potentials to interior of cell so all myofibrils can be activated simultaneouslyo Action potential passing down T-tubule opens nearby calcium channels located on the sarcoplasmic reticulum, flooding the area surrounding the myofibrils (sarcoplasm) with calcium ionso Extensiveness of the sarcoplasmic reticulum assures that when calcium is released it quickly reaches all areas of the myofibrils- Role of Ca 2+ ions in sarcoplasm:o No calcium present means that tropomyosin blocks actin binding sites, keeping cross bridges from binding to actin moleculeso Raise in concentration of calcium ions rotates actin and revealing the binding sites, allowing cross bridgesto bind to actin and initiate contractiono Re-uptake of calcium into S.R. causes tropomyosin to go back to blocking actin binding sites causing relaxation of the muscle- Action potential initiates Excitation-Contraction Coupling1. Action potential generated and propagated along the sarcolemma and down the T-tubule via voltage gatedion channels (same as unmyelinated axon)2. Action potential triggers Ca 2+ release from sarcoplasmic reticulum3. Calcium ions bind to troponin, removing the blocking action of tropomyosin, exposing actin binding sites4. Myosin cross bridges alternately attach to actin and detach, pulling the actin filaments toward the center of the sarcomere; release of energy by ATP hydrolysis powers the cycling process5. Removal of Ca 2+ by active transport into SR after the action potential ends, causing tropomyosin to blockthe actin binding sites, causing muscle to relaxo Active State: response to AP in which actin binding sites are exposed and cycling of cross bridges occurs- Motor end plate: specialized region (post synaptic membrane) of sarcolemma directly under lower motor neuronBio 312o Packed full of nicotinic acetylcholine receptors, chemically gated ion channels, contains no voltage gated channels1. Action potential propagated in motor neuron, causing voltage gated calcium channels to open causing the release of neurotransmitter into the neuromuscular junction/synaptic cleft by exocytosis2. Nicotinic receptors on motor end plate bind to the acetylcholine released by neuron3. Binding of Ach causes the opening of chemically gated ion channels causing depolarization to occur (end plate potential)4. Adjacent voltage gated ion channels then propagate the action potential down the muscle fibero One end plate potential is enough to propagate signal, does not require summationo Acetylcholinesterase embedded in motor end plate rapidly breaks down Ach and allows for reuptake of choline, acetate diffuses away- Drugs & Toxins affecting NMJo Botulism: most toxic poison known Blocks release of Ach, produces flaccid paralysis Responsible for botox Treatment for crossed eyes, causing crooked eyeball to relax and point straight forwardo Black widow spider venom: triggers massive release of Ach causing spastic paralysiso Paralytics: neuromuscular blocking agents Nicotinic receptor antagonists Many clinical applications requiring muscle relaxtion/paralysis Do not diminish perception of pain Cholinesterase inhibitors used to reverse neuromuscular blocking agents after surgery/procedureo Myasthenia Gravis: characterized by muscle weakness and possible paralysis Progressive autoimmune disease that destroys nicotinic receptors and associated chemically gated ion channels Over time, motor end plate loses ability to generate depolarization and ability to generate AP’s Treatment is cholinesterase inhibitorSkeletal Muscle Mechanics: characteristics of muscle contractions- When motor neuron approaches target muscle, neuron will branch and stimulate many different muscle fibers- Motor unit: single motor neuron and all of the muscle fibers it controlso Any given muscle is composed of many motor unitso Strength of contraction is proportional to the number of motor units that get activatedo Muscles have mixture of large (many muscle fibers) and small (few muscle fibers) motor units The larger the motor unit, the larger the force generatedo Activity is all-or-none- Contraction: generation of tension within a muscle by cross bridge activityo External muscle tension: tension exerted by contracting muscle on some object (barbell)o (After)load: force exerted by external object on the muscle after contraction beginso External muscle tension > afterload, then muscle shortenso External muscle tension < or = afterload, then no shortening- Types of Contraction:o Isometric: muscle develops tension but doesn’t contract or extend. Muscle holds load in constant positiono Isotonic: muscle changes length while afterload on the muscle remains constant Concentric: muscle shortens during contraction Eccentric: unsupported load on muscle is greater than external muscle tension causing muscle to


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