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fundamentals of hbk > day 11 - muscle anatomy + phys. > Flashcards

day 11 - muscle anatomy + phys. Flashcards

1
Q

heart “wants to” beat at BLANKbpm

A

100bpm

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2
Q

is skelital muscle striated or non-striated

A

striated

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3
Q

skelital muscles are under voluntary/involuntary control

A

voluntary (exept respiratory muscles are weird)

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4
Q

name the three types of muscle tissue

A

skelital muscle, cardiac muscle, smooth muscle

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5
Q

cardiac muscles are striated/smooth

A

striated

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6
Q

cardiac muscles are under voluntary/involuntary control

A

involuntary

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7
Q

smooth muscle is striated/non-striated

A

non-striated (smooth)

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8
Q

smooth muscle is voluntary/involuntary

A

involuntary

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9
Q

what type(s) of muscle cells are multinucleated

A

skelital muscles

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10
Q

what type(s) of muscle cells are not ultinucleated

A

cardiac + smooth muscle

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11
Q

action potential(s) can/cannot go through connective tissue

A

canNOT

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12
Q

in what type of muscle cell does an action potential travel as a wave accross the whole muscle (as opposed to action potentials effecting only one motor unit)

A

cardiac muscle

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13
Q

in skelital muscle, muscle fibers are structurally BLANK from neighboring fiber(s)

A

structurally INDEPENDANT

fibers contract without the fiber next to it contracting

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14
Q

neuromuscular junction (def)

A

synapse between a neuron and muscle fiber

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15
Q

what neurotransmitter is released at neuromuscular junction

A

ACh

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16
Q

what happens when ACh is released into a neuromuscular junction

A

ACh stimulates muscle fiber(s) by causing action potential

action potential starts cascade of events that causes contraction through that entire muscle CELL

muscle cell contracts, producing maximal force, until action potential is stopped (muscle cells are all or none force production)

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17
Q

force production of a full muscle contracting is due to BLANK

A

the amount of muscle fibers recruited NOT how hard the fibers are pulling – muscle fibers are all or none force production

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18
Q

muscle twitch (def)

A

contraction as the result of one action potential from a single stimulus

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19
Q

tetanus (def)

A

high frequency stimulation that leads to a sustained contraction

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20
Q

electromyography (def)

A

recording of electrical signals being sent to the muscle (NOT measuring what the muscle is actually doing)

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21
Q

myocyte (def)

A

muscle cell

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22
Q

sarcolemma (def)

A

muscle cell membrane

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23
Q

sarcoplasm (def)

A

muscle cell cytoplasm

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24
Q

connective tissue (def)

A

very strong supporting tissue(s)

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25
Q

what connective tissue connects bone to bone

A

ligaments

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26
Q

what connective tissue connects muscle to bone

A

tendons

27
Q

tendon (def)

A

connect muscle to bone and transfer force production from muscle to bone

28
Q

how is connective tissue organized in a muscle

A

connective tissue wraps around each indivdual muscle fiber in many layers then wraps around groups of muscle fibers and eventually wraps around whole muscle

connective tissue wraps extend past the end of the muscle fibers/last muscle fiber to connect to bone

29
Q

true/false: tendons are stuck onto the ends of muscles and attach muscle to bone

A

FALSE THEY ARNT JUST STUCK ON THE END THEY ARE WRAPPED

30
Q

tendons are vascular/avascular

A

avascular – take much longer than muscle to heal

31
Q

myofiliment (def)

A

structural proteins in muscle fibers that cause shortening

32
Q

myofiliment types

A

actin and myosin

33
Q

actin (def)

A

thin filament, double helix shape

has CA2+ binding site, when CA2+ binds it causes conformational change

34
Q

myosin (def)

A

thick filament, arm like cross bridges that firm strong bonds with actin when CA2+ is bound (conformational change makes it possible for myosin to get a good grip/strong bond w/actin)

35
Q

how many actin per each myosin

A

6 actin per one myosin

36
Q

sarcomere (def)

A

section of muscle, structural + functional unit of muscle cell

37
Q

how do you define a sarcomere

A

from one z-line to the next z-line

38
Q

explain the basic mechanism of muscle contraction

A

action potential occurs (due neural stimulation)

ACh released into the neuromuscular junction which causes the release of Ca2+ in the muscle cell from the sarcoplasmic reticulum

Ca2+ binds to binding site on acting, causing conformational change

myosin binds to actin after conformational change (can now get a good grip)

myosin pulls on actin toward the midline, z-lines become closer to eachother = sarcomeres shorten

39
Q

who developed the sliding filament theory

A

huxely

40
Q

sarcoplasmic reticulum (def)

A

organell that acts as a storage site for Ca2+ in muscle cells + sucks Ca2+ back in once neural stimulation ends

41
Q

step one in sliding filament theory (diagram)

A

energized, but weak bond (myosin in wrong position to pull)

42
Q

step two in sliding filament theory (diagram)

A

energized, Ca2+ binds to binding sites on actin = strong bond (myosin in position to pull)

43
Q

steps three + four in sliding filament theory (diagram)

A

myosin uses strong bond formed with actin and pulls

now un energized, and uncocked

44
Q

what happens to muscle contraction if there is no atp

A

always contracted (rigor mortis)

45
Q

best/most accepted theory of fatigue in muscles at a cellular level

A

H+ ions associated with lactate production may interfere with muscle contraction

46
Q

how do H+ ions possibly cause peripheral fatigue

A

H+ interferes with Ca2+ binding sites on actin and blocks Ca2+ from binding

H+ blocking Ca2+ = less force production = cant do another rep etc.

47
Q

central fatigue (def)

A

“i just dont want to do this anymore” even if one physically could

48
Q

periferal fatigue (def)

A

accumulation fatigue (accumulation of H+ due to lactate production)

muscle fatigue

49
Q

what type of muscle fibers have the most mitochondria

A

slow oxidative

50
Q

what type of muscle fiber is best at adaptation

A

FOG

51
Q

henneman size principle (def)

A

increased frequency/magnitude of stimulation will sum to reach threshold of more and faster fibers

52
Q

true/false: body will let you recruit all FG fibers but only after all SO and FOG fibers are also recruited

A

FALSE

your body will NEVER let you recruit all you FG fibers because then you would tear the muscle from the tendon

53
Q

fiber type and performance: elite power atheletes

A

ex. sprinters, jumpers, throwers, volleyball, american football, etc.

high percentage of FG fibers, up to 70%

54
Q

fiber type and performance: elite endurance atheletes

A

ex. distance running, nordic skiing, cyclists, triathletes, etc.

high percentage of SO fibers, up to 85%

55
Q

why do elite endurance atheletes have up to 85% SO fibers but elite power atheletes only have up to 70% FG fibers

A

because all postural muscles are SO and everyone has postural muscles so those get lumped in with the SO fibers in endurance atheletes althogh they dont actually have to do with thier sport and eveyrone has them

56
Q

fiber types and performance: regular people/the rest of us

A

have more ballanced mix of slow + fast fibers determined by genetics

can adapt, but there is genetic ceiling (not going to be elite)

muscle fibers can change characteristics (FOG look + act more like FG), but cannot actually change type

57
Q

adaptation of muscle fiber types to training: endurance (aerobic/oxidative) training

A
  • greatest adaptation in SO fibers (increased mitochondria)
  • can result in a shift in characteristics of FOG + FG fibers toward more oxidative capacity
  • possible increase in muscle size due to additional acting + myosin
58
Q

adaptation of muscle fiber types to training: resistance/high intensity (anaerobic/glycolydic) training

A
  • greatest adaptation in FG + FOG fibers (more phosphocreatine stores, greater increase in muscle size from additional actin + myosin)
  • can result in a shift in characteristics of SO + FOG fibers (more glycolidic capacity + increased muscle size)
59
Q

muscle fiber adaptation through overload (greater than normal physical stress)

A

causes microtears in fibers and trigger immune response including inflamation and formation of new proteins (DOMS)

60
Q

delayed onset muscle soreness (DOMS) steps

A

1) structural damage to muscle cells (microtears)

2) membrane damage

3) calcium leaks from sarcoplasmic reticulum

4) protease activated which results in breakdown of cellular proteins

5) inflammatory response

6) edema (swelling) and pain (particularly when moving bc swelling hits free nerve endings)

61
Q

overtraining (def)

A

accumulation of training stress that is detramental to ones health and performanceo

62
Q

overtraining symptoms

A
  • elevated HR at rest + at fixed work rate
  • physchological staleness
  • increased rate of illness
  • loss of appetite + decrease in bodyweight
  • decrease(s) in performance
63
Q

progression causes BLANK

A

hypertrophy (increase in cell size due to additional actin + myosin)

fundamentals of hbk (18 decks)

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