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Adam Clarke www.brain-freeze.co.uk

Biology Unit 5 Revision Summary
Slow twitch muscle fibres Fast twitch muscle fibres
Red colour rich in oxygen storing myoglobin White less myoglobin therefore less oxygen
stored
Long-term maintaining posture/ long-distance
running
Short-term sprinting, eye movement
Aerobic respiration releases energy slowly Anaerobic respiration using glucose from
glycogen
Lots of mitochondria/myoglobin and rich blood
to supply oxygen to muscle
Fewer mitochondria/myoglobin more
myofibrils
Contract slowly Contract quickly
Myoglobin protein that holds oxygen required for muscles
Myofibrils long cylindrical organelles made of proteins specialised for contraction made of units
of sarcomeres
Sarcomeres- made of myosin and actin
Sarcoplasm muscle cells cytoplasm
Sarcolemma cell membrane of muscle fibre cells

Myosin two long polypeptide chains twisted together ending with a globular head that has ADP
and Pi attached to it. make up thick myofilaments
Actin made up of actin monomers has myosin binding sites at regular intervals - make up thin
myofilaments

Tropomyosin wraps around double actin chains, in a relaxed muscle it covers up the myosin
binding sites
Troponin attached regularly along tropomyosin chain

How muscles contract
1) calcium ions bind to troponin molecules changing their shape
2) Troponin molecules pull on the tropomyosin molecules they are attached to.
3) The tropomyosin moves from the myosin binding sites exposing them ready for action.
4) Myosin head binds to the actin forming an actomyosin bridge
5) ATP and inorganic phosphate are released from the myosin head causing the myosin to change
shape with the head bending forward moving the actin filament along the myosin filament
shortening the sarcomere.
6) Free ATP binds to the head causing another shape change in the myosin so the binding of the
head to the actin strand is broken.
7) This alongside the use of calcium ions activates ATPase in the myosin head
8) ATP is hydrolysed releasing energy to return the myosin head to its original position primed with
ADP and Pi, ready for the process to restart.
9) Calcium ions remain in the sarcoplasm and the cycle is repeated. Some are pumped into the
sarcoplasmic reticulum using ATP energy.
10) Troponin and tropomyosin return to their original positions and the contraction is complete, the
muscle fibre becomes relaxed.
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Movement
1) Muscle contraction exerts a pull on a bone
2) When they relax they stop contracting and become capable of being pulled back to their original
shape
3) Muscles are found in pairs
4) One pulls the bone in one direction, the other pulls it back to its original position - working in
opposition to each other as antagonistic pairs

Antagonistic pair muscles work in opposition of one another
Bones matrix of collagen and calcium salts
Cartilage chondrocytes collagen fibrils elastic
Tendons- bundles of collagen fibres connects muscle to bone
Ligaments bone to bone
Joints ball and socket, pivot, saddle, hinge

Control of heartbeat
1)The sinoatrial node (SAN the hearts pacemaker) sends a wave of electrical excitation causing the
atria to contract
2)Excitation spreads to similar tissue called the atrioventricular node.
3)The AVN is excited as a result of the SAN from which the wave of depolarisation passes to the
bundle of His
4)The bundle of His carries the electrical excitation from the AVN down to the Purkyne tissue.
(The Purkyne tissue penetrates through the septum of the heart spreading between and around the
ventricles)
5) As the depolarisation travels through the tissue it sets of the contraction of the ventricles starting
at the bottom and so squeezing blood out of the heart.

Bodily response to exercise
1) Atria fill with blood at start of cardiac cycle with stretch receptors in the muscle walls of the heart
responding to the stretching by sending nerve impulses to the cardiovascular control centre.
2) At the start of a period of exercise more blood than usual returns to the heart because the big
muscle blocks in the legs and arms squeeze more blood along the veins when they work
3) Increased blood flow into the atria causes the receptors to be more stretched than usual making
them send more nerve impulses to the cardiovascular centre of the brain.
4) This consequently sends more nerve impulses along the sympathetic nerve to the SAN causing an
increase in heart rate.
5) An increase in stretching of the heart atrial muscle as blood returns from the body also makes the
muscles contract harder to increase the volume of blood released in every stroke.
6) Baroreceptors found in the sinuses of the carotid arteries in the neck are also important in the
feedback control of the heart rate particularly as exercise ends.
7) An increase in blood pressure of the arteries stretches the baroreceptors which send nerve
impulses to the cardiovascular centre causing the parasympathetic system to slow down the heart
rate and cause a widening of the blood vessels to lower blood pressure.

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Adam Clarke www.brain-freeze.co.uk
8) The reverse process occurs when exercise starts as the blood vessels dilate with adrenaline
causing the blood pressure to fall
9) The stretching of the baroreceptors is reduced and when they dont stimulate the cardiovascular
control centre it immediately sends signals along the sympathetic nerve to stimulate the heart rate
and increase blood pressure again.

Control and regulation of breathing
1) Inhalation occurs when impulses from the respiratory centre (medulla) travel along sympathetic
nerves causing the intercostal muscles and the diaphragm to contract.
2)As the lungs inflate, stretch receptors in the walls of the bronchi send nerve impulses increasingly
rapidly to the respiratory centre.
3)These impulses eventually inhibit the respiratory centre and stop stimulating the breathing
muscles.
4) Breathing in stops and with the relaxation of the muscles, exhalation occurs.

Homeostasis maintenance of a steady internal state in the body regardless of changes in the
internal or external conditions
Negative feedback system a change is conditions is registered by receptors and results in effectors
stimulated to restore equilibrium
Positive feedback effectors work to increase the effect which has triggered the response

Cardiac volume volume of blood pumped in each heartbeat
Cardiac output cardiac volume x heart rate

Sympathetic nervous system excitatory speeds up heart rate
Parasympathetic inhibitory slows heart rate
Baroreceptor sensors sensitive to pressure

Components of lung volume
Ventilation rate = tidal volume x frequency of respiration

Control and regulation of breathing
1) The respiratory centre (in the medulla of the hindbrain) sends impulses along sympathetic nerves
causing the intercostal muscles and diaphragm to contract.
2) As the lungs inflate stretch receptors in the walls of the bronchi send nerve impulses to the
respiratory centre
3) Eventually the nerve impulses inhibit the respiratory centre causing it to stop stimulating
breathing muscles.
4) As breathing in stops, the muscles relax and exhalation starts.





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Adam Clarke www.brain-freeze.co.uk
Homeostasis and breathing
1) Chemoreceptors sensitive to the level of carbon dioxide send impulses back to the main
respiratory centre when carbon dioxide levels rise.
2) Impulses are then sent out to the breathing muscles so the breathing rate changes to remove the
extra carbon dioxide.
3) The chemical sensors and the stretch receptors of the muscles and lungs act on the respiratory
centre to maintain the increase in ventilation until exercise is complete.

Temperature limits
Low critical temperature this is the point at which thermoregulatory mechanisms are no longer
sufficient in conserving heat.
Low lethal temperature- individual dies due to low temperature
High critical temperature thermoregulation can no longer keep temperatures down - faster
metabolic rate with increase in temperature continues the increase in metabolic rate.

Mechanisms to increase temperature Mechanisms to decrease temperature
Vasoconstriction = arterioles constrict less
blood to surface less heat loss
Vasodilation arterioles near surface of skin
dilate more blood flows so heat can be lost
More Subcutaneous fat Less subcutaneous fat
Shivering involuntary muscle contraction Sweating high specific heat capacity of water
allows absorption of heat
Increased metabolism more respiration more
heat released
Lowered metabolism

Control of core blood temperature
1) Hypothalamus contains temperature receptors to detect changes in temperature of the blood
flowing through it
2) At higher temperatures a heat loss centre is activated sending impulses along motor nerves to
effectors that increase blood flow and sweating/ lower metabolic rates.
3) If the temperature drops the heat gain centre reacts sending nerve impulses to the skin for
vasoconstriction / for involuntary muscles contractions (shivering) and increased metabolism.

Heart rate
ECG - Electrocardiograph
P wave depolarisation of the SAN / related tissue in the atrium
QRS complex spread of excitation through the ventricles
T wave- rapid repolarisation of the Purkyne tissue in the ventricles

Arrhythmia normal electrical activity of the heart is disrupted and the rhythm of the contraction
of the muscles will change.

Ischaemic restriction in blood supply

Atrial fibrillation atria beating too fast and ineffectively
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Adam Clarke www.brain-freeze.co.uk

Tachycardia heart beats too fast

Ventricular fibrillation ventricles lose rhythm contract erratically and weakly little blood is
pumped into the arteries fall in blood pressure heart attack / body brain starved of blood

Defibrillator large electric shock to normalise abnormal heart rhythm

Osteoarthritis
1) Cartilage roughens and erodes
2) Bone ends thicken and the synovial membrane makes more fluid joint swells and the joint
capsule thickens too.
3) The whole joint becomes swollen and painful
4) The cartilage wears away completely until the bone ends touch
5)The bone ends wear away changing the shape of the joint causing severe pain

Anabolic steroids
1) Steroids pass through the cell surface membrane
2) In the cell they bind with receptor molecules
3) The complex formed acts as a transcription factor
4) the complex binds to the DNA and switches on particular genes linked to protein synthesis.
5) The RNA produced is affected changing the type and numbers of proteins and subsequently the
enzymes produced.

Erythropoietin
1) The erythropoietin peptide hormone binds to a receptor in the cell surface membrane
2) The membrane bound complex activates a second messenger in the cell cytoplasm
3) A protein kinase cascade is triggered.
4) Different proteins are activated until final product
5) This enters the nucleus and acts as a transcription factor switching on the genes linked to protein
synthesis of the enzymes required for the production of more red blood cells.


Hormones can switch on genes
1) Proteins called transcription factors in cells control the transcription of genes
2) These bind to DNA sites near the start of the genes and increase (activator) /decrease (repressor)
the rate of transcription
3) Hormones can bind to transcription factors to change body temperature
4) At cold temperatures thyroxine is released which binds to the thyroid hormone receptor causing it
to act as activator.
5) The transcription rate increases to produce more protein which increases the metabolic rate to
increase body temperature


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Adam Clarke www.brain-freeze.co.uk
Ethical issues regarding performance-enhancing drugs


For Against
Athletes have the right to make their own
decision
Some are illegal

Drug-free sport isnt fair anyway different
athletes have access to various training facilities,
coaches, equipment.
Some may gain an advantage by taking drugs
not through hard work or training
Athletes that want to compete at high levels may
only be able to using performance enhancing
drugs
Serious health risks blood pressure and heart
problems
Some may not be fully informed about the risks


























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Adam Clarke www.brain-freeze.co.uk
Sensitivity in plants
Meristem areas of cell division and elongation which occur behind the tip of a root or shoot

Red light (580 to 660nm) stimulates germination
Far red light (700-730nm) inhibits germination

Phytochrome plant photoreceptor blue-green pigment that reacts with different types of light
Pr - absorbs red light (leads to flowering)
Pfr absorbs far red light (in this form the plant is germinating, growth of internodes are inhibited as
etiolation is not necessary)
(Pfr to Pr in dark)

When one form absorbs light it converts reversibly into the other form.

Photoperiods
Long-day plants build up of Pfr during daylight hours stimulates flowering
Short-day plants lack of Pfr stimulates flowering

Tropism plant growth in response to an environmental cue
Phototropism growth of plant in response to light
Positive tropism growth towards the stimulus e.g. shoots grow towards the light
Negative tropism growth away from stimulus roots grow away from light
Geotropism growth of plant in response to gravity shoots negatively geotropic / roots positively
geotropic.

Auxins growth factor that stimulates growth of shoots by cell wall elongation.
Unilateral light light affecting plant from one side
Indoleacetic acid auxin in tips of shoots that controls tropisms causing uneven growth
Phototropism IAA moves to shaded parts to increase growth towards light














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Adam Clarke www.brain-freeze.co.uk
Myelin sheath fatty layer around nerve fibre made of Schwann cells repeatedly wrapped around
themselves.

Nodes of ranvier gaps between the Schwann cells

Axon fibres that carry impulses away from nerve cell body

Dendrons fibres that carry impulses towards the cell body


Action potential
1) Stimulus excitation of the neurone cell membrane causing sodium ion channels to open
making it permeable to sodium with ions diffusing into the neurone down the electrochemical
gradient making the inside of the neurone less negative.

2) Depolarisation if potential reaches the threshold of -55mv, more sodium channels open with
ions diffusing into the neurone.

3) Repolarisation when potential difference is +30mv, sodium channels close and potassium
channels open with the membrane being more permeable to potassium ions leading them to diffuse
out of the neurone causing the neurone to progress towards resting potential.

4) Hyperpolarisation potassium ion channels are slow to close so too many potassium ions diffuse
out of the neurone with the potential difference becoming more negative than the resting potential
at -70mV.

5) Resting potential ion channels are reset with the sodium-potassium pump returning the
membrane to its resting potential until the membrane is excited by another stimulus.

There is a refractory period during which ion channels cant be opened acting as a time delay
between one action potential and the next, ensuring that action potentials are unidirectional and
pass along as discrete impulses.












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Adam Clarke www.brain-freeze.co.uk
Synapses
1) The arrival of an impulse at a synaptic knob increases the permeability of the presynaptic
membrane to calcium ions as calcium ion channels open up.
2) Calcium ions then move into the synaptic knob down their concentration gradient.
The effect of an influx of calcium ions is to cause the synaptic vesicles which contain a transmitter
substance or neurotransmitter to move to the presynaptic membrane.
3) Each vesicle contains around 3000 neurotransmitters. Some vesicles fuse with the presynaptic
membrane releasing transmitter substance into the synaptic cleft.
4) The molecules diffuse across the gap and become attached to specific protein receptor sites on
the post-synaptic membrane.
5) This opens sodium ion channels in the membrane and there is an influx of sodium ions into the
fibre causing a change in the potential difference across the membrane and an excitatory post-
synaptic potential to be set up.
6) With sufficient EPSPs the positive charge in the post-synaptic cell exceeds the threshold level and
an action potential is set up which then travels on along the post-synaptic neurone.
7) The neurotransmitter can also have the opposite effect if different ion channels open in the
membrane allowing inwards movement of negative ions causing the inside to be more negative than
the normal resting potential.
8) An inhibitory post-synaptic potential results which makes it less likely that an action potential will
occur in the post-synaptic fibre.

The ISPs play a part in the way we hear patterns of sound
Once a neurotransmitter has had an effect it is destroyed by enzymes in the synaptic cleft so that
the receptors on the post-synaptic membrane are emptied and can react to a subsequent impulse.

Nervous system communication
Sensory neurones - transmit electrical impulses from receptors to the CNS
Relay neurons - transmit electrical impulses between sensory neurons and motor neurons
Motor neurones - transmit electrical impulses from CNS to effectors

e.g.
Dim light > light receptors detect lack of light > CNS processes info > radial muscles in the iris are
stimulated by motor neurones > radial muscles contract to dilate your pupils making them bigger

Stimulus > Receptors > CNS > effectors > response








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Adam Clarke www.brain-freeze.co.uk
Hormonal system communication
Gland - is a group of cells specialised to secrete a hormone e.g. pancreas secretes insulin
Hormones chemical messengers proteins/peptides or steroids
Glands can be stimulated by change in concentration or by electrical impulses, working by diffusing
directly into blood taken around the body to diffuse and bind to specific receptors on the
membranes of target cells causing a response in them.

e.g.
Low blood glucose concentration > receptors on pancreas cells detect low blood glucose
concentration > pancreases releases hormone glucagon into the blood > target cells in the liver
detect glucagon and convert glycogen into glucose > glucose is released into blood so glucose
concentration increases

Computerised tomography
These use x-ray radiation to produce cross-sectional images of the brain
Denser structures in the brain absorb more radiation than the less dense structures and so show up
with a lighter colour on screen.
Brain structure major structures
Brain function- can see loss of function alongside diseased/damaged part of brain
Medical diagnosis damaged/diseased part of brain e.g. stroke blood has different density so
shows up lighter colour where blood from damaged blood vessels can be seen and loss of function
determined.

MRI
These use strong magnetic fields and radio waves to produce cross-section images of the brain

Investigating structure more detail difference between normal and abnormal parts
Function damaged parts loss of function- find relationship
Medical diagnosis show damaged or diseased areas of brain tumour cells show up different to
magnetic field than healthy cells find location and size and determine what functions are affected
FMRI
Shows brain activity more oxygenated blood in active areas (to supply neurons with glucose and
oxygen). Molecules with oxygenated blood respond differently to a magnetic field than
deoxygenated blood. More active areas of the brain can be identified on an fMRI scan.

Investigating structure detailed structure similar to MRI
Brain function function carried out whilst person is in the scanner part of the brain involved will be
more active
Medical diagnosis show damaged and diseased areas as well as conditions caused by abnormal
activity in the brain where structural cause isn't obvious.


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Adam Clarke www.brain-freeze.co.uk
Receptors 1) Light enters the eye through the pupil where the amount of light that enters is
controlled by the muscle of the iris.
2) Light rays are focused by on the retina lining the inside of the eye by the lens
3) It is the retina that contains photoreceptor cells that detect light
4) In the retina the fovea is an area where lots of photoreceptors are contained
5) When light hits the photoreceptors they bleach the light-sensitive pigments causing a chemical
change.
6) A nerve impulse is triggered along a bipolar neurone (which connects photoreceptors to the optic
nerve) consequently taking impulses to the brain.

Rods (peripheral parts of retina) - only give information in black and white sensitive to low light/
movement
Cones (in fovea) give information in colour red-sensitive, green-sensitive and blue-sensitive which
are stimulated in different proportions so different colours are seen involving the pigment iodopsin.

Rods contain a light-sensitive pigment called rhodopsin which is made of retinal and opsin.
When it is dark the rods are not stimulated: 1) sodium ions are pumped out of the cell using active
transport but sodium ions diffuse back in to the cell through open sodium channels.
2) The inside of the cell is only slightly negative compared to the outside so the cell membrane is
said to be depolarised, triggering the release of neurotransmitters.
3) These neurotransmitters inhibit the bipolar neurone so it cant fire an action potential therefore
no information goes to the brain.

The process when the rods are stimulated by light.
1) Light energy causes rhodopsin to break apart into retinal and opsin in a process called bleaching
(where light energy changes cis-retinal into trans-retinal) causing the sodium ion channels to close.
2) Sodium ions are actively transported out of the cell so they cant diffuse back in.
3) Sodium ions build up on the outside of the cell making the inside of the membrane
hyperpolarised.
4) In this state it stops releasing neurotransmitters meaning that theres no inhibition of the bipolar
neurone.
5) The bipolar neurone is no longer inhibited causing it to depolarise. If the change in potential
difference reaches the threshold with an action potential transmitted to the brain via optic nerve.

Pupil reflex
1) Light enters the eye
2) the brighter the light the more action potentials travel along neurones in the optic nerve to the
brain
3) This is detected by a control centre in the midbrain
4) The impulses then travel along two neurones into further control centres where they synapse
with branches of the parasympathetic cranial nerve (the oculomotor) which transmits impulses to
the iris
5) These stimulate the effects i.e. the muscles of the iris with the circular muscles contracting and
the radial muscles relaxing so the pupil constricts.
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Adam Clarke www.brain-freeze.co.uk
Visual Cortex development
This is an area of the cerebral cortex which is used to receive and process visual information.
Neurones in the visual cortex receive information from either your left or right eye.
Neurones are grouped together in columns called ocular dominance columns with the right eye
receiving information from the right ocular dominance / left eye from left ocular dominance
columns.
The columns are the same size and are arranged in alternating pattern across the visual cortex.

Study investigating how the visual cortex develops (Hubel and Wiesel)
They used cats and monkeys to study the electrical activity of the neurones in the visual cortex.
They found that the left ocular dominance columns were stimulated when an animal used its left eye
/ the right ocular dominance columns are stimulated when an animal uses its right eye.

The experiment involved very young kittens:
1) One eye was stitched
2) Their eye was kept like this for several months
3) When the eye was unstitched, that eye was blind.
4) The ocular dominance columns for the stitched up eye were also a lot smaller than normal /
ocular dominance columns larger than normal
5) The ocular dominance columns for the open eye had expanded to take over the other columns
that werent being stimulated neurones in the visual cortex are said to have switched dominance.
6) This experiment was repeated in adult cats where it was found that they had not gone blind in the
stitched eye and that their ocular dominance columns remained the same.
7) This demonstrates how we have a critical window in which the visual cortex must develop during
infancy, because if prevented from growing then, it does not do so later in life. Additionally where
children have a cataract and are unable to develop their visual cortex they will be blind however
adults with cataracts can recover their sight.

Habituation
1) Use a stimulus to elicit a response from an organism
2) Time how long it takes to withdraw from the response
3) Evoke the response as regular intervals and record how long it takes to withdraw
4) If habituation has taken place with withdrawal time should decrease at each interval
5) If a novel stimulus is used, the response should increase the time taken to withdraw its response.









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Adam Clarke www.brain-freeze.co.uk

Ethics of using animals in medical research
For Against
Some animals share a lot of similarities to
humans and have lead to breakthroughs
Difficult to generalise results from animals
Animals are looked after - painkillers /
anaesthetics used
Pain and distress can be caused in animals
Cell cultures and computer models arent a true
representation of how cells may react animals
are the only way to study behaviour
Computer models/ cultures of human cells can
be used as safer alternatives
We have a greater right to life than other
animals
Animals right activitists say that animals have the
right not to be experimented on

L-Dopa
Because dopamine cant cross the blood-brain barrier a precursor to it is used, which allows the
sythnesis of more dopamine in the substantia nigra.
MDMA
Ecstasy blocks the serotonin reuptake transport system so synapses are completely flooded with
serotonin which cant be returned to the presynaptic knob. Alternatively the drug may make the
transport system release all the serotonin from the presynaptic knob into the synapse affecting the
post-synaptic membrane by flooding the brain with impulses.

Genetically modified microorganisms
1) Isolate and cut out required gene
2) Place gene into plasmid vector using DNA ligase
3) Place plasmid into host bacterial cell
4) Downstream processing- use bioreactor to remove human insulin for use
Genetically modified plants
1) Insert required gene into bacterium plasmid
2) Infect plant with modified bacteria so the gene becomes part of the plant chromosome.
3) Tumour develops in the plant with cells containing gene tumour cells are cultured with new
plants grown containing the new genes.

Ethics of using genetic modification
For Against
Technology may be used only for wealthy Genetic modification violates rights of organism
GM Crops higher yield / more nutrition
reduce famine
Transmission of genetic material crossover
with wild organisms
Pest resistant save money Safety of genetically modified food
Use GMO to make enzymes
GM bacteria human insulin
Vaccines in plant tissue environment already
suitable

Cheaper drugs more available