Muscles Flashcards

1
Q

3 types of muscle

A
  1. skeletal
  2. cardiac
  3. smooth
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2
Q

function of 3 types of muscle

A
  1. smooth = line organs and vessels
  2. cardiac = contract the heart
  3. skeletal = move/contract limbs
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3
Q

overall skeletal structure

A
  1. muscle fibre
  2. myofibrils (Thick = myosin, Thin = actin) (Thin contains = troponin and myosin) (Titin filamentous molecules) (surrounded by sarcolemma, t tubules in sarcolemma)
  3. sarcomere (z disc, m line, myofibrils, a band, I band, sarcoplasmic reticulum)

= long, striated fibres, multinuclear cells

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4
Q

describe the different parts of myofibrils

A
  1. Thick filaments (1500) = 2 molecules of heavy chain myosin with heads
  2. Thin filaments (3000) = 2 actin chains in alpha helix

Thin filaments contain:

  1. troponin= double stranded alpha helix protein
  2. tropomyosin = triad of 3 proteins

holding the filaments together:
Titian filamentous molecules

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5
Q

what does mutation in the titin filamentous molecules cause?

A

myopathy

early respiratory failure

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6
Q

describe the structure of the sarcomere (draw on paper if u have some nearby)

A

z discs separating each sarcomere - present in the I band
m line in the centre of the sarcomere - present in the A band
Thin actin filaments - present in the A and I band
Thick myosin filaments - present in the A band
sarcoplasmic reticulum surrounding the sarcomere

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7
Q

describe the band of the sarcomere

A

A band - thin actin and thick myosin filaments present (mainly thick = darker)
does not change size during contraction

I band - thin actin only (lighter)
shortens during contraction as the thin actin overlap more with the thick myosin filaments in the A band

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8
Q

describe skeletal contraction - excitation-contraction coupling (summary)

A
  1. ACh released at neuromuscular junction = depolarises end plate and sets of AP
  2. AP travels down sarcolemma and down t tubules in the triad (cistenae, t tubule, cisternae)
  3. depolarisation of t tubules causes voltage gated calcium channels to open = initiates a conformational change in the ryanodine receptors
  4. calcium ions released fro the sarcoplasmic reticulum cisternae
  5. calcium binds to troponin
  6. troponin removes tropomyosin from the actin binding sites on the thin filament so that the myosin heads of the thick filaments can attach to them
  7. cross bridges are formed = contraction so long as calcium is uptaken again
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9
Q

describe the formation of crossbridges

A
  1. ATP in the muscle bind to the head of the heavy chains of the thick filaments.
  2. This causes myosin to disengage from actin whilst the ATP is hydrolysed by the myosin head
  3. The myosin head pivots to be perpendicular to the thin filaments and form a cross bridge with an actin monomer that is 2 positions away
  4. Phosphate and ADP is released from myosin causing the head to then move by 45 degree. As such, actin is drawn past the myosin filaments. It is the hydrolysis of ATP that gives the head the energy to adopt the perpendicular position, and the release of phosphate that causes a conformational change in the myosin head.
  5. This conformational change propels the thin and thick filaments in opposite directions (thin towards the m line) and thus causes a contraction
  6. This repeats whilst calcium levels are elevated, and actin sites are available for cross bridges to form with the myosin
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10
Q

how are muscles relaxed?

A

ACh esterase stops EACh from triggering more action potentials and releasing more calcium

the calcium present is uptaken back into the sarcoplasmic reticulum by Ca2+ ATPase

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11
Q

describe the structure of cardiac muscle

A
  1. striated
  2. short, branched fibres
  3. intercalated disks instead of z lines = transmit mechanical forces
  4. gap junctions between intercalated disks = synchronised and faster
  5. t tubules = fewer but more prominent = more forceful movement as calcium can move between cells
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12
Q

function of cardiac muscle

A
  1. myogenic = involuntary contraction of the heart = controls its own contraction rate = hear rate
  2. many mitochondria so doesn’t fatigue
  3. uses stored and extracellular calcium to contract - Calcium ions which enter during the plateau phase of the action potential activate channels in the membrane to open more channels and let more calcium in
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13
Q

describe the structure of smooth muscle

A
  1. not striated (thick and thin filaments aren’t parallel), uninuclear
  2. dense bodies instead of z lines = they bind to actin via actinin
  3. no troponin (tropomyosin is present)
  4. cytoskeletal filaments present = transmit force
  5. less developed calcium stores
    a. visceral = sheets of cells with same innervation = connected by gap junctions like cardiac
    b. multi-unit = individually innervated
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14
Q

describe the function (contraction) of smooth muscle

A

no troponin = cross bridge formation is instead regulated by a protein called calmodulin

  1. The membrane depolarises. This causesvoltage-gated calcium channels to open and extracellular calcium ions diffuse into the cell
  2. calcium ions bind to calmodulin, forming the calcium-calmodulin complex.
  3. This activates myosin light chain kinase.
  4. MLC kinase activates the myosin heads by phosphorylating them as ATP is hydrolysed.
  5. myosin heads attach to actin-binding sites and pull on the thin filaments.
  6. These filaments are anchored to the dense bodies in the sarcoplasm. When thin filaments slide past the thick filaments, they pull on the dense bodies, causing the entire muscle fibre to contract.
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15
Q

DIAGRAM, CLINICAL AND EXPERIMENTAL
draw the diagrams of
1. a muscle fibre
2. a sarcomere

explain the clinical relevance of Titian filamentous molecules

no experimental

A

clinical = mutations can cause myopathy and early respiratory failure

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