3.6 Chapter 15- Nervous Coordination and Muscles

Question 1

Why is coordination important?

Answer 1

• Specialised cells lose the ability to perform some functions so different groups of cells carry out their own functions.
• Cells become dependent on others to carry out the function they no longer specialise in.
• E.g. obtaining oxygen for respiration, providing glucose, or removing waste.
• Different functions must be coordinated to be performed efficiently as no body system works in isolation.
• Coordination is performed by the nervous system and the hormonal system. Although they are different, both systems work together and interact with one another.

Question 2

What is a neurone?

Answer 2

Specialised cells adapted to carrying electrochemical changes (nerve impulses).

Question 3

What is the structure of a myelinated motor neurone?

Hint: 6 points

Answer 3

• Cell body- contains cell organelles (nucleus and large amounts of rough endoplasmic reticulum to produce proteins and neurotransmitters)/
• Dendrons- extensions of the cell body- branch out into smaller fibres called dendrites- carry impulses to cell body.
• Axon- long fibre that carries nerve impulses away from the cell body. Axons carries the impulse away from the cell body.
• Schwann cell- surround the axon- protect it and provide electrical insulation, provide phagocytosis to remove cell debris and regenerate cells. Wrap around the axon many times so that layers of their membrane build up.
• Myelin sheath- covers the axon- membrane of Schwann cells- rich in lipids called myelin- electrical insulator- made up of Schwann cells.
• Nodes of Ranvier- constrictions- adjacent Schwann cells have constrictions where there is no myelin sheath- sodium ion channels concentrated here

Question 4

What are the different types of neurone and describe their structure.

Answer 4

• Sensory neurones- carry nerve impulses (electrical signals) from receptors to intermediate or motor neurones (in the CNS). One very long dendron-carries impulses towards the cell body.
• Relay or intermediate neurones- transmit electrical impulses between neurones (usually sensory and motor neurones). Have numerous short processes.
• Motor neurones- transmit nerve impulses away from relay or intermediate neurones to effectors e.g. glands and muscles. Long axon, many short dendrites.

Question 5

Draw and label the different types of neurone.

Answer 5

Answer on revision card

Question 6

What are nerve impulses?

Answer 6

• Nerve impulses are self-propagating waves of electrical activity that travel along the axon membrane.
• Nerve impulses involve the temporary reversal in potential difference across the membrane from the resting potential to the action potential.

Question 7

What is the resting potential

Answer 7

• In a resting state, the axons inside is negatively charged compared to its outside- more positive ions outside the cell than inside the cell. The axon is polarised- negative difference in charge across it.
• The resting potential is usually -70mV (millivolts) in humans- this is the voltage across the membrane (difference in charge).

Question 8

How is the resting potential of the axon maintained?

Answer 8

• Maintained by the movement of sodium and potassium ions across the membrane which is controlled by:
• The phospholipid bilayer- hydrophobic- barrier to lipid insoluble substances- ions can’t diffuse through- prevents them from entering and leaving the cell except through proteins.
• Channel proteins- span phospholipid bilayer- have ion channels that enable facilitated diffusion. Selective -only open in the presence of specific water soluble ions otherwise closed. Some have gates- open or close in different conditions. Some remain open all the time so ions diffuse unhindered through them.
• Carrier proteins- actively transport ions in and out of the axon e.g. sodium- potassium pump.

Question 9

How is a resting potential established?

Answer 9

• The membrane permeability is differential to sodium and potassium ions, this establishes an electrochemical gradient that forms the resting potential difference.
• Membrane isn’t permeable to sodium or potassium ions so they can’t simply diffuse- have to move through facilitated diffusion/ active transport through carrier proteins.
• Sodium-potassium pump actively transports 3 sodium ions out of the axon for every two potassium ions in- creates a sodium ion electrochemical gradient- more positive sodium ions outside the cell than inside.
• Voltage-gated sodium ion channels and potassium ion channels are both closed.
• More permanently open potassium ion leak channels than sodium ion leak channels- membrane more permeable to potassium ions- potassium ions diffuse out of the axon by facilitated diffusion down concentration gradient after being pumped in by the sodium-potassium pump. Whereas, membrane is less permeable to sodium ions- little diffusion of sodium ions in.
• Higher concentration of sodium ions outside and potassium ions inside the neurone creates an electrochemical gradient.
• Sodium and potassium ions- both positive.
• Outward movement of positive ions is greater than the inward movement- overall movement of more positive ions out of the cell than inside the cell- outside of the cell more positively charged compared to the inside, which is relatively negatively charged- decreases potential.

Question 10

When is an action potential created?

Answer 10

• An action potential occurs after the membrane is stimulated.
• When a neurone is stimulated, voltage gated sodium ion channels open. If the stimulus is big enough to create a generator potential that reaches threshold, it triggers a rapid change in potential difference (an action potential) and the membrane transmits a nerve impulse.
• Changes in electrical activity- cause voltage-gated channels in axon membrane change shape- open or close depending on the voltage across membrane.

Question 11

Give a brief overview of the changes in charge during the action potential.

Answer 11

• Changes in membrane permeability lead to depolarisation and the generation of an action potential.
• This involves a temporary reversal of the charges either side of the part of the axon potential.
• The membrane becomes positively charged to around +40 mV and becomes depolarised.

Question 12

How is an action potential different to a resting potential?

Answer 12

The action potential occurs by diffusion, while the resting potential is mostly maintained by active transport.

Question 13

Describe an action potential.

Hint: 6 steps

Answer 13

1. At resting potential, voltage-gated potassium ion channels and voltage-gated sodium ion channels are both closed. However, some permanently open potassium channels are open (more than sodium ion channels).
2. Energy from the stimulus (the generator potential) excites the neurone cell membrane, causing some sodium ion channels to open (e.g. stretch-mediated sodium ion channels). The membrane becomes more permeable to sodium. Sodium ions diffuse into the axon through facilitated diffusion down the sodium ion electrochemical gradient. Their positive charge causes a reversal in the potential difference across the membrane- potential difference becomes less negative.
3. If the potential difference increases enough to reach threshold of -55mV, voltage-gated sodium ion channels open and sodium ions rush into the axon through these channels by facilitated diffusion. The membrane becomes depolarised and can reach +40mV.
4. At a p.d. of +40mV, the voltage-gated sodium ion channels close, preventing a further influx of sodium ions. The voltage-gated potassium ion channels open. Membrane is more permeable to potassium so potassium ions diffuse out of the axon down the potassium ion concentration gradient. The electrochemical gradient preventing further outward movement of potassium ions is reversed, causing more voltage-gated potassium ion channels to open, The membrane begins to return to resting potential- repolarisation.
5. Potassium ion channels are slow to close- overshoot if the electrochemical gradient- too many potassium ions diffuse out of the neurone- potential difference becomes more negative than the resting potential- hyperpolarisation.
6. All ion channels are reset- sodium-potassium pump cause more sodium ions to be pumped out than potassium ions in, re-establishing the resting potential of -70mV. The resting potential is maintained until the membrane is excited by another stimulus.

Question 14

What is a nerve impulse?

Answer 14

Transmission of action potential along the axon of a neurone.

Question 15

How is an action potential passed along?

Answer 15

• The action potential is passed along different sections of the membrane one at a time, not the whole membrane.
• Action potential- moves rapidly along axon- size stays the same.
• One region of the axon produces an action potential and becomes depolarised- stimulates depolarisation of the next region- action potentials generated along each small region of the axon membrane- travelling wave of depolarisation.
• The previous region of the membrane undergoes repolarisation, resulting in hyperpolarisation (the refractory potential) so that impulses aren’t sent back as the membrane reaches resting potential.

Question 16

Describe the passage of an action potential along an unmyelinated neurone.

Answer 16

1. A stimulus causes a sudden influx of sodium ions and reverses the charge on the axon so it is positive inside, negative outside- action potential- membrane depolarised.
2. Sodium ions diffuse sideways. If enough sodium ions diffuse in to reach threshold of -55mV, the voltage-gated sodium ion channels in the next region of the neurone to open and sodium ions rush in- causing an action potential- depolarisation.
3. This happens again further along the axon and causes a wave of depolarisation to travel along the neurone- moves away from parts of the membrane in the refractory period.
4. Outward movement of potassium ions continues so that the axon membrane behind the action potential returns to it’s original state- repolarised.
5. Repolarisation allows the membrane to go back to the resting potential, ready for another stimulus.

Question 17

Describe the passage of an action potential along a myelinated neurone.

Answer 17

• Occurs by saltatory conduction.
• Myelin (fatty sheath) around the axon- electrical insulator- prevents action potentials.
• Breaks in myelin- nodes of Ranvier- where action potentials can happen.
• Myelinated neurone- depolarisation only happens at nodes of Ranvier (where sodium ions are concentrated).
• Localised circuits- between adjacent nodes of Ranvier- cytoplasm conducts enough electrical charge to depolarise the next node- action potential jump from node to node through saltatory conduction.

Question 18

Compare the passage of an action potential in a myelinated vs. unmyelinated neurone and explain why.

Answer 18

• Action potential passes along myelinated neurone faster than in unmyelinated neurone.
• In unmyelinated neurone- depolarisation travels as a wave along length of the whole axon membrane- depolarisation has to occur all the way along the axon membrane- takes more time- more stages- less rapid- slower than saltatory conduction.

Question 19

How can damage to the myelin sheath lead to musclular disease?

Answer 19

• Depolarisation occurs along whole length of neurone/ across more of the membrane.
• Less saltatory conduction.
• Nerve impulses slowed- unable to jump node to node.
• Slower to reach neuromuscular junctions.

Question 20

What factors affect the speed of an action potential?

Answer 20

• Myelin sheath- electrical insulator- allows action potential to jump between nodes of Ranvier through saltatory conduction- increases speed of conduction.
• Diameter- greater= faster, less leakage of ions from a large axons as less leak channels per unit of volume (leakage makes membrane potential harder to maintain). Less resistance to the flow of ions than in the cytoplasm of smaller axons- depolarisation reaches parts of neurone membrane faster.
• Temperature- higher= faster- increases rate of diffusion- sodium potassium pump- controlled by enzymes for active transport- enzymes function more rapidly at higher temperatures. Speed only increases to around 40°C- proteins denature (including enzymes) and speed decreases/ impulses can’t be conducted. In cold-blooded animals, temperature therefore affects the speed of response and strength of muscle contractions.

Question 21

Which principle describes nerve impulses?

Answer 21

The all or nothing principle.

Question 22

Describe the all-or-nothing principle.

Answer 22

• Threshold value- level of stimulus that triggers an action potential.
• Below threshold- no action potential generated- occurs in any stimulus below the threshold (nothing).
• Any stimulus above threshold- generates action potential the same size no matter the strength of the stimulus- strength of stimulus can’t be detected by size of action potential- all principle.
• If threshold is reached, all or nothing principle means the action potential will always be the same size.

Question 23

How does an organism detect the strength of a stimulus?

Answer 23

• Detects the strength of the stimulus not by the size of the action potential but by:
• Frequency of impulses- larger= higher frequency.
• Different neurones with different thresholds- brain detects number and type of neurones stimulated and therefore the size of the stimulus.

Question 24

What is the refractory period?

Answer 24

• After action potential- neurone cell membrane can’t be excited again straight away- as voltage-gated potassium ion channels are slow to close- hyperpolarisation- voltage gated sodium ion channels can’t be made to open until the membrane is repolarised by sodium-potassium pumps.
• Period of time when inward movement of sodium ions prevented due to voltage-gated sodium ion channels closed- membrane can’t be depolarised and action potential can’t be created.
• Impossible to generate an action potential.
• Recovery period- time of delay between action potentials.

Question 25

Why is a refractory period important?

Answer 25

• Ensures action potentials only occur in one direction- unidirectional- action potentials can’t be stimulated in refractory region- only move forwards.
• Produces discrete impulses- new action potential can’t be formed immediately behind the first one- ensures action potentials are separate and don’t overlap.
• Limits number of action potentials- limits possible frequency of action potentials- impulse transmission- and therefore strength of stimulus.

Question 26

What is a synapse?

Answer 26

• Where one neurone connects with another or with an effector.
• Link neurones and coordinate activities.

Question 27

Describe the structure of a synapse.

Answer 27

• Transmit information through neurotransmitters.
• Separated by synaptic cleft- small gap- short diffusion pathway- quick diffusion.
• o Presynaptic neurone:
• Axon has a swollen portion- synaptic knob
• Releases chemical neurotransmitter stored in synaptic vesicles.
• Large amount of mitochondria and endoplasmic reticulum to manufacture neurotransmitter.
• Neurotransmitter- released from vesicles- diffuses across postsynaptic neurone. Effects depend on which specific receptors they bind to.
• Postsynaptic neurone- specific receptor proteins to receive neurotransmitters and generate action potential. Many different types of receptor due to specificity to neurotransmitters.

Question 28

What are the features of a synapse?

Answer 28

• Unidirectional- pass information in one direction- from presynaptic to postsynaptic neurone.
• Discrete response- Enzymes are released into the synaptic cleft to break down neurotransmitters or the neurotransmitters are returned back to the presynaptic neurone- Prevents continuous generation of action potential- discrete transfer of information.
• Summation- see other card
• Inhibition- see other card.

Question 29

What is the importance of summation and describe it’s features.

Answer 29

• Low frequency action potentials (due to weak stimulus)- lead to insufficient release of neurotransmitter to reach threshold and trigger a new action potential in the postsynaptic neurone.
• Summation- effect of neurotransmitters- added together with buildup of neurotransmitter.
• Sometimes inhibitory and excitatory neurones can be summated at a synapse to make the threshold for action potential higher- need to balance effects of inhibitory and excitatory to gain a response.
• Allows fine tuning of response and accurate processing of information.
• Two types- spatial and temporal.

Question 30

Describe spatial summation.

Answer 30

Different presynaptic neurones release neurotransmitters at the same time into the same synaptic cleft- more likely to reach threshold in postsynaptic neurone and cause an action potential.

Question 31

Describe temporal summation?

Answer 31

One presynaptic neurone receives nerve impulses in quick succession- releases neurotransmitter many times over short period- concentration builds up and is more likely to reach threshold of postsynaptic neurone and cause action potential.

Question 32

What are the different types of neurotransmitter?

Answer 32

• Neurotransmitters can be excitatory, inhibitory or both.
• Excitatory neurotransmitters- depolarise the postsynaptic membrane- make it fire an action potential if threshold is reached.
• Inhibitory neurotransmitters- hyperpolarise postsynaptic membrane- make potential more negative- less likely to fire an action potential.

Question 33

What is an inhibitory synapse?

Answer 33

Uses inhibitory neurotransmitters- make it less likely for a postsynaptic neurone to transmit an action potential- cause hyperpolarisation.

Question 34

Describe the process of an inhibitory synapse.

Hint: 6 steps

Answer 34

1. Presynaptic neurone- releases neurotransmitter- binds to chloride ion channels on postsynaptic neurone.
2. Neurotransmitter causes chloride ion proton channels open.
3. Chloride ions- move into postsynaptic neurone by facilitated diffusion.
4. Binding of neurotransmitter- opens potassium ion channels- potassium ions move out of postsynaptic neurone into synapse.
5. Negatively charged chloride ions moving in and positively charged potassium ions moved out- make the postsynaptic neurone more negative and outside more positive.
6. Membrane potential decreases to -80mV- hyperpolarisation- larger influx of sodium ions- needed to produce an action potential/ depolarise the membrane- less likely new action potential created.

Question 35

What is the role of a synapse.

Answer 35

• Synapses transmit information- one neurone to another.
• Single impulse- along one neurone- initiate new impulses in number of different neurones at a synapse- single stimulus creates a number of simultaneous responses.
• Number of impulses- combined at synapse- allows impulses from receptors reacting to different stimuli contribute to a single response.

Question 36

What is the role of neurotransmitter in an excitatory synapse?

Answer 36

• Chemical neurotransmitters are only made in the presynaptic neurone.
• Neurotransmitter- stored in synaptic vesicles- action potential in synaptic knob- causes vesicles to fuse with pre-synaptic membrane- release neurotransmitter.
• Neurotransmitter- diffuses across synaptic cleft- binds to receptor proteins- only on postsynaptic neurone.
• Each receptor is a protein- binds specifically to neurotransmitter- complementary shapes.
• Neurotransmitter- binds with receptor protein- leads to new action potential- synapses that do this are called excitatory synapses.

Question 37

What is a cholinergic synapse?

Answer 37

• Neurotransmitter- acetylcholine (ACh).
• Occurs in vertebrates- in CNS and neuromuscular junctions (another form of synapse to muscles).

Question 38

Describe the sequence of events of synaptic transmission (e.g. across a cholinergic synapse.

Answer 38

1. Action potential at presynaptic neurone-** depolarises presynaptic membrane**- stimulates voltage-gated calcium ion protein channels in the presynaptic membrane to open- calcium ions enter synaptic knob by facilitated diffusion (pumped out later by active transport).
2. Calcium ion influx- causes synaptic vesicles of neurotransmitter (e.g. acetylcholine) to fuse with presynaptic membrane- releases neurotransmitter into synaptic cleft by exocytosis.
3. Neurotransmitter- diffuses across synaptic cleft- short diffusion pathway- diffusion quick.
4. Neurotransmitter binds to receptors on sodium ion protein channels in the postsynaptic neurone membrane- causes sodium ion protein channels to open- sodium ions diffuse rapidly into the postsynaptic neurone down the concentration gradient- depolarisation.
5. This influx of sodium ions generates a new action potential in the postsynaptic neurone if the depolarisation reaches threshold.
6. Enzymes (e.g. acetylcholinesterase) hydrolyse the neurotransmitter and the products diffuse back across the synaptic cleft into the presynaptic neurone- recycled. Sodium ion protein channels close in the absence of the neurotransmitter. Prevents continuous generation of action potential- discrete transfer of information.
7. Most of the time, ATP is used to recombine the components of the neurotransmitter. It is then stored in synaptic vesicles ready for future use.

Question 39

What are the excitatory effects of drugs on synaptic transmission?

Answer 39

• Create more action potentials in postsynaptic neurone- enables more sodium ions to enter and reach threshold for action potential.
• Mimic a neurotransmitter by being a similar shape- activate receptors.
• Stimulate release of more neurotransmitter so more receptors are activated.
• Inhibit the enzyme that break down the neurotransmitter- more neurotransmitters in synaptic cleft to bind to receptors- neurotransmitters there for longer- allows sodium ions to enter to reach threshold for action potential.
• Enhance body’s responses to impulses passed along pre-synaptic neurone.

Question 40

What are the inhibitary effects of drugs on synaptic transmission?

Answer 40

• Create fewer action potentials.
• Some inhibit release of neurotransmitter from the presynaptic neurone- fewer receptors activated.
• Blocks receptors- so can’t be activated by neurotransmitters- few receptors can be activated.
• Mimics inhibitory neurotransmitters- similar shape.
• Reduce the body’s response to impulses passed along the pre-synaptic neurone.

Question 41

What are muscles?

Answer 41

Effectors- respond to nervous stimulation by contraction- cause movement.

Question 42

What are the types of muscle?

Answer 42

• Cardiac muscle- in the heart- not under conscious control.
• Smooth muscles- in walls of internal organs e.g. blood vessels and gut- not under conscious control.
• Skeletal muscle (a ka. striated muscle)- under conscious control- attached to skeleton- used for movement.

Question 43

Describe the structure of muscles.

Hint: 7 points

Answer 43

• Muscles- made up of muscle fibres- large bundles of long cells containing myofibrils- grouped together to provide powerful force.
• Contain lots of long cylindrical organelles- myofibrils- made of protein and are specialised for contraction- bundled together into progressively larger units- organised parallel to each other.
• Not made up of individual cells- junction between cells- too weak- instead separate cells fused together into muscle fibres- share nuclei and cytoplasm (sarcoplasm).
• Sarcoplasm- large concentration of mitochondria- provide ATP needed for muscle contraction.
• Cell membrane of muscle fibre- sarcolemma- fold inwards across the membrane into the sarcoplasm- called T-tubules- extensions of cell-surface membrane that branch throughout sarcoplasm- spread electrical impulses throughout the sarcoplasm so reach all parts of muscle fibre.
• Sarcoplasmic reticulum- muscles endoplasmic reticulum- network of membranes through the sarcoplasm- stores and releases calcium ions needed for muscle contraction.
• Muscle fibres- multinucleate- many nuclei.

Question 44

What are the features of looking at muscles under a microscope.

Answer 44

• Depends on how stained and longitudinal or transverse cross section.
• Look out for nuclei.
• Cross-striations- are A bands and I bands.

Question 45

How do muscles interact with each other and bone.

Answer 45

• Muscles attached to bones by tendons.
• Muscles- attached to skeleton- incompressible- rigid- acts as levers and gives muscle something to pull against- if muscle exerts force via tendons on the bone- the bone moves rather than the muscle or bone changing shape.
• Parts of skeleton- move relative to each other around points called joints.
• Pairs of muscle relax and contract to move bones at a joint.
• Ligaments attach bones to other bones- hold them together.
• Skeletal muscles work as antagonistic pairs- one contracts and one relaxes to move bones into correct position as muscles can only pull not push. Contracting muscle- agonist. Relaxing muscle- antagonist.

Question 46

What is an ultrastructure and a gross structure?

Answer 46

• Ultrastructure= high magnification structure.
• Gross structure= large structure- visible with naked eye.

Question 47

Describe the structure of myofibrils.

Answer 47

• Myofibrils are made up of bundles of thick and thin myofilaments- move past each other for muscle contraction.
• Myofibrils are made of two protein filaments:
• Actin- thinner- two strands twisted around each other.
• Myosin- thicker- long rod-shaped tails- bulbous heads project from each side.

Question 48

Describe the structure of the different muscle filaments.

Answer 48

• Myosin- made up of 2 types of protein- Fibrous protein- arranged into a filament made up of several hundred molecules (the tail). Globular protein- 2 bulbous structures at one end- hinged heads- move back and forth- each head has a binding site for actin and ATP.
• Actin- globular protein- one long chain- twisted around one another- form helical strand- has binding site for myosin- actin-myosin binding site.
• Tropomyosin- long thin protein threads- fibrous strands around actin filaments- blocks myosin binding sites- have calcium ion receptors.

Question 49

Why do myofibrils appear striped?

Answer 49

Myofibrils- appear striped under microscope due to alternating coloured bands of light and dark.

Question 50

Describe the bands in myofibrils.

Answer 50

• I-bands- Light bands- only actin in this region.
• A-bands- Dark bands- actin and myosin overlap in this region.
• M-line- middle of each sarcomere and middle of myosin filaments.
• H-zone- lighter coloured- around M-line- only contains myosin.
• Z line- centre of each I band.
• Distance between adjacent Z-lines- sarcomere.
• Muscle contraction- causes sarcomere to shorten and pattern of I and A bands to change.

Question 51

Describe neuromuscular junctions.

Answer 51

• Specialised cholinergic synapse between motor neurone and muscle fibre.
• Stimulates muscle using acetylcholine neurotransmitter- binds to cholinergic receptors.

Question 52

Why are neuromuscular junctions important?

Answer 52

• Many neuromuscular junctions spread throughout the muscle.
• Ensure that all fibres contract simultaneously as the wave of contraction does not take long to travel along the muscle.
• Allows fast and powerful movement.
• Rapid and coordinated muscle contraction- essential for survival.

Question 53

Describe motor units and their importance.

Answer 53

• Muscle fibres supplied by a single motor neurone- act as a single unit- known as motor unit- gives control over force muscle exerts:
• Slight force needed- only few units stimulated.
• Strong force needed- large number of units stimulated.

Question 54

Describe the process of transmission at a neuromuscular junction.

Hint: 6 steps.

Answer 54

1. Nerve impulse is received at the neuromuscular junction.
2. This causes synaptic vesicles to fuse with the presynaptic membrane and release acetylcholine by exocytosis.
3. Acetylcholine diffuses across the synaptic cleft to the postsynaptic membrane (the sarcolemma) which opens sodium ion channels- if enough enter to reach threshold- sodium ions enter rapidly and cause depolarisation.
4. The depolarisation leads to muscle contraction.
5. Acetylcholine is broken down by acetylcholinesterase to ensure the muscle isn’t over-stimulated.
6. Resulting choline and ethanoic acid diffuse back into the neurone- recombine to form acetylcholine using energy from ATP.

Question 55

List the similarities between a neuromuscular junction and a synapse.

Answer 55

• Neurotransmitters transported by diffusion.
• Receptors- bind with neurotransmitter and cause influx of sodium ions.
• Use sodium-potassium pump to repolarise axon.
• Use enzymes to breakdown the neurotransmitter.

Question 56

Compare the differences of neuromuscular junctions and synapses.

Answer 56

• Only excitatory/ May be excitatory or inhibitory.
• Links neurones to muscles. / Links neurones to other neurones or effector organs.
• Only motor neurone. / Motor, sensory, and intermediate (relay) neurones.
• Action potential ends. / New action potential may be produced.
• Acetylcholine binds to receptors on membrane of muscle fibre. / Acetylcholine binds to receptors on post-synaptic neurone’s membrane.
• Postsynaptic membrane- has lots of folds- form clefts that store acetylcholinesterase. / Postsynaptic membrane doesn’t have folds.
• Has more receptors. / Has less receptors.

Question 57

Describe the role of pairs of muscle.

Answer 57

• Skeletal muscles work as antagonistic pairs- pull in opposite directions- one contracts and one relaxes to move bones into correct position. Contracting muscle- agonist. Relaxing muscle- antagonist.
• Contraction of skeletal muscle- moves part of the skeleton in one direction but muscle can’t pull it the opposite direction as they can’t push only pull.
• Moving in opposite direction- requires second muscle- antagonistic- works in opposite direction- stretches other relaxed muscle to return it to its original state ready for contraction.

Question 58

Give an overview of muscle contraction.

Answer 58

• Process of muscle contraction involves arrangement of muscle fibres- actin and myosin filaments slide past one another in the sliding filament mechanism- make sarcomeres contract.
• Simultaneous contraction of sarcomeres- muscle fibres contract at same time.
• Sarcomeres return to original length when muscle relaxes (and antagonistic muscle pulls it back to shape).

Question 59

What is the evidence for the sliding filament mechanism?

Answer 59

• Sliding filament- more overlap of actin and myosin in contracted muscle then relaxed- changes of myofibrils.
• A-band remains the same width- width determined by length of myosin filaments- shows have not become shorter- so muscle contraction isn’t due to filaments shortening.

Question 60

Desribe the effect on a sarcomere of muscle contraction.

Answer 60

• I-band narrows.
• Z-lines move closer together (sarcomere shortens).
• H-Zone becomes narrower.
•  A-band remains the same width-

Question 61

Describe the interaction between proteins in muscles breiefly.

Answer 61

Myosin bulbous heads form cross-bridges with actin- attach themselves to binding sites on actin filaments- flexing in unison- pull actin along myosin. Detach, use ATP as energy to return to original angle, re-attach further along the actin. Repeated a lot very fast.

Question 62

What is the name for the process of muscle contraction and name the steps.

Answer 62

• Filaments slide past one another- sliding filament mechanism.
• Muscle stimulation, muscle contraction, muscle relaxation.

Question 63

Describe muscle stimulation.

Answer 63

• Action potential reaches neuromuscular junction from the motor neurone.
• Causes calcium ion protein channels to open and calcium ions to diffuse into synaptic knob.
• Calcium ions- synaptic vesicles fuse with presynaptic membrane- release acetylcholine into synaptic cleft.
• Acetylcholine- diffuses across synaptic cleft- binds with receptors on muscle cell-surface membrane- depolarisation of the sarcolemma.
• Action potential (depolarisation)- travels deep into fibre through T-tubules.
• T-tubules- in contact with sarcoplasmic reticulum- have actively transported calcium ions inside leading to very low calcium concentration in sarcoplasm.
• Action potential- opens voltage- gated calcium ion protein channels on sarcoplasmic reticulum. Calcium ions diffuse into sarcoplasm of myofibrils down a concentration gradient.
• Calcium ions bind to receptors on tropomyosin- causes change in tertiary structure- tropomyosin molecules blocking the actin-myosin binding sites on actin filaments pulls away- reveals myosin binding sites on actin- allows myosin head to bind and form actinomyosin cross bridges.

Question 64

Describe muscle contraction.

Answer 64

• ADP molecules attached to myosin heads- able to bind to actin filament- form an actinomyosin cross bridge.
• Once attached to actin filaments- myosin heads change angle- bend and pull actin filament in power stroke- releases molecule of ADP.
• ATP binds to myosin head causing it to detach from the actin, breaking the actinomyosin cross bridge.
• Calcium ions- activate ATP hydrolase- hydrolyses the ATP to ADP- provides energy for myosin heads to return to original position.
• Myosin head- with ADP- reattaches further along the actin filament to another actin-myosin binding site and forms a new actinomyosin cross bridge.
• Cycle is repeated as long as concentration of calcium ions in myofibril remains high.
• Actinomyosin cross bridges form and break rapidly- pull actin along- shortens sarcomere- causes muscle to contract.
• Myosin- joined tail to tail- oppositely facing sets- movement of one set opposite direction to other- actin filaments move in opposite directions- move towards each other- shorten distance between Z-lines.
• Takes place repeatedly and simultaneously- shortens muscle to move the bone.

Question 65

Describe muscle relaxation.

Answer 65

• Nervous stimulation ceases- calcium ions actively transported back into sarcoplasmic reticulum using ATP hydrolysis.
• Reabsorption of calcium ions- tropomyosin moves back and blocks actin-myosin binding sites on actin again- myosin unable to bind with actin.
• Contraction ceases as no myosin heads are attached to actin filaments- no actinomyosin cross bridges. and muscle relaxes.
• Force from antagonistic muscles- pull actin filaments out from between the myosin- slide back to their original relaxed position - lengthens sarcomere.

Question 66

Where does the energy for muscle contraction come from?

Answer 66

• Comes from hydrolysis of ATP to ADP and Pi.
• ATP- continually generated so contraction can continue to happen.

Question 67

Why is energy needed for muscle contraction.

Answer 67

• ATP used up quickly.
• Needed to move myosin heads past actin.
• Break actinomyosin bridges.
• Reabsorb calcium ions into the sarcoplasmic reticulum by active transport.
• To reabsorb/ resynthesise neurotransmitter.
• Active muscles- greater demand for ATP- muscles working intensely can be life saving e.g. escaping from danger.

Question 68

Describe aerobic respiration in muscles.

Answer 68

• **Aerobic respiration- **regenerates ATP through oxidative phosphorylation in cells mitochondria- requires oxygen- good for long periods of low-intensity exercise.
• Require **large amounts of mitochondria to supply ATP. **
• Aerobic respiration produces more ATP than anaerobic.

Question 69

Why is anaerobic respiration needed in some muscles and describe it’s features.

Answer 69

• Very active muscles- demand for ATP and oxygen greater than rate blood can supply oxygen- ATP need to be generated anaerobically. Partly through glycolysis and partly through phosphocreatine.
• Anaerobic respiration- ATP made rapidly by glycolysis- end product of pyruvate converted to lactate. Lactate- build-up causes muscle fatigue- good for short periods of intense exercise.
• Anaerobic respiration also includes the use of phosphocreatine.

Question 70

Describe phosphocreatine as an energy source.

Answer 70

• ATP- made by phosphorylating ADP by adding a phosphate group taken from phosphocreatine (PCr).
• Phosphocreatine- regenerates ATP- stored in muscles.
• Acts as a reserve supply of phosphate- immediately combines with ADP to reform ATP- generates ATP very quickly.
• Phosphocreatine runs out after a few seconds- used for short bursts of vigorous exercise.
• Anaerobic- doesn’t need oxygen and doesn’t produce lactate.
• ADP + Phosphocreatine –> ATP+ Creatine.
• Creatine gets broken down into creatinine which is removed by the kidneys.
• Phosphocreatine- replenished using phosphate from ATP when muscle relaxed and aerobic respiration is occurring at a fast enough rate.

Question 71

What are the two types of muscle fibre and how do they vary?

Answer 71

• Slow twitch.
• Fast twitch.
• Proportions vary in muscles and in people.

Question 72

Describe the features of slow-twitch fibres.

Answer 72

• Contract more slowly- less powerful contractions over a longer period.
• Adapted to endurance- work for a long time and don’t tire easily.
• Common in muscles that constantly contract to maintain posture or are used in endurance activities such as long-distance running e.g. calf muscles, back muscles.
• Adapted for aerobic respiration to avoid build- up of lactic acid- tires muscles- causes them to function less effectively and prevents long-duration contractions.
• Energy released slowly through aerobic respiration.

Question 73

What adaptions do slow-twitch muscle fibres have?

Answer 73

• Adapted to aerobic respiration.
• Large store of myoglobin- stores oxygen.
• Rich supply of blood vessels- delivers oxygen and glucose for aerobic respiration.
• Large numbers of mitochondria- produce ATP.
• Mitochondria- near edge of muscle fibres- short diffusion pathway for oxygen from the blood vessels to mitochondria.
• Glycogen for respiration to produce ATP- hydrolysed into glucose.

Question 74

Describe the features of fast-twitch muscle fibres.

Answer 74

• Contract rapidly and powerfully over a short period.
• Tire quickly due to build-up of lactic acid.
• Good for short, intense bursts of exercise.
• Common muscles that contract in short bursts of intense activity to produce fast movement e.g. legs/ arms.
• Energy- released quickly through anaerobic respiration using glycogen in muscle fibres.
• Also have stores of phosphocreatine- energy generated quickly when needed.

Question 75

How are fast-twitch muscle fibres adapted?

Answer 75

• Adapted for anaerobic respiration:
• Thicker and numerous myosin filaments.
• High concentration of glycogen- store of glucose for anaerobic respiration to produce ATP.
• Fewer mitochondria or blood vessels.
• Little myoglobin- don’t store much oxygen.
• High concentration of enzymes for anaerobic respiration- provide ATP rapidly.
• Phosphocreatine store- rapidly generates ATP from ADP in anaerobic conditions- provides energy for muscle contraction.