UWL BIO 312 - Muscle contraction (3 pages)

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Muscle contraction

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Muscle contraction


Lecture notes describing the anatomy and physiology of muscular synapses, pharmacology of neuro-muscular interactions, as well as intro to muscle mechanics, motor unit, external muscle tension, load, isometric, isotonic, concentric, eccentric

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Lecture Note
University of Wisconsin-La Crosse
Bio 312 - Human Anatomy and Physiology I
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Bio 312 Lecture 20 Lecture Outline 1 Muscular contraction a Anatomy of synapses b Physiology of contraction c Pharmacology 2 Muscle Mechanics a Motor units b Types of contraction Muscular Contraction Neuromuscular junction where nerve cell axon synapses with skeletal muscle o Always excitatory somatic muscles are always nicotinic o Synapse in middle of muscle fiber for most uniform action potential throughout fiber Sarcoplasmic reticulum membranous sac surrounding every myofibril stores Ca2 when not stimulated o Releases calcium during stimulation o Active re uptake of calcium when relaxed Transverse tubules invaginations of sarcolemma that occur at regular intervals throughout sarcolemma o Rapidly conduct action potentials to interior of cell so all myofibrils can be activated simultaneously o Action potential passing down T tubule opens nearby calcium channels located on the sarcoplasmic reticulum flooding the area surrounding the myofibrils sarcoplasm with calcium ions o 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 molecules o Raise in concentration of calcium ions rotates actin and revealing the binding sites allowing cross bridges to bind to actin and initiate contraction o 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 Coupling 1 Action potential generated and propagated along the sarcolemma and down the T tubule via voltage gated ion channels same as unmyelinated axon 2 Action potential triggers Ca 2 release from sarcoplasmic reticulum 3 Calcium ions bind to troponin removing the blocking action of tropomyosin exposing actin binding sites 4 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 process 5 Removal of Ca 2 by active transport into SR after the action potential ends causing tropomyosin to block the actin binding sites causing muscle to relax o 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 neuron Packed full of nicotinic acetylcholine receptors chemically gated ion channels contains no voltage gated channels 1 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 exocytosis 2 Nicotinic receptors on motor end plate bind to the acetylcholine released by neuron 3 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 fiber o One end plate potential is enough to propagate signal does not require summation o Acetylcholinesterase embedded in motor end plate rapidly breaks down Ach and allows for reuptake of choline acetate diffuses away Drugs Toxins affecting NMJ o 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 forward o Black widow spider venom triggers massive release of Ach causing spastic paralysis o 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 procedure o 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 inhibitor Skeletal 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 controls o Any given muscle is composed of many motor units o Strength of contraction is proportional to the number of motor units that get activated o Muscles have mixture of large many muscle fibers and small few muscle fibers motor units The larger the motor unit the larger the force generated o Activity is all or none Contraction generation of tension within a muscle by cross bridge activity o 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 begins o External muscle tension afterload then muscle shortens o 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 position o Isotonic muscle changes length while afterload on the muscle remains constant Concentric muscle shortens during contraction o Eccentric unsupported load on muscle is greater than external muscle tension causing muscle to lengthen

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