Chapter10 part 3
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The document discusses skeletal muscle contraction and the neuromuscular junction. It describes how a motor neuron impulse stimulates a muscle fiber, causing the release of acetylcholine at the neuromuscular junction. This triggers an action potential in the muscle fiber membrane and the subsequent release of calcium ions from the sarcoplasmic reticulum, activating muscle contraction. It also summarizes the steps involved in muscle tension generation and lists several clinical conditions that can affect skeletal muscle function such as polio, tetanus, botulism, and myasthenia gravis.
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Chapter10 part 3
- 1. © 2015 Pearson Education, Inc. Chapter 10 part 3
- 2. © 2015 Pearson Education, Inc. Motor end plate Synaptic terminal Sarcoplasmic reticulum Myofibril Motor neuron Axon Motor end plate Path of electrical impulse (action potential) Neuromuscular junction Myofibril The structural relationship between a skeletal muscle fiber and its lone neuromuscular junction
- 3. 3 Muscle contraction begins when a motor neuron impulse stimulates an impulse in a muscle fiber. Nerve impulse is generated and sent as an electrical current (action potential) along sarcolemma The neuromuscular junction is the region where the motor neuron comes into close proximity to the muscle fiber. The neuromuscular junction (NMJ) Special intercellular connection between the nervous system and skeletal muscle fiber Controls calcium ion release into the sarcoplasm
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- 10. © 2015 Pearson Education, Inc. Excitation-contraction coupling, the dumping of calcium ions onto sarcomeres as a result of the movement of an action potential down the T tubule T tubule Sarcoplasm Sarcoplasmic reticulum (SR) Ca2+ Ca2+
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- 18. 18 Summary of Steps from Stimulation of the Nerve to the Production of Tension 1. A stimulus is propagated down the alpha motor neuron. 2. Acetylcholine (Ach) is released from the endplate and crosses the synapse. 3. Ach causes Na+ and K+ channels to open up on the sarcolemma. 4. Na+ flows into the cell and K+ flow out of the cell, generating a muscle fiber action potential. 5. Na+ spreads downward into the T-tubule system causing Ca++ to be released from the sarcoplasmic reticulum. 6. Ca++ binds with troponin, a change in configuration of actin that exposes the actin binding site. 7. A cross-bridge is formed between actin and myosin. 8. The ATP in the myosin head is downgraded to ADP + Pi. 9. Once the Pi is released the myosin head is tightly bound to actin. 10. The myosin arm does work on actin and tension is generated.
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- 21. Tension = pulling force • Tension Production by Muscles Fibers • As a whole, a muscle fiber is either contracted or relaxed The all–or–none principal: as a whole, a muscle fiber is either contracted or relaxed Amount of tension in a muscle is determined by the following: Resting length of the sarcomere at the time of stimulation (how much overlap) Frequency of stimulation….which impacts the concentration of calcium ions
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- 44. © 2015 Pearson Education, Inc. The production of lactate during peak activity, its conversion to glucose in the liver, and the rebuilding of glycogen reserves in the muscles during recovery Lactate Pyruvate Glucose Glucose Pyruvate Lactate Glucose 70–80% 20–30% LIVER MUSCLE Glycogen reserves in muscle Peak Activity Recovery Much of the large amounts of lactate produced during peak exertion diffuses out of the muscle fibers and into the bloodstream. The liver absorbs this lactate and begins converting it into pyruvate. This process continues after exertion has ended, because lactate levels within muscle fibers remain relatively high, and lactate continues to diffuse into the bloodstream. After the absorbed lactate is converted to pyruvate in the liver, roughly 30 percent of the new pyruvate molecules are broken down in the mitochondria, providing the ATP needed to convert the remaining 70 percent of pyruvate molecules into glucose. The glucose molecules are then released into the circulation, where they are absorbed by skeletal muscle fibers and used to rebuild their glycogen reserves.
- 45. While creatine phosphate can sustain contraction longer than the ATP reserves, long-term contraction requires breakdown of glycogen (what is glycogen?)
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- 50. Slow (R)—more mitochondria (M) and capillaries (cap) than fast (W)
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- 55. Figure 10-22 • individual cells (NOT fused into fibers) • connected by intercalated discs • striated, with single central nucleus • short, broad T tubules encircle Z lines • no terminal cisternae in SR • rich in mitochondria and myoglobin • totally dependent on aerobic metabolism-functional syncitium
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- 61. © 2015 Pearson Education, Inc. Factors and clinical conditions affecting muscles • Hypertrophy – Increase in muscle size due to: • Increase in myofilaments • Increase in myofibril size • Increase in mitochondria • More glycogen and glycolytic enzymes – As a result of repeated exhaustive stimulation • Can be promoted by administration of steroid hormones
- 62. © 2015 Pearson Education, Inc. Factors and clinical conditions affecting muscles • Atrophy – Decrease in muscle size, tone, and power – As a result of decreased stimulation such as during: • Paralysis by spinal injury • Damage to nervous system • Having body part in cast after bone fracture – Initially reversible, but after prolonged disuse, muscle fibers can die and not be replaced
- 63. © 2015 Pearson Education, Inc. Factors and clinical conditions affecting muscles • Clinical conditions – Polio • Virus attacks motor neurons of brain and spinal cord causing paralysis (lost of voluntary movement) – Tetanus • Toxin from bacteria (Clostridium tetani) that suppresses the mechanism inhibiting motor neuron activity • Thrives in low-oxygen areas like deep punctured tissues • Results in sustained, powerful contractions of affected muscles • Severe tetanus can have 40%–60% mortality – Deaths rare due to immunization in U.S.
- 64. © 2015 Pearson Education, Inc. Factors and clinical conditions affecting muscles • Clinical conditions • Botulism • Toxin from bacteria (Clostridium botulinum) that blocks ACh release at neuromuscular junctions • Acquired through bacteria-contaminated food – Myasthenia gravis • Loss of ACh receptors at neuromuscular junctions • Results in progressive weakness
- 65. © 2015 Pearson Education, Inc. Factors and clinical conditions affecting muscles • Clinical conditions Rigor mortis • Generalized muscle contraction shortly after death (2–7 hours) • Begins with small muscles of face, neck, and arms • Due to depletion of ATP, leaving myosin cross-bridges attached to actin • Ends 1–6 days later as muscular tissue decomposes
- 66. © 2015 Pearson Education, Inc. Figure 9.12 3 Four clinical conditions that affect skeletal muscles Polio: a virus affects motor neurons in the spinal cord and brain, causing muscle atrophy and paralysis Tetanus: the bacterium Clostridium tetani releases a powerful toxin that suppresses the mechanism that inhibits motor neuron activity, causing sustained, powerful contraction of skeletal muscles throughout the body Botulism: ingestion of a toxin produced by the bacterium Clostridium botulinum paralyzes skeletal muscles by preventing ACh release at neuromuscular junctions Myasthenia gravis: loss of ACh receptors at the neuromuscular junctions results in progressive muscular weakness
Editor's Notes
- Figure 9.4.1 A skeletal muscle fiber contracts when stimulated by a motor neuron
- Figure 9.4.8 A skeletal muscle fiber contracts when stimulated by a motor neuron
- ATP Provides Energy for Muscle Contraction Sustained muscle contraction uses a lot of ATP energy Muscles store enough energy to start contraction Muscle fibers must manufacture more ATP as needed ATP Generation Cells produce ATP in two ways Aerobic metabolism of fatty acids in the mitochondria Anaerobic glycolysis in the cytoplasm Energy demands: ATP consumption: trillions of molecules per second per fiber sustained contraction requires continuous regeneration of ATP Production of ATP for muscle contraction. (a) Creatine phosphate, formed from ATP while the muscle is relaxed, transfers a high-energy phosphate group to ADP, forming ATP during muscle contraction. (b) Breakdown of muscle glycogen into glucose and production of pyruvic acid from glucose via glycolysis produce both ATP and lactic acid. Because no oxygen is needed, this is an anaerobic pathway. (c) Within mitochondria, pyruvic acid, fatty acids, and amino acids are used to produce ATP via aerobic respiration, an oxygen-requiring set of reactions.
- Figure 9.10.3 Muscles are subject to fatigue and may require an extended recovery period
- Skeletal muscle fibers are not all alike in composition and function. For example, muscle fibers vary in their content of myoglobin, the red-colored protein that binds oxygen in muscle fibers. Skeletal muscle fibers that have a high myoglobin content are termed red muscle fibers and appear darker (the dark meat in chicken legs and thighs); those that have a low content of myoglobin are called white muscle fibers and appear lighter (the white meat in chicken breasts). Red muscle fibers also contain more mitochondria and are supplied by more blood capillaries. Skeletal muscle fibers also contract and relax at different speeds, and vary in which metabolic reactions they use to generate ATP and in how quickly they fatigue. For example, a fiber is categorized as either slow or fast depending on how rapidly the ATPase in its myosin heads hydrolyzes ATP. Based on all these structural and functional characteristics, skeletal muscle fibers are classified into three main types: (1) slow oxidative fibers, (2) fast oxidative–glycolytic fibers, and (3) fast glycolytic fibers.
- Within a particular motor unit, all of the skeletal muscle fibers are of the same type. The different motor units in a muscle are recruited in a specific order, depending on need. For example, if weak contractions suffice to perform a task, only SO motor units are activated. If more force is needed, the motor units of FOG fibers are also recruited. Finally, if maximal force is required, motor units of FG fibers are also called into action with the other two types. Activation of various motor units is controlled by the brain and spinal cord. The relative ratio of fast glycolytic (FG) and slow oxidative (SO) fibers in each muscle is genetically determined and helps account for individual differences in physical performance. For example, people with a higher proportion of FG fibers (see Table 10.4) often excel in activities that require periods of intense activity, such as weight lifting or sprinting. People with higher percentages of SO fibers are better at activities that require endurance, such as long-distance running.
- Although the total number of skeletal muscle fibers usually does not increase with exercise, the characteristics of those present can change to some extent. Various types of exercises can induce changes in the fibers in a skeletal muscle. Endurance-type (aerobic) exercises, such as running or swimming, cause a gradual transformation of some FG fibers into fast oxidative–glycolytic (FOG) fibers. The transformed muscle fibers show slight increases in diameter, number of mitochondria, blood supply, and strength. Endurance exercises also result in cardiovascular and respiratory changes that cause skeletal muscles to receive better supplies of oxygen and nutrients but do not increase muscle mass. By contrast, exercises that require great strength for short periods produce an increase in the size and strength of FG fibers. The increase in size is due to increased synthesis of thick and thin filaments. The overall result is muscle enlargement (hypertrophy), as evidenced by the bulging muscles of body builders. A certain degree of elasticity is an important attribute of skeletal muscles and their connective tissue attachments. Greater elasticity contributes to a greater degree of flexibility, increasing the range of motion of a joint. When a relaxed muscle is physically stretched, its ability to lengthen is limited by connective tissue structures, such as fasciae. Regular stretching gradually lengthens these structures, but the process occurs very slowly. To see an improvement in flexibility, stretching exercises must be performed regularly—daily, if possible—for many weeks.
- Between the layers of cardiac muscle fibers, the contractile cells of the heart, are sheets of connective tissue that contain blood vessels, nerves, and the conduction system of the heart. Cardiac muscle fibers have the same arrangement of actin and myosin and the same bands, zones, and Z discs as skeletal muscle fibers. However, intercalated discs (in-TER-ka-lāt-ed; intercal- = to insert between) are unique to cardiac muscle fibers. These microscopic structures are irregular transverse thickenings of the sarcolemma that connect the ends of cardiac muscle fibers to one another. The discs contain desmosomes, which hold the fibers together, and gap junctions, which allow muscle action potentials to spread from one cardiac muscle fiber to another. Cardiac muscle tissue has an endomysium and perimysium, but lacks an epimysium.
- Cardiac muscle cells (cardiocytes): individual cells (NOT fused into fibers) connected by intercalated discs striated, with single central nucleus short, broad T tubules encircle Z lines no terminal cisternae in SR rich in mitochondria and myoglobin totally dependent on aerobic metabolism In response to a single action potential, cardiac muscle tissue remains contracted 10 to 15 times longer than skeletal muscle tissue. The long contraction is due to prolonged delivery of Ca2+ into the sarcoplasm. In cardiac muscle fibers, Ca2+ enters the sarcoplasm both from the sarcoplasmic reticulum (as in skeletal muscle fibers) and from the interstitial fluid that bathes the fibers. Because the channels that allow inflow of Ca2+ from interstitial fluid stay open for a relatively long time, a cardiac muscle contraction lasts much longer than a skeletal muscle twitch.
- Intercalated Discs Are specialized contact points between cardiocytes Join cell membranes of adjacent cardiocytes (gap junctions, desmosomes) Functions of intercalated discs Maintain structure Enhance molecular and electrical connections Conduct action potentials Coordination of cardiocytes Because intercalated discs link heart cells mechanically, chemically, and electrically, the heart functions like a single, fused mass of cells We have seen that skeletal muscle tissue contracts only when stimulated by acetylcholine released by a nerve impulse in a motor neuron. In contrast, cardiac muscle tissue contracts when stimulated by its own autorhythmic muscle fibers. Under normal resting conditions, cardiac muscle tissue contracts and relaxes about 75 times a minute. This continuous, rhythmic activity is a major physiological difference between cardiac and skeletal muscle tissue. The mitochondria in cardiac muscle fibers are larger and more numerous than in skeletal muscle fibers. This structural feature correctly suggests that cardiac muscle depends largely on aerobic respiration to generate ATP, and thus requires a constant supply of oxygen. Cardiac muscle fibers can also use lactic acid produced by skeletal muscle fibers to make ATP, a benefit during exercise. Like skeletal muscle, cardiac muscle fibers can undergo hypertrophy in response to an increased workload. This is called a physiological enlarged heart and it is why many athletes have enlarged hearts. By contrast, a pathological enlarged heart is related to significant heart disease.
- Action potentials: long duration compared to skeletal muscle slow calcium channels delay repolarization (return to a relaxed state) long refractory period during which these cells cannot be stimulated (NO wave summation or tetany)
- spindle-shaped, non-striated single, central nucleus no T tubules; SR forms a loose network filaments NOT arranged in sarcomeres thin filaments attach to dense bodies Like cardiac muscle tissue, smooth muscle tissue is usually activated involuntarily. Of the two types of smooth muscle tissue, the more common type is visceral (single-unit) smooth muscle tissue (Figure 10.16a). It is found in the skin and in tubular arrangements that form part of the walls of small arteries and veins and of hollow organs such as the stomach, intestines, uterus, and urinary bladder. Like cardiac muscle, visceral smooth muscle is autorhythmic. The fibers connect to one another by gap junctions, forming a network through which muscle action potentials can spread. When a neurotransmitter, hormone, or autorhythmic signal stimulates one fiber, the muscle action potential is transmitted to neighboring fibers, which then contract in unison, as a single unit.
- Figure 9.12.3 Many factors can result in muscle hypertrophy, atrophy, or paralysis