Body Movement in Skeletal Muscles PDF

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MemorableSpatialism

Uploaded by MemorableSpatialism

CMMS - AGU

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skeletal muscle body movement anatomy biology

Summary

This document explains skeletal muscle contraction and body movement, covering neuromuscular control, excitation-contraction coupling, and the molecular basis of skeletal muscle contraction. It also discusses disorders of the neuromuscular junction and rigor mortis.

Full Transcript

Learning Objects Skeletal Muscle Contraction & Body Movement Skeletal muscles contract and relax to mechanically move the body. Walking, running, and manipulating objects with the hands. Skeletal muscle works in conjunction with the bones of the skeleton t...

Learning Objects Skeletal Muscle Contraction & Body Movement Skeletal muscles contract and relax to mechanically move the body. Walking, running, and manipulating objects with the hands. Skeletal muscle works in conjunction with the bones of the skeleton to create body movements. The fibers contract and generate tension (force) which is transmitted through the tendons to bones. This allows the muscles to move bones, and different movements Neuromuscular Control Signaling from the Nervous System Excitation signals from the neurons (motor neurons in the spinal cord or brainstem) are the only way to functionally activate the skeletal muscle fibers to contract. The Neuromuscular Junction (NMJ) The neuromuscular junction (NMJ) is the point of synaptic contact between the axon terminal of a motor neuron and the muscle fiber it controls. Synaptic Cleft: 20-30 nm wide gap containing acetylcholinesterase (AChE). The Motor End Plate forms the postsynaptic part of NMJ. It is the thickened portion of the sarcolemma that is folded to form depressions called junctional folds. Invaginations (clefts or folds) increase the surface area of the postsynaptic membrane. Contain ACh receptors and voltage- gated Na+ channels. Acetylcholine Release Voltage-gated sodium channels (VGSCs) facilitate action potential generation during Main Schema for Neuromuscular Transmission Disorders of the Neuromuscular Junction In presynaptic membrane In post-synaptic 1. Eaton-Lambert syndrome membrane is an autoimmune disorder of 1. Myasthenia Gravis: the neuromuscular junction. an autoimmune It is caused by antibodies to disorder of calcium channels in the neuromuscular junction presynaptic axon terminal. caused by antibodies to cholinergic receptors in 2. Botulism: Toxin made by the postsynaptic Clostridium botulinum membrane. bacteria inhibits the release of ACh from the presynaptic membrane. Neuromuscular Junction disorder patients present with complaints of muscle fatigue and weakness that fluctuate with episodes of worsening after physical activity. Excitation-Contraction Coupling Ca+2 for Excitation-Contraction Coupling Release of Ca+2 from Sarcoplasmic Reticulum Dihydropyridine (DHP) receptors sense the action potential in the muscle fiber membrane. They are physically linked to Ca+2 release channels (ryanodine receptor channels; RyR) of the SR. Activation of DHP receptors of T- tubules triggers the opening of Ca+2 channels of SR. After a few msecs, repolarization of the T-tubule occurs and Ca+2 release channels on the SR are closed. The SR is the primary source of Ca+2 influx in skeletal muscle. ECF calcium influx does not play a major role. Organization of Skeletal Muscle Skeletal Muscle Structure- Gross to Cellular The Myofilaments The arrangement of thin and thick filaments gives skeletal muscle its microscopic striated appearance and creates functional units called sarcomeres. The thick myosin filaments are anchored in place by Titin fibers. The thin actin filaments are anchored directly to Z-lines. A cross-section through a sarcomere shows that each myosin can interact with 6 actin filaments, and each actin can interact with 3 myosin filaments. The Sarcomere The sarcomere is the fundamental unit of contraction and is defined as the region between two Z-lines (discs). Each sarcomere consists of a central A- band (thick filaments) and two halves of the I-band (thin filaments). The I-band from two adjacent sarcomeres meets at the Z-line. The central portion of the A-band is the M-line, which does not contain actin. The Sliding Filament Theory of Contraction A muscle fiber contracts when myosin filaments pull actin filaments closer together and thus shorten sarcomeres within a fiber. When all the sarcomeres in a muscle fiber shorten, the fiber contracts. The sliding of actin past myosin generates muscle tension (force). Changes in sarcomere during contraction Ultrastructure of Skeletal Muscle Molecular Basis of Contraction Contractile Proteins of Skeletal Muscle The thick filament called myosin is a polymer of myosin molecules, each of which has a flexible cross- bridge that binds ATP and actin. The Molecular Basis of Skeletal Muscle Contraction The Contraction Cycle - Role of Ca+2 and ATP Hydrolysis of ATP by myosin energizes the cross bridges, providing the energy for force generation. Binding of ATP to myosin separates cross- bridges from actin, allowing the bridges to repeat their cycle of activity. This cycle will continue if ATP is available and Ca+2 levels in the sarcoplasm are high.. SERCA (Sarcoendoplasmic Reticulum Calcium ATPase) transfers Ca2+ from the cytosol of the cell to the lumen of the SR. In order for a skeletal muscle contraction to occur: 1. There must be a neural stimulus. 2. There must be Ca+2 in the cytosol of the muscle cells. 3. ATP must be available for energy. Relaxation occurs when stimulation of the nerve stops. Relaxation of skeletal muscle fibers, and ultimately, the skeletal muscle, begins when the motor neuron stops releasing its chemical signal, ACh, into the synapse at the NMJ. The muscle fiber will repolarize, which closes the Ca+2 release channels in the sarcoplasmic reticulum (SR). Also, Ca+2 is pumped back into the SR by Ca+2 - ATPase. Rigor Mortis The process of rigor mortis is the increase of stiffness of the body due to changes in the muscle tissue. After death, aerobic respiration in an organism ceases, depleting the source of oxygen used in the making of ATP. ATP is required to cause separation of the actin-myosin cross-bridges during relaxation of muscle. When oxygen is no longer present, the body may continue to produce ATP via anaerobic glycolysis. When the body's glycogen is depleted, the ATP concentration diminishes, and the body enters rigor mortis because it is unable to break those cross bridges.

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