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Chap11 Muscle Tissue

The document discusses the anatomy and physiology of the muscular system, describing the microscopic structure of skeletal muscle including muscle fibers, myofilaments, sarcomeres, and motor units. It explains how skeletal muscle cells are made up of bundles of myofibrils containing thick and thin filaments that overlap to allow contraction, and are innervated by motor neurons to allow voluntary movement. The different types of muscle tissue and their functions are also introduced.

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11-1 Chapter 11 Muscular System
11-2 Muscle Tissue • Types and characteristics of muscular tissue • Microscopic anatomy of skeletal muscle • Nerve-Muscle relationship • Behavior of skeletal muscle fibers • Behavior of whole muscles • Muscle metabolism • Cardiac and smooth muscle
11-3 Introduction to Muscle • Movement is a fundamental characteristic of all living things; • Cells capable of shortening and converting the chemical energy of ATP into mechanical energy; • Types of muscle 1. Skeletal 2. Cardiac 3. smooth • Physiology of skeletal muscle – basis of warm-up, strength, endurance and fatigue
11-4 Characteristics of Muscle 1. Responsiveness (excitability) – to chemical signals, stretch and electrical changes across the plasma membrane 1. Conductivity – local electrical change triggers a wave of excitation that travels along the muscle fiber 1. Contractility -- shortens when stimulated 2. Extensibility -- capable of being stretched 3. Elasticity -- returns to its original resting length after being stretched
11-5 Skeletal Muscle • Voluntary (conscience control) striated muscle attached to bones • Typical muscle cell can be as long as 30 cm (12 inches). Due to the cells length they are called muscle fibers or myofibrils. • Exhibits alternating light and dark transverse bands or striations – reflects overlapping arrangement of internal contractile proteins
11-6 Connective Tissues of a Muscle • Epimysium – covers whole muscle belly – blends into CT between muscles • Perimysium – slightly thicker layer of connective tissue – surrounds bundle of cells called a muscle fascicle • Endomysium – thin areolar tissue around each muscle cell (myofibril) – allows room for capillaries and nerve fibers
11-7 Connective Tissue Elements Tendon Deep fascia Epimysium Perimysium Endomysium
11-8
11-9 Tendon anatomyTendon anatomy Tendon Epimysium Fascicle Fiber Fibril Collagen Microfibril Perimysium Endomysium
11-10 Connective Tissue Elements Superficial Fascia Deep Fascia Location of Fascia 2 types: 1. Deep fascia – found between adjacent muscles 2. Superficial fascia (hypodermis) – adipose between skin and muscles
11-11 Connective Tissue Elements Collagen component is (not excitable) extensible and elastic; – stretches slightly under tension and recoils when released Function of this property: • protects muscle from injury (by providing resistance to stretch) • Upon relaxation of muscle, elastic recoil returns muscle to its resting length & keeps it from becoming to flaccid.
11-12 Connective Tissue Elements Elastic components of collagen 2 types 1. parallel elastic components – runs parallel with the contractile parts of the muscle. Including endomysium, perimysium, epimysium. 2. series elastic components - joined end to end with the muscle and constitutes the tendons or other connections that bind muscle to bone.
11-13 Connective Tissue Elements Elastic recoil adds: Significant power output and efficiency of the mucsle How? Some of the pull exerted on the bone results from this recoil rather than from using ATP. Example: Running. Recoil of calcaneal tendon helps lift the heel from the ground after heal strike allowing for some of the thrust as you push off with the toes.
11-14 Reflection Questions • Answer the following questions: 1. Define responsiveness, conductivity, contractility, extensibility, and elasticity. 2. State why each of the above properties is necessary for muscle function. 3. How is skeletal muscle different from the other types of muscles? 4. Why would the skeletal muscles perform poorly without their series elastic components?
11-15 Muscle Attachments • Direct (fleshy) attachment to bone – epimysium is continuous with periosteum; – intercostal muscles; • Indirect attachment to bone – epimysium continues as tendon or aponeurosis that merges into periosteum as perforating fibers; – biceps brachii or abdominal muscle; • Stress will tear the tendon before pulling the tendon loose from either muscle or bone.
11-16 Parts of a Skeletal Muscle • Origin – attachment to stationary end of muscle • Belly – thicker, middle region of muscle • Insertion – attachment to mobile end of muscle
11-17 Skeletal Muscle Shapes Fusiform muscles thick in middle and tapered at ends biceps brachii m. Parallel muscles have parallel fascicles rectus abdominis m. Convergent muscle broad at origin and tapering to a narrower insertion Pennate muscles fascicles insert obliquely on a tendon unipennate, bipennate or multipennate palmar interosseus, rectus femoris and deltoid Circular muscles ring around body opening orbicularis oculi
11-18 Learning Strategy • Explore the location, origin, insertion and innervation of 160 skeletal muscles – use tabular information in this chapter. • Increase your retention – examining models and atlases – palpating yourself – observe an articulated skeleton – say the names aloud and check your pronunciation
11-19 Microscopic Anatomy of Skeletal Muscle
11-20 Muscle Fibers Exemplify form following function at its best! Small, complex, organized structure of protein molecules that are related to contractile function!
11-21
11-22 The Muscle Fiber
11-23 Muscle Fibers • Have multiple flattened nuclei pressed against the inside plasma membrane. • The plasma membrane is called: Sarcolemma • The cytoplasm is called: Sarcoplasm
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11-25 Muscle Fibers • Sarcoplasm is filled with – Long proteins called myofibrils (bundles of myofilaments) – glycogen for stored energy and myoglobin for binding oxygen • Smooth ER = Sarcoplasmic Reticulum – network around each myofibril – dilated end-sacs (terminal cisternea) store calcium – Transverse (T) tubules that penetrate the interior of the cell.
11-26 Muscle Fibers • Sarcoplasmic Reticulum Reservior of Ca+, gated channels, that will release Ca+ into the cytosol, where Ca+ activate the muscle contraction process. The T tubules penetrate the interior of the cell and emerge on the other side. It will surround a myofibril A pair of terminal cisternae run along side a T- tubule constituting the Triad
11-27 Myofilaments Each myofibril is bundle of parallel protein microfilaments called myofilaments 3 types of myofilaments: 1. Thick Filaments 2. Thin Filaments 3. Elastic Filaments
11-28 1. Thick Filaments • Made of 200 to 500 molecules of protein called myosin – 2 entwined polypeptides (golf clubs) • Arranged in a bundle with heads directed outward in a spiral array around the bundled tails – central area is a bare zone with no heads
11-29 2. Thin Filaments • Composed of two intertwined strands of protein called - fibrous (F) actin • Each F actin is made up of subunits called globular (G) proteins. (resembles a beaded necklace) • Each G protein has an active site that will enable it to bind to the myosin protein. • All of the active sites are covered by a protein called Tropomyosin. (especially during relaxation of muscle, thus preventing myosin from binding to the actin). • Each tropomyosin molecule has a calcium binding protein called Troponin.
2. Thin Filaments 11-30
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11-32 3. Elastic Filaments Composed of – springy protein called Titin Function: – Anchor each thick filament to Z disc – Stabilizes the thick filament, – Centers the thick filament between the thin – Prevents overstretching of sarcomere
11-33 Regulatory and Contractile Proteins • Contractile proteins = Myosin and Actin, they do the work of shortening the muscle fibers • Regulatory Proteins = Tropomyosin and Troponin – switch that starts and stops shortening of muscle cell – contraction activated by release of calcium into sarcoplasm and its binding to troponin, – troponin moves tropomyosin off the actin active sites
11-34 Overlap of Thick and Thin Filaments
11-35 Striations • Myosin and actin are not unique to muscle cells. These proteins occur in other cells, and function in cellular motility, mitosis, and transport of intracellular materials. • However, in skeletal and cardiac muscles the proteins are arranged in a precise manner that is characteristic of the striations in both types of muscles.
Sarcomere Functional contractile unit of a muscle fiber goes from one Z disc to the other Z disc. Z lines – thin filament attachment I bands – area of thin filament only A bands – length of thick filament H band – only contains only thick filaments, no thin filaments. A muscle will shorten because the individual sacomeres shorten and pull the Z disc closer to each other. 11-36
11-37 Striations = Organization of Filaments Neither thick nor thin filaments change length during shortening
11-38
11-39 Reflection Questions • Answer the following questions: 1. What special terms are given to the plasma membrane, cytoplasm, and smooth ER of a muscle cell. 2. What is the difference between a myofilament and myofibril? 3. List five proteins of the myofilaments and describe their physical arrangement. 4. Sketch the overlapping pattern of myofibrils to explain how they account for the A bands, I bands, H bands, and Z discs.
11-40 Nerve-Muscle Relationships
11-41 Motor Neurons • Skeletal muscle must be stimulated by a nerve or it will not contract (innervated by somatic motor neurons) • Cell bodies of somatic motor neurons in brainstem or spinal cord • Axons of somatic motor neurons = somatic motor fibers – terminal branches supply one muscle fiber
11-42 Motor Unit As a nerve signal stimulates the nerve fibers they all contract in unison. One nerve and all the muscle fibers innervated by it are called a Motor Unit.
11-43 Motor Units • A motor neuron and the muscle fibers it innervates – dispersed throughout the muscle – when contract together causes weak contraction over wide area • Fine control – small motor units contain as few as 20 muscle fibers per nerve fiber – eye muscles • Strength control (gross) – gastrocnemius muscle has 1000 fibers per nerve fiber
11-44 Motor Units What would be the advantage of having multiple motor units in the same muscle? Able to work in shifts. Muscles fatigue with constant stimuli. If all muscle fibers of one of your postural muscles was under the control of only one motor unit then if those muscles fatigued you may collapse. Prevented: multiple motor units for one muscle group. The fatigued motor units can rest while other motor units work. Allowing the postural muscles to always maintain stability.
11-45 The Neuromuscular Junction
11-46 The Neuromuscular Junction Synapse – functional connection between nerve fiber and target cell. Neuromuscular Junction- When target cell is a muscle fiber. Synaptic Knob- end of motor nerve. Motor End Plate- the knob sits is a depression of the sarcolemma. Synaptic Cleft- tiny gap between the motor nerve and muscle fiber. Acetylcholine (ACh)- chemical that functions as a neurotransmitter. Synaptic vesicles- stores ACh. Junctional folds- infolding of sarcolemma to surface area. Acetylcholinesterase (AChE)- enzyme found in basal lamina and part of sarcolemma, breaks down ACh, thus shutting down the stimulation of muscle fibers and allowing a muscle to relax
11-47 Neuromuscular Toxins • Pesticides (cholinesterase inhibitors) – bind to acetylcholinesterase and prevent it from degrading ACh – spastic paralysis and possible suffocation • Tetanus or lockjaw is spastic paralysis caused by toxin of Clostridium bacteria – blocks glycine release in the spinal cord and causes overstimulation of the muscles • Flaccid paralysis (limp muscles) due to curare that competes with ACh – respiratory arrest
11-48 Electrically Excitable Cells • Plasma membrane is polarized or charged – resting membrane potential (RMP) due to Na+ outside of cell and K+ and other anions inside of cell – difference in charge across the membrane = resting membrane potential (-90 mV cell) • Stimulation opens ion gates in membrane – ion gates open (Na+ rushes into cell and K+ rushes out of cell) • quick up-and-down voltage shift = action potential – spreads over cell surface as nerve signal
11-49 Behavior of Skeletal Muscle Fibers
11-50 Muscle Contraction and Relaxation • Four phases: 1. excitation = nerve action potentials lead to action potentials in muscle fiber 2. excitation-contraction coupling = action potentials on the sarcolemma activate myofilaments 3. contraction = shortening of muscle fiber 4. relaxation = return to resting length • Images will be used to demonstrate the steps of each of these actions quick up-and-down voltage shift = action potential
11-51 Excitation of a Muscle Fiber
11-52 Excitation (steps 1 and 2) 1. Nerve signal opens voltage-gated calcium channels. 2. Calcium stimulates exocytosis of synaptic vesicles containing ACh = ACh release into synaptic cleft.
11-53 Excitation (steps 3 and 4) 3. ACh diffuses across the synaptic cleft and binds to receptor proteins on the sarcolemma. 4. Receptors are ligand-gated ion channels. Binding of ACh (ligand) to receptor proteins opens Na+ and K+ channels resulting in jump in RMP from -90mV to +75mV forming an end-plate potential (EPP).
11-54 Excitation (step 5) 5. In response to the EPP, voltage gated ion channels in the sarcolemma open, causing Na+ to enter muscle fiber and K+ exit muscle fiber, creating an action potential. (Excitation)
11-55 Excitation-Contraction Coupling Link the action potential on the sarcolemma to activation of the myofilaments.
11-56 Excitation-Contraction Coupling (steps 6 and 7) 6. Action potential (AP) spreading over sarcolemma (ripples on a pond) enters T tubules and continues down into sarcoplasm. 7. AP opens voltage-gated channels in T tubules causing calcium gates in the terminal cisternae of the SR to open, thus Ca+ will diffuse out of SR down its [ ] gradient into the cell.
11-57 Excitation-Contraction Coupling (steps 8 and 9) 8. Calcium released by SR binds to troponin of thin filament 9. Troponin-tropomyosin complex changes shape and exposes active sites on actin
11-58 Sliding Filament Theory
11-59
11-60 Contraction (steps 10 and 11) 10. Myosin must have an ATP molecule bound to it in order to initiate contraction. Myosin ATPase in myosin head hydrolyzes an ATP molecule, activating the head and “cocking” it in an extended position, high energy position. 11. It binds to actin active site forming a cross-bridge
11-61 Contraction (steps 12) 12. Myosin releases ADP and phosphate as it flexes (low energy position) pulling the thin filament past the thick called the Power stroke. Myosin remains bound to actin until it binds a new ATP
11-62 Contraction (Step 13) 13. With the binding of more ATP, the myosin head releases the actin and is ready to repeat process – hydrolyze the ATP, recock (recovery stroke) and bind to a new active site farther down the thin filament. – half of the heads are bound to a thin filament at one time preventing slippage – thin and thick filaments do not become shorter, just slide past each other (sliding filament theory)
11-63 Relaxation Fibers returning to resting length
11-64 Relaxation (steps 14 and 15) 14. Nerve stimulation stops arriving at NMJ, so the synaptic knob stop releasing ACh. 15. Acetylcholinesterase removes ACh from receptors. Breaks it down and knob reabsorbs it. Stimulation of the muscle cell ceases.
11-65 Relaxation (step 16) 16. SR uses active transport to pump calcium back from cytosol (cell) into the cisternae to bind to protein called calsequestrin and stored. • ATP is needed for muscle contraction as well as muscle relaxation
11-66 Relaxation (steps 17 and 18) 17. Ca+ ions dissociate from troponin, pumped back to SR. 18. Tropomyosin moves back into position and blocks the active site of the actin filament. Myosin can no longer bind, muscle fiber ceases to produce or maintain tension.
11-67 Rigor Mortis • Stiffening of the body beginning 3 to 4 hours after death • Deteriorating sarcoplasmic reticulum releases calcium • Calcium activates myosin-actin cross-bridging and muscle contracts, but can not relax. • Muscle relaxation requires ATP and ATP production is no longer produced after death • Fibers remain contracted until myofilaments decay
11-68 Length-Tension Relationship • Amount of tension generated, therefore the force of contraction depends on length of muscle before it was stimulated – length-tension relationship (see graph next slide) • Overly contracted (weak contraction results) – thick filaments too close to Z discs and can’t slide • Too stretched (weak contraction results) – little overlap of thin and thick does not allow for very many cross bridges too form • Optimum resting length produces greatest force when muscle contracts – central nervous system constantly monitors and adjusts the length of resting muscles maintains optimal length producing muscle tone or partial contraction
11-69 Length-Tension Curve
11-70 Behavior of Whole Muscle
11-71 Threshold, Latent period, Twitch Threshold - minimum amount of voltage needed to generate an action potential in the muscle fiber and produce a contraction. Twitch- At theshold, a stimulus creates a quick cycle of contraction and relaxation. Latent Period- between the onset of the stimulus and onset of the twitch. The force generated during this time is called Internal tension. (no shortening of muscle or recorded on myogram All experiments are performed on the gastrocnemius of a frog
11-72 Threshold, Latent period, Twitch Once the elastic components are taut, the muscle begins to generate External tension and move a resistant load = Contraction phase. Relaxation Phase- the myosin releases the thin filaments as the Ca2+ is reabsorbed back into the SR. Note: the muscle is quicker to contract than relax.
11-73
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11-80 Isometric and Isotonic Contractions • Isometric muscle contraction – develops tension without changing length – important in postural muscle function and antagonistic muscle joint stabilization • Isotonic muscle contraction – tension while shortening = 1. concentric – tension while lengthening = 2. eccentric
11-81 ATP Sources • All muscle contraction depends on ATP • Pathways of ATP synthesis – anaerobic fermentation (ATP production limited) • without oxygen, produces toxic lactic acid – aerobic respiration (more ATP produced) • requires continuous oxygen supply, produces H2O and CO2
11-82 Immediate Energy Needs • Short, intense exercise (100 m dash) – oxygen need is supplied by myoglobin • Phosphagen system – myokinase transfers Pi groups from one ADP to another forming ATP – creatine kinase transfers Pi groups from creatine phosphate to make ATP • Result is power enough for 1 minute brisk walk or 6 seconds of sprinting
11-83 Short-Term Energy Needs • Glycogen-lactic acid system takes over – produces ATP for 30-40 seconds of maximum activity • playing basketball or running around baseball diamonds – muscles obtain glucose from blood and stored glycogen
11-84 Long-Term Energy Needs • Aerobic respiration needed for prolonged exercise – Produces 36 ATPs/glucose molecule • After 40 seconds of exercise, respiratory and cardiovascular systems must deliver enough oxygen for aerobic respiration – oxygen consumption rate increases for first 3-4 minutes and then levels off to a steady state • Limits are set by depletion of glycogen and blood glucose, loss of fluid and electrolytes
11-85 Fatigue • Progressive weakness from use – ATP synthesis declines as glycogen is consumed – sodium-potassium pumps fail to maintain membrane potential and excitability – lactic acid inhibits enzyme function – accumulation of extracellular K+ hyperpolarizes the cell – motor nerve fibers use up their acetylcholine
11-86 Endurance • Ability to maintain high-intensity exercise for >5 minutes – determined by maximum oxygen uptake • VO2 max is proportional to body size, peaks at age 20, is larger in trained athlete and males – nutrient availability • carbohydrate loading used by some athletes – packs glycogen into muscle cells – adds water at same time (2.7 g water with each gram/glycogen) » side effects include “heaviness” feeling
11-87 Oxygen Debt • Heavy breathing after strenuous exercise – known as excess postexercise oxygen consumption (EPOC) – typically about 11 liters extra is consumed • Purposes for extra oxygen – replace oxygen reserves (myoglobin, blood hemoglobin, in air in the lungs and dissolved in plasma) – replenishing the phosphagen system – reconverting lactic acid to glucose in kidneys and liver – serving the elevated metabolic rate that occurs as long as the body temperature remains elevated by exercise
11-88 Slow- and Fast-Twitch Fibers • Slow oxidative, slow-twitch fibers – more mitochondria, myoglobin and capillaries – adapted for aerobic respiration and resistant to fatigue – soleus and postural muscles of the back (100msec/twitch)
11-89 Slow and Fast-Twitch Fibers • Fast glycolytic, fast-twitch fibers – rich in enzymes for phosphagen and glycogen-lactic acid systems – sarcoplasmic reticulum releases calcium quickly so contractions are quicker (7.5 msec/twitch) – extraocular eye muscles, gastrocnemius and biceps brachii • Proportions genetically determined
11-90 Strength and Conditioning • Strength of contraction – muscle size and fascicle arrangement • 3 or 4 kg / cm2 of cross-sectional area – size of motor units and motor unit recruitment – length of muscle at start of contraction • Resistance training (weight lifting) – stimulates cell enlargement due to synthesis of more myofilaments • Endurance training (aerobic exercise) – produces an increase in mitochondria, glycogen and density of capillaries
11-91 Contraction Strength of Twitches
11-92 Contraction Strength of Twitches • Threshold stimuli produces twitches • Twitches unchanged despite increased voltage • “Muscle fiber obeys an all-or-none law” contracting to its maximum or not at all – not a true statement since twitches vary in strength • depending upon, Ca2+ concentration, previous stretch of the muscle, temperature, pH and hydration • Closer stimuli produce stronger twitches
11-93 Recruitment and Stimulus Intensity • Stimulating the whole nerve with higher and higher voltage produces stronger contractions • More motor units are being recruited – called multiple motor unit summation – lift a glass of milk versus a whole gallon of milk
11-94 Twitch and Treppe Contractions • Muscle stimulation at variable frequencies – low frequency (up to 10 stimuli/sec) • each stimulus produces an identical twitch response – moderate frequency (between 10-20 stimuli/sec) • each twitch has time to recover but develops more tension than the one before (treppe phenomenon) – calcium was not completely put back into SR – heat of tissue increases myosin ATPase efficiency
11-95 Incomplete and Complete Tetanus • Higher frequency stimulation (20-40 stimuli/second) generates gradually more strength of contraction – each stimuli arrives before last one recovers • temporal summation or wave summation – incomplete tetanus = sustained fluttering contractions • Maximum frequency stimulation (40-50 stimuli/second) – muscle has no time to relax at all – twitches fuse into smooth, prolonged contraction called complete tetanus – rarely occurs in the body
11-96 Muscle Contraction Phases • Isometric and isotonic phases of lifting – tension builds though the box is not moving – muscle begins to shorten – tension maintained
11-97 Cardiac Muscle 1 • Thick cells shaped like a log with uneven, notched ends • Linked to each other at intercalated discs – electrical gap junctions allow cells to stimulate their neighbors – mechanical junctions keep the cells from pulling apart • Sarcoplasmic reticulum less developed but large T tubules admit Ca+2 from extracellular fluid • Damaged cells repaired by fibrosis, not mitosis
11-98 Cardiac Muscle 2 • Autorhythmic due to pacemaker cells • Uses aerobic respiration almost exclusively – large mitochondria make it resistant to fatigue – very vulnerable to interruptions in oxygen supply
11-99 Smooth Muscle • Fusiform cells with one nucleus – 30 to 200 microns long and 5 to 10 microns wide – no striations, sarcomeres or Z discs – thin filaments attach to dense bodies scattered throughout sarcoplasm and on sarcolemma – SR is scanty and has no T tubules • calcium for contraction comes from extracellular fluid • If present, nerve supply is autonomic – releases either ACh or norepinephrine
11-100 Types of Smooth Muscle • Multiunit smooth muscle – largest arteries, iris, pulmonary air passages, arrector pili muscles – terminal nerve branches synapse on myocytes – independent contraction
11-101 Types of Smooth Muscle • Single-unit smooth muscle – most blood vessels and viscera as circular and longitudinal muscle layers – electrically coupled by gap junctions – large number of cells contract as a unit
11-102 Stimulation of Smooth Muscle
11-103 Stimulation of Smooth Muscle • Involuntary and contracts without nerve stimulation – hormones, CO2, low pH, stretch, O2 deficiency – pacemaker cells in GI tract are autorhythmic • Autonomic nerve fibers have beadlike swellings called varicosities containing synaptic vesicles – stimulates multiple myocytes at diffuse junctions
11-104 Features of Contraction and Relaxation • Calcium triggering contraction is extracellular – calcium channels triggered to open by voltage, hormones, neurotransmitters or cell stretching • calcium ions bind to calmodulin • activates light-chain myokinase which activates myosin ATPase • power stroke occurs when ATP hydrolyzed • Thin filaments pull on intermediate filaments attached to dense bodies on the plasma membrane – shortens the entire cell in a twisting fashion
11-105 • Contraction and relaxation very slow in comparison – slow myosin ATPase enzyme and slow pumps that remove Ca+2 • Uses 10-300 times less ATP to maintain the same tension – latch-bridge mechanism maintains tetanus (muscle tone) • keeps arteries in state of partial contraction (vasomotor tone) Features of Contraction and Relaxation
11-106 Contraction of Smooth Muscle
11-107 Responses to Stretch 1 • Stretch opens mechanically-gated calcium channels causing muscle response – food entering the esophagus brings on peristalsis • Stress-relaxation response necessary for hollow organs that gradually fill (urinary bladder) – when stretched, tissue briefly contracts then relaxes
11-108 • Must contract forcefully when greatly stretched – thick filaments have heads along their entire length – no orderly filament arrangement -- no Z discs • Plasticity is ability to adjust tension to degree of stretch such as empty bladder is not flabby Responses to Stretch 2
11-109 Muscular Dystrophy • Hereditary diseases - skeletal muscles degenerate and are replaced with adipose • Disease of males – appears as child begins to walk – rarely live past 20 years of age • Dystrophin links actin filaments to cell membrane – leads to torn cell membranes and necrosis • Fascioscapulohumeral MD -- facial and
11-110 Myasthenia Gravis • Autoimmune disease - antibodies attack NMJ and bind ACh receptors in clusters – receptors removed – less and less sensitive to ACh • drooping eyelids and double vision, difficulty swallowing, weakness of the limbs, respiratory failure • Disease of women between 20 and 40 • Treated with cholinesterase inhibitors, thymus removal or immunosuppressive agents
11-111 Myasthenia Gravis Drooping eyelids and weakness of muscles of eye movement

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Chap11 Muscle Tissue

  • 1.
  • 2.
    11-2 Muscle Tissue • Typesand characteristics of muscular tissue • Microscopic anatomy of skeletal muscle • Nerve-Muscle relationship • Behavior of skeletal muscle fibers • Behavior of whole muscles • Muscle metabolism • Cardiac and smooth muscle
  • 3.
    11-3 Introduction to Muscle •Movement is a fundamental characteristic of all living things; • Cells capable of shortening and converting the chemical energy of ATP into mechanical energy; • Types of muscle 1. Skeletal 2. Cardiac 3. smooth • Physiology of skeletal muscle – basis of warm-up, strength, endurance and fatigue
  • 4.
    11-4 Characteristics of Muscle 1.Responsiveness (excitability) – to chemical signals, stretch and electrical changes across the plasma membrane 1. Conductivity – local electrical change triggers a wave of excitation that travels along the muscle fiber 1. Contractility -- shortens when stimulated 2. Extensibility -- capable of being stretched 3. Elasticity -- returns to its original resting length after being stretched
  • 5.
    11-5 Skeletal Muscle • Voluntary(conscience control) striated muscle attached to bones • Typical muscle cell can be as long as 30 cm (12 inches). Due to the cells length they are called muscle fibers or myofibrils. • Exhibits alternating light and dark transverse bands or striations – reflects overlapping arrangement of internal contractile proteins
  • 6.
    11-6 Connective Tissues ofa Muscle • Epimysium – covers whole muscle belly – blends into CT between muscles • Perimysium – slightly thicker layer of connective tissue – surrounds bundle of cells called a muscle fascicle • Endomysium – thin areolar tissue around each muscle cell (myofibril) – allows room for capillaries and nerve fibers
  • 7.
    11-7 Connective Tissue Elements Tendon Deepfascia Epimysium Perimysium Endomysium
  • 8.
  • 9.
    11-9 Tendon anatomyTendon anatomy TendonEpimysium Fascicle Fiber Fibril Collagen Microfibril Perimysium Endomysium
  • 10.
    11-10 Connective Tissue Elements SuperficialFascia Deep Fascia Location of Fascia 2 types: 1. Deep fascia – found between adjacent muscles 2. Superficial fascia (hypodermis) – adipose between skin and muscles
  • 11.
    11-11 Connective Tissue Elements Collagencomponent is (not excitable) extensible and elastic; – stretches slightly under tension and recoils when released Function of this property: • protects muscle from injury (by providing resistance to stretch) • Upon relaxation of muscle, elastic recoil returns muscle to its resting length & keeps it from becoming to flaccid.
  • 12.
    11-12 Connective Tissue Elements Elasticcomponents of collagen 2 types 1. parallel elastic components – runs parallel with the contractile parts of the muscle. Including endomysium, perimysium, epimysium. 2. series elastic components - joined end to end with the muscle and constitutes the tendons or other connections that bind muscle to bone.
  • 13.
    11-13 Connective Tissue Elements Elasticrecoil adds: Significant power output and efficiency of the mucsle How? Some of the pull exerted on the bone results from this recoil rather than from using ATP. Example: Running. Recoil of calcaneal tendon helps lift the heel from the ground after heal strike allowing for some of the thrust as you push off with the toes.
  • 14.
    11-14 Reflection Questions • Answerthe following questions: 1. Define responsiveness, conductivity, contractility, extensibility, and elasticity. 2. State why each of the above properties is necessary for muscle function. 3. How is skeletal muscle different from the other types of muscles? 4. Why would the skeletal muscles perform poorly without their series elastic components?
  • 15.
    11-15 Muscle Attachments • Direct(fleshy) attachment to bone – epimysium is continuous with periosteum; – intercostal muscles; • Indirect attachment to bone – epimysium continues as tendon or aponeurosis that merges into periosteum as perforating fibers; – biceps brachii or abdominal muscle; • Stress will tear the tendon before pulling the tendon loose from either muscle or bone.
  • 16.
    11-16 Parts of aSkeletal Muscle • Origin – attachment to stationary end of muscle • Belly – thicker, middle region of muscle • Insertion – attachment to mobile end of muscle
  • 17.
    11-17 Skeletal Muscle Shapes Fusiformmuscles thick in middle and tapered at ends biceps brachii m. Parallel muscles have parallel fascicles rectus abdominis m. Convergent muscle broad at origin and tapering to a narrower insertion Pennate muscles fascicles insert obliquely on a tendon unipennate, bipennate or multipennate palmar interosseus, rectus femoris and deltoid Circular muscles ring around body opening orbicularis oculi
  • 18.
    11-18 Learning Strategy • Explorethe location, origin, insertion and innervation of 160 skeletal muscles – use tabular information in this chapter. • Increase your retention – examining models and atlases – palpating yourself – observe an articulated skeleton – say the names aloud and check your pronunciation
  • 19.
  • 20.
    11-20 Muscle Fibers Exemplify formfollowing function at its best! Small, complex, organized structure of protein molecules that are related to contractile function!
  • 21.
  • 22.
  • 23.
    11-23 Muscle Fibers • Havemultiple flattened nuclei pressed against the inside plasma membrane. • The plasma membrane is called: Sarcolemma • The cytoplasm is called: Sarcoplasm
  • 24.
  • 25.
    11-25 Muscle Fibers • Sarcoplasmis filled with – Long proteins called myofibrils (bundles of myofilaments) – glycogen for stored energy and myoglobin for binding oxygen • Smooth ER = Sarcoplasmic Reticulum – network around each myofibril – dilated end-sacs (terminal cisternea) store calcium – Transverse (T) tubules that penetrate the interior of the cell.
  • 26.
    11-26 Muscle Fibers • SarcoplasmicReticulum Reservior of Ca+, gated channels, that will release Ca+ into the cytosol, where Ca+ activate the muscle contraction process. The T tubules penetrate the interior of the cell and emerge on the other side. It will surround a myofibril A pair of terminal cisternae run along side a T- tubule constituting the Triad
  • 27.
    11-27 Myofilaments Each myofibril isbundle of parallel protein microfilaments called myofilaments 3 types of myofilaments: 1. Thick Filaments 2. Thin Filaments 3. Elastic Filaments
  • 28.
    11-28 1. Thick Filaments •Made of 200 to 500 molecules of protein called myosin – 2 entwined polypeptides (golf clubs) • Arranged in a bundle with heads directed outward in a spiral array around the bundled tails – central area is a bare zone with no heads
  • 29.
    11-29 2. Thin Filaments •Composed of two intertwined strands of protein called - fibrous (F) actin • Each F actin is made up of subunits called globular (G) proteins. (resembles a beaded necklace) • Each G protein has an active site that will enable it to bind to the myosin protein. • All of the active sites are covered by a protein called Tropomyosin. (especially during relaxation of muscle, thus preventing myosin from binding to the actin). • Each tropomyosin molecule has a calcium binding protein called Troponin.
  • 30.
  • 31.
  • 32.
    11-32 3. Elastic Filaments Composedof – springy protein called Titin Function: – Anchor each thick filament to Z disc – Stabilizes the thick filament, – Centers the thick filament between the thin – Prevents overstretching of sarcomere
  • 33.
    11-33 Regulatory and ContractileProteins • Contractile proteins = Myosin and Actin, they do the work of shortening the muscle fibers • Regulatory Proteins = Tropomyosin and Troponin – switch that starts and stops shortening of muscle cell – contraction activated by release of calcium into sarcoplasm and its binding to troponin, – troponin moves tropomyosin off the actin active sites
  • 34.
    11-34 Overlap of Thickand Thin Filaments
  • 35.
    11-35 Striations • Myosin andactin are not unique to muscle cells. These proteins occur in other cells, and function in cellular motility, mitosis, and transport of intracellular materials. • However, in skeletal and cardiac muscles the proteins are arranged in a precise manner that is characteristic of the striations in both types of muscles.
  • 36.
    Sarcomere Functional contractile unitof a muscle fiber goes from one Z disc to the other Z disc. Z lines – thin filament attachment I bands – area of thin filament only A bands – length of thick filament H band – only contains only thick filaments, no thin filaments. A muscle will shorten because the individual sacomeres shorten and pull the Z disc closer to each other. 11-36
  • 37.
    11-37 Striations = Organizationof Filaments Neither thick nor thin filaments change length during shortening
  • 38.
  • 39.
    11-39 Reflection Questions • Answerthe following questions: 1. What special terms are given to the plasma membrane, cytoplasm, and smooth ER of a muscle cell. 2. What is the difference between a myofilament and myofibril? 3. List five proteins of the myofilaments and describe their physical arrangement. 4. Sketch the overlapping pattern of myofibrils to explain how they account for the A bands, I bands, H bands, and Z discs.
  • 40.
  • 41.
    11-41 Motor Neurons • Skeletalmuscle must be stimulated by a nerve or it will not contract (innervated by somatic motor neurons) • Cell bodies of somatic motor neurons in brainstem or spinal cord • Axons of somatic motor neurons = somatic motor fibers – terminal branches supply one muscle fiber
  • 42.
    11-42 Motor Unit As anerve signal stimulates the nerve fibers they all contract in unison. One nerve and all the muscle fibers innervated by it are called a Motor Unit.
  • 43.
    11-43 Motor Units • Amotor neuron and the muscle fibers it innervates – dispersed throughout the muscle – when contract together causes weak contraction over wide area • Fine control – small motor units contain as few as 20 muscle fibers per nerve fiber – eye muscles • Strength control (gross) – gastrocnemius muscle has 1000 fibers per nerve fiber
  • 44.
    11-44 Motor Units What wouldbe the advantage of having multiple motor units in the same muscle? Able to work in shifts. Muscles fatigue with constant stimuli. If all muscle fibers of one of your postural muscles was under the control of only one motor unit then if those muscles fatigued you may collapse. Prevented: multiple motor units for one muscle group. The fatigued motor units can rest while other motor units work. Allowing the postural muscles to always maintain stability.
  • 45.
  • 46.
    11-46 The Neuromuscular Junction Synapse– functional connection between nerve fiber and target cell. Neuromuscular Junction- When target cell is a muscle fiber. Synaptic Knob- end of motor nerve. Motor End Plate- the knob sits is a depression of the sarcolemma. Synaptic Cleft- tiny gap between the motor nerve and muscle fiber. Acetylcholine (ACh)- chemical that functions as a neurotransmitter. Synaptic vesicles- stores ACh. Junctional folds- infolding of sarcolemma to surface area. Acetylcholinesterase (AChE)- enzyme found in basal lamina and part of sarcolemma, breaks down ACh, thus shutting down the stimulation of muscle fibers and allowing a muscle to relax
  • 47.
    11-47 Neuromuscular Toxins • Pesticides(cholinesterase inhibitors) – bind to acetylcholinesterase and prevent it from degrading ACh – spastic paralysis and possible suffocation • Tetanus or lockjaw is spastic paralysis caused by toxin of Clostridium bacteria – blocks glycine release in the spinal cord and causes overstimulation of the muscles • Flaccid paralysis (limp muscles) due to curare that competes with ACh – respiratory arrest
  • 48.
    11-48 Electrically Excitable Cells •Plasma membrane is polarized or charged – resting membrane potential (RMP) due to Na+ outside of cell and K+ and other anions inside of cell – difference in charge across the membrane = resting membrane potential (-90 mV cell) • Stimulation opens ion gates in membrane – ion gates open (Na+ rushes into cell and K+ rushes out of cell) • quick up-and-down voltage shift = action potential – spreads over cell surface as nerve signal
  • 49.
  • 50.
    11-50 Muscle Contraction and Relaxation •Four phases: 1. excitation = nerve action potentials lead to action potentials in muscle fiber 2. excitation-contraction coupling = action potentials on the sarcolemma activate myofilaments 3. contraction = shortening of muscle fiber 4. relaxation = return to resting length • Images will be used to demonstrate the steps of each of these actions quick up-and-down voltage shift = action potential
  • 51.
  • 52.
    11-52 Excitation (steps 1and 2) 1. Nerve signal opens voltage-gated calcium channels. 2. Calcium stimulates exocytosis of synaptic vesicles containing ACh = ACh release into synaptic cleft.
  • 53.
    11-53 Excitation (steps 3and 4) 3. ACh diffuses across the synaptic cleft and binds to receptor proteins on the sarcolemma. 4. Receptors are ligand-gated ion channels. Binding of ACh (ligand) to receptor proteins opens Na+ and K+ channels resulting in jump in RMP from -90mV to +75mV forming an end-plate potential (EPP).
  • 54.
    11-54 Excitation (step 5) 5.In response to the EPP, voltage gated ion channels in the sarcolemma open, causing Na+ to enter muscle fiber and K+ exit muscle fiber, creating an action potential. (Excitation)
  • 55.
    11-55 Excitation-Contraction Coupling Link theaction potential on the sarcolemma to activation of the myofilaments.
  • 56.
    11-56 Excitation-Contraction Coupling (steps6 and 7) 6. Action potential (AP) spreading over sarcolemma (ripples on a pond) enters T tubules and continues down into sarcoplasm. 7. AP opens voltage-gated channels in T tubules causing calcium gates in the terminal cisternae of the SR to open, thus Ca+ will diffuse out of SR down its [ ] gradient into the cell.
  • 57.
    11-57 Excitation-Contraction Coupling (steps8 and 9) 8. Calcium released by SR binds to troponin of thin filament 9. Troponin-tropomyosin complex changes shape and exposes active sites on actin
  • 58.
  • 59.
  • 60.
    11-60 Contraction (steps 10and 11) 10. Myosin must have an ATP molecule bound to it in order to initiate contraction. Myosin ATPase in myosin head hydrolyzes an ATP molecule, activating the head and “cocking” it in an extended position, high energy position. 11. It binds to actin active site forming a cross-bridge
  • 61.
    11-61 Contraction (steps 12) 12.Myosin releases ADP and phosphate as it flexes (low energy position) pulling the thin filament past the thick called the Power stroke. Myosin remains bound to actin until it binds a new ATP
  • 62.
    11-62 Contraction (Step 13) 13.With the binding of more ATP, the myosin head releases the actin and is ready to repeat process – hydrolyze the ATP, recock (recovery stroke) and bind to a new active site farther down the thin filament. – half of the heads are bound to a thin filament at one time preventing slippage – thin and thick filaments do not become shorter, just slide past each other (sliding filament theory)
  • 63.
  • 64.
    11-64 Relaxation (steps 14and 15) 14. Nerve stimulation stops arriving at NMJ, so the synaptic knob stop releasing ACh. 15. Acetylcholinesterase removes ACh from receptors. Breaks it down and knob reabsorbs it. Stimulation of the muscle cell ceases.
  • 65.
    11-65 Relaxation (step 16) 16.SR uses active transport to pump calcium back from cytosol (cell) into the cisternae to bind to protein called calsequestrin and stored. • ATP is needed for muscle contraction as well as muscle relaxation
  • 66.
    11-66 Relaxation (steps 17and 18) 17. Ca+ ions dissociate from troponin, pumped back to SR. 18. Tropomyosin moves back into position and blocks the active site of the actin filament. Myosin can no longer bind, muscle fiber ceases to produce or maintain tension.
  • 67.
    11-67 Rigor Mortis • Stiffeningof the body beginning 3 to 4 hours after death • Deteriorating sarcoplasmic reticulum releases calcium • Calcium activates myosin-actin cross-bridging and muscle contracts, but can not relax. • Muscle relaxation requires ATP and ATP production is no longer produced after death • Fibers remain contracted until myofilaments decay
  • 68.
    11-68 Length-Tension Relationship • Amountof tension generated, therefore the force of contraction depends on length of muscle before it was stimulated – length-tension relationship (see graph next slide) • Overly contracted (weak contraction results) – thick filaments too close to Z discs and can’t slide • Too stretched (weak contraction results) – little overlap of thin and thick does not allow for very many cross bridges too form • Optimum resting length produces greatest force when muscle contracts – central nervous system constantly monitors and adjusts the length of resting muscles maintains optimal length producing muscle tone or partial contraction
  • 69.
  • 70.
  • 71.
    11-71 Threshold, Latent period,Twitch Threshold - minimum amount of voltage needed to generate an action potential in the muscle fiber and produce a contraction. Twitch- At theshold, a stimulus creates a quick cycle of contraction and relaxation. Latent Period- between the onset of the stimulus and onset of the twitch. The force generated during this time is called Internal tension. (no shortening of muscle or recorded on myogram All experiments are performed on the gastrocnemius of a frog
  • 72.
    11-72 Threshold, Latent period,Twitch Once the elastic components are taut, the muscle begins to generate External tension and move a resistant load = Contraction phase. Relaxation Phase- the myosin releases the thin filaments as the Ca2+ is reabsorbed back into the SR. Note: the muscle is quicker to contract than relax.
  • 73.
  • 74.
  • 75.
  • 76.
  • 77.
  • 78.
  • 79.
  • 80.
    11-80 Isometric and IsotonicContractions • Isometric muscle contraction – develops tension without changing length – important in postural muscle function and antagonistic muscle joint stabilization • Isotonic muscle contraction – tension while shortening = 1. concentric – tension while lengthening = 2. eccentric
  • 81.
    11-81 ATP Sources • Allmuscle contraction depends on ATP • Pathways of ATP synthesis – anaerobic fermentation (ATP production limited) • without oxygen, produces toxic lactic acid – aerobic respiration (more ATP produced) • requires continuous oxygen supply, produces H2O and CO2
  • 82.
    11-82 Immediate Energy Needs •Short, intense exercise (100 m dash) – oxygen need is supplied by myoglobin • Phosphagen system – myokinase transfers Pi groups from one ADP to another forming ATP – creatine kinase transfers Pi groups from creatine phosphate to make ATP • Result is power enough for 1 minute brisk walk or 6 seconds of sprinting
  • 83.
    11-83 Short-Term Energy Needs •Glycogen-lactic acid system takes over – produces ATP for 30-40 seconds of maximum activity • playing basketball or running around baseball diamonds – muscles obtain glucose from blood and stored glycogen
  • 84.
    11-84 Long-Term Energy Needs •Aerobic respiration needed for prolonged exercise – Produces 36 ATPs/glucose molecule • After 40 seconds of exercise, respiratory and cardiovascular systems must deliver enough oxygen for aerobic respiration – oxygen consumption rate increases for first 3-4 minutes and then levels off to a steady state • Limits are set by depletion of glycogen and blood glucose, loss of fluid and electrolytes
  • 85.
    11-85 Fatigue • Progressive weaknessfrom use – ATP synthesis declines as glycogen is consumed – sodium-potassium pumps fail to maintain membrane potential and excitability – lactic acid inhibits enzyme function – accumulation of extracellular K+ hyperpolarizes the cell – motor nerve fibers use up their acetylcholine
  • 86.
    11-86 Endurance • Ability tomaintain high-intensity exercise for >5 minutes – determined by maximum oxygen uptake • VO2 max is proportional to body size, peaks at age 20, is larger in trained athlete and males – nutrient availability • carbohydrate loading used by some athletes – packs glycogen into muscle cells – adds water at same time (2.7 g water with each gram/glycogen) » side effects include “heaviness” feeling
  • 87.
    11-87 Oxygen Debt • Heavybreathing after strenuous exercise – known as excess postexercise oxygen consumption (EPOC) – typically about 11 liters extra is consumed • Purposes for extra oxygen – replace oxygen reserves (myoglobin, blood hemoglobin, in air in the lungs and dissolved in plasma) – replenishing the phosphagen system – reconverting lactic acid to glucose in kidneys and liver – serving the elevated metabolic rate that occurs as long as the body temperature remains elevated by exercise
  • 88.
    11-88 Slow- and Fast-TwitchFibers • Slow oxidative, slow-twitch fibers – more mitochondria, myoglobin and capillaries – adapted for aerobic respiration and resistant to fatigue – soleus and postural muscles of the back (100msec/twitch)
  • 89.
    11-89 Slow and Fast-TwitchFibers • Fast glycolytic, fast-twitch fibers – rich in enzymes for phosphagen and glycogen-lactic acid systems – sarcoplasmic reticulum releases calcium quickly so contractions are quicker (7.5 msec/twitch) – extraocular eye muscles, gastrocnemius and biceps brachii • Proportions genetically determined
  • 90.
    11-90 Strength and Conditioning •Strength of contraction – muscle size and fascicle arrangement • 3 or 4 kg / cm2 of cross-sectional area – size of motor units and motor unit recruitment – length of muscle at start of contraction • Resistance training (weight lifting) – stimulates cell enlargement due to synthesis of more myofilaments • Endurance training (aerobic exercise) – produces an increase in mitochondria, glycogen and density of capillaries
  • 91.
  • 92.
    11-92 Contraction Strength ofTwitches • Threshold stimuli produces twitches • Twitches unchanged despite increased voltage • “Muscle fiber obeys an all-or-none law” contracting to its maximum or not at all – not a true statement since twitches vary in strength • depending upon, Ca2+ concentration, previous stretch of the muscle, temperature, pH and hydration • Closer stimuli produce stronger twitches
  • 93.
    11-93 Recruitment and StimulusIntensity • Stimulating the whole nerve with higher and higher voltage produces stronger contractions • More motor units are being recruited – called multiple motor unit summation – lift a glass of milk versus a whole gallon of milk
  • 94.
    11-94 Twitch and TreppeContractions • Muscle stimulation at variable frequencies – low frequency (up to 10 stimuli/sec) • each stimulus produces an identical twitch response – moderate frequency (between 10-20 stimuli/sec) • each twitch has time to recover but develops more tension than the one before (treppe phenomenon) – calcium was not completely put back into SR – heat of tissue increases myosin ATPase efficiency
  • 95.
    11-95 Incomplete and CompleteTetanus • Higher frequency stimulation (20-40 stimuli/second) generates gradually more strength of contraction – each stimuli arrives before last one recovers • temporal summation or wave summation – incomplete tetanus = sustained fluttering contractions • Maximum frequency stimulation (40-50 stimuli/second) – muscle has no time to relax at all – twitches fuse into smooth, prolonged contraction called complete tetanus – rarely occurs in the body
  • 96.
    11-96 Muscle Contraction Phases •Isometric and isotonic phases of lifting – tension builds though the box is not moving – muscle begins to shorten – tension maintained
  • 97.
    11-97 Cardiac Muscle 1 •Thick cells shaped like a log with uneven, notched ends • Linked to each other at intercalated discs – electrical gap junctions allow cells to stimulate their neighbors – mechanical junctions keep the cells from pulling apart • Sarcoplasmic reticulum less developed but large T tubules admit Ca+2 from extracellular fluid • Damaged cells repaired by fibrosis, not mitosis
  • 98.
    11-98 Cardiac Muscle 2 •Autorhythmic due to pacemaker cells • Uses aerobic respiration almost exclusively – large mitochondria make it resistant to fatigue – very vulnerable to interruptions in oxygen supply
  • 99.
    11-99 Smooth Muscle • Fusiformcells with one nucleus – 30 to 200 microns long and 5 to 10 microns wide – no striations, sarcomeres or Z discs – thin filaments attach to dense bodies scattered throughout sarcoplasm and on sarcolemma – SR is scanty and has no T tubules • calcium for contraction comes from extracellular fluid • If present, nerve supply is autonomic – releases either ACh or norepinephrine
  • 100.
    11-100 Types of SmoothMuscle • Multiunit smooth muscle – largest arteries, iris, pulmonary air passages, arrector pili muscles – terminal nerve branches synapse on myocytes – independent contraction
  • 101.
    11-101 Types of SmoothMuscle • Single-unit smooth muscle – most blood vessels and viscera as circular and longitudinal muscle layers – electrically coupled by gap junctions – large number of cells contract as a unit
  • 102.
  • 103.
    11-103 Stimulation of SmoothMuscle • Involuntary and contracts without nerve stimulation – hormones, CO2, low pH, stretch, O2 deficiency – pacemaker cells in GI tract are autorhythmic • Autonomic nerve fibers have beadlike swellings called varicosities containing synaptic vesicles – stimulates multiple myocytes at diffuse junctions
  • 104.
    11-104 Features of Contractionand Relaxation • Calcium triggering contraction is extracellular – calcium channels triggered to open by voltage, hormones, neurotransmitters or cell stretching • calcium ions bind to calmodulin • activates light-chain myokinase which activates myosin ATPase • power stroke occurs when ATP hydrolyzed • Thin filaments pull on intermediate filaments attached to dense bodies on the plasma membrane – shortens the entire cell in a twisting fashion
  • 105.
    11-105 • Contraction andrelaxation very slow in comparison – slow myosin ATPase enzyme and slow pumps that remove Ca+2 • Uses 10-300 times less ATP to maintain the same tension – latch-bridge mechanism maintains tetanus (muscle tone) • keeps arteries in state of partial contraction (vasomotor tone) Features of Contraction and Relaxation
  • 106.
  • 107.
    11-107 Responses to Stretch1 • Stretch opens mechanically-gated calcium channels causing muscle response – food entering the esophagus brings on peristalsis • Stress-relaxation response necessary for hollow organs that gradually fill (urinary bladder) – when stretched, tissue briefly contracts then relaxes
  • 108.
    11-108 • Must contractforcefully when greatly stretched – thick filaments have heads along their entire length – no orderly filament arrangement -- no Z discs • Plasticity is ability to adjust tension to degree of stretch such as empty bladder is not flabby Responses to Stretch 2
  • 109.
    11-109 Muscular Dystrophy • Hereditarydiseases - skeletal muscles degenerate and are replaced with adipose • Disease of males – appears as child begins to walk – rarely live past 20 years of age • Dystrophin links actin filaments to cell membrane – leads to torn cell membranes and necrosis • Fascioscapulohumeral MD -- facial and
  • 110.
    11-110 Myasthenia Gravis • Autoimmunedisease - antibodies attack NMJ and bind ACh receptors in clusters – receptors removed – less and less sensitive to ACh • drooping eyelids and double vision, difficulty swallowing, weakness of the limbs, respiratory failure • Disease of women between 20 and 40 • Treated with cholinesterase inhibitors, thymus removal or immunosuppressive agents
  • 111.
    11-111 Myasthenia Gravis Drooping eyelidsand weakness of muscles of eye movement