Section 6 - Organisms respond to changes in their environment: 15. Nervous coordination and muscles Flashcards

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1
Q

What are the two main forms of coordination in animals and what are the main differences between them

A

Nervous coordination:
- Electrical signals pass along neurons
- Targets are stimulated as the nerve cell secretes chemicals (neurotransmitters)
- Results in rapid communication between parts of the organism
- Responses are shot-lived and localised
- eg. Reflex

Hormonal coordination:
- Chemicals are produced (hormones) and transported in the blood plasma
- Specific receptors on the cell-surface membrane of target cells are stimulated by a change in hormone conc.
- Results in slower and less specific communication within an organism
- Responses are longer-lasting and widespread
- eg. Control of blood glucose conc.

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2
Q

What are neurones (nerve cells)

A

Specialised cells adapted to rapidly carry electrochemical changes (nerve impulses) from one part of the body to another

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3
Q

What are the main features of nerve cells

A
  • Cell body: Contains organelles, and is associated with the production of neurotransmitters
  • Dendrons: Extensions of the cell body that subdivide into ‘dendrites’, carrying the nerve impulse towards the cell body
  • Axon: Single long fibre that carries nerve impulses away from the cell body, with ‘Axon terminals’ at the other end
  • Schwann cells: Surround the axon in layers, forming the myelin sheath
  • Myelin sheath: Layers of Schwann cells that cover periodic sections of the membrane, providing electrical insulation
  • Nodes of Ranvier: Constrictions between Schwann cells where there is no myelin sheath
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4
Q

What is the role of the Schwann cells

A

Surround the axon, with the membrane wrapped around many times, forming layers of lipids (myeline) resulting in a myelin sheath.
- Provides electrical insulation
- Cells carry out phagocytosis to remove cell debris
- Play a role in nerve regeneration

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5
Q

What is the structure and function of a sensory neurone

A

Transmit nerve impulses from a receptors to the central nervous system (intermediate or motor neurone)
- Have one very long dendron that carries the impulse to the cell body
- Have one axon that carries the impulse away
- Cell body is in ‘dorsal root ganglion’ (on the side…)

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6
Q

What is the structure and function of an intermediate (relay) neurone

A

Transmits nerve impulses between neurones (sensory to motor) within the central nervous system
- Have many short dendrons surrounding the cell body, carrying impulses towards it
- Have one short axon that carries impulses away

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7
Q

What is the structure and function of a motor neurone

A

Transmits nerve impulses from the central nervous system (intermediate neurone) to an effector such as a muscle or gland
- Have many short dendrites that carry impulses to the cell body
- Have one long axon to carry the impulse away

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8
Q

What is a nerve impulse

A

A self-propagating wave of electrical activity that travels along the membrane of a neurone

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9
Q

How is the movement of ions across the axon membrane controlled

A
  • Phospholipid bilayer prevents Na+ and K+ moving across the membrane by simple diffusion
  • Channel proteins allow ions to move by facilitated diffusion (Some are ‘gated’ and open under certain conditions, such as when the pd increase, but others are permanently open)
  • Some carrier proteins actively transport Na+ out of the membrane and K+ into the membrane
    (Sodium-potassium pump)
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10
Q

What is the resting potential of an axon

A

When the inside of the axon membrane is negative relative to the outside (~65mV)
∴ Axon is said to be polarised

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11
Q

How is a resting potential established across the axon membrane

A
  • Na+ are actively transported out of the axon by the sodium-potassium pump
  • K+ are actively transported into the axon by the sodium-potassium pump
  • 3Na+ move out for every 2K+ that move in
  • ∴ An electrochemical gradient is established (negative inside)
  • There are now more Na+ in the tissue fluid surrounding the axon than in the cytoplasm, and more K+ in the cytoplasm than in the tissue fluid
  • The sodium channels are gated and closed, so no Na+ can diffuse, whereas the ‘leaky potassium gates’ remain open and allow K+ to diffuse back out
  • This all establishes a negative potential across the axon (Polarised)
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12
Q

What is an action potential

A

Temporary reversal of the potential difference across the axon membrane due to a stimulus of sufficient size

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13
Q

What is the process of an action potential

A
  • Resting potential is maintained by sodium-potassium pump
  • The energy from the stimulus causes some Na+ gates to open (eg. Stretch mediated sodium channels in the ‘Pacinian corpuscle’)
  • Na+ then diffuse into the axon through these channels, beginning to reverse the pd across the membrane
  • If the stimulus was sufficient, the pd will increase to the threshold potential, causing all of the voltage-gated Na+ channels to open.
  • This will increase the diffusion of Na+ into the axon, further increasing the pd, depolarising the membrane (positive feedback)
  • Once a pd of +40mV is reached, the voltage gated Na+ channels close, preventing a further influx of sodium
  • Also at this point, the voltage gated potassium channels open, and now there is a positive potential inside, the K+ diffuse out through these channels, and the ‘leaky-channels’ that are always open.
  • This results in the repolarisation of the membrane and negative potential is re-established
  • Eventually, the outward movement of K+ ions causes a temporary overshoot of electrical gradient, as the inside of the axon becomes more negative than at resting potential (Hyperpolarisation)
  • The voltage-gated potassium channels then close, and the excess K+ diffuse back in through the leaky-channels due to their attraction to the negative charge
  • Sodium-potassium pumps re-establish a resting potential (-65mV) and the axon is now said to be repolarised
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14
Q

How is an action potential propagated along an unmyelinated axon

A
  • A stimulus results in the depolarisation of a small region at the end of an axon, creating an action potential
  • The Na+ ions that moved into the axon now diffuse a little way along the cell, establishing a localised electric current
  • This increases the charge in the adjacent region of the axon, causing the voltage gated sodium channels to open, depolarising this adjacent region of the axon
  • Once the initial region reaches a potential of +40mV, the Na+ gates close and K+ gates open, repolarise this section
  • The cycle repeats as the action potential is propagated further along the axon
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15
Q

How is an action potential propagated along a myelinated axon (Saltatory conduction)

A
  • The myelin sheath acts as an electrical insulator, preventing the formation of an action potential in the regions that it is present
  • There are gaps between adjacent sheaths ever 1-3mm (nodes of Ranvier) where the action potential can form
  • This results in a localised current arising between two nodes, as the increased potential at one node repels the positive ions in the myelinated section of the axon, so the action potential ‘jumps’ to the next node
  • This jumping of action potentials between nodes is called ‘Saltatory conduction’ and occurs as the positive ions being repelled across the gap begin to depolarise the next node.
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16
Q

What are the main factors that effect the speed of an action potential

A
  • Myelin sheath
  • Diameter of the axon
  • Temperature
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17
Q

How does a myelin sheath effect the speed of an action potential

A

The myelin sheath results in ‘saltatory conduction’ where the action potential jumps between adjacent Nodes of Ranvier, and this increases the speed of the action potential, as depolarisation doesn’t need to occur at every point along the axon
(Increases the speed from ~30ms^-1 in an unmyelinated neurone to ~90ms^-1 in a myelinated neurone)

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18
Q

How does the diameter of the axon effect the speed of an action potential

A

The greater the diameter of the axon, the faster the conductance, as there is less leakage of ions which make the positive potential harder to establish/maintain

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19
Q

How does temperature effect the speed of an action potential

A

The higher the temperature, the faster the action potential
- Increases the kinetic energy of the ions, so faster diffusion across the membrane
- Increases rate of enzyme activity, so respiration rate increases to produce more ATP for the sodium-potassium pump
- However, if temp is too high, enzymes and membrane proteins can be denatured, so no conduction occurs
- Temp also effects speed and strength of muscle contractions, so effects response time

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20
Q

What is the ‘All-or-nothing’ Principle for an action potential

A

For a nerve impulse, there is a certain level of stimulus (threshold potential) that will trigger an action potential
- If the stimulus is of any strength below this value, no action potential will be caused
- If the stimulus is of any strength above this value, an action potential of the same size will form
∴ There can’t be ‘large’ or ‘small’ action potential, all are the same size regardless of the strength of the stimulus

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21
Q

How can the strength of a stimulus be detected, as all action potentials are the same size

A
  • Frequency of impulses ∝ Stimulus strength
  • Different neurones will have different threshold values, so the brain interprets the number and type of neurones that pass impulses to determine the stimulus size
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22
Q

What is the refractory period of an action potential and why does it occur

A

When an action potential has been created in a region of an axon, there is a period afterwards in which no further action potentials can be generated
- Voltage gated Na+ channels are closed, so depolarisation can’t occur
- Hyperpolarisation of this region (too many K+ ions leave) decreases the relative charge, so any positive ions won’t increase the pd enough to reach threshold from this ‘extra-negative’ state

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23
Q

What is the purpose of the refractory period of an action

A

Ensures the action potential is only propagated in one direction
- Hyperpolarisation of previous regions means that the action potential will only travel in one direction, as Na+ ions that diffuse backwards won’t increase the pd enough to reach threshold from this ‘extra-negative’ state

Results in discrete impulses
- Due to the refractory period, a new action potential can’t be formed in the same region of the axon immediately after another
- ∴ Ensures action potentials are separate

Limits the number of action potentials
- As the action potentials are discrete and separate, there is a limit to the number that can pass along an axon in a given time
- ∴ Limits the strength of stimulus that can be detected

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24
Q

What is a synapse

A

The point where one neurone communicates with another, or with an effector

25
Q

What are the main features of synapse

A
  • Neurotransmitters (chemicals) transmit information from one neurone to another
  • Neurones are separated by a synaptic cleft (gap 20-30nm wide)
  • End of the presynaptic neurone is swollen, known as the presynaptic knob (Possesses many mitochondria and ER to manufacture neurotransmitters)
  • Neurotransmitters are stored in synaptic vesicles, within the presynaptic knob, which bind to the membrane in the presence of an action potential and release the chemicals into the synaptic cleft.
  • Neurotransmitters diffuse across to receptors on the postsynaptic neurone, where they lead to the formation of an action potential so the nerve impulse can continue
26
Q

How do synapses ensure that a nerve impulse is only propagated in one direction

A

Synapses are unidirectional, as neurotransmitters are only produced in the synaptic knob, so information can only be passed in one direction

27
Q

What is an ‘excitatory synapse’

A

A synapse at which the neurotransmitters lead to the formation of an action potential in the postsynaptic neurone

28
Q

What is a cholinergic synapse

A

Synapse with the chemical ‘Acetylcholine’ as the neurotransmitter
- Acetylcholine = Acetyl (ethanoic acid) + Choline
- Common in vertebrates (CNS and Neuromuscular junctions)

29
Q

What is the process of transmission across a cholinergic synapse (excitatory synapse)

A

1) The arrival of an action potential at the end of a presynaptic neurone causes calcium ion protein channels to open
∴ Ca2+ enter the synaptic knob
2) This influx of Ca2+ causes the synaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine into the synaptic cleft
3) The Acetylcholine diffuses across and binds to the sodium ion protein channels on the postsynaptic membrane
4) This causes the sodium channels to open, allowing Na+ to diffuse into the postsynaptic neurone, down the conc. gradient
∴ Depolarises the post synaptic neurone and generates a new action potential
5) The enzyme ‘Acetylcholinesterase’ hydrolyses acetylcholine into choline and ethanoic acid, which diffuse back across the synaptic cleft
∴ Neurotransmitter is recycled, and prevents a continuous generation of new action potentials in the postsynaptic neurone (Na+ gates close when no acetylcholine is present)
6) ATP released by mitochondria in the synaptic knob is used to reform acetylcholine

30
Q

What is an ‘inhibitory synapse’

A

A synapse at which the neurotransmitters inhibits the formation of an action potential in the postsynaptic neurone

31
Q

How do inhibitory synapses work

A
  • The synaptic knob releases a type of neurotransmitter that binds to chloride ion protein channels
  • This causes the Cl- channels to open, as well as nearby K+ channels
  • This allows Negative Cl- to diffuse into the postsynaptic neurone, while positive K+ diffuses out
  • The combined effect of this is that the postsynaptic membrane is hyperpolarised (-85mV)
  • This hyperpolarisation means a larger influx of Na+ is required to cause an action potential in this region, making it less likely that one will occur (inhibition)
32
Q

What is summation in a synapse

A

The process of increasing the information (Neurotransmitters) received by the post synaptic neurone
- For an Excitatory synapse, this increases the change of an action potential forming (and nerve impulse continuing), as enough Na+ channels will be open to exceed the threshold value
- For an Inhibitory synapse, this decreases the change of an action potential forming, as a greater hyperpolarisation will occur

33
Q

What are the two types of summation in a synapse

A
  • Spatial summation
  • Temporal summation
34
Q

What is spatial summation in a synapse

A

When a number of different presynaptic neurones together release more neurotransmitters to be received by one postsynaptic neurone

35
Q

What is temporal summation in a synapse

A

When a single presynaptic neurone has an increased frequency of action potentials travelling along it, so more neurotransmitters are released in a given time and the conc. in the synaptic cleft increases

36
Q

What effects can drugs have on synapses

A

Can stimulate the nervous system by creating more action potentials on the postsynaptic membrane
- Mimic neurotransmitter
- Stimulate the release of more neurotransmitters
- Inhibit the enzymes that break down neurotransmitters

Can inhibit the nervous system by creating fewer action potentials on the postsynaptic membrane
- Inhibits the release of neurotransmitters
- Blocking receptors on the postsynaptic membrane

37
Q

What is the effect of drugs such as Morphine and Codeine on synapses with endorphins as neurotransmitters

A

Endorphins are neurotransmitters on sensory nerve pathways that block the sensation of pain
- Drugs such as Morphine and Codeine can bind to the same receptors so mimic the effect of endorphins

38
Q

What is the effect the drug Prozac on synapses with serotonin as a neurotransmitter

A

Serotonin is a neurotransmitter involved in the regulation of sleep and certain emotional states.
∴ Decline in serotonin is thought to be a cause of clinical depression
- The drug Prozac affects serotonin in the synaptic cleft to increase the number that bind with the post synaptic membrane

39
Q

What is the effect the drug Valium on synapses with GABA as a neurotransmitter

A

GABA is a neurotransmitter that inhibits the formation of an action potential in the postsynaptic neurone
- The drug Valium enhances the binding for GABA to it’s receptors, further inhibiting the transmission of a nerve impulse

40
Q

What are muscles

A

Effector organs that respond to nervous stimulation by contracting and so cause movement

41
Q

What are the three main types of muscles

A

Cardiac muscles
- Found only in the heart
- Not under conscious control

Smooth muscles
- Found in the wall of blood vessels and the gut
- Not under conscious control

Skeletal muscles
- Makes up the bulk of body muscle in vertebrates, attached to the bones
- Under voluntary, conscious control

42
Q

What is the macro structure of a skeletal muscle

A
  • Made up of lots of tiny fibres (myofibrils)
  • To increase strength, myofibrils bundle together to form a single muscle fibre
  • A Whole muscle fibre shares one nucleus and cytoplasm (=Sarcoplasm, containing lots of mitochondria and ER)
  • Muscle fibres bundle together, surrounded by nerves and capillaries, and these bundles group together to form the whole muscle
43
Q

What are the 3 types of protein filaments that make up myofibrils

A
  • Actin filaments: Thin, consisting of two strands of actin molecules twisted around one another
  • Myosin filaments: Thicker, consisting of long rod-shaped tails with bulbous head that projects on one side
  • Tropomyosin: Long thin threads wound around actin filaments
44
Q

What is the microscopic structure of myofibrils

A
  • Made up of repeating striped sections called Sarcomeres, due to the overlapping myosin and actin filaments
  • 2 myosin filaments are end-to-end, in-between actin filaments, holding the 2 sides of the sarcomere together
  • Tropomyosin filaments are wrapped around the actin, blocking the myosin-head binding sites until a stimulation for contraction occurs
45
Q

What are the different bands within one Sarcomere of a myofibril

A

Light bands = I Bands (Isotropic bands)
- Appear light as the filaments don’t overlap in this section
- Occur between sarcomeres, so have half at each end of one
- At the centre of each I band is a Z-line (distance between adjacent z-lines = sarcomere)

Dark bands = A Bands (Anisotropic bands)
- Appear darker as the thick and thin filaments overlap in this region
- At the centre of each A band is a lighter coloured region called a H-zone, where only myosin is present

When a muscle contracts, the sarcomeres shorten and the pattern of light and dark bands changes

46
Q

What are the 2 types of muscle fibres

A
  • Slow-twitch fibres
  • Fast-twitch fibres

Vary in proportion from muscle to muscle and person to person

47
Q

What are slow-twitch muscle fibres

A
  • Contract more slowly, with less powerful contractions
  • Contract over long periods, so are adapted for endurance work
  • Adapted for aerobic respiration to avoid build up of lactic acid:
    • Large store of Myoglobin (stores O(2))
    • Rich supply of blood to deliver glucose and O(2)
    • Numerous mitochondria to produce ATP
  • eg. Common in human calf muscles
48
Q

What are fast-twitch muscle fibres

A
  • Contract more rapidly to produce more powerful contractions
  • Contract over short period, so are adapted for intense exercise
  • Adapted for intense work:
    • Thicker and more numerous myosin filaments
    • High conc. of glucose
    • High conc. of enzymes involved in anaerobic respiration to rapidly produce ATP
    • Contain a store of phosphocreatine (Molecule that can rapidly generate ATP from ADP in anaerobic conditions, by acting as a phosphate molecule, providing energy for contractions)
  • eg. Common in human Biceps
49
Q

What is a Neuromuscular junction

A

The point where a motor neurone meets a skeletal muscle fibre (many spread throughout the muscle, to ensure that fibres contract simultaneously)

50
Q

What is a motor unit

A

All the muscle fibres attached to a single motor neurone, which therefore act as a single functional unit

51
Q

What is the process of transmission across a Neuromuscular junction

A
  • When an impulse reaches the junction, the synaptic vesicles fuse with the presynaptic membrane and release acetylcholine (neurotransmitter)
  • These chemicals then diffuse across to the post synaptic membrane (muscle fibre) and bind to receptors
  • This alters the membranes permeability to sodium ions, so Na+ rushes in, depolarising the membrane, leading to the muscle contracting
  • The Acetylcholine is broken down into Ethanoic acid and Choline by the acetylcholinesterase enzyme, recycling the neurotransmitter and avoiding and over-stimulation of the muscle
52
Q

What are the main similarities between a neuromuscular junction and a synapse

A
  • Both have neurotransmitters that are transported by diffusion
  • Both rely on receptors that cause an influx of Na+
  • Both have a sodium-potassium pump to repolarise the axon
  • Both use enzymes that break down neurotransmitters to be recycled
53
Q

What are the main differences between a neuromuscular junction and a synapse

A
  • Neuromuscular junctions are only ever excitatory, whereas synapses can be excitatory or inhibitory
  • Neuromuscular junctions only link neurones to muscles, whereas synapses can link neurones to neurones of neurones to other effector organs
  • Neuromuscular junction only involve motor neurones, whereas synapses can involve motor, sensory and intermediate (relay) neurones
  • Neuromuscular junctions are always at the end of a neural pathway (action potential ends), whereas a new action potential is generated in the postsynaptic neurone at a synapse
54
Q

What is the sliding filament mechanism of muscle contractions

A
  • The bulbous heads of myosin filaments form cross-bridges with actin filaments
  • The heads attach to binding sites on the actin, and then flex in unison, pulling the actin filaments along the myosin filaments
  • They then become detached and, using ATP, return to their original angle and reattach further along the actin
  • This process is repeated up to 100 times per second, resulting in a muscle contraction
55
Q

What is the evidence for the sliding filament mechanism

A
  • The myofibrils appear darker where the actin and myosin overlap
  • When a contraction occur, the following visible changes occur:
    • I Bands become narrower
    • Z-line become closer together (sarcomere shortens)
    • H-zone becomes narrower
    • A Band remains the same width

∴ Evidence for the sliding filament mechanism is that the I band becomes narrower, as more of the actin now overlaps with the myosin
Also, the A bands remain the same with, determined by the length of the myosin, proving that the contraction isn’t due to shortening fibres

56
Q

How are muscles stimulated to contract (process of transmission across a neuromuscular junction)

A
  • Action potential reaching the neuromuscular junction cause calcium ion protein channels to open, so Ca2+ diffuses into the synaptic knob
  • This causes synaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine
  • The neurotransmitter then diffuses across to receptors on the muscle cell-surface membrane, opening sodium channels
  • Na+ then rushes in, depolarising the membrane
57
Q

What is the process of muscle contractions

A
  • After the neuromuscular junction, the action potential travels deep into the fibre through a system of tubules called T-tubules (extensions of the cell-surface membrane that branch throughout the sarcoplasm)
  • The tubules are in contact with the ER of the muscle (sarcoplasmic reticulum), which has been actively transporting Ca2+ out of the sarcoplasm
  • The action potential causes calcium ion protein channels in the sarcoplasmic reticulum to open, so Ca2+ diffuses out of them and into the muscle sarcoplasm
  • The Ca2+ bind to troponin molecules on the Tropomyosin, causing it to pull away from the actin, unblocking the binding sites for the myosin to attach
  • ADP molecules bind to the myosin heads, which means they can now attach to the binding sites on the actin filaments, forming cross-bridges
  • Once attached, the myosin heads change their angle, pulling the actin molecules along, and releasing the ADP molecule (+ Pi)
  • Another ATP molecule then binds to the myosin head, causing it to become detached from the actin
  • The hydrolysis of this ATP then provides the energy for the myosin head to return to it’s original angle
  • The ADP left attached to the myosin head now means it is able to reattach to the actin further along
  • This process repeats, contracting the muscle as long as the actin binding sites remain exposed.
58
Q

What is the process of muscle relaxation after the stimulus stops

A
  • When the nervous stimulation ceases, Ca2+ is actively transported back into the sarcoplasmic reticulum (using energy from the hydrolysis of ATP)
  • This reabsorption of Ca2+ causes tropomyosin to move back and block the binding sites on the actin
  • ∴ Myosin heads are no longer able to bind, so the contraction ceases and the muscles relax
    • In this state, antagonistic muscles can pull actin filaments out from between the myosin (to a point)
59
Q

How is energy supplied for muscle contractions

A
  • Supplied by the hydrolysis of ATP into ADP
    (needed for the movement of the myosin heads and the active transport of Ca2+ into the sarcoplasmic reticulum)
  • Most ATP is regenerated during the aerobic respiration of Pyruvate, but this requires O(2), which is at a lower conc. in very active muscles
  • ∴ Some ATP is regenerated anaerobically in glycolysis
  • ∴ Some ATP is regenerated through the use of phosphocreatine:
    • Stored in the muscles and acts as a reserve supply of phosphate to bind to ADP and immediately form ATP (can’t supply energy directly)
    • Store replenished using phosphate from ATP when muscle is relaxed