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MUSCLES

MUSCLE TYPES. Skeletal. Smooth. Cardiac. OVERVIEW. Skeletal and smooth muscle cells are elongated

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MUSCLES

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    1. MUSCLES AND MUSCLE TISSUE

    2. MUSCLE TYPES Skeletal Smooth

    3. OVERVIEW Skeletal and smooth muscle cells are elongated “Muscle fibers” Muscle contraction depends on two kinds of myofilaments Actin fibers Myosin fibers

    4. SKELETAL MUSCLES Skeletal muscles Tissue packaged into organs Skeletal muscle fibers longest muscle cells Striated Obvious stripes due to overlapping of filaments Contraction involves movement of filaments Voluntary control Voluntary muscles Only type of muscle subject to conscious control

    5. CARDIAC MUSCLES Cardiac muscles Tissue packaged into organs Present only in heart Constitutes bulk of heart wall Striated Obvious stripes due to overlapping of filaments Contraction involves movement of filaments Involuntary Involuntary muscles Not subject to conscious control

    6. SMOOTH MUSCLES Smooth muscles Tissue packaged into organs Present in walls of hollow visceral organs Forces substances through internal body channels Nonstriated Filaments present, but no stripes apparent Involuntary Involuntary muscles Not subject to conscious control

    7. MUSCLE CHARACTERISTICS Excitability (Irritability) Ability to receive and respond to a stimulus e.g., chemical, pH change, etc. Response is generation of an electrical impulse Contractility Ability to shorten forcibly when stimulated Extensibility Ability to be stretched/extended when relaxed Elasticity Ability of muscle fiber to recoil and resume resting length after being stretched

    8. MUSCLE FUNCTIONS Produce movement Most movements result of muscular contraction Movement of body and within body Maintain posture Muscles continuously active Stabilize joints Major force stabilizing many joints Generate heat Contraction generates heat Heat required to maintain constant body temperature

    9. SKELETAL MUSCLE Gross Anatomy Each skeletal muscle is a discrete organ Composed of several kinds of tissues Skeletal muscle fibers Blood vessels Nerve fibers Connective tissue

    10. SKELETAL MUSCLE Gross Anatomy: Nerve & Blood Supply Muscle served by Single nerve Single artery One or more veins All branch profusely through connective tissue sheaths

    11. SKELETAL MUSCLE Gross Anatomy: Connective Tissue Sheaths Individual muscle fibers wrapped and held together by multiple connective tissue sheaths Endomysium Perimysium Epimysium Support each cell and reinforce muscle

    12. SKELETAL MUSCLE Gross Anatomy: Connective Tissue Sheaths Endomysium Surround each individual muscle fiber Fibers mainly reticular fibers

    13. SKELETAL MUSCLE Gross Anatomy: Connective Tissue Sheaths Perimysium Fibrous connective tissue Surrounds bundles wrapped muscle fibers Endomysium- wrapped bundles are “fasicles”

    14. SKELETAL MUSCLE Gross Anatomy: Connective Tissue Sheaths Epimysium Dense irregular connective tissue Surrounds entire muscle

    15. SKELETAL MUSCLE Gross Anatomy: Connective Tissue Sheaths All connective tissue sheaths are continuous with each other and with tendons Muscle fibers contract ? Contraction pulls on sheaths ? Sheaths transmit force to bones ? Bones move Contribute to natural elasticity of muscle tissue

    16. SKELETAL MUSCLE Gross Anatomy: Muscle Attachments Skeletal muscles span joints Attachment to bones in two places Insertion More movable bone Origin Less movable bone

    17. SKELETAL MUSCLE Gross Anatomy: Muscle Attachments Direct attachments Epimysium is attached to the bone’s periosteum Indirect attachments More common than direct attachments Smaller, more durable Connective tissue sheaths extend beyond the muscle Rope-like tendon Sheet-like aponeurosis Anchors muscle to the connective tissue covering of a bone, cartilage, or the fascia of another muscle

    18. SKELETAL MUSCLE Microscopic Anatomy: Skeletal Muscle Fiber Long, cylindrical cell 10 – 100 mm width ~10X that of average body cell Up to 30 cm length Plasma membrane is termed “sarcolemma” Cytoplasm is termed “sarcoplasm”

    19. SKELETAL MUSCLE Microscopic Anatomy: Skeletal Muscle Fiber Sarcoplasm Large amounts of stored glycogen “Glycosomes” Large amount of myoglobin Oxygen-storing pigment similar to hemoglobin Hemoglobin genes descended from duplicated ancestral myoglobin gene “Molecular evolution” What is the function of these two components?

    20. SKELETAL MUSCLE Microscopic Anatomy: Skeletal Muscle Fiber Organelles The usual organelles are present Multiple nuclei beneath sarcolemma Skeletal muscles are syncytia, fusions of hundreds of embryonic cells Myofibrils Sarcoplasmic reticulum T-tubules

    21. SKELETAL MUSCLE Microscopic Anatomy: Skeletal Muscle Fiber Myofibrils Many myofibrils densely packed in each muscle cell More than 105 per cell 80% of cell volume Run parallel to length of cell Diameter of 1-2 mm Contain contractile elements

    22. SKELETAL MUSCLE Microscopic Anatomy: Myofibrils Striations Repeating pattern of dark and light bands Dark “A bands” Light “I bands” Near-perfect alignment of bands between myofibrils gives entire cell striped appearance

    23. SKELETAL MUSCLE Microscopic Anatomy: Myofibril Striations A-bands (dark bands) Lighter stripe in center “H-zone” Bisected by M line I-bands (light bands) Bisected by Z disc Sarcomere Region of a myofibril between two Z discs

    24. SKELETAL MUSCLE Microscopic Anatomy: Myofibril Striations Sarcomere Region of a myofibril between two Z discs A band flanked by half of an I band on each end ~2 mm long Smallest contractile unit of a muscle fiber Myofibril consists of linked sarcomeres

    25. SKELETAL MUSCLE Microscopic Anatomy: Myofibril Striations Banding pattern results from an orderly arrangement of thick (myosin) and thin (actin) filaments Thick filaments extend entire length of A band Thick filaments absent across I band Z disc composed of the protein nebulin Anchors thin filaments M line in H zone darker due to protein strands linking adjacent thick filaments

    26. SKELETAL MUSCLE Microscopic Anatomy: Thick Filaments Composed mainly of ~200 myosin molecules Rod-like tail Two interwoven polypeptide chains Form central part of thick filament Globular heads Present on ends of thick filaments “Business end” of myosin Cross bridges linking thick filaments to thin filaments during contraction

    27. SKELETAL MUSCLE Microscopic Anatomy: Thin Filaments Composed mainly of the protein actin Possess sites to which myosin heads bind during contraction Also contains regulatory proteins Tropomyosin Surround and stiffen actin core Block myosin binding sites in relaxed muscle Troponin Three-polypeptide complex TnI: inhibitory subunit TnT: helps position tropomyosin on actin TnC: binds to Ca2+

    28. SKELETAL MUSCLE Microscopic Anatomy: Other Filaments Elastic filaments Comprised of the giant protein titin Extends from Z disc to the thick filament Functions Holds thick filaments in place Resists excessive stretching Assists the muscle cell in springing back into shape after being stretched

    29. SKELETAL MUSCLE Microscopic Anatomy: Sarcoplasmic Reticulum Elaborate smooth endoplasmic reticulum Interconnecting tubules loosely surround each myofibril Regulates intracellular Ca2+ levels Stores Ca2+ Ca2+ released on demand during stimulation

    30. SKELETAL MUSCLE Microscopic Anatomy: T Tubules Invagination of plasma membrane (sarcolemma) Elongated tube penetrating cell interior Intimate contact with SR Electrical impulses traveling along sarcolemma also travel along T tubules Conduct impulses to deepest regions of muscle Transmit to every sarcomere Impulses signal Ca2+ release from SR

    31. SKELETAL MUSCLE Sliding Filament Model of Contraction During contraction, thin filaments slide past thick filaments Involves activation of myosin’s cross bridges Increases overlap between actin and myosin Relaxed muscle: slight overlap Stimulated muscle: increased overlap

    32. SKELETAL MUSCLE Sliding Filament Model of Contraction How do filaments slide? Each myosin cross bridge attaches and detaches several times during a contraction Ratcheting action generates tension Thin filaments propelled toward center of sarcomere Occurs simultaneously in all sarcomeres throughout the cell Not all cells of the muscle Cell shortens

    33. MUSCLE PHYSIOLOGY Excitation - Contraction Coupling Muscle contraction requires stimulation by nerve Electrical current is propagated “Action potential” Intracellular Ca2+ rises Contraction is triggered

    34. MUSCLE PHYSIOLOGY Neuromuscular Junction Skeletal muscles stimulated by motor neurons Components of somatic nervous system Nerves “reside” in brain or spinal cord Threadlike extensions travel to muscle cells “Axon” Divides profusely as it enters the muscle Each axonal ending forms branching neuromuscular junction with a single muscle fiber Only one neuromuscular junction per muscle fiber

    35. MUSCLE PHYSIOLOGY Neuromuscular Junction Axonal ending and muscle fiber very close Not touching 1 – 2 nanometers (nm) apart Separating space termed “synaptic cleft” Gel-like extracellular substance rich in glycoproteins

    36. MUSCLE PHYSIOLOGY Neuromuscular Junction Axonal ending contains synaptic vesicles Membrane-enclosed sacs Contain neurotransmitter acetylcholine (Ach) Ach can be released into synaptic cleft by exocytosis

    37. MUSCLE PHYSIOLOGY Neuromuscular Junction Nerve impulse reaches end of axon Voltage-gated Ca2+ channels in axonal membrane open Ca2+ enters axon from extracellular fluid Ca2+ influx signals exocytosis Synaptic vesicles fuse with axonal membrane ACh enters synaptic cleft

    38. MUSCLE PHYSIOLOGY Neuromuscular Junction Muscle cell’s sarcolemma highly infolded “Junctional folds” Increased surface area Membrane rich with ACh receptors

    39. MUSCLE PHYSIOLOGY Neuromuscular Junction Released ACh diffuses across synaptic cleft ACh binds to sarcolemma’s ACh receptors ACh ? acetic acid and choline Catalyzed by the enzyme acetylcholinesterase Sarcolemma-bound enzyme Binding triggers electrical events Muscle ultimately contracts

    40. MUSCLE PHYSIOLOGY Homeostatic Imbalance: Myasthenia Gravis Disease characterized by a shortage of ACh receptors Autoimmune disease Body destroys its own Ach receptors Interferes with neuromuscular junction events Drooping eyelids, difficulty swallowing & talking, generalized weakness

    41. MEMBRANE POTENTIAL A voltage exists across the plasma membrane “Membrane potential” Due to separation of oppositely charged ions Resting potential exhibited in cell’s resting state From -5 to -100 millivolts (mV) Inside of cell is negative relative to outside Cells are “polarized”

    42. MUSCLE PHYSIOLOGY Neuromuscular Junction: Depolarization Resting sarcolemma is polarized “Resting potential” Interior face slightly negatively charged Binding of ACh to receptors opens ligand-gated Na+ channels Na+ enters myofibril K+ exits cell, but to lesser degree Interior face of sarcolemma becomes less negative “Depolarization” “End plate potential” is formed

    43. MUSCLE PHYSIOLOGY Action Potential Depolarization is initially a local electrical event End plate potential becomes action potential, which spreads rapidly along sarcolemma Membrane areas adjacent initial depolarization become depolarized Voltage-gated Na+ channels are activated Na+ enters cell, initiation action potential Depolarization wave spreads to adjacent areas, opening additional Na+ channels Action potential results in contraction

    44. MUSCLE PHYSIOLOGY Action Potential Repolarization wave quickly follows depolarization wave Na+ channels close Voltage-gated K+ channels open K+ rapidly exits myofibril Electrical conditions of cell restored Na+-K+ pump will restore ionic conditions Several contractions can occur before ionic imbalances adversely impact contractile activity

    45. MUSCLE PHYSIOLOGY Action Potential Muscle cannot be stimulated again until repolarization is complete “Refractory period”

    46. MUSCLE PHYSIOLOGY Excitation-Contraction Coupling Action potential propagates along sarcolemma Transmitted down T tubules Brief (1-2 milliseconds [ms]) Ends prior to visible signs of contraction AP triggers SR to release Ca2+ into sarcoplasm Ca2+ channels opened

    47. MUSCLE PHYSIOLOGY Excitation-Contraction Coupling Ca2+ binds to troponin TnC Shape altered, blocking action of tropomyosin removed Myosin heads attach to thin filaments “Ratcheting” pulls thin filaments toward center of sarcomere

    48. MUSCLE PHYSIOLOGY Excitation-Contraction Coupling Ca2+ actively pumped back into SR Ca2+ signal ends within ~30 ms Tropomyosin blockade reestablished Cross bridge activity ends Relaxation occurs

    49. MUSCLE PHYSIOLOGY Excitation-Contraction Coupling Repeat Requires additional nerve impulse When nerve impulses are delivered rapidly Ca2+ levels increase greatly Muscle cells do not completely relax between stimuli Contraction is stronger and more sustained

    50. MUSCLE PHYSIOLOGY Sarcoplasmic Ca2+ Concentrations Sarcoplasmic Ca2+ levels are very low Phosphate levels in sarcoplasm are higher Ca2+ and PO43- react to form crystals These crystals would kill the cell Ca2+ and PO43- must be kept separated Intracellular Ca2+ is tightly regulated by proteins e.g., calsequestrin, calmodulin

    51. MUSCLE PHYSIOLOGY Muscle Fiber Contraction Cross bridge attachment of actin requires Ca2+ Low intracellular Ca2+ Muscle cell is relaxed Myosin binding sites on actin are physically blocked by tropomyosin molecules Rising Ca2+ levels Ca2+ ions bind to regulatory sites on troponin TnC TnC shape changes Tropomyosin removed from binding site Binding sites on actin are exposed

    52. MUSCLE PHYSIOLOGY Muscle Fiber Contraction Once binding sites on actin are exposed: Myosin head is already “cocked” Cocking fueled by hydrolysis of bound ATP molecule ADP & Pi remain covalently bound to myosin

    53. MUSCLE PHYSIOLOGY Muscle Fiber Contraction Once binding sites on actin are exposed: Cross bridge formation Myosin heads attach to binding sites Approximately half of the myosin heads on a given thick filament are bound at any given time

    54. MUSCLE PHYSIOLOGY Muscle Fiber Contraction Once binding sites on actin are exposed: Power stroke Myosin head pivots, moving through 70o angle ADP & Pi released from myosin

    55. MUSCLE PHYSIOLOGY Muscle Fiber Contraction Once binding sites on actin are exposed: Cross bridge detachment New ATP molecule covalently binds to myosin head Myosin and actin disassociate

    56. MUSCLE PHYSIOLOGY Muscle Fiber Contraction Once binding sites on actin are exposed: Myosin head is again “cocked” Repeat ~30 times or more during a muscle contraction Continues as long as Ca2+ and ATP concentrations are sufficient

    57. MUSCLE PHYSIOLOGY Muscle Fiber Relaxation As Ca2+ pumps of the SR reclaim Ca2+ Troponin again changes shape Myosin binding sites on actin again blocked by tropomyosin Contraction ends Muscle fiber relaxes

    58. MUSCLE PHYSIOLOGY Muscle Fiber Contraction: Rigor Mortis Muscles begin to stiffen 3 – 4 hours after death Peak rigidity at ~12 hours Dying cells are unable to exclude Ca2+ Intracellular [Ca2+] normally low Ca2+ influx promotes formation of cross bridges What step requires ATP binding? How much ATP is made by dead cells? Why don’t the muscles relax?

    59. MUSCLE PHYSIOLOGY Contraction of a Skeletal Muscle A skeletal muscle consists of many muscle cells Principles governing the contraction of a muscle fiber and of a skeletal muscle are similar All contractions are not equal In response to different stimuli, muscles contract With varying force For varying periods of time

    60. MUSCLE PHYSIOLOGY Contraction of a Skeletal Muscle Muscle tension The force exerted by a contracting muscle Load The opposing force exerted by the weight of the object being moved Isometric contraction Muscle tension develops, but load is not moved Isotonic contraction Muscle tension developed overcomes the load Muscle shortening occurs

    61. MUSCLE PHYSIOLOGY Each muscle is served by one or more motor nerves Consist of axons of hundreds of motor neurons The axon of each motor neuron branches upon entering muscle Each branch ends at a neuromuscular junction

    62. MUSCLE PHYSIOLOGY Motor Unit A single motor neuron and its associated muscle fibers From four to hundreds of muscle fibers per motor unit Multiple motor units per muscle Not clustered within muscle Firing of motor neuron causes contraction of all muscle fibers in motor unit Not all muscle fibers of muscle Entire muscle contracts More motor units = stronger contraction

    63. MUSCLE TWITCH Response of motor unit to single action potential Three phases Latent period Few msec following stimulation Muscle tension begins to increase Period of contraction 10 – 100 msec Cross bridges are active Tension develops, muscle may shorten Period of relaxation 10 – 100 msec Initiated by reentry of Ca2+ into SR Muscle tension decreases to zero

    64. MUSCLE TWITCH Twitch contractions of some muscles are rapid and brief e.g., muscles controlling eye movement Some muscles contract more slowly and remain contracted for longer periods e.g., calf muscles

    65. GRADED RESPONSES Normal muscle contractions Not jerky Relatively smooth Vary in strength based on demand “Graded muscle responses” Graded muscle responses achieved by Altering the frequency of stimulation Altering the strength of the stimulus

    66. GRADED RESPONSES Changes in Stimulation Frequency Two stimuli in rapid succession Second twitch will be stronger than the first Appears to “ride on shoulders” of first “Wave summation” Second contraction occurs before the muscle is completely relaxed following the first contraction Second contraction causes more shortening that first

    67. GRADED RESPONSES Changes in Stimulation Frequency Multiple stimuli in rapid succession Relaxation time between twitches shortens Sarcoplasmic [Ca2+] increases Degree of summation increases Quivering contraction termed “incomplete tetanus” a.k.a., “unfused tetanus”

    68. GRADED RESPONSES Changes in Stimulation Frequency Multiple stimuli in rapid succession Relaxation time between twitches shortens Sarcoplasmic [Ca2+] increases Degree of summation increases Quivering contraction termed “incomplete tetanus” Ultimately fused into smooth “complete tetanus”

    69. GRADED RESPONSES Response to Stronger Stimuli Wave summation increases contractile force Main function is to produce smooth, continuous contractions Force of contraction increased by “multiple motor unit summation” Threshhold stimulus recruits first motor units Maximal stimulus recruits all of a muscle’s motor units

    70. GRADED RESPONSES Smallest motor units Fewest and smallest muscle fibers Controlled by small, highly excitable motor neurons Tend to get activated first Larger motor units Contain large, coarse muscle fibers Controlled by larger, less excitable motor neurons Activated only when a stronger contraction is necessary DON’T REALLY DO THIS, JUST PRETEND!!!!! Caress your neighbor, then slap him/her. What motor units are you activating?

    71. GRADED RESPONSES Treppe Why do muscle contractions become slightly stronger with each successive stimulus during the initial phases of muscle activity? Increasing sarcoplasmic [Ca2+] More binding sites exposed More heat liberated Enzymes work more efficiently Muscles become more pliable

    72. MUSCLE TONE Relaxed skeletal muscles are always slightly contracted This state is termed “muscle tone” Stretch receptors in muscles and tendons are activated Spinal reflexes continually activate an alternating subset of motor neurons No active movement produced Mucles kept firm, healthy, and ready to respond to stimulation Helps stabilize joints and maintain osture

    73. ISOTONIC CONTRACTIONS Muscle length changes and moves the load Cross bridges are moving thin filaments Once tension is sufficient to move load, tension remains relatively constant Two types Concentric contractions Muscle shortens and does work Eccetric contractions Muscle contracts as it lengthens e.g., calf muscle while walking up a hill More forceful than concentric contractions

    74. ISOMETRIC CONTRACTIONS Tension builds but muscle length remains constant Muscle attempts to move a load greater than the force the muscle is able to develop (Try to lift your car or push this building over) Cross bridges are generating force but are not moving the thin filaments

    75. MUSCLE METABOLISM Muscular contraction requires energy Actually, they require TONS of energy Energy for the movement of the cross bridges Energy for the operation fo the calcium pump Energy sources Stored ATP Creatine phosphate Aerobic respiration Fermentation

    76. MUSCLE METABOLISM Stored ATP ATP provides the energy for Movement of the cross bridges Operation of the calcium pump ATP reserves provide this ATP for a little while Reserves depleted in 4 – 6 seconds at most How is this ATP get regenerated?

    77. MUSCLE METABOLISM Phosphorylation of ADP by Creatine Phosphate Creatine phosphate is a high-energy molecule stored in muscle Amount stored exceeds ATP reserves Phosphate readily transferred to ADP ADP + creatine-P ? ATP + creatine (A-P-P + creatine-P ? A-P-P-P + creatine) Creatine phosphate provides ATP for a while Creatine phosphate deplete in up to 10 – 15 seconds Now what do we do?

    78. MUSCLE METABOLISM Aerobic Respiration Provides most of the ATP during rest and light to moderate exercise Sugar +O2 ? ATP + CO2 + H2O Provides ~36 ATP molecules per glucose Sugar Easily liberated from glycogen stored in muscle Present in blood Can be replaced by other fuels (e.g., fatty acids, amino acids) Oxygen Carried by hemoglobin in blood Stored by myoglobin in muscle Ultimately limits aerobic respiration

    79. MUSCLE METABOLISM Fermentation Does not require O2 Aerobic respiration does require O2 Much less efficient than aerobic respiration 2 ATP per sugar as opposed to 30-something Faster than aerobic respiration Important early in strenuous exercise Glycolysis occurs as usual Glucose ? 2 pyruvate + 2 ATP + 2 NADH Pyruvate is reduced to form lactic acid Process regenerates NAD+ (which is required for glycolysis) Pyruvate + 2 NADH ? lactic acid + 2 NAD+

    80. MUSCLE METABOLISM Order of use of the various energy sources Stored ATP Creatine phosphate Fermentation Aerobic respiration Fermentation

    81. MUSCLE FATIGUE O2 ultimately becomes limiting ATP use exceeds ATP production Intracellular [lactic acid] increases Intracellular pH drops Ionic imbalances occur (e.g., K+, Ca2+) Muscles contract less effectively Muscles ultimately become physiologically unable to contract even when receiving stimuli “Muscle fatigue” Do cardiac muscles experience fatigue? Why or why not?

    82. OXYGEN DEBT For a muscle to return to its resting state Lactic acid must be removed O2 reserves must be replenished ATP reserves must be replenished Creatine phosphate must be replenished The amount of oxygen required for these processes is termed the oxygen debt Represents the difference between the amount of O2 needed for aerobic muscle activity and the amount of O2 actually used All non-aerobic sources of ATP contribute to debt

    83. HEAT PRODUCTION Heat production is an incidental consequence of muscle contraction ~40% of the energy released during muscle contraction is converted to useful work Remainder is given off as heat This heat is used to maintain a constant body temperature Excess heat is shed Do you remember how? Shivering produces additional heat when required

    84. FORCE OF CONTRACTION Force of muscle contraction is affected by Number of muscle fibers stimulated More motor units = greater force Relative size of fibers Larger fibers produce greater force Regular exercise causes muscle fiber hypertrophy Frequency of stimulation Force transferred from muscle to load Repeated stimulations produce sustained contraction Transfer more complete during sustained contractions Degree of muscle stretch Greatest force when muscle is slightly stretched

    85. CONTRACTION Velocity and Duration of Contraction Affected by load Faster contractions with no added load Greater load causes: Longer latent period Slower contraction Shorter contraction duration Affected by recruitment More motor units ? faster & more prolonged contractions Affected by muscle fiber type Detailed on next image

    86. CONTRACTION Velocity and Duration of Contraction Classification of muscle type by major ATP formation pathways Oxidative fibers Rely mainly on aerobic pathways for ATP generation Glycolytic fibers Rely mainly on fermentation for ATP generation Classification of muscle type by speed of contraction Slow fibers vs. fast fibers Differences reflect speed enzymatic hydrolysis of ATP Slow oxidative fibers Fast oxidative fibers Fast glycolytic fibers

    87. EFFECTS OF EXERCISE Muscles change in response to the amount of work they do e.g., active muscles may increase in size and strength e.g., inactive muscles atrophy

    88. EFFECTS OF EXERCISE Effects of aerobic (endurance) exercise (e.g., swimming, jogging, etc.) Increased # of capillaries surrounding muscle fibers Increased number of mitochondria in muscle fibers Increased myoglobin synthesis Most dramatic changes in slow oxidative fibers Changes result in More efficient muscle metabolism Greater endurance and strength Greater resistance to fatigue NO significant muscle hypertrophy

    89. EFFECTS OF EXERCISE Effects of resistance exercise (e.g., weight lifting, etc.) Significant muscle hypertrophy Individual muscle fibers increase in size Increase in number of mitochondria in muscle fibers Increase in number of myofilaments in muscle fibers Increased amount of connective tissue in muscle

    90. SMOOTH MUSCLE Present in the walls of all hollow organs (Not including the heart) Contractions similar to those of skeletal muscle Smooth muscle has several differences

    91. SMOOTH MUSCLE Spindle-shaped cells Smaller than skeletal muscle cells 2 – 5 micrometer diameter 100 – 400 micrometer length Single, centrally located nucleus Lack coarse connective tissue sheaths Possess small amount of fine connective tissue (endomysium) secreted by muscle cells Vascular, innervated

    92. SMOOTH MUSCLE Generally organized into two sheets Fibers organized perpendicular to each other Why are no striations visible? Alternating contraction and relaxation of opposing layers mixes and moves substances in organ’s lumen “Peristalsis”

    93. SMOOTH MUSCLE Lacks highly structured neuromuscular junctions Possess “diffuse junctions” Neurotransmitter released into wider area Sarcoplasmic reticulum less developed T-tubules absent Sarcolemma posesses Ca2+-containing infoldings “Caveoli”

    94. SMOOTH MUSCLE Organization of filaments differs No sarcomeres Thick:thin ratio 1:13, not 1:2 Thick filaments longer than skeletal counterparts Myosin heads on entire length of thick filaments Tropomyosin present, troponin absent Filaments arranged diagonally * Contain noncontractile intermediate filaments Resist tension Attach to “dense bodies”

    95. SMOOTH MUSCLE Slow, synchronized contractions Entire sheet responds to stimulus in unison Electrically coupled via gap junctions Some fibers in stomach and small intestine act as “pacemakers” Set contraction pace for other cells Some are self-excitatory Contract even without external stimulus Contract in response to neuronal or hormonal stimuli

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