Human Anatomy and Physiology Eleventh Edition, Global Edition PDF

Human Anatomy and Physiology Eleventh Edition, Global Edition Chapter 09 Part A Muscles and Muscle Tissue PowerPoint® Lectures Slides prepared by Karen Dunbar Kareiva, Ivy Tech Co...

Human Anatomy and Physiology Eleventh Edition, Global Edition Chapter 09 Part A Muscles and Muscle Tissue PowerPoint® Lectures Slides prepared by Karen Dunbar Kareiva, Ivy Tech Community College Copyright © 2020 Pearson Education Ltd. All Rights Reserved Why This Matters Understanding skeletal muscle tissue helps you to treat strained muscles effectively with RICE Copyright © 2020 Pearson Education Ltd. All Rights Reserved Video: Why This Matters Copyright © 2020 Pearson Education Ltd. All Rights Reserved 9.1 Overview of Muscle Tissue Nearly half of body’s mass Can transform chemical energy (ATP) into directed mechanical energy, which is capable of exerting force To investigate muscle, we look at: – Types of muscle tissue – Characteristics of muscle tissue – Muscle functions Copyright © 2020 Pearson Education Ltd. All Rights Reserved Types of Muscle Tissue (1 of 4) Terminologies: Myo, mys, and sarco are prefixes for muscle – Example: sarcoplasm: muscle cell cytoplasm Three types of muscle tissue – Skeletal – Cardiac – Smooth Only skeletal and smooth muscle cells are elongated and referred to as muscle fibers Copyright © 2020 Pearson Education Ltd. All Rights Reserved Types of Muscle Tissue (2 of 4) Skeletal muscle – Skeletal muscle tissue is packaged into skeletal muscles: organs that are attached to bones and skin – Skeletal muscle fibers are longest of all muscle and have striations (stripes) – Also called voluntary muscle: can be consciously controlled – Contract rapidly; tire easily; powerful – Key words for skeletal muscle: skeletal, striated, and voluntary Copyright © 2020 Pearson Education Ltd. All Rights Reserved Types of Muscle Tissue (3 of 4) Cardiac muscle – Cardiac muscle tissue is found only in heart § Makes up bulk of heart walls – Striated – Involuntary: cannot be controlled consciously § Contracts at steady rate due to heart’s own pacemaker, but nervous system can increase rate – Key words for cardiac muscle: cardiac, striated, and involuntary Copyright © 2020 Pearson Education Ltd. All Rights Reserved Types of Muscle Tissue (4 of 4) Smooth muscle – Smooth muscle tissue: found in walls of hollow organs § Examples: stomach, urinary bladder, and airways – Not striated – Involuntary: cannot be controlled consciously – Key words for smooth muscle: visceral, nonstriated and involuntary Copyright © 2020 Pearson Education Ltd. All Rights Reserved Table 9.3-1 Comparison of Skeletal, Cardiac, and Smooth Muscle Copyright © 2020 Pearson Education Ltd. All Rights Reserved Characteristics of Muscle Tissue All muscles share four main characteristics: – Excitability (responsiveness): ability to receive and respond to stimuli – Contractility: ability to shorten forcibly when stimulated – Extensibility: ability to be stretched – Elasticity: ability to recoil to resting length Copyright © 2020 Pearson Education Ltd. All Rights Reserved Muscle Functions Four important functions 1. Produce movement: responsible for all locomotion and manipulation § Example: walking, digesting, pumping blood 2. Maintain posture and body position 3. Stabilize joints 4. Generate heat as they contract Copyright © 2020 Pearson Education Ltd. All Rights Reserved 9.2 Skeletal Muscle Anatomy Skeletal muscle is an organ made up of different tissues with three features: nerve and blood supply, connective tissue sheaths, and attachments Copyright © 2020 Pearson Education Ltd. All Rights Reserved Nerve and Blood Supply Each muscle receives a nerve, artery, and veins – Consciously controlled skeletal muscle has nerves supplying every fiber to control activity Contracting muscle fibers require huge amounts of oxygen and nutrients – Also need waste products removed quickly Copyright © 2020 Pearson Education Ltd. All Rights Reserved Connective Tissue Sheaths Each skeletal muscle, as well as each muscle fiber, is covered in connective tissue Support cells and reinforce whole muscle Sheaths from external to internal: – Epimysium: dense irregular connective tissue surrounding entire muscle; may blend with fascia – Perimysium: fibrous connective tissue surrounding fascicles (groups of muscle fibers) – Endomysium: fine areolar connective tissue surrounding each muscle fiber Copyright © 2020 Pearson Education Ltd. All Rights Reserved Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium (1 of 2) Epimysium Epimysium Bone Perimysium Tendon Endomysium Muscle fiber in middle of a fascicle Blood vessel Perimysium wrapping a fascicle Endomysium (between individual muscle fibers) Muscle fiber Fascicle Copyright © 2020 Pearson Education Ltd. All Rights Reserved Attachments Muscles span joints and attach to bones Muscles attach to bone in at least two places – Insertion: attachment to movable bone – Origin: attachment to immovable or less movable bone Attachments can be direct or indirect – Direct (fleshy): epimysium fused to periosteum of bone or perichondrium of cartilage – Indirect: connective tissue wrappings extend beyond muscle as ropelike tendon or sheetlike aponeurosis Copyright © 2020 Pearson Education Ltd. All Rights Reserved Aponeuroses are sheet-like, Epicranial aponeurosis pearly-white fibrous tissues that are similar to tendons. 8 They connect sheet-like muscles that need a wide area of attachment to other body parts that the muscles act upon, e.g., bones, cartilage, other muscles. The epicranial aponeurosis External originates from the external occipital occipital protuberance and protuberance attaches to the occipitofrontalis muscle (2, 5) and anterior & superior auricular muscles (8). The occipitofrontalis muscle is responsible for facial expressions like raising the eyebrows and wrinkling the forehead. Copyright © 2020 Pearson Education Ltd. All Rights Reserved Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium (2 of 2) Bone Epimysium Tendon Blood vessel Perimysium wrapping a fascicle Endomysium (between individual muscle fibers) Muscle fiber Fascicle Copyright © 2020 Pearson Education Ltd. All Rights Reserved Table 9.1-1 Structure and Organizational Levels of Skeletal Muscle Copyright © 2020 Pearson Education Ltd. All Rights Reserved 9.3 Muscle Fiber Microanatomy and Sliding Filament Model Skeletal muscle fibers are long, cylindrical cells that contain multiple nuclei Sarcolemma: muscle fiber plasma membrane Sarcoplasm: muscle fiber cytoplasm Contains many glycosomes for glycogen storage, as well as myoglobin for O2 storage Modified organelles – Myofibrils – Sarcoplasmic reticulum – T tubules Copyright © 2020 Pearson Education Ltd. All Rights Reserved Myofibrils (1 of 7) Myofibrils are densely packed, rodlike elements – Single muscle fiber can contain 1000s – Accounts for ~80% of muscle cell volume Myofibril features – Striations – Sarcomeres – Myofilaments – Molecular composition of myofilaments Copyright © 2020 Pearson Education Ltd. All Rights Reserved Microscopic anatomy of a skeletal muscle fiber (1 of 4) Diagram of part of a Sarcolemma muscle fiber showing the myofibrils. One myofibril extends from the cut end of the fiber. Mitochondrion Myofibril Dark A band Light I band Nucleus Copyright © 2020 Pearson Education Ltd. All Rights Reserved Myofibrils (2 of 7) Striations: stripes formed from repeating series of dark and light bands along length of each myofibril – A bands: dark regions § H zone: lighter region in middle of dark A band – M line: line of protein (myomesin) that bisects H zone vertically – I bands: lighter regions § Z disc (line): coin-shaped sheet of proteins on midline of light I band Copyright © 2020 Pearson Education Ltd. All Rights Reserved Microscopic anatomy of a skeletal muscle fiber (2 of 4) Photomicrograph of portions Nuclei of two muscle fibers (7003). Notice the striations (alternating dark and light bands). Dark A band Light I band Fiber Copyright © 2020 Pearson Education Ltd. All Rights Reserved Myofibrils (3 of 7) Sarcomere – Smallest contractile unit (functional unit) of muscle fiber – Contains A band with half of an I band at each end § Consists of area between Z discs – Individual sarcomeres align end to end along myofibril, like boxcars of train Copyright © 2020 Pearson Education Ltd. All Rights Reserved Microscopic anatomy of a skeletal muscle fiber (3 of 4) Thin (actin) filament Z disc H zone Z disc Small part of one myofibril enlarged to show the myofilaments responsible for the banding pattern. Each sarcomere extends from one Z disc to the next. Thick (myosin) I band A band I band M line filament Sarcomere Copyright © 2020 Pearson Education Ltd. All Rights Reserved Myofibrils (4 of 7) Myofilaments – Orderly arrangement of actin and myosin myofilaments within sarcomere – Actin myofilaments: thin filaments § Extend across I band and partway in A band § Anchored to Z discs – Myosin myofilaments: thick filaments § Extend length of A band § Connected at M line – Sarcomere cross section shows hexagonal arrangement of one thick filament surrounded by six thin filaments Copyright © 2020 Pearson Education Ltd. All Rights Reserved Microscopic anatomy of a skeletal muscle fiber (4 of 4) Z disc M line Z disc Enlargement of one Thin (actin) sarcomere (sectioned filament lengthwise). Elastic (titin) filaments Thick (myosin) filament Cross sections of a Myosin sarcomere cut through filament in different locations. Actin filament I band M line Outer edge of A band thin filaments H zone thick thick filaments linked thick and thin only by accessory proteins filaments overlap filaments only Copyright © 2020 Pearson Education Ltd. All Rights Reserved Myofibrils (5 of 7) Molecular composition of myofilaments – Thick filaments: composed of protein myosin that contains two heavy and four light polypeptide chains § Heavy chains intertwine to form myosin tail § Light chains form myosin globular head – During contraction, heads link thick and thin filaments together, forming cross bridges § Myosins are offset from each other, resulting in staggered array of heads at different points along thick filament Copyright © 2020 Pearson Education Ltd. All Rights Reserved Myofibrils (6 of 7) Molecular composition of myofilaments (cont.) – Thin filaments: composed of fibrous protein actin § Actin is polypeptide made up of kidney-shaped G actin (globular) subunits – G actin subunits bears active sites for myosin head attachment during contraction § G actin subunits link together to form long, fibrous F actin (filamentous) § Two F actin strands twist together to form a thin filament – Tropomyosin and troponin: regulatory proteins bound to actin Copyright © 2020 Pearson Education Ltd. All Rights Reserved Composition of thick and thin filaments (1 of 4) Thick filament Each thick filament consists of many myosin molecules whose heads protrude at opposite ends of the filament. Portion of a thick filament Myosin head Actin-binding sites Tail Heads ATP binding site Flexible hinge region Myosin molecule Copyright © 2020 Pearson Education Ltd. All Rights Reserved Composition of thick and thin filaments (2 of 4) Thin filament A thin filament consists of two strands of actin subunits twisted into a helix plus two types of regulatory proteins (troponin and tropomyosin). Portion of a thin filament Actin Tropomyosin Troponin Myosinbinding sites Actin subunits Copyright © 2020 Pearson Education Ltd. All Rights Reserved Myofibrils (7 of 7) Molecular composition of myofilaments (cont.) – Other proteins help form the structure of the myofibril § Elastic filament: composed of protein titin – Holds thick filaments in place; helps recoil after stretch; resists excessive stretching § Dystrophin – Links thin filaments to proteins of sarcolemma § Nebulin, myomesin, C proteins bind filaments or sarcomeres together – Maintain alignment of sarcomere Copyright © 2020 Pearson Education Ltd. All Rights Reserved Clinical – Homeostatic Imbalance 9.1 (1 of 3) Duchenne muscular dystrophy (DMD) is most common and serious form of muscular dystrophies, muscle-destroying diseases that generally appear during childhood Inherited as a sex-linked recessive disease, so almost exclusively in males (1 in 3600 births) Appears between 2 and 7 years old when boy becomes clumsy and falls frequently Disease progresses from extremities upward, finally affecting head, chest muscles, and cardiac muscle. With supportive care, people with DMD can live into 30s and beyond Copyright © 2020 Pearson Education Ltd. All Rights Reserved Clinical – Homeostatic Imbalance 9.1 (2 of 3) Caused by defective gene for dystrophin, a protein that links thin filaments to extracellular matrix and helps stabilize sarcolemma Sarcolemma of DMD patients tear easily, allowing entry of excess calcium which damages contractile fibers Inflammation follows and regenerative capacity is lost resulting in increased apoptosis of muscle cells and drop in muscle mass Copyright © 2020 Pearson Education Ltd. All Rights Reserved A boy with Duchenne muscular dystrophy (DMD) Copyright © 2020 Pearson Education Ltd. All Rights Reserved Clinical – Homeostatic Imbalance 9.1 (3 of 3) chest muscles, and cardiac muscle. The weakness continues to progress, but with supportive care, DMD patients are living into their 30s and beyond. Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sarcoplasmic Reticulum and T Tubules Sarcoplasmic reticulum: network of smooth endoplasmic reticulum tubules surrounding each myofibril – Most run longitudinally – Terminal cisterns form perpendicular cross channels at the A–I band junction + – SR functions in regulation of intracellular 𝐶𝑎2 levels + – Stores and releases 𝐶𝑎2 Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sarcoplasmic Reticulum and T Tubules (1 of 3) T tubules – Tube formed by protrusion of sarcolemma deep into cell interior § Increase muscle fiber’s surface area greatly § Lumen continuous with extracellular space § Allow electrical nerve transmissions to reach deep into interior of each muscle fiber – Tubules penetrate cell’s interior at each A–I band junction between terminal cisterns § Triad: area formed from terminal cistern of one sarcomere, T tubule, and terminal cistern of neighboring sarcomere Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sarcoplasmic Reticulum and T Tubules (2 of 3) Triad relationships – T tubule contains integral membrane proteins that protrude into intermembrane space (space between tubule and muscle fiber sarcolemma) § Tubule proteins act as voltage sensors that change shape in response to an electrical current – SR cistern membranes also have integral membrane proteins that protrude into intermembrane space § SR integral proteins control opening of calcium channels in SR cisterns Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sarcoplasmic Reticulum and T Tubules (3 of 3) Triad relationships (cont.) – When an electrical impulse passes by, T tubule proteins change shape, causing SR proteins to change shape, causing release of calcium into cytoplasm Copyright © 2020 Pearson Education Ltd. All Rights Reserved Relationship of the sarcoplasmic reticulum and T tubules to myofibrils of skeletal muscle Part of a skeletal I band A band I band muscle fiber (cell) H zone Z disc Z disc M line Sarcolemma Myofibril Triad: T tubule Terminal Sarcolemma cisterns of the SR (2) Tubules of the SR Myofibrils Mitochondria Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sliding Filament Model of Contraction (1 of 3) Contraction: the activation of cross bridges to generate force Shortening occurs when tension generated by cross bridges on thin filaments exceeds forces opposing shortening Contraction ends when cross bridges become inactive Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sliding Filament Model of Contraction (2 of 3) In the relaxed state, thin and thick filaments overlap only slightly at ends of A band Sliding filament model of contraction states that during contraction, thin filaments slide past thick filaments, causing actin and myosin to overlap more – Neither thick nor thin filaments change length, just overlap more When nervous system stimulates muscle fiber, myosin heads are allowed to bind to actin, forming cross bridges, which cause sliding (contraction) process to begin Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sliding Filament Model of Contraction (3 of 3) Cross bridge attachments form and break several times, each time pulling thin filaments a little closer toward center of sarcome in a ratcheting action – Causes shortening of muscle fiber Z discs are pulled toward M line I bands shorten Z discs become closer H zones disappear A bands move closer to each other Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sliding filament model of contraction (1 of 2) 1 Fully relaxed sarcomere of a muscle fiber Z H Z A Copyright © 2020 Pearson Education Ltd. All Rights Reserved Sliding filament model of contraction (2 of 2) 2 Fully contracted sarcomere of a muscle fiber Z Z I I A Copyright © 2020 Pearson Education Ltd. All Rights Reserved 9.4 Muscle Fiber Contraction (2 of 2) Background and Overview Decision to move is activated by brain, signal is transmitted down spinal cord to motor neurons which then activate muscle fibers Neurons and muscle cells are excitable cells capable of action potentials – Excitable cells are capable of changing resting membrane potential voltages AP crosses from neuron to muscle cell via the neurotransmitter acetylcholine (ACh) Copyright © 2020 Pearson Education Ltd. All Rights Reserved Background and Overview (1 of 4) Ion Channels – Play the major role in changing of membrane potentials – Two classes of ion channels: § Chemically gated ion channels – opened by chemical messengers such as neurotransmitters – Example: ACh receptors on muscle cells § Voltage-gated ion channels – open or close in response to voltage changes in membrane potential Copyright © 2020 Pearson Education Ltd. All Rights Reserved “Chemically gated ion channel” and “Voltage-gated ion channel” Chemical messenger (e.g., ACh) Chemically gated ion Voltage-gated ion channel channel Copyright © 2020 Pearson Education Ltd. All Rights Reserved Background and Overview (2 of 4) Anatomy of Motor Neurons and the Neuromuscular Junction – Skeletal muscles are stimulated by somatic motor neurons – Axons (long, threadlike extensions of motor neurons) travel from central nervous system to skeletal muscle – Each axon divides into many branches as it enters muscle – Axon branches end on muscle fiber, forming neuromuscular junction or motor end plate § Each muscle fiber has one neuromuscular junction with one motor neuron Copyright © 2020 Pearson Education Ltd. All Rights Reserved Overview of skeletal muscle contraction (1 of 3) Brain Spinal cord Axon of motor neuron Motor neuron: The neuromuscular junction is the Cell body region where the motor neuron contacts the skeletal muscle. It Axon consists of multiple axon terminals Axon and the underlying junctional folds terminals of the sarcolemma. Muscle fiber Copyright © 2020 Pearson Education Ltd. All Rights Reserved Background and Overview (3 of 4) – Axon terminal (end of axon) and muscle fiber are separated by gel-filled space called synaptic cleft – Stored within axon terminals are membrane-bound synaptic vesicles § Synaptic vesicles contain neurotransmitter acetylcholine (ACh) – Infoldings of sarcolemma, called junctional folds, contain millions of ACh receptors – NMJ consists of axon terminals, synaptic cleft, and junctional folds Copyright © 2020 Pearson Education Ltd. All Rights Reserved Overview of skeletal muscle contraction (2 of 3) Axon of motor neuron Axon terminal of motor neuron Synaptic vesicle with ACh Synaptic cleft Cytoplasm of skeletal muscle fiber Junctional folds of the sarcolemma Copyright © 2020 Pearson Education Ltd. All Rights Reserved Background and Overview (4 of 4) The Big Picture - Four steps must occur for skeletal muscle to contract: 1. Events at neuromuscular junction 2. Muscle fiber excitation 3. Excitation-contraction coupling 4. Cross bridge cycling Copyright © 2020 Pearson Education Ltd. All Rights Reserved Overview of skeletal muscle contraction (3 of 3) Brain Spinal cord Axon of motor neuron Motor neuron: The neuromuscular junction is the Cell body region where the motor neuron contacts the skeletal muscle. It Axon consists of multiple axon terminals Axon and the underlying junctional folds terminals of the sarcolemma. Muscle fiber Sequence of events leading to contraction: Axon of motor A motor neuron fires an action potential neuron Axon terminal of (AP) down its axon. motor neuron Synaptic vesicle 1 Events at the The motor neuron’s axon terminal with ACh Synaptic cleft neuromuscular releases acetylcholine (ACh) into the Cytoplasm junction (see synaptic cleft. of skeletal Focus Figure 9.1) muscle fiber ACh binds receptors on the junctional folds of the sarcolemma. Junctional folds of the sarcolemma ACh binding causes a local depolarization called an end plate potential (EPP). 2 Muscle fiber The local depolarization (EPP) triggers an excitation (see AP in the adjacent sarcolemma. Figure 9.8) AP in sarcolemma travels down T tubules. 3 Excitation- contraction coupling Sarcoplasmic reticulum releases Ca2+. (see Focus Figure 9.2) Ca2+ binds to troponin, which shifts tropomyosin to uncover the myosin-binding sites on actin. Myosin heads bind actin. 4 Cross bridge cycle Contraction occurs via cross bridge cycling. (see Focus Figure 9.3) Copyright © 2020 Pearson Education Ltd. All Rights Reserved Events at the Neuromuscular Junction 1. AP arrives at axon terminal 2. Voltage-gated calcium channels open, calcium enters motor neuron 3. Calcium entry causes release of ACh neurotransmitter into synpatic cleft + 4. ACh diffuses across to ACh receptors (𝑁𝑎 chemical gates) on sarcolemma + 5. ACh binding to receptors, opens gates, allowing 𝑁𝑎 to enter resulting in end plate potential 6. Acetylcholinesterase degrades ACh Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Axon of Action motor neuron potential (AP) When a nerve impulse Axon terminal of neuromuscular junction reaches a Sarcolemma of neuromuscular junction, the muscle fiber acetylcholine (ACh) is released (1 of 6) 1 Action potential arrives at axon terminal of motor neuron. Ca2+ Ca2+ Axon terminal of motor neuron Fusing synaptic vesicles ACh Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Axon of Action motor neuron When a nerve impulse potential (AP) Axon terminal of neuromuscular reaches a junction Sarcolemma of neuromuscular junction, the muscle fiber acetylcholine (ACh) is released (2 of 6) 1 Action potential arrives at axon terminal of motor neuron. Ca2+ 2 Voltage-gated Ca2+ Ca2+ Synaptic vesicle channels open. Ca2+ enters the axon terminal, moving down its containing ACh electrochemical gradient. Axon terminal Synaptic cleft of motor neuron Fusing synaptic vesicles ACh Junctional folds of sarcolemma Sarcoplasm of muscle fiber Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Axon of Action motor neuron potential (AP) When a nerve impulse Axon terminal of neuromuscular junction reaches a Sarcolemma of neuromuscular junction, the muscle fiber acetylcholine (ACh) is released (3 of 6) 1 Action potential arrives at axon terminal of motor neuron. Ca2+ 2 Voltage-gated Ca2+ Ca2+ Synaptic vesicle channels open. Ca2+ enters the axon terminal, moving down its containing ACh electrochemical gradient. Axon terminal Synaptic cleft of motor neuron Fusing synaptic vesicles 3 Ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. Junctional ACh folds of sarcolemma Sarcoplasm of muscle fiber Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Axon of Action motor neuron potential (AP) When a nerve impulse Axon terminal of neuromuscular junction reaches a Sarcolemma of neuromuscular junction, the muscle fiber acetylcholine (ACh) is released (4 of 6) 1 Action potential arrives at axon terminal of motor neuron. Ca2+ 2 Voltage-gated Ca2+ Ca2+ Synaptic vesicle channels open. Ca2+ enters the axon terminal, moving down its containing ACh electrochemical gradient. Axon terminal Synaptic cleft of motor neuron Fusing synaptic vesicles 3 Ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. Junctional ACh folds of 4 ACh diffuses across the sarcolemma synaptic cleft and binds to ACh Sarcoplasm of receptors on the sarcolemma. muscle fiber Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Axon of Action motor neuron potential (AP) When a nerve impulse Axon terminal of neuromuscular junction reaches a Sarcolemma of neuromuscular junction, the muscle fiber acetylcholine (ACh) is released (5 of 6) 1 Action potential arrives at axon terminal of motor neuron. Ca2+ 2 Voltage-gated Ca2+ Ca2+ Synaptic vesicle channels open. Ca2+ enters the axon terminal, moving down its containing ACh electrochemical gradient. Axon terminal Synaptic cleft of motor neuron Fusing synaptic vesicles 3 Ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. Junctional ACh folds of 4 ACh diffuses across the sarcolemma synaptic cleft and binds to ACh Sarcoplasm of receptors on the sarcolemma. muscle fiber 5 ACh binding opens chemically gated ion channels that allow simultaneous Postsynaptic membrane Na+ K+ passage of Na+ into the muscle fiber and ion channel opens; K+ out of the muscle fiber. More Na+ Ions ions pass. enter than K+ ions exit, which produces a local change in the membrane potential called the end plate potential. Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Axon of Action motor neuron potential (AP) When a nerve impulse Axon terminal of neuromuscular junction reaches a Sarcolemma of neuromuscular junction, the muscle fiber acetylcholine (ACh) is released (6 of 6) 1 Action potential arrives at axon terminal of motor neuron. Ca2+ 2 Voltage-gated Ca2+ Ca2+ Synaptic vesicle channels open. Ca2+ enters the axon terminal, moving down its containing ACh electrochemical gradient. Axon terminal Synaptic cleft of motor neuron Fusing synaptic vesicles 3 Ca2+ entry causes ACh (a neurotransmitter) to be released by exocytosis. Junctional ACh folds of 4 ACh diffuses across the sarcolemma synaptic cleft and binds to ACh Sarcoplasm of receptors on the sarcolemma. muscle fiber 5 ACh binding opens chemically gated ion channels that allow simultaneous Na+ K+ Postsynaptic membrane passage of Na+ into the muscle fiber and ion channel opens; K+ out of the muscle fiber. More Na+ Ions ions pass. enter than K+ ions exit, which produces a local change in the membrane potential called the end plate potential. 6 ACh effects are terminated by ACh Degraded ACh Ion channel closes; its breakdown in the synaptic Na+ ions cannot pass. cleft by acetylcholinesterase and diffusion away from the junction. Acetylcholin- esterase K+ Copyright © 2020 Pearson Education Ltd. All Rights Reserved A&P Flix™: Events at the Neuromuscular Junction Copyright © 2020 Pearson Education Ltd. All Rights Reserved Clinical – Homeostatic Imbalance 9.2 Many toxins, drugs, and diseases interfere with events at the neuromuscular junction – Example: myasthenia gravis: disease characterized by drooping upper eyelids, difficulty swallowing and talking, and generalized muscle weakness – Involves shortage of Ach receptors because person’s ACh receptors are attacked by own antibodies – Suggests this is an autoimmune disease Copyright © 2020 Pearson Education Ltd. All Rights Reserved Generation of an Action Potential Across the Sarcolemma (1 of 4) Resting sarcolemma is polarized, meaning a voltage exists across membrane – Inside of cell is negative compared to outside Action potential is caused by changes in electrical charges Occurs in three steps 1. Generation of end plate potential 2. Depolarization 3. Repolarization Copyright © 2020 Pearson Education Ltd. All Rights Reserved Generation of an Action Potential Across the Sarcolemma (2 of 4) 1. End plate potential – ACh released from motor neuron binds to ACh receptors on sarcolemma – Causes chemically gated ion channels (ligands) on sarcolemma to open + – 𝑁𝑎 diffuses into muscle fiber + § Some 𝐾 diffuses outward, but not much + – Because 𝑁𝑎 diffuses in, interior of sarcolemma becomes less negative (more positive) – Results in local depolarization called end plate potential Copyright © 2020 Pearson Education Ltd. All Rights Reserved Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber (1 of 3) ACh-containing synaptic vesicle Axon terminal of neuromuscular Ca2+ junction Ca2+ Synaptic cleft Wave of depolarization 1 An end plate potential (EPP) is generated at the neuromuscular junction (see Focus Figure 9.1). The EPP causes a wave of depolarization that spreads to the adjacent sarcolemma. Copyright © 2020 Pearson Education Ltd. All Rights Reserved Generation of an Action Potential Across the Sarcolemma (3 of 4) 2. Depolarization: generation and propagation of an action potential (AP) – If end plate potential causes enough change in membrane voltage to reach critical + level called threshold, voltage-gated 𝑁𝑎 channels in membrane will open + – Large influx of 𝑁𝑎 through channels into cell triggers AP that is unstoppable and will lead to muscle fiber contraction + – AP spreads across sarcolemma from one voltage-gated 𝑁𝑎 channel to next one in adjacent areas, causing that area to depolarize Copyright © 2020 Pearson Education Ltd. All Rights Reserved Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber (2 of 3) ACh-containing Open voltagegated synaptic vesicle Na+ channel Axon terminal of neuromuscular Ca2+ junction Ca2+ Synaptic cleft K+ Action potential 2 Depolarization: Generating and propagating an action potential Wave of (AP). Depolarization of the sarcolemma opens voltage-gated depolarization sodium channels. Na1 enters, following its electrochemical gradient. 1 An end plate potential (EPP) is generated at At a certain membrane voltage, an AP is generated (initiated). The the neuromuscular junction (see Focus AP spreads to adjacent areas of the sarcolemma and opens Figure 9.1). The EPP causes a wave of voltage-gated Na1 channels there, propagating the AP. The AP depolarization that spreads to the adjacent propagates along the sarcolemma in all directions, just like ripples sarcolemma. from a pebble dropped in a pond. Copyright © 2020 Pearson Education Ltd. All Rights Reserved Generation of an Action Potential Across the Sarcolemma (4 of 4) 3. Repolarization: restoration of resting conditions + + – 𝑁𝑎 voltage-gated channels close, and voltage-gated 𝐾 channels open + – 𝐾 efflux out of cell rapidly brings cell back to initial resting membrane voltage – Refractory period: muscle fiber cannot be stimulated for a specific amount of time, until repolarization is complete + + – Ionic conditions of resting state are restored by 𝑁𝑎 −𝐾 pump + + § 𝑁𝑎 that came into cell is pumped back out, and 𝐾 that flowed outside is pumped back into cell Copyright © 2020 Pearson Education Ltd. All Rights Reserved Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber (3 of 3) ACh-containing Open voltagegated synaptic vesicle Na+ channel Axon terminal of neuromuscular Ca2+ junction Ca2+ Synaptic cleft K+ Action potential 2 Depolarization: Generating and propagating an action potential Wave of (AP). Depolarization of the sarcolemma opens voltage-gated depolarization sodium channels. Na1 enters, following its electrochemical gradient. 1 An end plate potential (EPP) is generated at At a certain membrane voltage, an AP is generated (initiated). The the neuromuscular junction (see Focus AP spreads to adjacent areas of the sarcolemma and opens Figure 9.1). The EPP causes a wave of voltage-gated Na1 channels there, propagating the AP. The AP depolarization that spreads to the adjacent propagates along the sarcolemma in all directions, just like ripples sarcolemma. from a pebble dropped in a pond. Closed voltagegated Open voltagegated Na+ channel K+ channel Na+ ++++++ + ++ + + +++++++++ - - - - - - - - - - - - - - - - - - - k+ 3 Repolarization: Restoring the sarcolemma to its initial polarized state (negative inside, positive outside). The repolarization wave is also a consequence of opening and closing ion channels—voltage-gated Na1 channels close and voltage-gated K1 channels open. The potassium ion concentration is substantially higher inside the cell than in the extracellular fluid, so K1 diffuses out of the muscle fiber. This restores the negatively charged conditions inside that are characteristic of a sarcolemma at rest. Copyright © 2020 Pearson Education Ltd. All Rights Reserved  + + Action potential tracing indicates changes in 𝑵𝒂 and 𝑲 ion channels +30 Na+ channels close, K+ channels open Depolarization due to Na+ entry 0 Repolarization due to K+ exit Na+ channels open K+ channels closed –90 0 5 10 15 20 Copyright © 2020 Pearson Education Ltd. All Rights Reserved Excitation-Contraction (E-C) Coupling Excitation-contraction (E-C) coupling: events that transmit AP along sarcolemma (excitation) are coupled to sliding of myofilaments (contraction) AP is propagated along sarcolemma and down into T tubules, where voltage-sensitive + proteins in tubules stimulate 𝐶𝑎2 release from SR + – 𝐶𝑎2 release leads to contraction AP is brief and ends before contraction is seen Copyright © 2020 Pearson Education Ltd. All Rights Reserved Excitation-contraction (E-C) coupling is the sequence of events by which transmission of an action potential along the sarcolemma leads to the sliding of myofilaments (1 of 3) Axon of Action motor neuron potential (AP) Axon terminal of neuromuscular junction Sarcolemma of the muscle fiber Action potential arrives at 1 axon terminal of motor neuron. Ca2+ 2 Voltage-gated Ca2+ Ca2+ channels open. Ca2+ enters the Synaptic vesicle axon terminal, moving down its electrochemical gradient. containing ACh Axon terminal of motor neuron Synaptic cleft Ca2+ entry causes ACh (a Fusing 3 neurotransmitter) to be released synaptic by exocytosis. vesicles ACh Junctional ACh diffuses across the folds of 4 synaptic cleft and binds to ACh receptors on the sarcolemma. sarcolemma Sarcoplasm of muscle fiber 5 ACh binding opens chemically gated ion channels that allow simultaneous passage of Na+ into Na+ N+ the muscle fiber and K+ out of Postsynaptic membrane the muscle fiber. More Na+ ions ion channel opens; enter than K+ ions exit, which produces a local change in the ions pass. membrane potential called the end plate potential. Degraded ACh 6 ACh effects are terminated by ACh Na+ Ion channel closes; its breakdown in the synaptic cleft by acetylcholinesterase and ions cannot pass. diffusion away from the junction. Acetylcholinesterase K+ Copyright © 2020 Pearson Education Ltd. All Rights Reserved Excitation-contraction (E-C) coupling is the sequence of events by which transmission of an action potential along the sarcolemma leads to the sliding of myofilaments (2 of 3) Copyright © 2020 Pearson Education Ltd. All Rights Reserved Excitation-contraction (E-C) coupling is the sequence of events by which transmission of an action potential along the sarcolemma leads to the sliding of myofilaments (3 of 3) Copyright © 2020 Pearson Education Ltd. All Rights Reserved A&P Flix™: Excitation-Contraction Coupling Copyright © 2020 Pearson Education Ltd. All Rights Reserved Muscle Fiber Contraction: Cross Bridge Cycling (1 of 3) + At low intracellular 𝐶𝑎2 concentration: – Tropomyosin blocks active sites on actin – Myosin heads cannot attach to actin – Muscle fiber remains relaxed Voltage-sensitive proteins in T tubules change shape, causing sarcoplasmic reticulum + (SR) to release 𝐶𝑎2 to cytosol Copyright © 2020 Pearson Education Ltd. All Rights Reserved Muscle Fiber Contraction: Cross Bridge Cycling (2 of 3) + + At higher intracellular 𝐶𝑎2 concentrations, 𝐶𝑎2 binds to troponin Troponin changes shape and moves tropomyosin away from myosin-binding sites Myosin heads is then allowed to bind to actin, forming cross bridge Cycling is initiated, causing sarcomere shortening and muscle contraction + When nervous stimulation ceases, 𝐶𝑎2 is pumped back into SR, and contraction ends Copyright © 2020 Pearson Education Ltd. All Rights Reserved Muscle Fiber Contraction: Cross Bridge Cycling (3 of 3) Four steps of the cross bridge cycle 1. Cross bridge formation: high-energy myosin head attaches to actin thin filament active site 2. Working (power) stroke: myosin head pivots and pulls thin filament toward M line 3. Cross bridge detachment: ATP attaches to myosin head, causing cross bridge to detach 4. Cocking of myosin head: energy from hydrolysis of ATP “cocks” myosin head into high-energy state § This energy will be used for power stroke in next cross bridge cycle Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Actin Ca2+ Thin filament The cross bridge cycle ADP is the series of events Myosin cross bridge Pi during which myosin Thick filament heads pull thin Myosin filaments toward the 1 Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. center of the sarcomere (1 of 4) Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Actin Ca2+ Thin filament The cross bridge cycle ADP is the series of events Myosin cross bridge Pi during which myosin Thick filament heads pull thin Myosin filaments toward the 1 Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. center of the sarcomere (2 of 4) ADP Pi 2 The power (working) stroke. ADP and P i are released and the myosin head pivots and bends, changing to its bent low-energy state. As a result it pulls the actin filament toward the M line. In the absence of ATP, myosin heads will not detach, causing rigor mortis. ATP Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Actin Ca2+ Thin filament The cross bridge cycle ADP is the series of events Myosin cross bridge Pi during which myosin Thick filament heads pull thin Myosin filaments toward the 1 Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. center of the sarcomere (3 of 4) ADP Pi 2 The power (working) stroke. ADP and P i are released and the myosin head pivots and bends, changing to its bent low-energy state. As a result it pulls the actin filament toward the M line. In the absence of ATP, myosin heads will not detach, causing rigor mortis. ATP ATP 3 Cross bridge detachment. After ATP attaches to myosin, the link between myosin and actin weakens, and the myosin head detaches (the cross bridge “breaks”). Copyright © 2020 Pearson Education Ltd. All Rights Reserved  Actin Ca2+ Thin filament The cross bridge cycle ADP is the series of events Myosin cross bridge Pi during which myosin Thick filament heads pull thin Myosin filaments toward the 1 Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. center of the sarcomere (4 of 4) ADP ADP ATP Pi Pi hydrolysis 4 Cocking of the myosin head. As 2 The power (working) stroke. ADP myosin hydrolyzes ATP to ADP and Pi , and P i are released and the myosin head the myosin head returns to its prestroke pivots and bends, changing to its bent high-energy, or “cocked,” position. * low-energy state. As a result it pulls the actin filament toward the M line. In the absence of ATP, myosin heads will not detach, causing rigor mortis. ATP ATP *This cycle will continue as long as ATP is 3 Cross bridge detachment. After ATP available and Ca2+ is bound to troponin. If attaches to myosin, the link between myosin ATP is not available, the cycle stops between and actin weakens, and the myosin head steps 2 and 3. detaches (the cross bridge “breaks”). Copyright © 2020 Pearson Education Ltd. All Rights Reserved A&P Flix™: Cross Bridge Cycle Copyright © 2020 Pearson Education Ltd. All Rights Reserved Clinical – Homeostatic Imbalance 9.3 Rigor mortis – 3–4 hours after death, muscles begin to stiffen § Peak rigidity occurs about 12 hours postmortem – Intracellular calcium levels increase because ATP is no longer being synthesized, so calcium cannot be pumped back into SR § Results in cross bridge formation – ATP is also needed for cross bridge detachment § Results in myosin head staying bound to actin, causing constant state of contraction – Muscles stay contracted until muscle proteins break down, causing myosin to release Copyright © 2020 Pearson Education Ltd. All Rights Reserved