Brunel University London - Introduction to Medical Sciences 1 - Sarcomeres and Sliding Filament Theory Part 3 PDF

Introduction to Medical Sciences 1 Cell Signalling and Movement Sarcomeres and Sliding Filament Theory Part 3 Copyright © Brunel University London v.3 2024. All rights reserved. Cell Signalling and Movement Dr Julianna Gal Version 3 2024 Copyrig...

Introduction to Medical Sciences 1 Cell Signalling and Movement Sarcomeres and Sliding Filament Theory Part 3 Copyright © Brunel University London v.3 2024. All rights reserved. Cell Signalling and Movement Dr Julianna Gal Version 3 2024 Copyright © Brunel University London v.3 2024. All rights reserved. Cell Signalling and Movement Sarcomeres and Sliding Filament Theory Part 3 Copyright © Brunel University London v.3 2024. All rights reserved. Sarcomeres and Sliding Filament Theory Part 1: Skeletal muscle organisation and structure of sarcomeres Part 2: Skeletal muscle contraction and the sliding filament theory Part 3: Control of skeletal muscle force and role of calcium Copyright © Brunel University London v.3 2024. All rights reserved. Sarcomeres and Sliding Filament Theory Part 3: Control of skeletal muscle force and role of calcium Overview Calcium ions and regulation of cross-bridge formation T-tubules, the sarcoplasmic reticulum and calcium ion movement Copyright © Brunel University London v.3 2024. All rights reserved.  Force-length properties of sarcomeres provide a platform for thinking about how muscle force is influenced by geometry, joint angle and therefore posture How is sliding filament mechanism enabled to occur in a controlled way? Recall from our statements introducing the sliding filament theory: Thick filament myosin head binds to thin filament: cross-bridge formed Calcium ions are key! Copyright © Brunel University London v.3 2024. All rights reserved. Thin filament actin with tropomyosin and troponin Now, thick filament myosin head can bind to thin filament actin Cross-bridge formation is blocked until calcium binds to troponin and displaces tropomyosin Copyright © Brunel University London v.3 2024. All rights reserved. Action potential (AP) generated at neuromuscular junction by sodium (Na+) influx into sarcoplasm (acetylcholine receptor-sensitive sodium channels) AP arrival at T-tubules causes shape change in membrane receptors, which open Ca2+ channels in sarcoplasmic reticulum (voltage-sensitive dihydropyridine (DHP) receptors and ryanodine (RyR) Ca2+ release channels) Calcium (Ca2+) flows from higher to lower concentration into sarcomeres, allowing cross-bridge formation Copyright © Brunel University London v.3 2024. All rights reserved.  High concentration of calcium ions within sarcomeres allows continued cross-bridge formation If ATP is available, the power-stroke can proceed and sarcomere, muscle fibre, and whole muscle tension can increase Muscle relaxation begins with ending neural stimulation, so action potentials stop Voltage-sensitive DHP receptors return to their relaxed state when the sarcolemma is repolarized and close the Ca2+ release RyR channels in the sarcoplasmic reticulum (SR) However, calcium ions, which have accumulated within sarcomeres must be pumped back into the sarcoplasmic reticulum Copyright © Brunel University London v.3 2024. All rights reserved. Sarcoplasm is repolarised by stopping of Na+ influx at the neuromuscular junction. Na+ is continually being removed from sarcoplasm by Na+ ATPase protein pumps Calsequestrin helps to hold calcium ions in sarcoplasmic reticulum SERCA is Sarco/endoplasmic reticulum Ca2+ ATPase, a protein pump which uses ATP energy to move calcium ions back into the SR. Copyright © Brunel University London v.3 2024. All rights reserved. Summary Troponin and tropomyosin are regulatory proteins associated with thin-filament actin Calcium binds to troponin, displaces tropomyosin, and allows binding of thick-filament myosin to form cross-bridge Voltage-sensitive receptors in T-tubule are stimulated by action potential and open calcium channels in sarcoplasmic reticulum Muscle relaxation requires removal of calcium ions back into sarcoplasmic reticulum by calcium-ATPase pumps Calcium is concentrated in sarcoplasmic reticulum by calsequestrin Copyright © Brunel University London v.3 2024. All rights reserved. Slide figures adapted from the following sources Slide 7 Hall, Samuel, Crash Course Anatomy and Physiology, 9, 239- 280. Copyright 2019, Elsevier Ltd. Slide 8 and 10 Hall, John E. Guyton and Hall Textbook of Medical Physiology, Chapter 7, 93-100. Copyright 2021, Elsevier, Inc. Copyright © Brunel University London v.3 2024. All rights reserved. Dr Julianna Gal Copyright © Brunel University London v.3 2024. All rights reserved.