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Objectives: After studying this course, you should be able to:

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1 Objectives: After studying this course, you should be able to:
Differentiate the major classes of muscle in the body. Describe the molecular and electrical makeup of muscle cell excitation–contraction coupling. Define thin and thick filaments and how they slide to create contraction. Differentiate the role(s) for Ca2+ in skeletal and smooth muscle contraction.

2 انواع عضله صاف اسکلتی قلبی

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5 رتیکولوم سارکوپلاسمیک

6 ساختمان رشته میوزین

7 رشته های ضخیم و نازک

8 Walk-along mechanism for contraction

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10 Effect of Amount of Actin and Myosin Filament Overlap on Tension Developed by the Contracting Muscle

11 Relation of muscle length to tension in the muscle both before and during muscle contraction.

12 Relation of Velocity of Contraction to Load
skeletal muscle contracts extremely rapidly when it contracts against no load The velocity of contraction becomes progressively less as the load increases when the load has been increased to equal the maximum force that the muscle can exert, the velocity of contraction becomes zero and no contraction results, despite activation of the muscle fiber.

13 Sources of Energy for Muscle Contraction
ATP: sufficient to maintain full contraction for only 1 to 2 seconds at most Phosphocreatine: five times as great as the ATP Glycolysis of glycogen: Oxidative metabolism. Efficiency of Muscle Contraction: the percentage of energy input that is converted into work instead of heat.

14 Isometric Versus Isotonic Contraction

15 Fast Fibers. (1) Large fibers for great strength of contraction.
(2) Extensive sarcoplasmic reticulum for rapid release of calcium ions to initiate contraction. (3) Large amounts of glycolytic enzymes for rapid release of energy by the glycolytic process. (4) Less extensive blood supply because oxidative metabolism is of secondary importance. (5) Fewer mitochondria, also because oxidative metabolism is secondary.

16 Slow Fibers. (1) Smaller fibers.
(2) Also innervated by smaller nerve fibers. (3) More extensive blood vessel system and capillaries to supply extra amounts of oxygen. (4) Greatly increased numbers of mitochondria, also to support high levels of oxidative metabolism. (5) Fibers contain large amounts of myoglobin, an iron-containing protein similar to hemoglobin in red blood cells.

17 Muscle twitch

18 Summation of contractions
(1) by increasing the number of motor units contracting simultaneously, which is called multiple fiber summation, (2) by increasing the frequency of contraction, which is called frequency summation and can lead to tetanization. Changes in Muscle Strength at the Onset of Contraction—The Staircase Effect (Treppe). Skeletal Muscle Tone: muscle spindles role Muscle Fatigue: depletion of muscle glycogen, diminish of transmission of the nerve signal through the neuromuscular junction

19 Dystrophin–Glycoprotein Complex
The large dystrophin protein (427 KDa) forms a rod that connects the thin actin filaments to the transmembrane protein -dystroglycan in the sarcolemma by smaller proteins in the cytoplasm, syntrophins. β-dystroglycan is connected to merosin (merosin refers to laminins that contain the 2 subunit in their trimeric makeup) in the extracellular matrix by α-dystroglycan. This dystrophin–glycoprotein complex adds strength to the muscle by providing a scaffolding for the fibrils and connecting them to the extracellular environment.

20 فیزیولوژی انقباض

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27 واحد حرکتی

28 Drugs That Enhance or Block Transmission at the Neuromuscular Junction
Stimulate the Muscle Fiber by Acetylcholine-Like -action. Many compounds, including methacholine, carbachol, and nicotine Stimulate the Neuromuscular Junction by Inactivating Acetylcholinesterase. Three particularly well known drugs, neostigmine, physostigmine, and diisopropyl fluorophosphate, Drugs That Block Transmission at the Neuromuscular Junction: curariform drugs can prevent passage of impulses from the nerve ending into the muscle. Myasthenia Gravis


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