Biology Unit 5

Topic 7 Run for your life

Fast and Slow Twitch Fibres

Sliding Filament Theory

1.

When the muscle is relaxed, the binding sites on the

actin are covered by tropomyosin.

2.

When the membrane of the muscle is depolarised,

calcium ions are released from the sarcoplasmic
reticulum and bind with the troponin which displaces
tropomyosin from the binding site, exposing the myosin
binding sites on the actin filaments.

3.

The myosin head binds to the myosin binding sites on

the actin, using energy from ATP and forming cross
bridges.

4.

As the myosin heads attach to the actin filaments, ADP

and Pi on the myosin head are released.

5.

The myosin changes shape, causing the myosin head to

nod forward. The attached actin moves over the myosin.

6.

An ATP molecule binds to the myosin head. This causes

the myosin head to detach.

7.

An ATPase on the myosin head hydrolyses the ATP,

forming ADP and Pi.

8.

This hydrolysis causes a change in the shape of the

myosin head. It returns to its upright position. This
enables the cycle to start again.

Questions:
1. Name 2 roles for ATP in the contraction of muscle fibres
Disconnecting myosin head from actin
Active transport of calcium ions back to the
sarcoplasmic reticulum.
2. How does rigor mortis occur?
Lack of ATP means cells are unable to use active
transport to pump calcium ions back to the
sarcoplasmic reticulum
Myosin head unable to detach from actin

Joints and Movements

Muscles bring about movement at a joint. Muscles can only
pull; they cannot push, so at least two muscles are needed to

move a bone to and fro. Pair of muscles that work this way are
described as antagonistic.
A muscle that contracts to cause extension of a joint is called an
extensor; the corresponding flexor muscle contracts to reverse
the movement.

Joint Structure
Joints are separated by a cavity filled with synovial fluid, which
enables them to move freely. It also acts as a lubricant.
The bones are held in position by ligaments that control and
restrict the amount of movement in the joint. Ligaments join
bone to bone. They are strong and flexible.
Tendons attach muscles to the bones, enabling the muscles to
power joint movement.
Cartilage protects bones within joints. They absorb synovial
fluid and act as a shock absorber.
Muscle cells have several nuclei (multinucleate) because a
single nucleus cannot effectively control the metabolism of such
a long cell.

Reaction of aerobic respiration

In aerobic respiration, the hydrogen stored in glucose is

brought together with oxygen to form water again. Overall,
there is a release of energy and this can be used to generate
ATP.

ATP

Investigating respiration
Rate of respiration of an organism is an indication of its
demand for energy. Respiration rate is the uptake of oxygen per
unit time is measured by the means of a respirometer. A
respirometer detects changes in pressure or volume of a gas.

Potassium hydroxide or soda lime absorbs carbon dioxide

released by the organism. Therefore, only oxygen gas causes a
change in volume.

Glycolysis
The initial stages of carbohydrate breakdown known as
glycolysis occur in the cytoplasm of cells, including the
sarcoplasm of muscle cells. It starts with the breakdown of sixcarbon glucose molecule into two molecules of pyruvate (3C).
Glycolysis does not need oxygen. It is the first stage of aerobic
and anaerobic respiration and is the only stage of anaerobic
respiration.
The first reactions of glycolysis need an input of energy from
ATP to get things started, because glucose (a hexose sugar) is
quite stable and unreactive.
[Glucose is phosphorylated]. Two phosphate groups are added
to the glucose from two ATP molecules, and this increases the
reactivity of glucose. It can now be split into two molecules of 3carbon (3C) compounds.
Each 3C sugar is oxidised, producing a 3-carbon compound,
pyruvate.
Hydrogen is removed and transferred to the hydrogen acceptor
NAD. Enough energy is released at this stage to make two
molecules of ATP. Phosphate from the intermediate compounds
is transferred to ADP, creating ATP. This is substrate level
phosphorylation, because energy for the formation of ATP
comes from the substrates.
Glycolysis reactions yield a net gain of two ATPs, two pairs of
hydrogen atoms and two molecules of 3-carbon pyruvate.

The link reaction

If oxygen is available, the 3C pyruvate created at the end of

glycolysis passes into the mitochondria. There it is completely
oxidised, forming CO2 and H2O.
In the presence of oxygen, 3 things happen:
1. The pyruvate is decarboxylated (a molecule of CO2 is
removed released as a waste product).
2. The pyruvate is also dehydrogenated (hydrogen is
removed). The hydrogen is transferred to the hydrogen
acceptor NAD+ to form NADH + H+.
3. The resulting acetate (2C) combines with coenzyme A
(CoA) to form the 2-carbon molecule acetyl coenzyme A
(acetyl CoA), which then enters the Krebs cycle.

Krebs cycle
Krebs cycle takes place in the matrix of the mitochondria,
where the enzymes that catalyse the reactions are located and
includes the following reactions:
Acetyl CoA (2C) combines with a 4-carbon compound to create
one with six carbons.
A series of reactions take place where the 6-carbon compound
is both decarboxylised and dehydrogenated, recreating the 4carbon compound.
In addition, one of the steps in the cycle involves substrate level
phosphorylation with direct synthesis of a single ATP.
CO2 is released a waste product and the hydrogen acceptors
NAD and FAD.
As a result, the 4-carbon compound is regenerated to combine
with more acetyl CoA.

So after one turn of Krebs cycle, we have

3 molecules of reduced NAD

The electron transport chain
1 molecule of reduced FAD
1 molecule of ATP
2 molecules of CO2

Two molecules of acetyl CoA enter Krebs cycle for each

molecule of glucose, so the cycle turns twice for each glucose
molecule, so we get each of the products timed by two.
The most important role of Krebs cycle is to provide hydrogen
that can be used in the electron transport chain to provide
energy for the formation of ATP.

The electron transport chain

The electron transport chain provides the means by which the
energy from the hydrogen atoms removed from the compounds
in Krebs cycle, glycolysis and the link reaction by coenzymes
can be used to make ATP. For most hydrogen produced, the
coenzyme NAD is the hydrogen acceptor. But those released in
one step of the Krebs cycle are accepted by the coenzyme FAD
rather than NAD.
Oxygen is required for this final stage of aerobic respiration.
The reactions take place on the inner membrane of the
mitochondria.
When a coenzyme accepts the hydrogen with its electron, the
coenzyme is reduced, becoming reduced NAD or reduced FAD.
The reduced coenzyme shuttles the hydrogen atoms to the
electron transport chain on the mitochondrial inner membrane.

The electron transport chain involves a chain of carrier

molecules along which hydrogen atoms and electrons are
passed.
The hydrogen atoms are passed on to other carrier
molecules from the hydrogen carriers [reduced NAD and
FAD]
Reduced NAD is the first carrier in the chain; it passes its
hydrogen on to FAD.
The hydrogen atoms split into hydrogen ions (H+) and
electrons.
The electrons are transferred along a series of electron carriers.
The hydrogen ions stay in solution in the space between the
inner and outer membranes of the mitochondria.
Protons move across the inner mitochondrial membrane
creating high H+ concentrations in the intermembrane
space.
H+ diffuses back into the mitochondrial matrix down the
electrochemical gradient.
H+ diffusion allows ATPase to catalyse ATP synthesis.
Finally, the electrons recombine with the hydrogen ions to
form hydrogen atoms and are passed on to oxygen to form
water. Oxygen is therefore the final electron acceptor.
ATP is formed at 3 points along the chain, so for each
reduced NAD, 3 ATP molecules are made. For each
reduced FAD, 2 ATP molecules are made. Formation of
ATP in this way is called oxidative phosphorylation.
Stage

Site in Cell

Glycolysis

Cytoplasm

Link reaction

Matrix of
mitochondrion

Number of ATPs
made
2 [4 made, 2 used] per
glucose
None

Krebs cycle
Electron
transport chain

Matrix of
mitochondrion
Inner membrane if
mitochondrion

2 [one per turn] per

glucose
34 per glucose

ATP synthesis by chemiosmosis

The cristae on the mitochondrion give the inner membrane a
large surface area, so there is more room for electron carriers
and ATP formation.
The chemiosmosis theory provides a model to explain the
synthesis of ATP in oxidative phosphorylation.
The energy released by the electron transport chain is
linked to pumping hydrogen ions from the matrix into the
space between the two membranes of the mitochondrion.
This results in a higher concentration of hydrogen ions in
the intermembrane space than in the matrix of the
mitochondrion: an electrochemical gradient is set up.
The hydrogen ions pass back into the matrix through the
stalked granules, along the electrochemical gradient. As
they do, their electrical potential energy is sued to make
ATP from ADP and Pi. ATPase catalyses the reaction.

Anaerobic respiration
This is respiration in the absence of oxygen. In the absence of
oxygen, only glycolysis can operate. As a result, the energy
yield in anaerobic respiration is low.
Without oxygen to accept the hydrogen ions and electrons, the
electron transport chain ceases; the reduced NAD created
during glycolysis, the link reaction and the Krebs cycle is not

oxidised. Without a supply of oxidised NAD, most respiration

reactions cannot continue.
In muscle cells for example, glycolysis can occur, but the
pyruvate is converted into lactate. The reduced NAD made in
glycolysis again passes its hydrogen on to pyruvate, this time
reducing it to lactate and an oxidised form of NAD is produced.
Glucose lactate + 2ATP
The net yield is just 2 ATP molecules per glucose molecule. The
end product of anaerobic respiration is lactate, which builds up
in the muscles and must be disposed of later. As lactate
accumulates, [lactic forms lactic acid in solution] the pH of cell
falls, inhibiting enzymes that catalyse the glycolysis reactions.
They glycolysis reactions and the physical activity depending on
them cannot continue.
As pH reduces, substrate may no longer be able to bind to
enzymes active site.
After a period of anaerobic respiration, most of the lactate is
converted back into pyruvate. It is oxidised directly to CO2 and
H2O via the Krebs cycle, thus releasing energy to synthesise
ATP. As a result, oxygen uptake is greater than normal in the
recovery period after exercise. This excess oxygen requirement
is called the oxygen debt. It is needed to fuel the oxidation of
lactate.
When oxygen becomes available again, the lactate is broken
down. First it is carried in the bloodstream to the liver where it
is converted back into pyruvate. About 1/5 is used to release
energy in aerobic respiration and the rest is converted into
glycogen. The oxygen required to break down the lactate is
called the oxygen debt.

At the end of the activity, the oxygen debt is repaid by

continuous deep and rapid breathing.
Cardiac Output

Blood comes back from the body and it enters into the
heart via the vena cava into the right atrium.
As it enters into the right atrium, the atrium contracts,
which pushes the blood into the right ventricle.
Once the blood gets into the right ventricle, the right
ventricle contracts and that pushes the blood through the
semilunar valves into the pulmonary artery.

 That blood goes to the lungs and picks up oxygen,

because you are breathing in oxygen and that oxygenates the
blood.
Both processes happen simultaneously, blood is being
pumped to the lungs at the same time it's being pumped to the
rest of the body.
The volume of blood pumped in one minute is called the cardiac
output. This increases during exercise.
Cardiac output depends on the volume of blood ejected from
the left ventricle (the stroke volume) and the heart rate:
Cardiac output = Stroke volume x Heart rate

Stroke volume
The stroke volume is the volume of blood pumped out of the left
ventricle each time the ventricle contracts. How much blood the
heart pumps out with each contraction is determined by how
much blood is filling the heart, that is, the volume of blood
returning to the heart from the body.
In diastole, during exercise the heart fills with a larger volume
of blood. The heart muscle is stretched to a greater extent,
causing it to contract with a greater force and so more blood is
expelled. This increases stroke volume and cardiac output.
When the body is at rest, the ventricles do not completely
empty with each beat; approximately 40% of the blood volume
remains in the ventricles after contraction.

Heart rate
Differences in resting heart rate are caused by many factors.
For example, our hearts differ in size, owing to body differences
in body size and genetics. A larger heart will usually have a

lower resting heart rate. It will expel more blood with each
heart beat and so, other things being equal, does not have to
beat as frequently to circulate the same volume of blood around
the body.

Control of heart rate

The heart is myogenic; it can contract and relax without having
to receive impulses from the nervous system.
The cardiac cycle is started by specialised cardiac muscle tissue
in the wall of the right atrium called the sinoatrial node SAN.
The cells of the SAN set the rhythm at which all the other
cardiac muscle cells beat and so can control the speed of the
cycle.
SAN sends out electrical impulses to the rest of the atria. These
impulses spread out in a wave of depolarisation over the atrial
walls. The cardiac muscle in the walls of both atria contract in
rhythm with the impulses from the SAN, so both right and left
atria contract at the same time.
The impulse travels to some specialised cells called the
atrioventricular node AVN. From here, the impulse is
conducted to the ventricles after a delay of about 0.13 seconds.
The delay ensures that the atria have finished contracting and
that the ventricles have filled with blood before they contract.
After this delay, they signal reaches the Purkyne fibres. These
are large, specialised muscle fibres that conduct impulses
rapidly to the apex of the ventricles. There are left and right
bundles of fibres and they are collectively called the bundle of
His.
The first ventricular cell to be to be depolarised is at the apex of
the heart, so that contraction begins at this point and travels

upwards towards the atria. This produces a wave of contraction

moving up the ventricles, pushing the blood into the aorta and
the pulmonary artery.

Electrocardiograms ECG
The electrical activity of the heart can be detected and displayed
on an electrocardiogram ECG, a graphic record of the electrical
activity during the cardiac cycle. The ECG is a useful diagnostic
tool in that it can detect these irregularities.
In an ECG, electrodes are taped to the persons chest and limps
to record the electrical currents produced during the cardiac
cycle. When there is a change in polarisation of the cardiac
muscle, a small electrical current can be detected at the surface
of the skin. This is what an ECG measures.

The P wave shows depolarisation of the atria, leading to atrial

contraction (atrial systole)

The PR interval shows the time taken for impulse to be

conducted from the SAN across the atria to the ventricles,
through the AVN.
QRS complex shows the wave of depolarisation resulting in
contraction of the ventricles (ventricular systole)
T wave shows repolarisation of the ventricles during the hearts
relaxation phase (diastole).
ECG can be used to measure heart rate. A heart rate less than
60bpm is known as bradycardia. Tachycardia is heart rate
greater than 100bpm.
ECG can provide information about abnormal heartbeats, areas
of damage and inadequate blood flow.

Breathing and exercise

Oxygen diffuses from the alveoli into the blood and carbon
dioxide diffuses out of the blood capillaries into the alveoli.
The volume of air we breathe in and out at each breath is our
tidal volume. Ventilation rate is the total volume of air taken
into the lungs in 1 minute.
Ventilation rate = Breathing rate x Tidal volume

Nervous control of heart rate

Heart rate is under the control of the cardiovascular control
centre located in the medulla of the brain. Changes in cardiac
output are controlled by the autonomic nervous system. There
are 2 distinct parts to the autonomic nervous system: The
sympathetic SNS and the parasympathetic nervous system
PNS.

Stimulation of the sinoatrial node SAN by the sympathetic

nerve causes an increase in heart rate [increases cardiac output]
by:
Increasing the heart rate
Increasing the stroke volume
Stimulation of the sinoatrial node SAN by the parasympathetic
nerve causes a decrease in heart rate [decreases cardiac output]
by:
Decreasing the heartbeat rate
Decreasing the stroke volume
These 2 opposing systems work on a negative feedback
principle, involving 2 centres in the medulla of the brain.
During vigorous exercise, the CO2 level in the blood increases
as a result of increased respiration. This causes a lowering of
the blood pH, so it becomes more acidic. The cardiovascular
control centre detects accumulation of CO2 and lactate in the
blood, reduction of oxygen in the blood and increased
temperature.
Mechanical activity in muscles and impulses are sent to the
cardiovascular control centre. This changes result in a higher
heart rate [increase in cardiac output]. Blood flow to the lungs
increase, so the extra CO2 is removed.
As the sound of a pistol, skeletal muscles contract and stretch
receptors in the muscles and tendons are stimulated. They send
impulses to the cardiovascular control centre. This in turn
raises the heart rate via the sympathetic nerve. There is an
increase in venous return, which leads to a rise in the stroke
volume. The elevated heart rate and stroke volume result in

higher cardiac output, thus increasing transporting oxygen and

fuel to muscles more quickly.
Stretch muscles in the walls of the aorta can detect changes in
blood flow to them, due to blood pressure.
To prevent it rising too far, pressure receptors in the aorta and
in the carotid artery send nerve impulses back to the
cardiovascular control centre. Inhibitory nerve impulses are
then sent from here to the sinoatrial node. In this way, an
excessive rise in blood pressure is avoided through negative
feedback, which prevents further rise in heart rate.

Hormonal effects on heart rate

Fear, excitement and shock cause the release of the hormone
adrenaline into the bloodstream from the adrenal glands
located above the kidneys.
Adrenaline has an effect on the heart rate similar to stimulation
by the sympathetic nerve. It has a direct effect on the sinoatrial
node, increasing the heart rate to prepare the body for any
likely physical demands.

The control of breathing

The ventilation centre in the medulla oblongata of the brain
controls breathing.
Inhalation
The ventilation centre sends nerve impulses ever 2-3 seconds to
the external intercostal muscles and diaphragm muscles. Both
of these sets of muscles contract causing inhalation.
Exhalation

As the lungs inflate, stretch receptors in the bronchioles are

stimulated. The stretch receptors send inhibitory impulses back
to the ventilation centre. As a consequence, impulses to the
muscles stop and the muscles relax, stopping inhalation and
allowing exhalation.
Exhalation is caused by the elastic recoil of the lungs and by
gravity helping to lower the ribs.
During exercise, the rate of respiration increases in your cells,
so more oxygen is used up and more CO2 is produced. It is the
rise in CO2 that triggers the changes in your breathing.

Controlling breathing rate and depth

A small increase in blood CO2 concentration causes a huge
increase in ventilation.
CO2 dissolves in the blood plasma making carbonic acid
Carbonic acid lowers pH of the blood.
Chemoreceptors sensitive to hydrogen ions are located in the
ventilation centre of the medulla oblongata. They detect the rise
in hydrogen ion concentration.
Impulses are sent to other parts of the ventilation centre.
Impulses are sent from the ventilation centre to stimulate the
muscles involved in breathing.
Increasing CO2 and decrease in pH leads to an increase in rate
and depth of breathing, through the more frequent and
stronger contraction of the appropriate muscles. The more
frequent and deeper breaths maintain a steep concentration
gradient of CO2 between the alveolar air and the blood. This in
turn ensures the removal of CO2 and uptake of oxygen. The

opposite response occurs with a decrease in CO2 [negative

feedback].

Controlling breathing during exercise

The motor cortex of the brain controls movement. As soon as
exercise begins, impulses from the motor cortex have a direct
effect on the ventilation centre in the medulla, increasing
ventilation sharply.

Spirometer
A spirometer is used to measure the volume of air that moves in
and out of the lungs. It is basically a clear, plastic box, filled at
the bottom with water. The space inside the spirometer
contains oxygen.
When you breathe out, the box moves up (pen moves up) and
when you breathe in, the box moves down (pen moves down).
With most spirometers, the exhaled air passes through a
container of soda lime, a chemical that absorbs CO2.
Tidal volume is the volume of air breathed in and out during a
single breath.
Vital capacity is the maximum volume of air that can be
breathed in or out of the lungs.

Negative feedbacks
In humans, if cells are to function properly, the bodys internal
conditions must be maintained within a narrow range of cells
optimum conditions. The maintenance of this stable internal
environment is called homeostasis.
Each condition that is controlled has a norm value or set point
that the homeostatic mechanisms are trying to maintain.

Receptors are used to detect deviations from the norm. These

receptors are connected to a control mechanism, which turns
on or off effectors to bring the condition back to the norm
value. A deviation from the norm results in a change in the
opposite direction back to the norm, the process is known as
negative feedback. These corrections mean that the actual value
fluctuates in a narrow range around the norm.

Homeostasis Temperature control

Thermoregulation is the control of body temperature.
Each control system must have:
A receptor [sensor] which detects a stimulus. A stimulus is
a change in the level of the factor being regulated.
A coordinator, which receives and controls information
from the receptor and triggers the action that will correct
the change.
An effector, which carries out the action that brings about
the change.
Our core body temperature is very stable at 37.50C. This body
temperature allows enzyme controlled reactions to occur at a
reasonable rate. At lower temperatures, the reactions would
occur too slowly for the body to remain active; at higher
temperatures the enzymes would denature.
In humans, temperature is maintained by a negative feedback
system. This system involves receptors that detect changes in
the blood temperature. These receptors are located in a
structure in the brain called the hypothalamus. The
hypothalamus is the control mechanism and acts as a
thermostat, turning on the effectors necessary to return the
temperature to the norm.

There are also thermoreceptors in the skin that detect

temperature changes. If the skin is warm, then impulses are
sent to the hypothalamus initiating the heat-loss responses and
inhibiting heat-gain responses. If the skin is cold, the opposite
happens.