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Human Anatomy & Kinanthropometry > C3 - HMS - Skeletal Muscle > Flashcards

C3 - HMS - Skeletal Muscle Flashcards

1
Q

Where is muscle derived from?

A

Embryonic mesoderm

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2
Q

What is a fascicle?

A

A bundle of muscle fibres within the perimysium (connective tissue)

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3
Q

What is a muscle?

A

Bundle of fascicles surrounded by the epimysium (connective tissue)

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4
Q

What is a cell with many nuclei described as?

A

Coenocytic (if nuclei results from mitosis)

Syncytium (if nuclei results from fusion of many cells)

((MUSCLE FIBRES ARE BOTH)

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5
Q

What are thick + thin myofilaments usually?

A

Thick - Myosin

Thin - Actin

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6
Q

How long roughly is a sarcomere?

A

3 micrometers

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7
Q

Do the lengths of actin and myosin change?

A

NO

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8
Q

SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION

What is the A band?

A

Entire length of Myosin so also a bit of Actin.

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9
Q

SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION

What is the I band?

A

Actin up to the start of myosin

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10
Q

SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION

What is the H zone?

A

JUST myosin

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11
Q

SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION

What happens to the A band?

A

Same length

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12
Q

SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION

What happens to the I band

A

Shortens

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13
Q

SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION

What happens to the H zone

A

Shortens

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14
Q

How do nervous impulses cause muscles to contract?

A

In a process called ‘excitation-contraction coupling’.

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15
Q

What is the molecular mechanism of muscle contraction described by?

A

Sliding filament theory

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16
Q

What is meant by a Neuromuscular Junction?

A

Where motor neurones synapse w/ muscle fibres.

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17
Q

Describe the motor end plate at a NM junction

A

Folded to give large SA

Has receptor proteins for Acetylcholine

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18
Q

Describe what happens when an AP arrives at a NM junction

A

Vesicles of NT acetylcholine are released into synaptic cleft to then diff. across to bind to receptor proteins on motor end plate = Na+ channels to open = DEPOLARISES sarcolemma.

Sarcolemma carries depolarisation AWAY to the rest of the myofibril.

The ‘T tubule’ carries depolarisation deep into microfibril.

Sarcoplasmic reticulum releases Ca2+ = muscular contraction.

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19
Q

When does the sequence of the sliding filament theory repeat until?

A

Until the Ca2+ ions (ions that expose the myosin binding sites on the actin) are all actively pumped back into the sarcoplasmic reticulum.

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20
Q

Give an example of slow twitch (Type 1) muscles in humans

A

Back muscles + soleus muscle have about 80% slow twitch fibres.

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21
Q

Give an example of fast twitch (Type 2) muscles in humans

A

Eye muscles have about 85% fast twitch fibres.

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22
Q

Physiological features of slow twitch muscle fibres

A

Contract slowly

Contract for longer time before relaxing

Longer time before fatigue

23
Q

Give 2 myofibril features of fast twitch muscle fibres

A

Few mitochondria

High density of myofibrils

24
Q

Describe the respiration of slow twitch muscle fibres

A

Aerobic

High density of capillaries to deliver O2

Little glycogen as blood brings glucose

High conc. of myoglobin so O2 available even at low O2 pp.

Little lactate made

25
Q

Describe the respiration of fast twitch muscle fibres

A

Anaerobic

Low density of capillaries as little O2 needed

High glycogen store to generate glucose for glycolysis.

Low conc. of myoglobin as no need for O2 store.

Lactate removed quickly by oxidation to pyruvate or reversion to glucose.

26
Q

Colour difference of muscle fibre types

A

Slow twitch = Dark due to rich blood supply + high myoglobin con.

Fast twitch = Light due to little blood + low myoglobin conc.

27
Q

What are the 2 types of fatigue?

A

Neural (when nerves initiating contraction can’t generate a sustained signal)

Metabolic (i.e shortage of substrates to provide energy, i.e glucose OR accumulation of metabolites i.e lactate)

28
Q

Define a cramp

A

A severe, involuntary muscle contraction that can occur in striated or non-striated muscle.

29
Q

How can skeletal muscle cramps be caused?

A

By fatigue as the lactate build up can inhibit the Cl- effect but not the K+ effect, so muscles would tend to contract, leading to cramp.

30
Q

What does the amount of muscle glycogen store depend on?

A

Physical training

Basal metabolic rate

Eating habits

31
Q

How can ‘Hitting the wall’ be avoided? (3)

A

High glycemic index foods

Endurance training so that slow twitch muscle fibres become more efficient + use fats rather than glycogen for energy.

CHO loading

32
Q

Why is fat harder to transport in the blood than glycogen?

A

Non-polar and the oxidation of fat reserves requires more O2 than the oxidation of glycogen.

33
Q

Physiologists conducting experiments used tissue from the same organism. Suggest factors that would need to be controlled.

A

Temp of solution.

pH of solution

Conc. of solution

Same muscle type.

34
Q

Why might no tension be generated

A

Because the actin + myosin filaments don’t overlap so no cross-bridges can form to enable contraction.

35
Q

State 3 roles of ATP in muscle contraction

A

Actively pumps Ca2+ back into sarcoplasmic reticulum = muscle relaxes

ATP binds to myosin heads = erect high energy state.

Release of energy from hydrolysis of ATP causes change in shape of myosin cross bridge, resulting in a bending action = POWER STROKE

36
Q

Where do calcium ions come from?

A

Sarcoplasmic reticulum, from ‘T’ tubules

37
Q

What is the role of calcium ions?

A

Bind to troponin + change shape = tropomyosin changes position.

= Exposing myosin binding sites on actin.

= Heads on myosin can now attach too actin.

38
Q

What is the mechanism of muscle contraction called?

A

Ratchet mechanism

39
Q

What is myosin’s functional role in muscle movement

A

Has moveable head that provides a power stroke when activated.

40
Q

Rigor mortis is a state of partial contraction of the muscle that occurs after death. During rigor mortis, the muscles are locked and the body is stiff.

Suggest why muscle enters this state

A

Because there’s no longer ATP to provide energy to change the shape of the myosin cross bridge.

41
Q

What is the process in the sliding filament hypothesis

A

Actin binding sites are blocked by tropomyosin + troponin.

B4 muscle contraction, ATP binds to myosin heads = erect high energy state.

Arrival of AP = release of Ca2+ from sarcoplasmic ret.

Ca2+ binds to troponin + causes blocking molecules to move so that myosin binding sites on actin are exposed.

Myosin heads attach to binding sites on actin filament.

Release of energy from hydrolysis of ATP causes change in shape of myosin cross bridge, resulting in a bending action = POWER STROKE

== actin fil. slide past myosin fil.

New ATP attached to myosin, releasing them from binding sites + reprising them for repeat movement. They become attached further along actin chain as long as ATP + Ca2+ are available.

42
Q

What does muscle contraction require?

A

Ca2+ and ATP

43
Q

Define synergists

A

Muscles that assist the agonist + may be involved in the fine-tuning of the direction of the movement.

44
Q

What is the Muscle spindle?

Where can it be found?

A

A stretch receptor located in skeletal muscle, parallel to muscle fibres.

45
Q

What does the muscle spindle do?

A

Stimulated in response to sustained or sudden stretch on the central region of its specialised intrafusal fibres.

Sensory info from muscle spindle is relayed to spinal cord.

Motor response adjusts degree of stretch of the muscle. = Help in coordination + efficiency of contr.

46
Q

Why are muscle spindles important?

A

Maintenance of muscle tone, postural reflexes + movement control.

47
Q

What is the role of PC in providing energy for muscle contraction?

A

Produces ATP

48
Q

Are slow twitch muscle fibres found near the surface or deeply situated?

A

Deeply situated

49
Q

Damaged muscle fibres have an increased mRNA conc. and a higher rate of O2 consumption, at rest, than undamaged muscle fibres.

Explain the increased mRNA conc.

A

Proteins need repairing so protein synthesis is required.

== More transcription + translation i.e pf troponin or myosin

50
Q

Damaged muscle fibres have an increased mRNA conc. and a higher rate of O2 consumption, at rest, than undamaged muscle fibres.

Explain the higher rate of O2 consumption

A

Rest = aerobic resp which requires O2 so more ATP produced.

= For condensation formation of peptide bond formation of extra mRNA

51
Q

How does the body provide the muscle with more O2 to meet increased O2 consumption?

A

⬆️ HR, breathing + ventilation rate

Vasoconstriction/dilation

52
Q

What is the effect of the increase in lactate levels in the muscle?

A

⬆️ acidity = contractile proteins become less sensitive to Ca2+ = ⬇️ ability to contract

53
Q

Suggest why during prolonged exercise, i.e marathon, the blood urea conc increases

A

aa are deaminated in liver == ammonia is converted to urea whilst remainder is used in respiration as another source of energy

Human Anatomy & Kinanthropometry (27 decks)

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