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A-Level Biology A2 > Nervous Coordination > Flashcards

Nervous Coordination Flashcards

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1
Q

What happens to neurone cell membranes at rest?

A

They are polarised.

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2
Q

What charge is the membrane outside when the neurones in its resting state and why?

A

Positively charged because there is more positive ions outside the cell than inside.

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3
Q

Why is the membrane polarised at rest

A

due to the outside being postively charged compared to the inside

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4
Q

what does polarised mean?

A

there’s a difference in charge (potential difference/ voltage) across it.

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5
Q

What is the voltage across the membrane when it’s at rest called?

A

the resting potential

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6
Q

What is the voltage/ resting potential at rest across the membrane?

A

-70mV

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7
Q

What is the resting potential created and maintained by?

A
  1. Sodium potassium pumps
  2. Potassium ion channels
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8
Q

What does the sodium-potassium pump do?

A

Moves sodium ions out of the neurone, but they can’t diffuse back in due to the membrane not being permeable to sodium ions. That creates a sodium ion electrochemical gradient because there are more positive sodium ions outside the cell than inside.

Move potassium ions in to neurone but the membrane is permeable to potassium ions so they diffuse back out through potssium ion channels.

These pumps use active transport to move 3 sodium ions out of the neurone for every two potassium moved in. ATP is needed to do this.

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9
Q

What are three types of transport protein?

A
  1. The sodium-potassium pumps
  2. Potassium ion channel
  3. Sodium ion channel
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10
Q

When neurone cell membranes are stimulated what happens?

A

It becomes depolarised

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11
Q

What does a stimulus trigger

A

Ion channels, called sodium ion channels, to open

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12
Q

If the stimulus is big enough, what does it do?

A

Triggers a rapid change in potential difference which causes the cell membrane to become depolarised

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13
Q

What is the action potential?

A

The sequence of events caused if the stimulus is big enough to trigger a rapid change in potential difference.

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14
Q

What does the sodium potassium pump use

A

active transport to move 3 sodium ions out of the neurone for every two potassium moved in. ATP is needed to do this.

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15
Q

What does the potassium ion channel use/ allow

A

Facilitated diffusion of potassium ions out of the neurone, down their conc. gradient.

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16
Q

Explain the changes in potential difference during action potential

A
  1. Stimulus - excites neurones cell membrane, causing sodium ion channels to open. The membrane becomes more permeable to sodium, so sodium ions diffuse into neurone down the sodium ion electrochemical gradient. That makes the inside of the neurone less negative.
  2. Depolarisation - if the potential difference reaches the threshold (around -55mV), more sodium ion channels open. More sodium ions diffuse rapidly into the neurone.
  3. Repolarisation - At a potential difference of around +30mV, the sodium ions channels close and potassium ions channels open. The membrane is more permeable to potassium so potassium ions diffuse out of neurone down the potassium ion concentration gradient. It starts to get the membrane back to its resting potential.
  4. Hyperpolarisation - Potassium ion channels are slow to close/ are still recovering so there’s a slight overshoot where too many potassium ions diffuse out of the neurone. The potential difference becomes more negative than the resting potential. They can’t be excited straight away after an action potential.
  5. Resting potential - The ion channels are reset. The sodium potassium pump returns the membrane to its resting potential and maintains it until the membranes excited by another stimulus
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17
Q

What happens after an action potential?

A

The neurone cell membrane can’t be excited again straight away because the channels are recovering and can’t be made to open - sodium ion channels are closed during repolarisation and potassium ions close during hyperpolarisation.

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18
Q

What is the refractory period?

A

The period of recovery.

The neurone cell membrane can’t be excited again straight away because the channels are recovering and can’t be made to open - sodium ion channels are closed during repolarisation and potassium ions close during hyperpolarisation.

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19
Q

What acts as a time delay?

A

The refractory period

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20
Q

What does the refractory period act as?

A

The time delay between one action potential and the next, making sure action potentials don’t overlap but pass along as discrete impulse.

Means there’s a limit to the freq. at which the nerve impulse can be transmitted.

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21
Q

How does the action potential move along the neurone?

A

As waves of depolarisation.

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22
Q

How do the sodium ions diffuse when an action potential happens?

A

They diffuse sideways

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23
Q

Explain the waves of depolarisation

A
  1. Sodium ion channels in the next region of the neurone opens up and sodium ions diffuse into that part.
  2. That causes a wave of depolarisation to travel along the neurone.
  3. The waves move away from the parts of the membrane in the refractory period because these parts can’t fire an action potential.
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24
Q

What does the refractory period produce?

A

Discrete impulses

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25
Q

What happens during the refractory period?

A

Ion channels are recovering and can’t be opened.

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26
Q

What does it mean when the refractory period acts as a time delay?

A
  1. Action potentials don’t overlap but pass along as discrete impulses.
  2. There’s a limit to the frequency at which the nerve impulses can be transmitted.
  3. Action potentials are unidirectional.
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27
Q

What nature does action potentials have?

A

An all-or-nothing nature

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28
Q

What happens once a threshold is reached?

A

An action potential will always fire with the same change in voltage.

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29
Q

If the threshold isn’t reached what wn’t happen?

A

An action potential won’t fire. That’s the all or nothing nature.

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30
Q

What does a bigger stimulus cause?

A

Causes an action potential to fire more frequently. Doesn’t cause a bigger action potential.

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31
Q

What are the three factors affecting the speed of conduction of action potential?

A
  1. Myelination
  2. Axon diameter
  3. Temperature
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32
Q

How does myelination and saltatory conduction affect the speed of conduction of action potentials?

A
  1. Some neurones are myelinated - they have a myelin sheath.
  2. The myelin sheath is an electrical conductor.
  3. In the peripheral nervous system, the sheath is made up of a type of cell called schwann cell.
  4. Between the schwann cells are tiny patches of bare membrane called the nodes of ranvier. Sodium ion channels are concentrated at the nodes.
  5. In a myelinated neurone, depolarisation only happens at the nodes of ranvier.
  6. The neurones cytoplasm conducts enough electrical charge to depolarise the next node, so the impulse jumps from node to node.
  7. That is called saltatory conduction and it’s really fast.
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33
Q

What is non-myelinated neurone?

A
  1. In a non-myelinated neurone, the impulse travels as a wave along the whole length of the axon membrane. So you get depolarisation along the whole length of the membrane.
  2. This is slower than saltatory conduction.
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34
Q

What type of cell is the sheath made up?

A
  1. In the peripheral nervous system, the sheath is made up of a type of cell called schwann cell.
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35
Q

What is between the schwann cells?

A
  1. bare membrane called the nodes of ranvier.
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36
Q

How does axon diameter affect the speed of conductions of action potentials?

A
  1. Action potentials are conducted quicker along axons with bigger diameters due to less resistance to the flow of ions than in the cytoplasm of a smaller axon.
  2. With less resistance, depolarisation reaches other parts of the neurone cell membrane quicker.
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37
Q

How does temperature affect the speed of conduction of action potential?

A

The speed of conduction increases as the temperature increases too, because ions diffuse faster.

The speed only increases up to around 40oC. If it was hgher the proteins would denature and the speed decreases.

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38
Q

What is a synapse?

A

A junction between a neurone and the next neurone, or between a neurone and an effector cell i.e. muscle or gland.

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39
Q

What is a synaptic cleft?

A

The tiny gap between the cells at a synapse

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40
Q

What does the presynaptic neurone have?

A

A synpatic knob

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41
Q

What does the synaptic knob contain?

A

Neurotransmitters

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42
Q

What happens when an action potential reaches the end of a neurone?

A

Neurotransmitters are released into the synaptic cleft. They diffuse across to the postsynaptic membrane and bind to specific receptors.

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43
Q

When are muscle contraction or hormones secreted?

A

When a neurotransmitter bind to the receptors as they might trigger an action potential.

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44
Q

Why/ how are impulses unidirectional (only travel in one direction)?

A

Because the receptors are only on the postsynaptic membrane so synapses makes them unidirectional.

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45
Q

Why are neurotransmitters removed from the cleft?

A

so the response doesn’t keep happening. They’re taken back into the presynaptic neurone or they’re broken down by enzymes.

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46
Q

What are synapses called that use acetylcholine?

A

Cholinergic synapses

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47
Q

Where does ACh transmit the nerve impulses across?

A

A cholinergic synapses.

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48
Q

How are nerve impulses transmitted across a cholingeric synapse?

A
  1. An action potential arrive at synaptic knob of the presnaptic neurone.
  2. The action potential stimulates voltage-gated calcium ion channels in the presynaptic neurone to open.
  3. Calcium ions diffuse into the synaptic knob.
  4. The influx of calcium ions into the synaptic knob causes the synaptic vesicles to move to the presynaptic membrane. They then fuse with the presynaptic membrane.
  5. The vesicles release the neurotransmitter acetylcholine (ACh) into the synaptic cleft - exocytosis.
  6. Ach diffuses acrosss the synaptic cleft and binds to specific cholingeric receptors on the postsynaptic membrane.
  7. Sodium ion channels open in the postsynaptic membrane.
  8. The influx of sodium ions into the postsynaptic membrane causes depolarisation.
  9. An action potential on the postsynaptic membrane is generated if the threshold is reached.
  10. ACh is removed from the synaptic cleft so the response doesn’t keep happening. It’s broken down by an enzyme called AChE (acetylcholinesterase) and the products are re-absorbed by the presnaptic neurone and used to make more ACh.
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49
Q

Explain excitatory neurotransmitters

A
  • Depolarise the postsynaptic membrane, making it fire out an action potential if a threshold is reached.
  • i.e. ACh is an ex. neuro. at cholinergic synapses in the CNS - it binds to cholinergic receptors to cause an action potential in the postsynaptic membrane and at a neuromuscular junction.
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50
Q

Explain inhibitory neurotransmitters

A
  • Hyperpolarise the postsynaptic membrane, making potential difference more negative, preventing it from firing an action potential.
  • i.e. ACh is an inhib. neuro. at cholinergic synapses in the heart. When it binds to receptors here, it can cause potassium ion channels to open on the postsynaptic membrane, hyperpolarising it.
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51
Q

What is an inhibitory synapse?

A

A synapse where inhibitory neurotransmitters are released from the presynaptic membrane following an action potential.

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52
Q

If a stimulus is weak, how much neurotransmitter is released?

A

Small amount which might not be enough to excite the postsnyaptic membrane to the threshold level and stimulate an action potential.

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53
Q

What is summation?

A

Where the effect of neurotransmitter released from many neurones (or one neurone that’s stimulated a lot in a short period of time) is added together.

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54
Q

What are the two summations?

A
  • Spatial summation
  • Temporal summation
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55
Q

What is spatial summation?

A
  • Many neurones connect to one neurone.
  • The small amount of neurotransmitter released from each of the neurones can be enough altogether to reach a threshold in postsyn. and trigger an action potential.
  • If some neurones release inhibitatory neurotransmitters then the total effect of all the neurotransmitter might be no action potential as hyperpolarise the postsynaptic mem.
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56
Q

What is temporal summation?

A
  • Where two or more nerve impulses arrive in quick succession from the same presynaptic neurone.
  • Makes an action potential more likely because more neurotransmitter is released into the synaptic cleft.
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57
Q

How is information accurately processed?

A

Having both types of summation

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58
Q

What are neuromuscular junction?

A

Synapses between a motor neurone and muscle cell.

59
Q

What neurotransmitter does neuromuscular junctions use?

A

ACh

60
Q

What do ACh bind to?

A

Nicotinic cholinergic receptors

61
Q

Difference between cholinergic synapse and neuromuscular junction

A
  1. The postsynaptic membrane has lots of folds that form clefts. They store the enzyme that breaks down ACh.
  2. The postsynaptic membrane has more receptors than cholinergic synapses.
  3. ACh is always excitatory at a neuromuscular junction. So when a motor neurone fires an action potential, it triggers a response in a muscle cell.
62
Q

What affects the action of neurotransmitters at synapses?

A

Drugs

63
Q

What is the effect of a drug if it’s the same shape as neurotransmitters?

A

They mimic their action at receptors (agonists drugs).

So more receptors activated

i.e. nictoine mimics acetylcholine so binds to nicotinic cholinergic receptors in the brain.

64
Q

agonists drugs

A

mimics their action at receptors activating more receptors

65
Q

What is the effect of a drug that blocks the receptors?

A

They can’t be activated by neurotransmitters (antagonists).

Fewer receptors can be activated.

i.e. curare blocks effects of acetylcholine by blocking the nicotinic cholinergic receptors.

Results in muscle being paralysed.

66
Q

What is the effect of drugs that inhibits the enzyme that breaks down a neurotransmitter?

A

More neurotransmitters in the synaptic cleft to bind to receptors and they’re there for longer.

i.e. nerve gases stop acetylcholine from being broekn down in the synaptic cleft.

Leads to loss of muscle control.

67
Q

What is the effect of drugs that stimulate the release of neurotransmitter from presynaptic neurone?

A

More receptors are activated i.e. amphetamines.

68
Q

What is the effect of drugs that inhibit the release of neurotransmitters from the presynaptic neurone?

A

Fewer receptors are activated i.e. alcohol.

69
Q

Why are calcium ions important in synaptic transmission?

A

Action potentials open calcium channels in the membrane of the synaptic knob, which causes an inward movement of calcium ions .

Calcium ions trigger the release of neurotransmitter from synaptic vesicles into the synaptic cleft.

70
Q

What do muscles act as?

A

antagonistic pairs

71
Q

Skeletal muscle

A

Type of muscle you use to move

Attached to bones by tendons

72
Q

What do ligaments do

A

attach bones to other bones to hold them together

73
Q

what holds bones together

A

ligaments

74
Q

How to skeletal muscles move bones at joints

A

they contract and relax

75
Q

What does it mean when it says bones are incompressible

A

rigid

76
Q

What do bones act as

A

levels, giving the muscles something to pull against.

77
Q

What are contracting muscles known as

A

agonist

78
Q

Agonist

A

Contracting muscles

79
Q

What are relaxing muscles called?

A

Antagonist

80
Q

Antagonist

A

Relaxing muscles

81
Q

What are the bones of your lower arm attached to?

A

bicep muscles and tendon muscles by tendons

82
Q

What happens when your biceps contract?

A

Triceps relex.

That pulls the bone so your arm bends (flexes) at the elbow.

The biceps is the agonist and triceps is antagonist.

83
Q

What happens when your triceps contract?

A

Biceps relaxes.

This pulls the bone so your arm straightens (extends) at the elbow.

Triceps are agonist and biceps are antagonist.

84
Q

What are skeletal muscles made up of?

A

Long muscle fibres

85
Q

What is the cell membrane of muscle fibre cells called

A

sarcolemma

86
Q

The folds are called?

A

Transverse tubules

87
Q

What do transverse tubules help?

A

To spread electrical impulses throughout the sarcoplasm so they’ll reach all parts of the muscle fibres.

88
Q

Where do sarcoplasmic reticulum run through

A

the sarcoplasm

89
Q

What does the sarcoplasmic reticulum store and release?

A

Calcium ions that are needed for muscle contraction

90
Q

What do muscle fibres have?

A

lots of mitochondria to provide the ATP that’s needed for muscle contraction.

long, cylindrical organelles called myofibrils.

Made up of proteins and are highly specialised for contraction.

91
Q

What are muscle fibres known as

A

multinucleate

92
Q

What do myofibrils contain

A

thick myosin filaments and thin actin filaments

93
Q

What are thick myofilaments made up of

A

myosin protein

94
Q

What are thin myofilaments made up of

A

actin protein

95
Q

What do you see if you look at a myofibril under an electron microscope

A

dark and light bands

96
Q

What do dark bands contain?

A

The thick myosin filaments and some overlpaping thin actin filaments - A-bands

97
Q

A-bands

A

contain thick myosin filaments and some overlpaping thin actin filaments

98
Q

What are light bands

A

Contain thin actin filaments only

I-bands

99
Q

I-bands

A

light bands

thin actin filaments

100
Q

What is a myofibril made up of

A

many short units called sarcomeres

101
Q

The ends of each sarcomere are marked with a..

A

Z-line

102
Q

What is the middle of each sarcomere called

A

M-line

103
Q

what is the M-line

A

The middle of the myosin filament.

104
Q

What does the H-zone contain

A

only the myosin filaments

105
Q

How is muscle contraction explained

A

By the sliding filament theory

106
Q

What makes the sarcomeres contract

A

Myosin and actin filaments sliding over each other

107
Q

The simultaneous contraction of lots of sarcomeres means the _____ and ______ _____ contract

A

myofibrils

muscle fibres

108
Q

What happens as the muscles relax

A

the sarcomeres return to their orginial length

109
Q

Explain the sliding filament theory

A
  1. Myosin and actin filaments slide over each other to make sarcomeres contract. The myofilaments themselves don’t contract.
  2. The simultaneous contraction of lots of sarcomeres means the myofibrils and muscle fibres contract.
  3. As muscles relax sarcomeres return to their original length.
110
Q

What bands change size/ get shorter when the sarcomere contracts?

A

I-bands get shorter

H-zones get shorter

111
Q

What happens to the sarcomeres when it contracts

A

Gets shorter

112
Q

What band stays the same when the sacromere contracts

A

A-band, stays the same length

113
Q

What move back and forth on the myosin filaments

A

globular heads as they’re hinged

114
Q

What does each myosin head have?

A

A binding site for actin

A binding site for ATP

115
Q

What do actin filaments have?

A

actin-myosin binding sites

116
Q

Where is tropomyosin found

A

bewteen actin filaments

117
Q

what do tropomyosin help?

A

myofilaments to move past each other

118
Q

What are binding sites in resting muscles blocked by?

A

Tropomyosin

119
Q

What happens in a resting muscle

A

the actin myosin binding site is blocked by tropomyosin

120
Q

What happens due to the actin myosin binding site being blocked

A

Myofilaments can’t slide past each other because the myosin heads can’t bind to the actin myosin binding site on the actin filament

121
Q

Explain the process of muscle contraction

A
  1. When an action potential from a motor neurone stimulates a muscle cell, it depolarises the sarcolemma. Depolarisation spreads down the T-tubules to the sarcoplasmic reticulum.
  2. That causes the sarcoplasmic reticulum to release stored calcium ions (Ca2+) into the sarcoplasm.
  3. Calcium ions bind to a protein attached to tropomyosin, causing the protein to change shape. This pulls the attached tropomyosin out of the actin-myosin binding site on the actin filament.
  4. This exposes the binding site allowing myosin head to bind.
  5. The bond formed when a myosin head binds to an actin filament is called actin myosin cross bridge.
  6. Calcium ions also activate the enzyme ATP hydrolase which hydrolyses ATP to proivde the energy needed for muscle contraction.
  7. The energy released from ATP causes the myosin head to bend which pulls the actin filament along in a rowing action.
  8. Another ATP molecule provides the energy to break the actin-myosin cross bridge, so the myosin head detaches from the actin filament after its moved.
  9. The myosin head reattaches to a different binding site further along the actin filament. A new actin-myosin cross bridges is formed and the cycle is repeated.
  10. Many cross bridges form and break very rapidly pulling the actin filament along - which shortens the sarcomere, causing the muscle to contract.
  11. The cycle will continue as ling as calcium ions are present.
122
Q

When excitation stops, what leaves?

A

Calcium ions leave

123
Q

Explain what happens when muscles returning back to resting state

A
  1. When muscles stop being stimulated, calcium ions leave their binding sites and are moved by active transport back into the sarcoplasmic reticulum (needs ATP).
  2. That causes the tropomyosin molecules to move back so they block the actin-myosin binding sites again.
  3. Muscles aren’t contracted because no myosin heads are attached to actin filaments (so no actin myosin cross bridges).
  4. Actin filaments slide back to their relaxed position which lengthens sarcomere.
124
Q

What provides the energy for muscle contraction?

A

ATP

Phosphocreatine

125
Q

Why does ATP need to be continually generated?

A

So excercise can continue.

126
Q

What are the three different ways ATP is generated?

A
  1. Aerobic respiration
  2. Anaerobic respiration
  3. ATP-Phosphocreatine (PCr) system
127
Q

Explain how ATP is regenerated through aerobic respiration

A
  1. Via. oxidative phosphorylation in cell’s mitochondira.
  2. Aerobic respiration only works when there’s oxygen so it’s good for long periods of low-intensity excerise.
128
Q

Explain how ATP is regenerated through anaerobic respiration

A
  1. ATP made rapidly by glycolysis.
  2. The end product of glycolysis is pyruvate, which is converted to lactate by lactate fermentation.
  3. Lactate can quickly build up in the muscles and cause muscle fatigue.
  4. Anaerobic respiration is good for short periods of hard excercise.
129
Q

Explain how ATP is regenerated through ATP-Phosphocreatine (PCr) system

A
  1. ATP made by phosphorylating ADP, adding a Pi group taken from PCr.
  2. ADP + PCr -> ATP + Cr
  3. PCr stored inside cells and ATP-PCr system generates ATP quickly.
  4. Runs out after a few seconds so used for short bursts or vigorous excercise.
  5. Some PCr getrs broken down into creatinine which is removed from the body via. the kidneys.
130
Q

When are creatinine levels higher?

A

In people who

  1. Excercise regulary
  2. High muscle mass
  3. Possibly have kidney damage
131
Q

What twitches are skeletal muscles made up of

A

fast and slow twitch

132
Q

State the differences between slow (1) and fast (2) twitch skeletal muscle fibres

A
  1. In slow twitch muscle fibres they contract slowly.
  2. In fast twitch muscle fibres contract very quickly.
  3. Slow twitch - muscles you use for posture i.e. those in the back, have a high proportation of them.
  4. Fast twitch - muscles you use for fast movement i.e. eyes and legs have higher proportion.
  5. Good for endurance activities
  6. Good for short bursts of speed and power
  7. Can work for a long time without getting tired
  8. Get tired very quickly
  9. Energy is released slowly throughout aerobic respiration. Lots of mitochondira and blood vessels supply the muscles with oxygen.
  10. Energy is released quickly throughout anaerobic respiration using glycogen. There are few mitochondria or blood vessels.
  11. Reddish in colour because they’re rich in myoglobin.
  12. Whitish in colour because they don’t have much myoglobin.
133
Q

Damage to the myelin sheaths of neurones can lead to problems controlling the contraction of muscles.

Suggest one reason why.

A
  1. Action potentials travel more slowly / don’t travel;
  2. So delay in muscle contraction / muscles don’t contract / muscles contract slow(er);
134
Q

Both slow and fast muscle fibres contain ATPase.

Explain why.

A
  1. Splitting / breakdown / hydrolysis of ATP;
  2. (Muscle) contraction requires energy / ATP
  3. Use of ATP by myosin.
135
Q

The tissue in the diagram came from muscle with a high proportion of brown-staining fibres. Was the tissue removed from slow or fast skeletal muscle?

Explain your answer.

A
  1. Fast because (lots of) ATPase allows rapid hydrolysis of ATP
  2. Slow because (lots of) ATPase allows rapid synthesis of ATP.
136
Q

What is the evidence that it had been stained for viewing with an optical (light) microscope? Explain your answer.

A
  1. Need light to see colour / brown / yellow;
  2. Cannot see colour / brown / yellow with electrons / an electron microscope;
137
Q

One form of muscle disease is caused by a mutated allele of a gene. This leads to production of myosin molecules that are unable to bind to other myosin molecules.

If myosin molecules are unable to bind to other myosin molecules, this prevents muscle contraction.
Use the diagram and your knowledge of how muscles contract to suggest why.

A
  1. Can’t form myosin / thick filaments;
  2. Can’t pull / can’t move actin / slide actin past / (myosin) have to be joined / fixed to pull actin;
  3. Myosin moves / if attached doesn’t move;
  4. Can’t move actin towards each other / middle of sarcomere / between myosin / can’t shorten sarcomere / can’t pull Z lines together.
138
Q

The leg muscles of long-distance cyclists are usually larger than the leg muscles of non-athletes.

Suggest why.

A
  1. No (overall) change in number of fibres;
  2. Increase in diameter of fibres;
  3. (Due to) training / exercise;
  4. (Long-distance) cyclists have more / higher percentage of slow fibres (than fast);
  5. Slow fibres of wider diameter than fast fibres;
  6. (Long-distance) cyclists have more mitochondria;
  7. (Long-distance) cyclists have more capillaries (in muscles).
139
Q

Describe the roles of calcium ions and ATP in the contraction of a myofibril. (5)

A
  1. Calcium ions diffuse into myofibrils from (sarcoplasmic) reticulum;
  2. (Calcium ions) cause movement of tropomyosin (on actin);
  3. (This movement causes) exposure of the binding sites on the actin;
  4. Myosin heads attach to binding sites on actin;
  5. Hydrolysis of ATP (on myosin heads) causes myosin heads to bend;
  6. (Bending) pulling actin molecules;
  7. Attachment of a new ATP molecule to each myosin head causes myosin heads to detach (from actin sites).
140
Q

ATP is an energy source used in many cell processes. Give two ways in which ATP is a suitable energy source for cells to use.

A
  1. Releases relatively small amount of energy / little energy lost as heat;
  2. Releases energy instantaneously;
  3. Phosphorylates other compounds, making them more reactive;
  4. Can be rapidly re-synthesised;
  5. Is not lost from / does not leave cells.
141
Q

What is the role of phosphocreatine (PCr) in providing energy during muscle contraction?

A
  1. provides phosphate / phosphorylates;
  2. To make ATP;
142
Q



Use your knowledge of fast muscle fibres to explain the data in the figure.

A
  1. Fast muscle fibres used for rapid / brief / powerful / strong contractions;
  2. Phosphocreatine used up rapidly during contraction / to make ATP;
  3. (As people get older) slower metabolic rate / slower ATP production / slower respiration;
  4. ATP used to reform phosphocreatine;
143
Q

People who have McArdle’s disease produce less ATP than healthy people. As a result, they are not able to maintain strong muscle contraction during exercise. Use your knowledge of the sliding filament theory to suggest why.

A
  1. Attachment / cross bridges between actin and myosin;
  2. ‘Power stroke’ / movement of myosin heads / pulling of actin;
  3. Detachment of myosin heads;
  4. Myosin heads move back / to original position / ‘recovery stroke’

A-Level Biology A2 (11 decks)

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