josh musces - Flashcards

(42 cards)

1
Q

what are the three muscle types and list if the are volantary and striated.

A

skeletal - striated, volantary
smooth - not striated, involantary
cardiac - striated, involantary

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2
Q

decribe the flow of wraping of the muscle, begining with the mucle body and finishing at the protein fillaments (skeletal)

A

muscle body
->connective tissue wraps fascicle
-> groups of fibers
-> sarcolemma wraps muscle fiber
-> groups of myofibril
-> groups of protein filaments

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3
Q

what is the cytoplasm of the muscle fibre?

A

sarcoplasm

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4
Q

what is the sarcopasmic reticulum?

A

Specialized type of smooth ER that regulates the calcium ion concentration in the cytoplasm of skeletal muscle fibre

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5
Q

what are the transverse T tubules

A

The extensions of the cell membrane that penetrate into the centre of skeletal muscle fibres

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6
Q

a single sarcomere run from two lines, what are they

A

from Z line to Z line

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7
Q

what are the names of the thick and thin fillament

A

thick - myosin
thin - actin

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8
Q

describe the structure of the myosin

A

a thich band which have branches of myosin on the sides, these mysoin will bind to the actin fillament and cause contrations of the muscle.

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9
Q

describe the structure of the actin

A

actin is suronded by bands of tropomyosin (reguatory protein which overlaps the binding sites when rested) and troponin (regulatory protein which bind to myosin and actin using reverse binding to calcium.)

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10
Q

what are the three types of muscle twitchs and describe their diffrence of fuction

A

Slow twitch oxidative - Degrades glycogen in the Krebs cycle. This has high mitochondria count and high myoglobin.
Fast twitch oxidative - Degrades glycogen in the Krebs cycle. This has moderatly high mitochondria count and moderate myoglobin. as it can use glycolosis when needed.
Fast twitch glycolytic - Converts glycogen to lactic acid. Does not require oxygen, therefor it has low mitochondria and low myoglobin

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11
Q

describe the colour of the meat from the three twich types in muscles

A

slow oxidative - high myoglobin means it is very dark read, consider rumps and ‘bloody’ meats
fast oxidative - moderate myoglobin means it will have a dark tone, condier thigh and leg meat from chicken
fast glycolic - no myoglobin produces white meat, high in chicken breast

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12
Q

desrcibe the histology of the three muslce twitch types

A

slow oxidative - smallest diameter, which high enzymes activity, areobic
fast oxidative - share characteristic from both
fast glycolic - largest diameter, aneraobic.
the enzyme/ oxidative states will indicate how it will stain.

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13
Q

for each type of muscle twitch describe the real uses they have

A

slow oxidative - endurence based (long distance running), it has a slower fatuige
fast oxidative - mix of long term but still highly rapid action
fast glycolic -high burst of energy, (sprinting) focuses on rapid contractions/ relaxations, has poor fatiuge. short term

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14
Q

what are the two catergories of MRFs and they subfamilies

A

primary - MyoD and MYf5
secondary - myogenin, MRF4

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15
Q

what are MRF responsible for

A

Muscle regulatory factors
- induce commitment of myogenic lineage and myofiber differentiation
- postnatal myogenesis

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16
Q

list some growth factors important to muscles

A

insuin
Myostatin
TGF - Beta
FGF
Hepatocyte grief factor

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17
Q

describe insulins role in muscle growth

A

Central role in development, differentiation & maintenance of skeletal muscle
Produced by liver, myoblasts, satellite cells, myofibres & fibroblasts
its direct effects are:
Increases glucose & AA uptake
Decreased Proteolysis
Increases Protein synthesis

18
Q

describe myostatin effect on muscle growth

A

Plays a central role in physiological processes as a NEGATIVE regulator of muscle growth
Inhibits myogenic differentiation by inhibiting expression of myogenic transcription factors MyoD & myogenin
Naturally occurring mutation -> muscle hypertrophy “double muscling”

19
Q

describe FGF role in muscle growth

A

Fey role in early myoblast development
Proliferating myogenic cells, suppresses expression of MRFs, MyoD & myogenin
(if blocked we will have premature differentiation and decreased muscle weight)

20
Q

describe TGF- beta effect on muscle growth

A

Slows the proliferation of myoblasts & satellite cells
Inhibits expression of MyoD & myogenin

21
Q

describe the effects of hepatocyte growth factor

A

Autocrine and paracrine effects on myogenic cell lineage
Induces the initial conversion of mesenchymal cells to establish the somitic pool of myogenic precursors
Stimulate activation and early division of satellite cells

22
Q

what growth factor are involved in stem cells determination into myoblasts

23
Q

what growth factor transform myoblasts into myotubes. (inorder and labeled)

A

dermination - HGF
proliferation - TGF-Beta, IGF
differentiation IGF, myogenin/MFR4
fusion: IGF, HGF

24
Q

what growth factors are involved in myotubes formation into myofibers

A

Fusion and hypertrophy is controled by:
IGF, FGF, HGF

25
what regulative horomones are involved in muscle growth
Steroid and catecholamine derived Beta-agonists
26
what permissive hormones are involved in muscle growth
insulin, thyroid and glucocorticoids
27
what is insulins role and effect on muscle growth
regulate cellular glucose uptake (glycogen deposition). stimulates AA transport, protein synthesis and inhibits protein degrations during tissue growth. post nataly it will have an anabolic effect
28
if there is a defficency in insulin what occurs?
muscle wastage
29
what is thyroid horomes role and effect on muscle growth
muscle sythesis and sketetal muscle regulation. stimulate energy usage, oxidative metabolism and metabolic rate
30
what is adrenal glucocorticoids role and effect on muscle growth
inhibit growth Reduce glucose use by tissues Increases gluconeogenesis Induces hyperglycaemia Increases protein catabolism Inhibit secretion of GH and IGF, slowing growth
31
what happen if thyroid hormone is in excess and deficient
deficient - growth retardation excess - Protein degradation and muscle atrophy
32
what happens if there is a high dosage of adrenal glucocorticoids
muscle atrophy
33
when do most muscle fibres from?
during feotal development
34
postnatal hypertrophy of muscles are controlled by what
satellite cell proliferation
35
where are the muscle satellite cells kept post nataly
found at the basal lamina of mature myofibers, there are very samll amounts
36
what do satellite cells do any how
- muscle regeneration Satellite cells proliferate into myogenic cells that fuse & form new muscle fibres. They have the ability to replicate DNA, divide and fuse with adjacent fibres.
37
describe the proccess of muscle atrophy
when the rate of breakdown is higher than the rate of synthesis. Degradation of muscle protein results in decrease of myofibre cross sectional area Muscle nuclei are also lost during muscle atrophy degration is by: Calpain system Lysosomal system Proteasome pathway
38
where is muscle atrophy the most common
fast glycotic fibers
39
describe the process of muscle hypertrophy
Protein synthesis & degradation constantly occurring Rate of synthesis >> rate of breakdown = increased protein Rate of breakdown >> rate of synthesis = decreased protein Role of intracellular enzymes in maintaining balance between protein degradation & synthesis
40
what is the callipyge gene and how does it effect muscle
Callipyge gene: the presence of this gene in sheep results in skeletal muscle enlargement, most prominent in hindquarters. The callipyge gene results in overexpression of delta-like homologue 1 (Dlk1).
41
what id Dk1 and how does it cause mucle enlargment
Dlk1 is a cell membrane protein which activates pathways for satillite cells in tissues. overexression caused by the callipyge gene means that there will be an abnormal increase of satellite cells differention, increasing muscle mass.
42
what is Nutritional muscular dystrophy
known as white muscle disease / ridgid limb syndrome, the muscle exhibits white or grey areas of degeneration. This is due to the lipid oxidation (free radicals) induced damage to sarcoplasmic reticulum, this means the calcium is not separated anymore. This is caused by a selenium deficiency (Se), possibly combined with vitamin E. Se is crucial for the synthesis of glutathione peroxidase, which protects cells from free radicals.