6B - nervous coordination Flashcards
1
Q
how is information sent through the nervous system?
A
as nerve impulses – electrical signals that pass along nerve cells known as neurones
2
Q
what is a nerve?
A
a bundle of neurones
3
Q
what do neurones do?
A
coordinate the activities of sensory receptors, decision-making centres in the central nervous system, and effectors such as muscles and glands
4
Q
what features do neurones have?
A
-axon
-myelin sheath
-nodes of ranvier
-dendrite
-cell body
-axon terminal
-terminal buttons
5
Q
what is the axon and what does it do?
A
a long fibre
↳ allows electrical impulses from the neuron to travel away & be received by other neurons
6
Q
how is the axon of some neurones insulated?
A
-by a fatty sheath with small uninsulated sections along its length (called nodes of ranvier)
-the sheath is made of myelin, a substance made by schwann cells
7
Q
what is the benefit of the myelin sheath?
A
the electrical impulse does not travel down the whole axon, but jumps from
between nodes of ranvier → saltatory conduction
↳ this speeds up the conduction of the impulse and its transfer from one neurone to another
8
Q
what are dendrites and what is the benefit of them?
A
extensions from neurone cell bodies
↳ they can connect to many other neurones and receive impulses from them, forming a network for easy communication
9
Q
the three main types of neurone:
A
-sensory
-relay
-motor
10
Q
what do sensory neurones do?
A
carry impulses from receptors to the CNS (brain or spinal cord)
11
Q
what do relay neurones do?
A
they’re found entirely within the CNS and connect sensory and motor neurones
12
Q
what do motor neurones do?
A
carry impulses from the CNS to effectors (muscles or glands)
13
Q
motor neurone structure:
A
-a large cell body at one end, that lies within the spinal cord or brain
-a nucleus that is always in its cell body
-many highly-branched dendrites extending from the cell body, providing a large surface area for the axon terminals of other neurones
14
Q
what is a resting axon?
A
one that is not transmitting impulses
15
Q
what is resting potential?
A
the fact that in a resting axon, the inside of the axon always has a negative electrical potential compared to the outside of the axon
16
Q
what is the figure for testing potential?
A
-70mV (ie. the inside of the axon has an electrical potential about 70mV lower than the outside)
17
Q
which factors contribute to establishing & maintaining the resting potential?
A
-the active transport of sodium ions and potassium ions
-differential membrane permeability
18
Q
how are sodium ions and potassium ions actively transported?
A
-carrier proteins called sodium-potassium pumps are present in the membranes of neurones
-these pumps use ATP to actively transport 3 sodium ions out of the axon for every 2 potassium ions that they actively transport in
19
Q
what does the active transport of sodium ions and potassium ions result in?
A
there is a larger concentration of positive ions outside the axon than there are inside the axon
20
Q
a differential membrane permeability:
A
-the cell-surface membrane of neurones has selective protein channels that allow sodium and potassium ions to move across the membrane by facilitated diffusion
-the protein channels are less permeable to sodium ions than potassium ions
-this means that potassium ions can diffuse back down their concentration gradient, out of the axon, at a faster rate than sodium ions
21
Q
electrical impulses in neurones:
A
unlike a normal electric current, these
these impulses, known as action potentials, occur via very brief changes in the distribution of electrical charge across the cell surface membrane
22
Q
what are action potentials caused by?
A
the rapid movement of sodium ions and potassium ions across the membrane of the axon / changes in membrane permeability /
23
Q
what is in the axon membrane?
A
there are channel proteins that allow sodium ions or potassium ions to pass through
24
Q
steps of depolarisation:
A
1) a stimulus triggers an inflow of sodium ions into the cell (sodium ion channels in the axon membrane open)
2) sodium ions pass into the axon down the electrochemical gradient (there is a greater concentration of sodium ions outside the axon than inside / the inside of the axon is negatively charged, attracting the positively charged sodium ions) → this reduces the potential difference across the axon membrane as the inside of the axon becomes less negative (depolarisation)
3) depolarisation triggers more channels to open, allowing more sodium ions to enter and causing more depolarisation
(positive feedback)
4) if the potential difference reaches around -55mV (threshold potential), more channels open & more sodium ions enter, causing the inside of the axon to reach a potential of around +40mV
5) an action potential is generated
↳ depolarisation of the membrane at the site of the first action potential causes sodium ions to diffuse to along the axon (depolarising the membrane in the next section of the axon and causing sodium ion voltage-gated channel proteins to open there → conduction)
6) this triggers the production of another action potential in this section of the axon membrane and the process continues
25
what does conduction allow for?
it allows action potentials to begin at one end of an axon and then pass along the entire length of the axon membrane
26
how is an impulse is transmitted in one direction along the axon of a neurone?
1) in response to a signal (eg: from a receptor cell), the axon becomes depolarised
2) current flows to the next resting section of the axon membrane, depolarising it and generating further action potentials in this direction
3) the previous section of the axon membrane is temporarily unresponsive to depolarisation, as it is in a phase of repolarisation
4) the wave of depolarisation ensures that the action potentials continue in only one direction (towards the axon terminal)
27
steps of repolarisation and the refractory period:
1) very shortly after an action potential in a section of axon membrane is generated, all the sodium ion voltage-gated channel proteins in this section close, stopping any further sodium ions diffusing into the axon
2) potassium ion voltage-gated channel proteins in this section of axon membrane open, potassium ions diffuse out of the axon, down their concentration gradient
3) this returns the potential difference to normal (about -70mV) - repolarisation
4) there is a short period of hyperpolarisation, the potential difference across this section of axon membrane briefly becomes more negative than the resting potential
5) the potassium ion voltage-gated channel proteins then close and the sodium ion channel proteins in this section of membrane become responsive to depolarisation again
↳ until depolarisation occurs, this section of the axon membrane is in a period of recovery and is unresponsive
(refractory period)
6) resting potential is re-established by the sodium-potassium pump. this is called the refractory period
28
why is the refractory period important?
-it ensures that ‘new’ action potentials are generated ahead (ie. further along the axon), rather than behind the original action potential
↳ this means that the impulse can only travel in one direction (essential for the successful and efficient transmission of nerve impulses along neurones)
-it ensures that action potentials are discrete events (don’t merge into one another)
29
what is the refractory period?
the period during which no other action potential can be generated
30
What does it mean when the plasma membrane of the neuron is polarised?
-there is a separation of charge across the membrane
-the inside of the neurone is more negative and the outside is more positive (this is the state when the neuron is at rest)
31
explain how a resting potential is maintained in a neurone.
-the membrane is less permeable to sodium ions / fewer sodium ion channels are open
-sodium ions are pumped out by sodium ion carriers
-the inside is more negative than the outside (3 sodium ions out for two potassium ions in)
32
what happens when receptors are stimulated?
they are depolarised
33
what is the all or nothing principle?
if the intensity of a stimulus is below the threshold potential, no action potential will be initiated
34
what does the frequency of impulses suggest?
-a strong stimulus will generate a high frequency of impulses within the sensory neurone
-a weaker stimulus stimulus will generate a low frequency of impulses within the sensory neurone
-a very weak stimulus will fail to generate any impulses
35
how do threshold levels change?
instead than staying constant, threshold levels in receptors usually increase with continued stimulation, so that a greater stimulus is needed before impulses are sent along sensory neurones
36
what does the length of the refractory period determine?
the maximum frequency at which impulses can be transmitted along neurones
37
what is the speed of conduction?
how quickly the impulse is transmitted along a neurone
38
which factors determine the speed of conduction?
-the presence or absence of myelin
-the diameter of the axon
-temperature
39
what is the speed of conduction in unmyelinated neurones?
very slow as depolarisation must occur along the whole membrane of the axon
40
what is the speed of conduction in myelinated neurones?
the speed is much quicker
↳ in sections of the axon that are surrounded by a myelin sheath, depolarisation (and the action potentials that this would lead to) cannot occur, as the myelin sheath stops the diffusion of sodium ions and potassium ions
↳ action potentials can only occur at the nodes of Ranvier
↳ the action potentials jump from one node to the next (saltatory conduction)
41
benefits of saltatory conduction:
saltatory conduction allows the impulse to travel much faster than in an unmyelinated axon of the same diameter
42
how does diameter affect conduction speed?
-impulses are conducted at higher speeds along neurones with thicker axons
-thicker axons have an axon membrane with a greater surface area over which the diffusion of ions can occur
-this increases the rate of diffusion of sodium ions and potassium ions through protein channels, which increases the rate at which depolarisation and action potentials can occur
43
how does temperature affect conduction speed?
-colder conditions can slow down the conduction of nerve impulses
-the colder temperatures mean there is less kinetic energy available for the facilitated diffusion of potassium and sodium ions during an action potential
44
conduction speed in mammals vs reptiles
-some animals (such as mammals) maintain very stable body temperatures
-temperature does not usually affect the speed of nerve impulses in these animals
-the body temperature of other animals can vary with the environment (eg: cold-blooded reptiles)
45
what does the refractory period mean?
there is a minimum time between action potentials occurring at any one place along a neurone
46
equation for the maximum frequency of impulses within a certain time:
time ÷ duration of the refractory period
47
equation for the maximum frequency of impulses within a second:
1 ÷ duration of the refractory period
48
EXTRA: different units are used for these calculations
impulses sec-1
action potentials sec-1
hz (1 Hz is equal to one impulse per second)
49
Figure 1 shows the changes in the permeability of a section of an axon membrane to two ions that are involved in the production of an action potential. Use the information in Figure 1 to calculate the maximum frequency of action potentials per second along the axon. Show your working.
(GO LOOK AT GRAPH IN CAMERA ROLL)
**step 1:** determine the duration of the refractory period
↳ from the graph: 2.75 milliseconds
**step 2:** convert this to seconds
↳ 0.00275 seconds
**step 3:** insert relevant figures into the equation
↳ time ÷ duration of the refractory period
1 ÷ 0.00275 = 363.63
answer = 364 action potentials sec-1
50
milliseconds → seconds
1000 milliseconds = 1 seconds
(second x 1000 = millisecond)
51
for the same diameter of axon, the graph shows that the rate of conduction of the nerve impulse in myelinated neurones in the cat is faster than that in the lizard.
suggest an explanation for this.
cat has higher body temperature →
faster diffusion of ions / faster opening of ion channels
52
can electric impulses jump?
no
electric impulses can't jump across a synapse, they must be converted into chemical messengers
(neurotransmitters) in order to reach the post synaptic membrane
53
what happens where two neurones meet?
a very small gap, known as the synaptic cleft, separates them
(the ends of the two neurones, along with the synaptic cleft, form a synapse)
54
steps of synaptic transmission:
1) an electrical impulse (AP) arrives at the the presynaptic neurone
2) vesicles containing neurotransmitter
move towards the presynaptic membrane and bind
3) the vesicles release the neurotransmitters, which diffuse across the synapse and bind with receptor molecules on the postsynaptic membrane
4) this stimulates the postsynaptic neurone to generate another action potential that travels down the axon of the postsynaptic neurone
5) the excess neurotransmitters in the synapse are then destroyed or reuptaken
55
why are excess neurotransmitters destroyed or reuptaken?
to prevent continued stimulation of the second neurone, which could cause repeated impulses to be sent
56
what is a c____ synapse
a cholinergic synapse is one that uses acetylcholine as a neurotransmitter
57
symbol for acetylcholine:
Ach
58
steps of synaptic transmission at a cholinergic synapse:
1) action potential arrives at the presynaptic membrane, the membrane depolarises, this stimulates voltage-gated calcium ion channels to open
2) calcium ions flood into the pre-synaptic neurone (down the concentration gradient)
3) acetylcholine-containing vesicles move forwards & fuse with the presynaptic membrane, acetylcholine is released into the synaptic cleft
4) acetylcholine neurotransmitters diffuse across the synapse and temporarily bind to receptors on the postsynaptic membrane
5) the receptors change shape & open, allowing sodium ions to diffuse down an electrochemical gradient into the cytoplasm of the postsynaptic neurone
6) sodium ions rush into the post-synaptic neurone. if enough sodium ions diffuse in, the action potential threshold is reached and the neurone depolarises
7) to stop the sodium ion channels staying permanently open (& permanent depolarisation of the postsynaptic membrane), the ACh molecules are broken down and recycled
8) acetylcholinesterase catalyses the hydrolysis of the ACh molecules into acetate and choline
9) choline is recycled back into acetylcholine after reacting with acetyl coenzyme A
59
3 spec points related to transmission across a cholinergic synapse:
-unidirectionality
-temporal and spatial summation
-inhibition by inhibitory synapses
60
unidirectionality:
-synapses ensure the one-way transmission of impulses
-impulses can only pass in one direction at synapses because neurotransmitter is released on one side and its receptors are on the other
(chemical transmission cannot occur in the opposite direction)
61
what does unidirectionality do?
it prevents impulses from travelling the wrong way, back to where they were initiated
62
what happens when an impulse arrives at a synapse?
-it doesn’t always cause impulses to be generated in the next neurone / a single impulse isn’t always sufficient to generate an action potential in the post-synaptic neurone
63
what are some of the reasons why an impulse doesn’t generate an action potential in the post-synaptic neurone?
-only a small amount of acetylcholine is released into the synaptic cleft
-a small number of the gated sodium ion channels are opened in post synaptic axon membrane
-an insufficient number of sodium ions pass through the membrane → the threshold potential is not reached
-the small amount of acetylcholine attached to receptors is broken down rapidly by acetylcholinesterase
64
what is summation?
when the effect of multiple impulses are added together to become sufficient enough to generate an action potentoal
65
what are the benefits of summation?
-the effect of a stimulus can be magnified
-a combination of different stimuli can trigger a response
-it avoids the nervous system being overwhelmed by impulses
↳ synapses slow down the rate of transmission of a nerve impulse that has to travel along two or more neurones
66
what are the two types of summation?
-temporal
-spatial
67
what is temporal summation?
multiple nerve impulses from a single pre-synaptic neurone occur in succession
↳ increases the concentration of neurotransmitters in the synaptic cleft, increasing the likelihood of firing an action potential (reaching the threshold potential)
68
what is spatial summation?
multiple pre-synaptic neurones connect to the same post-synaptic neurone
↳ multiple impulses → large amount of acetylcholine released into the synaptic cleft → the generation of an action potential
69
what is inhibition?
when neurotransmitters prevent the generation of an action potential in a postsynaptic neurone
(the impulse stops at the synapse)
70
how can a neurotransmitter inhibit an impulse?
by opening the gated potassium ion channels in the membrane so that potassium ions are able to diffuse out of the cell body
71
excitatory neurotransmitters & their effect:
excitatory neurotransmitters make an action potential more likely to fire by depolarising the post-synaptic membrane
(closer to reaching threshold potential)
72
inhibitory neurotransmitters & their effect:
make an action potential less likely to fire by hyperpolarising the post-synaptic membrane
73
what do inhibitory synapses play a vital role in & how?
the nervous circuit
↳ they prevent random impulses from being sent around the body
↳ they allow for specific pathways to be stimulated
74
inhibitory pathways can…
-develop over time
-these pathways are very important for skills such as painting and drawing
inhibitory pathways help to refine their uncontrolled movement
75
different modes of action of drugs:
(synapse)
-stimulating the release of a neurotransmitter
-providing the chemicals needed to synthesise neurotransmitters
-acting in the same way as a neurotransmitter by binding to the same specific receptor
-preventing the reuptake of the neurotransmitter by the presynaptic neurone
76
dopamine:
-dopamine is a neurotransmitter involved in muscle control
-dopamine also plays a vital role in pain relief
77
morphine & dopamine
-chemicals called endorphins can stimulate the release of dopamine
-the endorphins attach to opioid receptors on presynaptic neurones that release dopamine
-morphine is a chemical very similar in structure to endorphins and so it can provide pain relief by stimulating the release of dopamine
78
what is a way of releasing endorphins?
exercise is a natural way to cause the release of endorphins
79
parkinson’s disease:
individuals that suffer from Parkinson's disease produce insufficient amounts of dopamine → there are two types of drugs that are used to treat this disease
1) a dopamine agonist - produces the same effect as dopamine by binding to the same receptors
2) a dopamine precursor - this can be used to synthesise dopamine in the neurones
80
cocaine & dopamine
-cocaine also affects levels of dopamine
-it binds to the dopamine transporter protein
-this prevents dopamine from binding to the transporter so it is not able to move through the membrane back into the presynaptic neurone
As a result dopamine builds up in the synapses which can lead to feelings of pleasure
81
cannabinoids & dopamine
-cannabinoids are found in cannabis
-cannabinoid receptors are located in the pre-synaptic membrane of neuromuscular junctions
-when a cannabinoid molecule binds to its specific receptor, it closes the calcium ion channels → decreased muscle contraction
82
where is a neuromuscular junction?
between a neurone and muscle
83
when does a striated muscle contract?
when it receives an impulse from a motor neurone via the neuromuscular junction
84
steps of transmission across a neuromuscular junction:
1) an action potential arrives at the pre-synaptic membrane of a motor neurone & causes calcium ions to diffuse into the neurone
2) vesicles containing acetylcholine fuse with the presynaptic membrane
3) the ACh that is released diffuses across the neuromuscular junction and binds to receptor proteins on the sarcolemma
4) stimulates ion channels in the sarcolemma to open, sodium ions to diffuse in
5) the sarcolemma depolarises, an action potential generates & passes down the T-tubules
6) action potentials cause voltage-gated calcium ion channel proteins in the membranes of the sarcoplasmic reticulum to open, calcium ions diffuse out of the sarcoplasmic reticulum and into the sarcoplasm
7) this leads to muscle contraction
85
where is acetylcholinesterase in muscles?
the muscle cell membrane contains clefts (folds of the membrane) containing acetylcholinesterase
86
neurotransmitters at cholinergic synapses vs neuromuscular junctions:
NJ:
only excitatory neurotransmitters
CS:
excitatory or inhibitory neurotransmitters
87
similarities of cholinergic synapses and neuromuscular junctions:
-both use acetylcholine as a neurotransmitter
-both are stimulated by an action potential on the presynaptic membrane
88
what does the effective movement of the human body require and why?
both muscle and an incompressible skeleton
→ muscles will only produce effective movement if they pull on a structure that does not shorten or bend - bone
89
what are muscles?
muscles are effectors, stimulated by nerve impulses from motor neurones / a block of many thousands of muscle fibres
90
the muscular system…
…is complex, with multiple muscles crossing over each other in multiple directions
91
what connects muscles to bone?
tendons
92
what are tendons?
lengths of strong connective tissue
93
features of tendons:
flexible but do not stretch when a muscle is contracting and pulling on a bone
94
can can muscles do?
muscles are only capable of contracting or pulling , they cannot push → this limitation means that muscles generally operate in pairs
95
antagonistic muscle action:
a muscle pulls in one direction at a joint and the other muscle pulls in the opposite direction / the two muscles work together by pulling in opposite directions
96
to raise the lower arm…
the bicep contracts and the tricep relaxes
as the bone can't be stretched the arm flexes around the joint, which brings the tricep into its full length so that it can contract again
97
how do muscles maintain posture?
antagonistic muscles both contract at joints to keep the joint at a certain angle → isometric contraction (a muscle contraction without motion)
98
what does striated muscle make up?
the muscles in the body that are attached to the skeleton (skeletal muscle)
99
what is striated muscle made up of?
multi nucleated muscle fibres, striated, tubular & usually attached to skeleton
100
what is a muscle fibre?
a highly specialised cell-like unit
→ each muscle fibre contains an organised arrangement of contractile proteins in the cytoplasm
→ each muscle fibre is surrounded by a cell surface membrane
→ each muscle fibre contains many nuclei
101
why isn’t a muscle fibre referred to as a cell?
because each muscle fibre contains many nuclei
102
different parts of a muscle fibre & their different names compared to the equivalent parts of a normal cell:
cell membrane = sarcolemma
cytoplasm = sarcoplasm
endoplasmic reticulum = sarcoplasmic reticulum (SR)
103
what does the sarcolemma have?
many deep tube-like projections that fold in from its outer surface and run close to the SR
(transverse system tubules or T-tubules)
104
what does the sarcoplasm contain?
mitochondria and myofibrils
105
functions of the mitochondria and microfibrils in the sarcoplasm:
-the mitochondria carry out aerobic respiration to generate the ATP required for muscle contraction
-myofibrils are bundles of actin and myosin filaments, which slide past each other during muscle contraction
106
what do the membranes of the sarcoplasmic reticulum contain?
protein pumps that transport calcium ions into the lumen of the sarcoplasmic reticulum
107
what is each myofibril is made up of?
two types of protein filament:
thick filaments made of myosin (darker)
thin filaments made of actin (lighter)
(the protein filaments are arranged in a particular order, creating different types of bands and line)
108
myosin and actin form…
repeating units called sarcomeres
109
protein filament arrangement…
protein filaments are arranged in a particular order, creating different types of bands and lines
110
what are all of the parts of a microfibril?
-the H band/zone
-the I band
-the A band
-the M line
-the Z line
-the sarcomere
111
H band/zone
“halfway area”
-only thick myosin filaments present
-part of the A band where there is no overlap between the actin and myosin filaments
112
I band
only thin actin filaments present
113
A band
-area where only myosin filaments are present
-part where actin and myosin filaments overlap
114
M line
“middle line”
-dark line through the middle of a sarcomere
-made of myosin
-attachment for myosin filaments
115
Z line
“end line”
-dark line between adjacent I-bands
-attachment/anchor for actin filaments
116
sarcomere
a segment of a myofibril (muscle cell) from one Z disk to the next
117
what are myosin molecules?
fibrous protein molecules with a globular head
118
myosin binding sites & structures:
-myosin filaments have binding sites for both actin and ATP on the globular head
-myosin heads are a globular shape that are hinged, allowing them to move back and forth to move actin closer towards it
119
what are actin molecules?
globular protein molecules
120
actin binding site:
actin filaments have binding sites for myosin heads (actin-myosin binding sites)
121
how do muscles cause movement?
by contracting
122
what happens during muscle contraction?
sarcomeres within myofibrils shorten as the Z discs are pulled closer together (the sliding filament model of muscle contraction)
123
PT 1
sliding filament theory (steps)
1) an action potential arrives at the neuromuscular junction
2) calcium ions are released from the sarcoplasmic reticulum (SR)
3) calcium ions bind to troponin molecules, stimulating them to change shape
4) troponin and tropomyosin proteins to change position on the actin (thin) filaments
5) myosin binding sites are exposed on the actin molecules because the troponin has moved
(myosin heads are cocked and in a starting position)
6) the myosin heads bind with the actin’s myosin binding site, forming cross-bridges between the two types of filament
7) the formation of the cross-bridges causes the myosin heads to spontaneously bend (releasing ADP and inorganic phosphate), pulling the actin filaments towards the centre of the sarcomere and causing the muscle to contract a little
124
PT 2
sliding filament theory (steps)
1) ATP binds to the myosin heads and causes a shape change that causes the myosin heads to release from the actin filaments
2) ATP hydrolase hydrolyses ATP into ADP and inorganic phosphate, the energy released is used to move the myosin heads to move back to their original positions (this is known as the recovery stroke)
3) the myosin heads can then bind to new binding sites on the actin filaments, closer to the Z line
4) the myosin heads move again, pulling the actin filaments even closer to the centre of the sarcomere, the sarcomere shortens and pulls the Z lines closer together
5) ATP binds to the myosin heads once more so they can detach again
6) if tropomyosin isn’t blocking the myosin-binding sites and the muscle has a supply of ATP, this process repeats until the muscle is fully contracted
125
sarcomere bands during contraction:
**A-bands**- remain the same length, as only the myosin is present and does not shorten
**I-bands** - shorten in length the myosin fibres move in, decreasing the length of the actin only segment
**H-zone** - shortens in length as the actin fibres move in, decreasing the length of the myosin only segment
126
actin & tropomyosin when a muscle is at rest:
-when the muscle is at rest, the protein tropomyosin prevents the actin and myosin filaments from sliding past each other
-tropomysin covers the actin-myosin binding site and is held in place by troponin
127
a supply of … is needed for muscle contraction
ATP
128
why is ATP needed for muscle contraction?
-energy is needed for the return movement of myosin heads that causes the actin filaments to slide
-the return of calcium ions back into the sarcoplasmic reticulum occurs via active transport
129
ATP in resting muscles:
resting muscles have a small amount of ATP stored that will only last for 3/4 seconds of intense exercise
130
mitochondria in muscle fibres:
the mitochondria present in the muscles fibres can aerobically respire and produce ATP
↳ this is slow and time-consuming
131
what other molecule is stored by muscle fibres?
phosphocreatine, which can be used for the rapid production of ATP
132
phosphate equation:
a phosphate ion from phosphocreatine is transferred to ADP:
ADP + phosphocreatine → ATP + creatine
133
phosphocreatine in muscle fibres:
different muscle fibre types contain different limited amounts of phosphocreatine so that muscles can continue contracting for a short period of time until the mitochondria are able to supply ATP
134
phosphocreatine & prolonged activity:
once the supply of phosphocreatine has been used up then the rate of muscle contraction must equal the rate of ATP production from both aerobic and anaerobic respiration
135
what are the two types of muscle fibres found in muscles?
fast fibres
slow fibres
136
human muscles & fibres:
-human muscles are made up of both types of muscle fibres
-some muscles have higher proportions of a particular fibre type due to their different properties
137
fast twitch muscle fibre properties:
-contract rapidly (need large amounts of calcium ions present to stimulate contraction)
-the myosin heads bind and unbind from the actin-binding sites five times faster than slow muscle fibres
138
what sort of respiration do fast muscle fibres rely on & what is the effect of this?
anaerobic respiration
↳ they are suited to short bursts of high-intensity activity as they fatigue quickly due to the lactate produced from anaerobic respiration
139
examples of locations of fast muscle fibres:
-often found in high proportions in the limbs of animals that flee a predator or hunt prey at high speeds
-there are high proportions of fast muscle fibres in human eyelids (they contract in short bursts and do not need to sustain the rapid movement)
140
features of fast muscle fibres:
-have fewer capillaries
-low amounts of myoglobin present
141
fast muscle fibres: fewer capillaries
-blood containing glucose and oxygen flow through the capillaries
-this means they have quite a slow supply of oxygen and glucose for aerobic respiration
142
fast muscle fibres: little myoglobin
-myoglobin is a red pigment molecule that is similar to haemoglobin
-myoglobin functions as a store of oxygen in muscles and increases the rate of oxygen absorption from the capillaries
143
colour of fast muscle fibres:
due to low amount of myoglobin and few capillaries, the fast muscle fibres appear paler in colour than slow muscle fibres
144
properties of slow muscle fibres:
contract more slowly and are suited to sustained activities like walking and perching
145
what sort of respiration do slow muscle fibres rely on & what is the effect of this?
they rely on aerobic respiration for ATP
↳ they fatigue less quickly due to less lactate production, making them ideal for endurance
146
examples of locations of slow muscle fibres:
-these muscle fibres are often found in high proportions in the limbs of animals that migrate or stalk prey over long distances
-human back muscles have a high proportion of slow muscle fibres
(these muscles have to contract for long periods of time in order to keep the skeleton erect when standing or sitting)
147
features of slow muscle fibres:
-denser network of capillaries
-high amounts of myoglobin, haemoglobin and mitochondria
148
slow muscle fibres: denser network of capillaries
-blood containing glucose and oxygen flow through the capillaries
-this means they have a short diffusion distance and a good supply of oxygen and glucose for aerobic respiration
149
slow muscle fibre: high amounts of myoglobin, haemoglobin and mitochondria
this increases the rate of oxygen supply, oxygen absorption and aerobic respiration
150
colour of slow muscle fibres:
due to the high amounts of red pigment, slow muscle fibres appear a dark red
151
distribution of muscle fibres in humans:
-most humans tend to have an equal amount of slow and fast fibres in their arm and leg muscles
-however, some people (commonly trained athletes and sportspeople) tend to have a higher proportion of one muscle fibre type in these muscles
152
why do athletes have higher proportions of one type of muscle fibre?
the higher proportion of the certain fibre type enhances their performance in their specific sport or event
153
specific athletes and their muscle fibre distributions:
athletes that train for short-burst, **high-intensity activities** (sprinting, weightlifting etc) tend to have higher proportions of fast muscle fibres and lower proportions of slow muscle fibres in their arms and legs
athletes that train for endurance activities (marathons, long-distance cycling etc) tend to have higher proportions of slow muscle fibres and lower proportions of fast muscle fibres in their arms and legs
154
how do athletes have different distributions of muscle fibres?
some individuals have muscles that are more suited to particular sports, but training can massively increase their success
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how have scientists stated that training can affect muscles?
-it can influence which fibre types develop
-it can increase the number of capillaries and mitochondria present in muscles
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EXAM TIP:
if an exam question asks how an individual's muscles get bigger as a result of exercise, remember that it is the size of the fibres and not the number of fibres that increase! an increase in the length and number of contractile units within each fibre causes this increase in size.
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what does prolonged exercise require?
the repeated contraction of muscles, over time this can cause muscles to fatigue so they are no longer able to contract at the same rate
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calcium ions & muscle fatigue:
the availability of calcium ions may decrease after repeated contractions
↳ calcium ions are essential in moving tropomyosin away from the actin-binding sites
↳ they are also responsible for activating ATPase
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lactate & muscle fatigue:
-lactate is also produced after repeated contractions
-anaerobic respiration provides a supply of ATP for muscles contraction, it also produces the waste product, lactate
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effects of lactate:
-lactate lowers the pH of muscles and affects the contraction of fibres
-it causes discomfort, muscle soreness, and fatigue → limits the duration of high-intensity activities the body can perform
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smooth muscle
-non-striated
-spindle shaped
-usually covers organs
-not nucleated
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ALT filament sliding theory:
1) an action potential arrived at the neuromuscular junction
2) calcium ions are released from the sarcoplasmic reticulum
3) calcium ions binds to troponin to molecules, stimulating them to change shape
4) this causes troponin and tropomyosin proteins to change position, myosin binding sites on the actin are exposed
5) the myosin head is cocked in its starting position and ready to bind to actin (because ATP is bound)
6) the myosin head attaches to the binding site and a cross bridge forms
7) the bound myosin rotates its head, producing a power stroke and causing actin to slide and move towards the sarcomere
8) ATP binds to the myosin head and allows it to detach and go back to its starting position (cocked head)
(1- cocked head / 2- cross bridge /
3- power stroke)
