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Neuro > Quiz 1 (Sep 8th Content) > Flashcards

Quiz 1 (Sep 8th Content) Flashcards

1
Q

Types of muscle

A

skeletal, cardiac, smooth

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2
Q

Characteristics of skeletal muscle

A

multinucleate, mitochondria, t-tubules, myofibrils, and sarcomeres, specific terms for intracellular structures

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3
Q

Specific terms for intracellular structures

A

sarcolemma = plasma membrane sarcoplasm = cytoplasm
sarcoplasmic reticulum = smooth ER

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4
Q

Connective tissue coverings

A

epimysium (large), perimysium (fascicles), endomysium (end)

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5
Q

Satellite cells (location & role)

A

located in the sarcolemma, regenerative cell growth, role in hypertrophy

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6
Q

Myofibrils

A

give striated appearance, arrangements of actin and myosin filaments

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7
Q

Myofibrils are made of

A

myosin & actin

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8
Q

Myosin is

A

thick

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9
Q

Actin is

A

thin

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10
Q

Tropomyosin

A

covers myosin binding sites on actin

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11
Q

Troponin

A

binds to tropomyosin and holds it over the myosin binding site

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12
Q

Skeletal muscle structure

A

muscle on bone, muscle, fascicle, myofibril, sarcomere, proteins

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13
Q

Study: Human Striated Muscle Ultrastructural changes accompanying increases in strength without hypertrophy –> Limitaion

A

Only study like this

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14
Q

Study: Human Striated Muscle Ultrastructural changes accompanying increases in strength without hypertrophy –> methods

A

2 biopsies prior to training, 1 after
Leg circumference, subcutaneous fat, leg ext strength
Five days/week for 10 weeks
Five reps 2/3 max leg ext & 5 max isometric contractions at 125º
20 round trips on stairs covering 3 floors
Remeasured for strength for new max loads

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15
Q

Study: Human Striated Muscle Ultrastructural changes accompanying increases in strength without hypertrophy –> results

A

No sig change in diameter of cells
Three sig measures: myosin filament concentration, distance between myosin filaments, # of actin around myosin
Change in ratio if unexplainable

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16
Q

Muscle Chemical Composition

A

75% water, 20% protein, 5% other

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17
Q

Neurotransmitter Release and Action (6 steps)

A
  1. AP reaches terminal
  2. Voltage-gated Ca channels open (Ca enters synaptic terminal and increases cytosolic Ca concentration)
  3. Ca eters terminal
  4. Release of ACh and diffuses into the cleft
  5. ACh binds to postsynaptic receptors
  6. ACh removed from synaptic cleft
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18
Q

Synaptic Transmission at NMJ (3 steps)

A
  1. Postsynaptic receptor (NAChR) allows diffusion of Na into the cell and K out
  2. Inactivation - ACh Esterase (AChE) is localized in folds of endplate and hydrolyses the ACh to choline and acetate
  3. Choline is taken back into the nerve terminal and is used to synthesize new ACh
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19
Q

Generation of action potentials

A

Current produced by EPP spreads to the surrounding muscle membrane

Local current depolarizes surrounding muscle membrane to a threshold and activates voltage-gated Na channels to produce action potentials

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20
Q

Voltage-dependent Ca channels located in

A

t-tubules

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21
Q

Activation of Ca release channels allows Ca to flow out of

A

cytosolic Ca into SR

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22
Q

Ca-ATPase in the SR membrane pumps out

A

cytosolic Ca into SR

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23
Q

Events of excitation-contraction coupling (6 steps)

A
  1. Action potential travels down into t-tubules
  2. Ca released from lateral sac
  3. Ca binds to troponin removing tropomyosin
  4. Cross-bridge binds and generates force
  5. Ca taken up
  6. Ca removal from troponin which restores tropomyosin
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24
Q

Sliding Filament Theory

A

Force generation produces shortening of skeletal muscle fiber, the overlapping of the thick and thin filament in each sarcomere propelled by movements of the cross-bridge

Ability of muscle fiber to generate force and movement depends on contractual proteins actin and myosin

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25
Q

A-band

A

thick

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26
Q

I-band

A

thin without thick

27
Q

H Zone

A

thick without thin

28
Q

Steps of Cross-Bridge Cycle (4)

A
  1. Cross bridge binds to actin
  2. Power stroke pulls actin toward the center of the sarcomere
  3. ATP binds to the myosin head and causes cross bridge to detach
  4. Hydrolysis of ATP energizes cross-bridge
29
Q

Role of ATP in Cross Bridge Cycle

A

Hydrolysis of ATP energizes the cycle
Binding of ATP breaks the linkage
No ATP means cross-bridge remains attached to actin producing rigor mortis

30
Q

Rigor Mortis

A

peaks 12 hours after death and disappears 48-60 hours after death due to breakdown of muscle

31
Q

Troponin’s three subunits

A

Inhibitory
Calcium-binding
Tropomyosin-binding

32
Q

Calcium binding sites are on

A

troponin

33
Q

Binding of calcium to the C subunit of troponin causes

A

conformational change of troponin which causes tropomyosin to move and expose myosin binding sites on actin

34
Q

As long as binding sites on actin remain exposed

A

cross-bridges will repeat and result in large displacements of the filaments

35
Q

SR

A

endoplasmic reticulum - like organelles that store calcium in skeletal muscle (and cardiac) muscle fibers

Surrounds myofibrils

36
Q

Lateral Sacs

A

enlargements at the end of ST and associated with t-tubules

37
Q

T-tubules

A

invaginations of muscle plasma membrane (sarcolemma)

38
Q

Sequence of Events in Activating Skeletal Muscle (13 steps)

A
  1. Activation of motor neuron cell body leads to action potential
  2. Action potential at the nerve terminal of a motor neuron causes the release of ACh at the neuromuscular junction
  3. ACh activated nicotine receptors in the endplate producing end-plate potential
  4. The end-plate potential depolarizes surrounding muscle membrane and produces an action potential
  5. Action potential propagates to the end of muscle fiber
  6. Action potential enters t-tubules and activates voltage-gated calcium channels
  7. Calcium is released from SR via calcium release channels
  8. Ca binds to troponin
  9. Tropomyosin moves to uncover myosin binding sites on actin
  10. Cross bridge cycling begins
  11. Calcium ATPase pumps calcium back into SR
  12. Calcium dissociates from troponin
  13. Tropomyosin covers myosin binding sites and cross-bridge cycling ends
39
Q

The plateau and descending limb of isometric/concentric force-length relationships are explained by

A

the amount of overlap between actin and myosin filaments

40
Q

When a muscle is stretched while activated and held at a final length long enough for force transients to cease, the steady force achieved is

A

always higher than steady force developed when the muscle is activated when held isometrically at the same final length

41
Q

When lengthened into a position you produce ______ force; after relaxing there is

A

greater; more tension in the muscle that was lengthened to get into position

42
Q

Force enhancement after active muscle stretching was maintained when muscles were

A

deactivated

43
Q

Passive force after deactivation of myofibrils was increased after

A

active stretching

44
Q

Passive force enhancement in muscle and fiber preparations occurs in

A

single myofibrils

45
Q

What is the main source of passive force in myofibrils it may be responsible for passive force enhancement in myofibrils

A

Titin

46
Q

Titin extends from ____________ & is fixed to the thick filament in the _______

A

sarcomere Z-disc to M band; A-band

47
Q

Titin runs freely in the

A

I-band region

48
Q

Skeletal muscles are activated by the release of

A

Ca from the SR

49
Q

Titin’s stiffness might be changed by

A

bringing calcium to specific attachment sites

50
Q

Stretching myofibrils results in

A

higher passive forces

51
Q

Passive structures of muscles are ____________ when passively stretched and become _____________ during active stretching

A

soft and compliant; hard and stiff

52
Q

Titin forces increase when _________ decreases

A

actin-myosin force

53
Q

Titin provides stability for sarcomeres on

A

descending limb of force-length relationship

54
Q

When titan is eliminated, all passive and active force transmission across sarcomeres is

A

lost

55
Q

Titin could increase its inherent stiffness upon activation and stretch by

A

binding calcium upon activation

56
Q

Titin could shorten its active spring length, becoming stiff, by

A

binding proximally to actin

57
Q

Training eccentrically is a longer energy demand for a

A

greater force output

58
Q

Genetics

A

Science focused on the transmission of traits of phenotypes across generations

59
Q

Quantitative traits such as _____________________ exhibit large inter-individual differences

A

total adiposity, heart size, or VO2max

60
Q

Evidence suggests there is a significant genetic component to human variation in

A

skeletal muscle strength and endurance

61
Q

Acute intervention data implies genes regulating translation initiation signaling influence progressive skeletal muscle hypertrophy in response to

A

RT

62
Q

Myostatin gene is expressed almost exclusively in cells of ___________ throughout embryonic development

A

skeletal-muscle lineage

63
Q

Systemic over-expression of the myostatin gene leads to a ________ characterized by extensive muscle loss

A

wasting syndrome

64
Q

A basic argument against generalized reliance on transgenic and/or knockout animals is that

A

rarely does a single gene control complex physiological systems

Neuro (2 decks)

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