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Muscle

Kristen C A & P I Exam 1 Englisch 71 Karten

Karten in diesem Stapel (71)

  1. 1Sarcolemmamuscle cell membrane
  2. 2Myoglobinred-colored, oxygen-binding protein
  3. 3Physical characteristics of muscle cellslong, striated, cylindrical, multinucleated
  4. 4t tubulescarry muscle action potential down into cell
  5. 5ATP attaches tomyosin
  6. 6Where are SR?around myofibrils
  7. 7What do SR contain?Ca2+
  8. 8Contractile proteins of muscleMyofilaments (thick and thin filaments)
  9. 9What does a Triad consist of?Terminal cisterns and T tubule
  10. 10What triggers muscle contraction?release of Ca2+
  11. 11What type of filaments are in I band?thin filaments
  12. 12Functional unit in muscleSarcomere
  13. 13proteins that make up myofibrilscontractile proteins (myosin & actin)
    regulatory proteins (troponin & tropomyosin - located on actin)
    structural proteins (titin, myomesin, nebulin, dystrophin)
  14. 14Titananchors thick filament to m line and z line
  15. 15NebulinInelastic protein that helps to align the thin filaments
  16. 16Dystrophinlinks think filaments to sarcolemma and trasmits the tension generated to the tendon
  17. 17M Line(myomesin) connects to titin and adjacent thick filaments
  18. 18How does contraction begin?1. Nerve impulse reaches axon terminal and synaptic vesicles release ACh
    2. ACh diffuses to receptors on the sarcolemma and Na+ channels open and Na+ rushes into cell
    3. A muscle action potential spreads over sarcolemma and down into T tubules
    4. SR releases Ca2+ into the sarcoplasm
    5. Ca2+ binds to toponin and causes troponin-tropomyosin complex to move and reveal myosin binding sites on actin -- the contraction cycle begins
  19. 19How do muscles relax?1. AChE breaks down ACh within synaptic cleft
    2. Muscle actin potential ceases
    3. Ca2+ release channels close
    4. Active transport pumps Ca2+ back into storage in SR
    5. Calcium-binding protein (calsequestrin) helps hold Ca2+ in SR
    6. Tropomyosin-troponin complex recovers binding site on the actin
  20. 20Rigor MortisState of muscular rigidity that begins 3-4 hours after death and lasts about 24 hrs. Ca2+ leaking out of SR allows myosin heads to bind to actin but they can't detach because ATP synthesis has ceased. Only release when proteolytic enzymes begin to digest decomposing cells.
  21. 21Superficial fascialoose connective tissue and fat underlying skin
  22. 22Rigor MortisCa2+ leaks out of SR and allows myosin heads to bind to actin. Since ATP synthesis has ceased, crossbridges cannot detach from actin until proteolytic enzymes begin to digest the decomposing cells.
  23. 23Resting muscle length70-130% of Optimal length
  24. 24What are the events occurring after a nerve signal?1. Release of ACh from synaptic vesicles after nerve impulse arrives at nerve terminal
    2. ACh binds to receptors on muscl motor end plate, opening gated ion channels so that Na+ can rush into the muscle cell
    3. Inside of muscle cell becomes more positive, triggering a muscle action potential that travels over the cell and down the T tubules
    4. Release of Ca2+ from SR
    5. Ca2+ binds to troponin, causing a conformation change that moves tropomyosin off the myosin binding site on actin. Power stroke follows.
    6. Acetylcholinesterase breaks down the ACh in synapse so the muslce action potential will cease and the muscle cell will relax
  25. 25Botulinum toxinblocks release of neurotransmitter at NMJ so muscle contraction can not occur
  26. 26Curarecauses muscle paralysis by blocking ACh receptors. Used to relax muscle in surgery.
  27. 27Neostigmineblocks removal of ACh from receptors so strengthens weak muscle contractions. Antidote for curare.
  28. 28What are the sources of ATP production in muscle?1. Creatine Phosphate
    2. Anaerobic Cellular Respiration
    3. Aerobic Cellular Respiration
  29. 29Creatine PhosphateExcess ATP within resting muscle is used to form creatine phosphate. Quick breakdown provides energy for creation of ATP when needed for short burst of activity.
  30. 30Anaerobic Cellular Respiration2 net gain of ATP. Glycolosis can continue anaerobically to provide ATP for 30 to 40 seconds of activity.
  31. 31Aerobic Cellular RespirationATP for any activity lasting over 30 seconds. When sufficient oxygen is avialabl,e pyruvic acid enters mitochondira to generate ATP, water and heat. yield is 36 ATP. Provides 90% of ATP energy if activity lasts more than 10 minutes.
  32. 32What is muscle fatigue and what factors contribute to muscle fatigue?Muscle fatigue is inability of muscles to contract after prolonged activity. Caused by:
    1. Insufficient oxygen or glycogen
    2. buildup of lactic acid and ADP
    3. insufficient release of acetylcholine from motor neurons
  33. 33Where do muscle tissues get oxygen?1. diffusion from blood
    2. myoglobin inside muscle fibers
  34. 34Motor unitone somatic motor neuron and all the skeletal muscle cells it stimulates (~150).
  35. 35Determinants of strength of muscle contraction1. Number of motor units activated
    2. Size of motor units
  36. 36Twitch contractionBrief contraction of all fibers in a motor unit in response to single action potential in its motor neuron or electrical stimulation of neuron or muscle fibers.
  37. 37Length of twitch20-200 msec
  38. 38Parts of a twitch contraction and what happens during each1. Latent period - Ca2+ is being released from SR, slack being removed from elastic components
    2. Contraction Period - Filaments slide past eachother
    3. Relaxation Period - active transport of Ca2+ into SR
    4. Refractory Period - muscle has lost excitability
  39. 39Unfused tetanusOnly partial relaxation between stimuli
  40. 40Fused tetanussustained contraction with no relaxation between stimuli
  41. 41Result of Ca2+ remaining in sarcoplasmWave summation and both types of tetanus result from Ca2+ remaining in sarcoplasm
  42. 42Muscle ToneInvoluntary contraction of a small number of motor units (alternately active and inactive in a constantly shifting pattern). Does not produce movement, keeps muscles firm. Maintains posture and blood pressure.
  43. 43Isotonic contractionA load is moved. Concentric (muscle shortens) and eccentric (muscle lengthens) contractions.
  44. 44Isometric contractionNo movement occurs. Maintains posture and supports objects in fixed position.
  45. 45Red muscle fibersmore myoglobin, capillaries and mitochondria
  46. 46White muscle fibersLess myoglobin and capillaries
  47. 47Classification of Muscle Fibers1. Slow oxidative (slow-twitch) - prolonged sustained contraction for maintaining posture.
    2. Fast oxidative-glycolytic (fast-twitch A) - red. split ATP quickly, used for walking and sprinting.
    3. Fast glycolytic (fast-twitch B) - white. anerobic movements for short duration.
  48. 48Anabolic Steroidsincrease muscle size, strength and endurance. Many serious side effects, including liver cancer, kidney damage, heart disease, mood swings, facial hair and voice deepening in females and atrophy of testicles and baldness in males.
  49. 49Characteristics of smooth muscle- lack T tubules
    - have little SR for Ca2+ storage
    - no sarcomeres
  50. 50calmodulinreplaces troponin in smooth muscle
  51. 51What type of muscle can regenerate?smooth muscle
  52. 52What are the effects on aging on muscle tissue?1. Skeletal muscle starts to be replaced by fat beginning at 30
    2. Slowing of reflexes
    3. Decrease in maximal strength
    4. Change in fiber type to slow oxidative fibers may be due to lack of use or may be result of aging.
  53. 53Myasthenia GravisProgressive autoimmune disorder that blocks ACh receptors at NMJ. Treatment includes steroids and ach-esterase inhibitors
  54. 54Muscular Dystrophiesinherited x chromosome mutation in which degeneration of individual muscle fibers produces atrophy of skeletal muscle
  55. 55Abnormal ContractionsSpasm - involuntary contraction of single muscle
    Cramp - painful spasm
    Tic - involuntary twitching of muscles usually under voluntary control
    Tremor - rhythmic involuntary contraction of opposing muscle groups
    Fasciculation - involuntary, brief twitch of a motor unit visible under the skin
  56. 56Originbone that does not move when muscle shortens
  57. 57Insertionmovable bone
  58. 58TenosynovitisInflammation of tendon and associated connective tissues
  59. 59Effort/loadWork done by muscle contraction
  60. 60ResistanceWeight of body part and perhaps an object
  61. 61Fulcrumfixed point of motion (like elbow joint)
  62. 62First-class leverex: Neck
  63. 63Second - class leverResistance closer to fulcrum than effort
  64. 64What are the characteristics of Cardiac muscle?Striated
    Short
    Quadrangular-shaped
    Branching fibers
    Single centrally located nucleus Intercalated discs connect adjacent cells with gap junctions
  65. 65Why are anabolic steroids taken?increase muscle size, strength, and endurance, but with very serious side effects
  66. 66What are some differences between cardiac muscle and skeletal muscle?More sarcoplasm and mitochondria
    Larger T tubles
    Less well developed SR and limited intracellular Ca2+ reserves
    Prolonged delivery of Ca2+ to sarcoplasm, producing contraction that lasts 10-15 times longer than in skeletal muscle
  67. 67What are the two types of smooth muscle?Visceral (single unit)
    Multiunit
  68. 68What are the characteristics of smooth muscle?small, tapering cells
    involuntary
    single, oval, centrally located nucleus
    lack T tubules and have little SR
  69. 69Troponin is to Skeletal muscle as _________ is to smooth muscleCalmodulin
  70. 70What regulates smooth muscle contraction?- nerve signals from autonomic nervous system
    - changes in local conditions
    hormones
    - stress-relaxation response
  71. 71—

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Beschreibung
Exam 1 A & P I Karteikarten am Muscle, erstellt von Kristen C am 20/06/2016.
Erstellt von
Kristen C · Jun 2016
Aktualisiert
3 Feb 2018
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1
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