Chapter 9 Muscular System Histology and Physiology PDF

Because learning changes everything. ® Chapter 9: Muscular System Histology and Physiology Seeley’s ANATOMY & PHYSIOLOGY Thirteenth Edition Cinnamon VanPutte, Jennifer Regan, Andrew Russo Lecturer: Mr. Rogers © 2023 McGraw Hill, LLC. All rights...

Because learning changes everything. ® Chapter 9: Muscular System Histology and Physiology Seeley’s ANATOMY & PHYSIOLOGY Thirteenth Edition Cinnamon VanPutte, Jennifer Regan, Andrew Russo Lecturer: Mr. Rogers © 2023 McGraw Hill, LLC. All rights reserved. Authorized only for instructor use in the classroom. No reproduction or further distribution permitted without the prior written consent of McGraw Hill, LLC.  Lecture Outline The hierarchical organization of a muscle is an excellent illustration of the relationship between form and function. Access the text alternative for slide images. © McGraw Hill, LLC 2  9.1 Functions of the Muscular System 1 Types of Muscle Tissue. Skeletal. Responsible locomotion, facial expressions, posture, respiratory movements, other types of body movement. Voluntary and controlled by the nervous system. Smooth. Walls of hollow organs, blood vessels, eye, glands, skin. Some functions: propel urine, mix food in digestive tract, dilating/constricting pupils, regulating blood flow. In some locations, autorhythmic. Controlled involuntarily by endocrine and autonomic nervous systems. Cardiac. Heart: major source of movement of blood. Autorhythmic. Controlled involuntarily by endocrine and autonomic nervous systems. © McGraw Hill, LLC 3  Comparison of Muscle Types 1 Skeletal Muscle Smooth Muscle Cardiac Muscle Location Attached to bones Walls of hollow organs, Heart blood vessels, eyes, glands, and skin Appearance Ed Reschke Victor P. Eroschenko Ed Reschke © McGraw Hill, LLC 4  Comparison of Muscle Types 2 Skeletal Muscle Smooth Muscle Cardiac Muscle Cell Shape Very long and Spindle-shaped (15– Cylindrical and cylindrical (1 mm–4 200 μm in length, 5–8 branched (100– cm, or as much as 30 μm in diameter 500 μm in length, cm in length, 10 μm– 12–20 μm in 100 μm in diameter) diameter) Nucleus Multiple nuclei, Single, centrally located Single, centrally peripherally located located Special None Gap junctions join Intercalated disks Cell-to-Cell some visceral smooth join cells to one Attachments muscle cells together another Striations Yes No © McGraw Hill, LLC 5  Comparison of Muscle Types 3 Skeletal Muscle Smooth Muscle Cardiac Muscle Control Voluntary and Involuntary Involuntary involuntary (reflexes) Capable of No Yes (some smooth Yes Spontaneous muscle) Contraction Function Controlling body Moving food through Pumping blood; movement the digestive tract, contractions emptying the urinary provide the major bladder, regulating force for blood vessel diameter, propelling blood changing pupil size, through blood contracting many gland vessels ducts, moving hair, and many other functions © McGraw Hill, LLC 6  9.1 Functions of the Muscular System 2 1. Movement of the body. 2. Maintenance of posture. 3. Respiration. 4. Production of body heat. 5. Communication. 6. Constriction of organs and vessels. 7. Contraction of the heart. © McGraw Hill, LLC 7  9.2 General Properties of Muscle Tissue Contractility: ability of a muscle to shorten with force. Excitability: capacity of muscle to respond to a stimulus (usually from nerves). Extensibility: muscle can be stretched beyond it normal resting length and still be able to contract. Elasticity: ability of muscle to recoil to original resting length after stretched. © McGraw Hill, LLC 8  9.3 Skeletal Muscle Anatomy Whole skeletal muscle anatomy. Connective tissue coverings: Epimysium. C.T. that surrounds a whole muscle (many fascicles). Merges with muscular fascia, the layer of C.T. between adjacent muscles and between muscles and skin. Perimysium. Loose C.T. surrounding a group of muscle fibers; passage for blood vessels and nerves. Bundles of muscle cells are called fascicles. Endomysium. Loose C.T. separating individual muscle fibers within each fascicle. Collagen from CT layers merge to form tendons or aponeuroses, which attach muscle to bone. © McGraw Hill, LLC 9  Nerves and Blood Vessels Motor neurons stimulate skeletal muscle contraction. Each motor neuron controls several muscle fibers. Each muscle fiber is supplied by a branch of the motor neuron. An artery and 1 to 2 veins extend with a nerve through the C T layers. Extensive capillary beds surround muscle fibers. © McGraw Hill, LLC 10  Whole Skeletal Muscle Fiber Structure: Connective Tissue, Innervation, and Blood Supply (b) Alvin Telser/Science Source; (c) Biophoto Associates/Science Source Access the text alternative for slide images. © McGraw Hill, LLC 11  Skeletal Muscle Fiber Anatomy Develop from fusion of myoblasts, resulting in large, multinucleated muscle cells. 1 to 4 mm avg length (can get up to 1 foot). 10 to 100 microns avg diameter. Have a striated appearance. Number of fibers remains relatively constant after birth; muscles get larger due to hypertrophy of muscle fibers. Ed Reschke © McGraw Hill, LLC 12  Histology of Muscle Fibers 1 Electrical component structures can respond to and transmit electrical signals; they include the following: Sarcolemma – plasma membrane; surrounds sarcoplasm (cytoplasm) and other contents of cell. Transverse tubules (T tubules) – inward folds of sarcolemma; project into the interior of muscle cell. Sarcoplasmic reticulum (SR) – specialized smooth endoplasmic reticulum (SER); stores calcium. Enlarged portions called terminal cisternae lie adjacent to T tubules. Two terminal cisternae and their associated T tubule form a triad. © McGraw Hill, LLC 13  Structure of the Triad Access the text alternative for slide images. © McGraw Hill, LLC 14  Histology of Muscle Fibers 2 Mechanical component structures allow muscles to contract; due to: Myofibrils – bundles of protein filaments; contain the protein filaments (myofilaments) that cause contraction. Myofilaments: Actin (thin) myofilaments. Myosin (thick) myofilaments. Myofilaments arranged into orderly units called sarcomeres. © McGraw Hill, LLC 15  Structure of a Muscle Access the text alternative for slide images. © McGraw Hill, LLC 16  Sarcomeres 1 Sarcomere: basic functional unit of muscle fiber; smallest part that can contract. Z disk: filamentous network of protein. Serves as attachment for actin myofilaments. Regions of sarcomere: I bands: lighter-staining regions, each containing a Z disk and extend to ends of myosin myofilaments. A bands: central dark-staining region; overlapping actin and myosin myofilaments (except at center). H zone: region in A band where actin and myosin do not overlap. M line: middle of H zone; delicate filaments holding myosin in place. © McGraw Hill, LLC 17  Sarcomeres 2 In muscle fibers, A and I bands of parallel myofibrils are aligned and so produce striated appearance. Titin filaments: elastic chains of amino acids; make muscles extensible and elastic. © McGraw Hill, LLC 18 Organization of Sarcomeres (a) Don W. Fawcett/Science Source Access the text alternative for slide images. © McGraw Hill, LLC 19  Actin (Thin) Myofilaments Two strands of fibrous (F) actin form a double helix extending the length of the myofilament; attached at either end at sarcomere. Composed of G actin monomers each of which has an active site. Actin site can bind myosin during muscle contraction. Tropomyosin: an elongated protein winds along the groove of the F actin double helix. Troponin is composed of three subunits: one that binds to actin, a second that binds to tropomyosin, and a third that binds to calcium ions. Spaced between the ends of the tropomyosin molecules in the groove between the F actin strands. The tropomyosin/troponin complex regulates the interaction between active sites on G actin and myosin. © McGraw Hill, LLC 20  Myosin (Thick) Myofilament Many elongated myosin molecules shaped like golf clubs. Molecule consists of myosin heavy chains wound together to form a rod portion lying parallel to the myosin myofilament and two myosin heads that extend laterally. Myosin heads. 1. Can bind to active sites on the actin molecules to form cross-bridges. 2. Attached to the rod portion by a hinge region that can bend and straighten during contraction. 3. Are ATPase enzymes: activity that breaks down adenosine triphosphate (ATP), releasing energy. Part of the energy is used to bend the hinge region of the myosin molecule during contraction. © McGraw Hill, LLC 21 Organization of the Sarcomere: Actin (e) Ed Reschke/Photolibrary/Getty Images Access the text alternative for slide images. © McGraw Hill, LLC 22  Neuromuscular Junction Structure 1 Motor neurons carry electrical signals called action potentials, which stimulate muscle fiber action potentials followed by muscle contraction. Points of contact between motor neuron and muscle fiber is the neuromuscular junction, or synapse, consisting of: Presynaptic terminal: axon terminal with synaptic vesicles containing the neurotransmitter acetylcholine (ACh). Neurotransmitters from one cell (for example, motor neuron) can bind to ligand-gated ion channels on another cell (for example, muscle fiber). Synaptic cleft: space. Postsynaptic membrane or motor end-plate. © McGraw Hill, LLC 23  Neuromuscular Junction Structure 2 (a) Don W. Fawcett/Science Source; (e) Ed Reschke/Photolibrary/Getty Images Access the text alternative for slide images. © McGraw Hill, LLC 24  Sliding Filament Model Actin myofilaments sliding over myosin to shorten sarcomeres. Actin and myosin do not change length. Shortening sarcomeres responsible for skeletal muscle contraction. During relaxation, sarcomeres lengthen because of some external force, like contraction of antagonistic muscles. Muscles that produce the opposite effect. © McGraw Hill, LLC 25  Sarcomere Shortening In a relaxed muscle, the actin and myosin myofilaments overlap slightly, and the H zone is visible. The sarcomere length is at its normal resting length. As a muscle contraction is initiated, actin myofilaments slide past the myosin myofilaments, the z disks are brought closer together, and the sarcomere begins to shorten. In a contracted muscle, the A bands do not narrow because the length of the myosin myofilaments does not change. The ends of the actin myofilaments are pulled to and overlap in the center of the sarcomere, shortening it and the H zone disappears. (a top image) Don W. Fawcett/ Science Source; (b top image) Biophoto Associates/Science Source Access the text alternative for slide images. © McGraw Hill, LLC 26  9.4 Skeletal Muscle Fiber Physiology Nervous system controls muscle contractions through action potentials. Resting membrane potentials. Membrane voltage difference across membranes (polarized). Inside cell more negative due to accumulation of large protein molecules. More K  on inside than outside. K  leaks out but not completely because negative proteins hold some back. Outside cell more positive and more Na  on outside than inside. Na  /K  pump maintains this situation. Must exist for action potential to occur. © McGraw Hill, LLC 27  Review of membrane permeabilities Phospholipid bilayer interior of the plasma membrane is hydrophobic and inhibits the movement of charged particles, particularly ions, yet ion movement is the basis for the electrical properties of the plasma membrane. Transport proteins play an important role in membrane permeability and contribute to the electrical properties of both the resting and the stimulated cell. © McGraw Hill, LLC 28  Ion Channels Types. Ligand-gated. Ligands are molecules that bind to receptors. Receptor: protein or glycoprotein with a receptor site. Example: neurotransmitters. Gate is closed until neurotransmitter attaches to receptor molecule. When Ach attaches to receptor on muscle cell, Na+ gate opens. Na+ moves into cell due to concentration gradient. Voltage-gated. Open and close in response to small voltage changes across plasma membrane. Each is specific for certain ions. © McGraw Hill, LLC 29  Measuring the Resting Membrane Potential 1. The concentration gradient for an ion determines whether it will enter or leave the cell after its ion channel opens. Because Na is in higher concentration outside the cell, when voltage-gated Na channels open, Na enters the cell. In a similar fashion, when gated K channels open, K  leaves the cell. Excitable cells have many K  leak ion channels. Thus, at rest, K  moves out of the cell faster than Na moves into the cell. In addition, negatively charged molecules, such as proteins, are “trapped” inside the cell because the plasma membrane is impermeable to them. For these reasons, the inside of the plasma membrane is more negatively charged than the outside. 2. Some K  is able to diffuse down the concentration gradient from inside to just outside the plasma membrane. Because K  is positively charged, its movement from inside the cell to outside causes the inside of the plasma membrane to become even more negatively charged compared with the outside. Potassium ions diffuse down their concentration gradient only until the charge difference across the plasma membrane is great enough to prevent any additional diffusion of K  out of the cell. Therefore, the resting membrane potential is an equilibrium in which the tendency for K  to diffuse out of the cell is opposed by the negative charges inside the cell. These negative charges inside the cell tend to attract the positively charged K  back into the cell. 3. It is the active transport of Na and K  by the sodium-potassium pump that maintains the uneven distribution of Na  and K  across the plasma membrane (see chapter 3). In a resting cell, the sodium-potassium pump transports K  from outside the cell to the inside and transports Na  from inside the cell to the outside. Access the text alternative for slide images. © McGraw Hill, LLC 30  Action Potentials Phases. Depolarization: Inside of plasma membrane becomes less negative. If change reaches threshold (when voltage-gated Na gates open), + depolarization occurs. Repolarization: return of resting membrane potential. Note that during repolarization, the membrane potential drops lower than its original resting potential, then rebounds. This is because Na plus K  together are higher, but then Na+ /K + pump restores the resting potential. All-or-none principle: If threshold is reached, the cell will respond completed. Propagate: Spread from one location to another. Action potential does not move along the membrane: new action potential at each successive location. Frequency: number of action potential produced per unit of time. Access the text alternative for slide images. © McGraw Hill, LLC 31  Voltage-Gated Ion Channels and the Action Potential 1 1. Resting membrane potential. Na voltage-gated channels (red) and + some, but not all, K  channels (purple) are closed. K  diffuses down its concentration gradient through the openK + channels (leak channels), making the inside of the cell membrane negatively charged compared to the outside. Access the text alternative for slide images. © McGraw Hill, LLC 32  Voltage-Gated Ion Channels and the Action Potential 2 2. Depolarization. Na channels (ligand-gated and voltage gated) are open. Na diffuses down its  concentration gradient through the open Na channels, making the inside of the cell membrane positively charged compared to the outside. 3. Repolarization. Na channels are closed, and Na movement into  the cells stops. More K  channels open. K  movement out of the cell increases, making the inside of the cell membrane negatively charged compared to the outside, once again. Access the text alternative for slide images. © McGraw Hill, LLC 33  Summary of Action Potential Generation 1. Before initiation of an action potential, the muscle fiber is in its resting membrane potential. 2. Depolarization occurs upon opening of voltage-gated Na+ channels. 3. Repolarization occurs when the Na+ channels close and the voltage-gated K+ channels open. 4. A period of hyperpolarization, also called the after-potential, occurs because the voltage-gated K+ channels stay open than longer than required to reach resting membrane potential. The Na+/K+ pump restores the resting ion balance. Access the text alternative for slide images. © McGraw Hill, LLC 34  Action Potential Propagation 1. An action potential in a local area of the plasma membrane is indicated by the green band. Note the reversal of charge across the membrane. 2. The depolarization of the membrane in one action potential location triggers the opening of voltage-gated Na+ channels in the adjacent plasma membrane. 3. The action potential propagates along the plasma membrane (green arrow). © McGraw Hill, LLC 35  Function of the Neuromuscular Junction 1. When an action potential reaches the presynaptic terminal of a motor neuron, it causes voltage-gated Ca2  channels in the presynaptic membrane to open. As a result, Ca diffuse into the 2 axon terminal. 2. Calcium ions cause s few synaptic vesicles to migrate to the presynaptic terminal where they fuse with the plasma membrane. 3. Acetylcholine (Ach) is released into synaptic cleft by exocytosis. 4. ACh diffuses across the synaptic cleft and binds to ligand-gated Na channels on the motor end plate causing them to open. 5. Na enters the muscle fiber, causing the postsynaptic membrane to depolarize. If depolarization passes threshold, an action potential is generated along the sarcolemma. 6. Ach detaches from the ligand-gated Na channels, which then close. 7. The enzyme, acetylcholinesterase, breaks down the Ach to acetic acid and choline. 8. Motor neurons actively reabsorb choline into the axon terminal and is rejoined with acetic acid to make more Ach. 9. Recycling choline molecules required less energy and is more rapid than continuously synthesizing new Ach. Acetic acid is an intermediate in the process of glucose metabolism which can be taken up and used by a variety of cells near the neuromuscular junction. Access the text alternative for slide images. © McGraw Hill, LLC 36  Excitation-Contraction Coupling Links electrical and mechanical components of contraction. Action potential produced on sarcolemma  propagated into T tubules  calcium channels on SR terminal cisternae open  calcium enters sarcoplasm, binds troponin  muscle contraction. Access the text alternative for slide images. © McGraw Hill, LLC 37  Action Potentials and Muscle Contraction 1. Excitation-contraction coupling begins at the neuromuscular junction with the production of an action potential in the sarcolemma. The action potential is propagated along the entire sarcolemma of the muscle fiber and into the T tubules. The T tubules wrap around sarcomeres where actin and myosin overlap and carry action potentials into the interior of the muscle fiber. There, the action potentials cause voltage-gated Ca 2 2. channels in the terminal cisternae of the sarcoplasmic reticulum to open. When the Ca2  channels open, Ca2  rapidly diffuses out of the sarcoplasmic reticulum and into the sarcoplasm surrounding the myofibrils. Once in the sarcoplasm, Ca binds to the troponin 2 3. molecules of the actin myofilaments. The binding of Ca2  to troponin causes the tropomyosin to move, which exposes active sites on the actin myofilaments. The myosin heads then bind to the exposed active sites on G actin to form cross-bridges. Muscles contract when cross- bridges move. 4. Cross-bridge formation. Access the text alternative for slide images. © McGraw Hill, LLC 38  Cross-Bridge Movement 1 Access the text alternative for slide images. © McGraw Hill, LLC 39  Cross-Bridge Movement 2 1. The myosin head stores energy from ATP breakdown that occurred during the previous cycle. The myosin head will remain in the high-energy position until the muscle fiber is stimulated by a motor neuron initiating the events of excitation- contraction coupling. Access the text alternative for slide images. © McGraw Hill, LLC 40  Cross-Bridge Movement 3 2. Once the Ca2 binds to the troponin and the active sites on the G actin are exposed, the myosin heads quickly bind to them. Access the text alternative for slide images. © McGraw Hill, LLC 41  Cross-Bridge Movement 4 3. Binding of the myosin heads to the active sites on the G actin forms the cross-bridges and triggers a rapid movement of the myosin heads at their hinged region. The movement of the myosin head is called the power stroke. Because the myosin head is bound to the G actin, the actin myofilament is pulled past the myosin myofilament toward the H zone of the sarcomere. Thus, the two myofilaments are “sliding” past each other. However, the myosin myofilament doesn’t move, it is the actin myofilament that moves. Access the text alternative for slide images. © McGraw Hill, LLC 42  Cross-Bridge Movement 5 4. Binding of ATP to the myosin head causes it to detach from the G actin. 5. The myosin head breaks down ATP into ADP and P, which remain attached to the myosin heads. Access the text alternative for slide images. © McGraw Hill, LLC 43  Cross-Bridge Movement 6 6. Breakdown of the ATP by the myosin head supplies the energy for the recovery stroke, which returns the myosin head to its “high- energy” position from its “low- energy” position. In the “high- energy” position, the myosin myofilament can bind farther down the actin myofilament to another active site, and pull the actin myofilament even closer to the H zone, further shortening the sarcomere. Access the text alternative for slide images. © McGraw Hill, LLC 44  Cross-Bridge Movement 7 During a single contraction, each myosin myofilament goes through the cycle of cross-bridge formation, movement, release, and return to its original position many times. Many cycles of power and recovery strokes occur during each muscle contraction. © McGraw Hill, LLC 45  Summary of Skeletal Muscle Contraction 1 Access the text alternative for slide images. © McGraw Hill, LLC 46  Summary of Skeletal Muscle Contraction 2 1. An action potential is propagated along the motor neuron. 2. The action potential in the motor neuron stimulates the opening of voltage-gated Ca2+ channels. 3. The influx of Ca into the motor neuron causes the secretion of acetylcholine. 4. The acetylcholine opens ligand-gated Ca2+ channels in the sarcolemma. 5. The resulting action potential in the muscle fiber travels along the entire sarcolemma. 6. The action potentials also move down the T tubule membranes. 7. The T tubules wrap around sarcomeres, where actin and myosin overlap and carry action potentials into the interior of the muscle fiber. There, the action potentials cause Ca2+gated channels in the terminal cisternae of the sarcoplasmic reticulum to open When the Ca channels open, 2+ rapidly diffuses out of the sarcoplasmic reticulum and into the sarcoplasm surrounding the myofibrils. 8. Once in the sarcoplasm, Ca2+ binds to the troponin molecules of the actin myofilaments. Binding of Ca2+ to troponin causes the tropomyosin to move, which exposes attachment sites on the actin myofilaments. The myosin heads then bind to the exposed attachment sites on actin to form cross- bridges. Muscles contract when cross-bridges move. 9. ATP molecules are broken down into ADP and P, which releases energy needed to move the myosin heads. The heads of the myosin myofilaments bend, causing the actin to slide past the myosin. As long as Ca2+ is present, the cycle repeats. © McGraw Hill, LLC 47  Muscle Relaxation Three major ATP-dependent events are required for muscle relaxation. 1. After an action potential has occurred in the muscle fiber, the sodium- potassium pump must actively transport Na+ out of the muscle fiber and K + into the muscle fiber to return to and maintain resting membrane potential. 2. ATP is required to detach the myosin heads from the active sites for the recovery stroke. 3. ATP is needed for the active transport of Ca2+ into the sarcoplasmic reticulum from the sarcoplasm. © McGraw Hill, LLC 48  9.5 Whole Skeletal Muscle Physiology Muscle twitch The response of a muscle fiber to a single action potential along its motor neuron. Phases. Lag or latent – from the stimulus to the beginning of the contraction. Contraction – Ca2+ released and cross- bridging cycling occurs. Relaxation – Ca2+ returns to SR and muscle fiber returns to precontraction length. Access the text alternative for slide images. © McGraw Hill, LLC 49  Types of Muscle Contractions Isometric: no change in length but tension increases. Postural muscles of body. Isotonic: change in length but tension constant. © McGraw Hill, LLC 50  Motor Units Motor unit: a single motor neuron and all muscle fibers innervated by it. An action potential in the neuron of a motor unit causes all the muscle fibers of that unit to contract. Motor Unit numbers: Large muscles have motor units with many muscle fibers. Small muscles that make delicate movements contain motor units with few muscle fibers. Access the text alternative for slide images. © McGraw Hill, LLC 51  Force of Contraction in Individual Muscle Fibers The strength of muscle contractions varies from weak to strong. The muscle responds in a graded fashion, depending on the force generated in the individual muscle fibers. Increasing the number of cross-bridges allows a fiber to contract with more force. Factors that increase the number of cross-bridges are: Frequency of stimulation Muscle fiber diameter Muscle fiber length at the time of contraction © McGraw Hill, LLC 52  Frequency of Stimulation - Treppe 1. The Ca2+ released in response to the first stimulus is not completely removed by the sarcoplasmic reticulum before the second stimulus causes the release of additional Ca2+ , even though the muscle relaxes completely between the muscle twitches. 2. As a consequence, during the next contraction of the muscle, the Ca2+ , concentration in the sarcoplasm increases slightly, making contraction more efficient because of the increased cross-bridge formation. For athletes, treppe achieved during warm-up exercises can contribute to improved muscle efficiency. Factors such as increased blood flow to the muscle and increased muscle temperature are probably involved because higher temperatures cause the enzymes in the muscle fibers to function more rapidly. Thus, muscle fibers do not normally display an all-or-none response to repeated stimuli. 3. However, after a few contractions, the level of tension produced by each contraction is equal to the previous contraction. Access the text alternative for slide images. © McGraw Hill, LLC 53  Wave Summation and Tetanus 1 As the frequency of action potentials increases beyond treppe, contraction occurs with greater force. Wave summation: muscle tension increases as contraction frequencies increase. Incomplete tetanus: muscle fibers partially relax between contraction. Complete tetanus: no relaxation between contractions. Wave summation and tetanus result because the mechanical events of muscle twitches take longer than the electrical events, allowing several action potentials to be generated in the time it takes for a single twitch. Calcium ions can not be removed fast enough; the muscle fiber is unable to relax. © McGraw Hill, LLC 54  Wave Summation and Tetanus 2 1. A single action potential arriving at a muscle fiber causes twitches that completely relax before the next action potential arrives. 2. As the action potential frequency increases, muscle fibers only partially relax before the next action potential arrives and the muscle fiber contracts again; this results in wave summation. 3. With continued stimulation, incomplete tetanus is the result. 4. Action potential frequency can increase to the point where the muscle fiber does not relax at all before the next action potential arrives, causing the muscle fiber to contract continuously; this results in complete tetanus. Access the text alternative for slide images. © McGraw Hill, LLC 55  Muscle Fiber Diameter The greater the muscle fiber diameter, the greater the force the muscle fiber can generate. In general, larger diameter fibers have more myofibrils and therefore can form more cross-bridges which provides more force of contraction. © McGraw Hill, LLC 56  Muscle Length at Time of Contraction Active tension: force applied to an object to be lifted when a muscle contracts. Active tension increases or decreases as a muscle fiber changes in length; active tension curve. Stretched too far – fewer cross-bridges can form. If not stretched at all – thick filaments touch Z disks and very little contraction can occur. Passive tension: tension applied to load when muscle stretches but is not stimulated. Total tension: sum of active and passive tension. © McGraw Hill, LLC 57  Muscle Length and Tension Access the text alternative for slide images. © McGraw Hill, LLC 58  Force of Contraction in Whole Muscles Strength of contraction is graded: ranges from weak to strong depending on stimulus strength. Multiple motor-unit recruitment: strength of contraction depends upon recruitment of motor units. A muscle has many motor units. Access the text alternative for slide images. © McGraw Hill, LLC 59  Recruitment Sub-threshold stimulus: no action potential; no contraction. Threshold stimulus: action potential; contraction. Submaximal stimuli: stronger stimuli that produce action potentials in axons of additional motor units. Maximal stimulus: action potentials are produced in axons of all motor units of a muscle. A greater stimulus (supramaximal stimulus) has no additional effect. © McGraw Hill, LLC 60  The Size Principle Size principle: during recruitment, small motor units are recruited first followed by large motor units. Muscle tone: constant tension by muscles for long periods of time; due to small percentage of all motor units contracting out of phase with one another. © McGraw Hill, LLC 61  Types of Isotonic Contractions Isotonic: change in length but tension constant. Concentric: overcomes opposing resistance and muscle shortens. Eccentric: tension maintained but the opposing resistance is great enough to cause the muscle to lengthen. © McGraw Hill, LLC 62  9.6 Muscle Fibers Types Slow-twitch (type I). Contract more slowly, smaller in diameter, better blood supply, more mitochondria, more fatigue-resistant than fast-twitch, large amount of myoglobin. Postural muscles, more in lower than upper limbs. Dark meat of chicken. Fast-twitch (type II). Respond rapidly to nervous stimulation, contain myosin that can break down ATP more rapidly than that in Type I, less blood supply, fewer and smaller mitochondria than slow-twitch. Lower limbs in sprinter, upper limbs of most people. White meat in chicken. Comes in oxidative and glycolytic (anaerobic) forms. © McGraw Hill, LLC 63  Muscle Fiber Types Most muscles have both types but varies for each muscle/person. Conversion from one type to the other not easily done. Effects of exercise: change in size of muscle fibers. Hypertrophy: increase in muscle size. Increase in myofibrils. Increase in nuclei due to fusion of satellite cells. Increase in strength due to better coordination of muscles, increase in production of metabolic enzymes, better circulation, less restriction by fat. Atrophy: decrease in muscle size. Reverse except in severe situations where cells die. © McGraw Hill, LLC 64  Heat Production Exercise: metabolic rate and heat production increase. Post-exercise: metabolic rate stays high due to oxygen debt. Excess heat lost because of vasodilation and sweating. Shivering: uncoordinated contraction of muscle fibers resulting in shaking and heat production. © McGraw Hill, LLC 65  9.7 Energy Sources for Muscle Contraction 1 Skeletal muscle fibers have three major ATP-dependent enzymes: The myosin head The Na  -K  pump to maintain the resting membrane potential The Ca2 reuptake pump in the sarcoplasmic reticulum Muscles fibers only have enough stored ATP for 5-6 seconds of contraction. Need to make more. © McGraw Hill, LLC 66  Energy Sources for Muscle Contraction 2 ATP provides immediate energy for muscle contractions. Produced through four processes: 1. Conversion of two ADP to one ATP and AMP Adenylate kinase 2. Transfer of phosphate from creatine kinase to ADP to form ATP Creatine kinase 3. Anaerobic respiration Occurs in absence of oxygen and results in breakdown of glucose to yield ATP and lactic acid 4. Aerobic respiration Requires oxygen and breaks down glucose to produce A TP, carbon dioxide and water More efficient than anaerobic © McGraw Hill, LLC 67  Production of ATP in Skeletal Muscle Access the text alternative for slide images. © McGraw Hill, LLC 68  Muscle Fatigue Fatigue - decreased capacity to work and reduced efficiency of performance. Mechanisms involved: Acidosis and ATP depletion due to either an increased ATP consumption or a decreased ATP production. Oxidative stress, which is characterized by the buildup of excess reactive oxygen species (ROS; free radicals). Local inflammatory reactions Physiological contracture - state of fatigue where due to lack of ATP neither contraction nor relaxation can occur. Psychological fatigue – most common type; comes from the central nervous system rather than the muscles. © McGraw Hill, LLC 69  Rigor Mortis and Muscle Soreness Rigor mortis: development of rigid muscles several hours after death. Ca2 leaks into sarcoplasm and attaches to myosin heads and crossbridges form. Rigor ends as tissues start to deteriorate. Soreness: due to the influx of inflammatory chemicals into the muscle fibers because injury has increased the permeability of the plasma membranes or ruptured them. © McGraw Hill, LLC 70  Oxygen Deficit and Excess Postexercise Oxygen Consumption Oxygen deficit: lag time between when a person begins to exercise and when he or she begins to breathe more heavily. Excess postexercise oxygen consumption: lag time before breathing returns to normal once exercise stops. Deficit must be repaid. Metabolic processes that restore homeostasis (body temp, ion concentrations, metabolite and hormone levels). © McGraw Hill, LLC 71  9.8 Smooth Muscle Not striated, fibers smaller than those in skeletal muscle. Spindle-shaped; single, central nucleus. More actin than myosin. Caveolae: indentations in sarcolemma; may act like T tubules. Dense bodies instead of Z disks as in skeletal muscle that actin attached to; also have noncontractile intermediate filaments. Ca2 required to initiate contractions; binds to calmodulin which regulates myosin kinase. Cross-bridging occurs. Relaxation: caused by enzyme myosin phosphatase. © McGraw Hill, LLC 72  Smooth Muscle Histology ©Victor Eroschenko © McGraw Hill, LLC 73  Actin and Myosin Proteins in a Smooth Muscle Cell Access the text alternative for slide images. © McGraw Hill, LLC 74  Smooth Muscle Contraction 1 1. Smooth muscle contraction is stimulated both neurally and hormonally. Regardless of the stimulus source, a G protein mechanism opens a Ca2  channel. 2. An α subunit opens the Ca2  channel in the plasma membrane, or depolarization opens Ca2  channels. Calcium ions diffuse through the Ca2  channels and combine with calmodulin. 3. Calmodulin with a Ca2  bound to it binds with myosin kinase and activates it. Access the text alternative for slide images. © McGraw Hill, LLC 75  Smooth Muscle Contraction 2 4. Activated myosin kinase transfers a phosphate from ATP to myosin heads to activate the contractile process. 5. A cycle of cross-bridge formation, movement, detachment, and cross-bridge formation occurs. 6. Relaxation occurs when myosin phosphatase removes phosphate from myosin. Access the text alternative for slide images. © McGraw Hill, LLC 76  Smooth Muscle Contraction 3 If the phosphate is removed from myosin while the cross- bridges are attached to actin, the cross-bridges release very slowly. This explains how smooth muscle is able to sustain tension for long periods and without extensive energy expenditure. This period of sustained tension is often called the latch state of smooth muscle contraction. © McGraw Hill, LLC 77  Types of Smooth Muscle Visceral: cells in sheets; function as a unit. Numerous gap junctions; waves of contraction. Often autorhythmic. Synapses are a series of dilations along the branching axons. Multiunit: cells or groups of cells act as independent units. Sheets (blood vessels); bundles (arrector pili and iris); single cells (capsule of spleen). Fewer gap junctions; synapses similar to skeletal muscle. © McGraw Hill, LLC 78  Electrical Properties of Smooth Muscle Slow waves of depolarization and repolarization transferred from cell to cell. Depolarization caused by spontaneous diffusion of Na  and Ca2 into cell. Does not follow all-or-none law. May have pacemaker cells. Contraction regulated by nervous system and by hormones. Access the text alternative for slide images. © McGraw Hill, LLC 79  Functional Properties of Smooth Muscle Some visceral muscle exhibits autorhythmic contractions. Tends to contract in response to sudden stretch but not to slow increase in length. Exhibits relatively constant tension: smooth muscle tone. Amplitude of contraction remains constant although muscle length varies © McGraw Hill, LLC 80  Regulation of Smooth Muscle 1 Innervated by autonomic nervous system (involuntary). Neurotransmitters are acetylcholine and norepinephrine. Hormones such as epinephrine and oxytocin. Other chemical regulators are histamine, prostaglandins, and by-products of metabolism. © McGraw Hill, LLC 81  Regulation of Smooth Muscle 2 Receptors present on plasma membrane; which neurotransmitters or hormones bind determines response. Receptor molecules that stimulate smooth muscle often open either sodium or calcium channels to cause depolarization. Receptor molecules that inhibit smooth muscle often close sodium and calcium channels or open potassium channels to cause hyperpolarization. © McGraw Hill, LLC 82  9.9 Cardiac Muscle Found only in heart. Striated and branched. Each cell usually has one nucleus. Has intercalated disks and gap junctions. Autorhythmic cells. Action potentials of longer duration and longer refractory period. Both Na  and Ca2 influx needed for depolarization, while Ca2 regulates contraction. © McGraw Hill, LLC 83  Cardiac Muscle Fibers (a) Ed Reschke Access the text alternative for slide images. © McGraw Hill, LLC 84  Effects of Aging on Skeletal Muscle Reduced muscle mass. Increased time for muscle to contract in response to nervous stimuli. Reduced stamina. Increased recovery time. Loss of muscle fibers, especially fast-twitch. Decreased density of capillaries in muscle. © McGraw Hill, LLC 85  Duchenne Muscular Dystrophy Access the text alternative for slide images. © McGraw Hill, LLC 86  End of Main Content Because learning changes everything. ® www.mheducation.com © 2023 McGraw Hill, LLC. All rights reserved. Authorized only for instructor use in the classroom. No reproduction or further distribution permitted without the prior written consent of McGraw Hill, LLC.