Unit 5: Energy, Exercise and Coordination

Topic 7: Run for your life.

7.1. Muscles and Movement:

7.1.1. Muscles:
Muscles connect and cause movement at a joint –
usually by working in co-ordination with other
muscles.

Muscles can only pull and cannot push, ∴ at any

joint two or more muscles are needed to cause
movement.

A pair of muscles that work together to cause movement is called: antagonistic muscles, as
they work together by working against each other. e.g.: lifting knee: hamstrings pull, quads
relax.

A muscle that:
Contracts to cause extension are called an
extensor.
The muscle that contracts to reverse this
movement is called the flexor.

7.1.2. Joints:
There is a type of joint that occupies the knee, hip and ankle joints. They are called the
Synovial joints as they are filled with Synovial fluid.

Structure and Function:

Structure – the arrangement of and relations to a complex something
Function – an activity or purpose natural to or intended for a person or thing

The joint consists of the following components and here’s what they do:

Muscle: organ that produces movement by

contraction.
Bone: Support and structure.
Tendon: Attaches muscle to bone and enables
muscle to power joint movement.
Cartilage: Tissue made of collagen that absorbs
synovial fluid, acts as a shock absorber and protects
bone ends within joints.
Pad of Cartilage: Additional protection.
Fibrous Capsule: Encloses joint.
Synovial membrane: Secretes synovial fluid.
Synovial fluid: Lubricant.
Ligament: Attaches bones to bone to stabilise joint,
and control and restrict movement in the joint.

Types of synovial joints include:

Ball and socket: Ball like surface in cup like end – movement in all three planes.
Hinge: Convex shape in concave - restricted to one plane.
Gliding: One flat surface slides on another flat surface.
Pivot: Part of bone fits into ring shaped structure.
1|Run for your life

Bones are usually susceptible to stresses such as:

Compression: Pushing
Tension: Pulling
Shear: Sliding

7.1.3. Structure of a skeletal muscle:

Skeletal muscles (voluntary muscles) are attached to bones or skin to control movement.
They are long and cylindrical and made up of bundles of muscle fibres (or muscle cells). A
muscle fibre is a single multinucleated cell. It may be several cm’s long but less than 0.1 nm
in diameter.

Multinucleated = More than one nucleus per cell (many cells fused to form one cell).

Muscles fibres appear striped ∴ are called striated or striped. These stripes make up the bulk
of the fibre and are striated due to the repeating bands of actin and myosin that run alongside
the myofibrils.

One muscle fibre is made up of mass of

myofibrils lined up in parallel and
covered with vast systems of tubes
called the Sarcoplasmic Reticulum.
These myofibrils are lined up alongside
mitochondria in the muscle cell and are
made up of a series of contractile units
called sarcomeres. These sarcomeres
contain two types of protein: Actin and
Myosin.

All of this is contained inside a muscle

cell matrix or ‘cytoplasm’ called the
sarcoplasm which is enclosed by the
sarcolemma.

Myofibrils are made of the 2 proteins:

Myosin:
-thick protein filaments (Bulbous ‘golf
club’ like heads)
Actin:
-thin protein filaments

A Sarcomere is one set of myosin and

actin fibres.
Many sarcomeres make up the
Myofibrils.
2|Run for your life

Structure of a sarcomere:

The Z-line is the imaginary line where one sarcomere joins another.
The thick myosin filaments with ‘golf club heads’ lie in central part. The actin and myosin
slide past each other, ∴ the sarcomere shortens and muscle contracts.

Actin can be further broken down

into Troponin (a protein that has
binding sites) which is covered by
Tropomyosin.

7.1.4. Sliding Filament Theory:

How it works:
When a muscle is stimulated/contracted, actin and myosin filaments slide between each
other. As a result of this movement, each sarcomere gets shorter and thus the whole muscle
fibre gets shorts (contracts):

Steps:
1. Action potential.
2. Ca2+ ions diffuse – from sarcoplasmic
reticulum.
3. Ca2+ binds to troponin – on actin.
4. Troponin moves – as a result tropomyosin
moves.
5. Binding sites exposed.
6. Myosin forms cross bridges.
7. ATPase hydrolyses ATP on myosin head
to ADP.
8. Energy release: angle of myosin head
changed.
9. Power stroke.
10. Myosin moves to the centre of sarcomere.
11. More ATP released – myosin to original
place.
12. If and when simulation stops, Ca2+ goes back to the sarcoplasmic reticulum.
3|Run for your life

The process explained:

1. An action potential arrives at the sarcolemma
(cell surface membrane) of a particular muscle
fibre. Here, the A.P. travels along the membranes
of the sarcoplasmic reticulum, deep into the muscle
fibre causing the release of an influx of Ca2+ ions
(which were stored in the S.R.) into the muscle
fibre.
2. In a relaxed myofibril, proteins called tropomyosin
and troponin cover binging sites on the actin
filaments. The calcium ions cause the
tropomyosin and troponin to change their original
shape, which uncovers the binding sites.
3. Heads of the myosin molecules, next to the
uncovered binding sites, now bind with the actin
filaments which form ‘cross-bridges’ between
them
4. Myosin heads tilt, pushing the actin filaments
along
5. ATP binds with the myosin heads and is
hydrolysed by ATPase, releasing some energy.
The synthesis of this energy causes the myosin
heads to disconnect themselves from the actin
filaments
6. The disconnected myosin heads flip back to their
original position, and bind with another exposed
binding site on the actin filament. They then tilt
again, pushing the actin filament along.
7. This process repeats over and over again, as long
as the action potentials continue to arrive
4|Run for your life

7.2. Cellular Respiration – the Energy Supply:

ATP (universal energy currency):

o storage of energy, made by respiration in sarcoplasm and cytoplasm
o energy used in all cellular reactions comes from ATP
o energy released by breaking 3rd phosphate from ATP molecule
o some already in muscles when exercising

Adenine Triphosphate (ATP):

o water soluble
o easily transported within cells
o contain many electrons around phosphate
groups ∴ high energy potential

Energy released when:

o Enzyne ATPase hydrolises ATP,
o ATP turns to ADP+Pi
o This seperation is what releases
energy.

Measuring the rate of respiration

1. Place organisms in a tube, with a non-living material of the same mass in another tube.
2. Soda lime or KOH is placed in each tube to absorb the CO2 produced, and cotton wool or
gauze is used to prevent contact with the organisms.
3. Coloured fluid is poured into the reservoir of each manometer and allowed to flow into the
capillary tube (make sure there are no air bubbles). You must end up with the same
quantity fluid in the two manometers.
4. Closing the spring clips, attach the manometers to bent glass tubing, ensuring a totally
airtight connection.
5. Next, place the bungs into the tops of the tubes.
6. As the organisms respire, they take oxygen from the air around them and give out CO2.
The removal of oxygen from the air inside the tube reduces the volume and pressure,
causing the manometer fluid to move towards the organisms to fill the pressure space.
The CO2 respired has been absorbed by the soda lime or KOH.
You would not expect the manometer with no organisms’ fluid to move but may do so because
of temperature changes. You must control this variable by subtracting the distance moved in
the control manometer from the distance moved in the experimental manometer, to give an
adjusted distance moved.
Calculate mean distance moved by the manometer per minute (volume of oxygen absorbed
by the organisms per minute):
Volume of liquid in a tube = length x πr2
 5|Run for your life

7.2.1. Respiration:
𝐺𝑙𝑢𝑐𝑜𝑠𝑒 + 𝑜𝑥𝑦𝑔𝑒𝑛 → 𝐶𝑎𝑟𝑏𝑜𝑛 𝐷𝑖𝑎𝑜𝑥𝑖𝑑𝑒 + 𝑤𝑎𝑡𝑒𝑟 + 𝑒𝑛𝑒𝑟𝑔𝑦
𝐶6 𝐻12 𝑂6 + 6𝑂2 → 6𝐶𝑂2 + 6𝐻2 𝑂 + 38𝐴𝑇𝑃
Respiration: a process in living organisms in which the chemical bond energy in glucose
molecules is used to convert 38 ADP molecules into 38 ATP molecules - the oxidation of
energy-containing organic molecules. Oxygen is required and CO2 and water are produced
as waste. There are two types, aerobic and anaerobic.

All cells obtain their useable energy through

respiration. The energy released from this process
combines ADP with an inorganic phosphate to
make ATP. It is with ATP that cells perform their
functions; it is the energy currency of cells.
Glycolysis is the starting point of both all
respiration.

Types of respiration (classified according to the

need of oxygen):
 Anaerobic respiration does not require oxygen
(O2).
 Aerobic respiration requires oxygen (O2).

Respiration occurs in 4 distinct steps:

Step Reactants Products Summary
2 x Pyruvate A 6C glucose molecule is split into two 3C pyruvate molecules.
1. Glycolysis 1 x Glucose
4 x ATP Some ATP used to split glucose molecule in the first part of
(cytoplasm) 2 x ATP
2 x NADH glycolysis.
1 x Acetyl CoA
2.1. Link Reaction 1 x Pyruvate 3C Pyruvate is split into a 2C molecule, which is attached to a CoA
1 x CO2
(mitochondria matrix) 1 x CoA enzyme to form Acetyl CoA. Remaining C atom is used to form CO2.
1 x NADH
1 x CoA CoA gives its 2C atoms to a 4C molecule to form a temporary 6C
1 x ATP molecule. In a series of steps the 6C molecule releases the two C
2.2. Krebs’ Cycle
1 x Acetyl CoA 2 x CO2 atoms as CO2,eventually re-forming the starting 4C compound.
(mitochondria matrix)
3 x NADH Cycle is then ready to repeat itself. As the cycle turns ATP, NADH &
1 x FADH 2 FADH2 are formed.
4.Oxidative 10 x NADH 34 x ATP
The electron transport chain uses the NADH and FADH2 made in
Phosphorylation 2 x FADH2 6 x H2 O
previous steps to make lots of ATP.
(mitochondria cristae) 6 x O2

1. Glycolysis:
 Takes place in the cytoplasm of cells and sarcoplasm of muscles.
 No oxygen needed (anaerobic respiration)
 6C glucose broken down into 3C pyruvates (requires 2 ATPs)
 Rapidly produces ATP

Process:
Galactose (glucose polymer) must first be split into Glucose
1. Glucose is unreactive,
- It’s phosphorylated – 2 phosphate groups removed from 2 ATP molecules to
release 2 ADP molecules
- Attached to the glucose molecule.
∴ makes active glucose: Fructose biphosphate
2. Fructose biphosphate undergoes lysis,
- Splitting of Fructose biphosphate.
- Makes Triose phosphate .
- A 3 carbon sugar.
6|Run for your life

3. Two inorganic phosphate groups are added to the Triose phosphate

- Triose Phosphate now oxidised by a dehydrogenase + NAD (Nicotinamide adenine
dinucleotide).
- 2NAD converted into 2 reduced NAD or 2NADH.
- NAD is reduced, gains electrons.
- 2 ATPs are produced by picking up the inorganic ATPs.
- As the hydrogen is removed by NAD the energy released is used to form 2ATPs.
- This extra energy is from the fact there is less energy in the triose phosphate so
therefore the remaining energy is transferred to the ATP formation: It is called,
substrate level phosphorylation

𝑁𝐴𝐷 + + 2𝐻 + + 2𝑒 − → 𝑁𝐴𝐷𝐻2

2 x Pyruvate released (3 carbon sugar)

4TPs are made with net gain of 2
2ATPs are made due to the substrate level phosphorylation.

Overall; 4ATP are made, 2NADH are made and 2ATPs are used.
Net gain: 2ATP and 2NADH

2. 1. Link Reaction:
If oxygen is available, the pyruvate now moves into a mitochondrion, where the Link
Reaction and the Krebs Cycle take place. During these processes, the glucose is completely
oxidised.
Carbon dioxide is removed from the pyruvate. This CO2 diffuses out of the mitochondrion
and out of the cell. Hydrogen is also removed from the pyruvate, and is picked up by NAD,
producing reduced NAD. This converts pyruvate into a two-carbon compound which
immediately combines with coenzyme A to produce acetyl coenzyme A (acetyl CoA).

In the Link Reaction a Pyruvate molecule (3C) is split into a 2C molecule and a CO2. The 2C
molecule is attached to a CoA enzyme, forming Acetyl CoA.

(Remember, two molecules of Pyruvate were made at the

end of Glycolysis, therefore the Link Reaction happens
twice)

Overall; 2NADH and 2 CO2 are made.

Net gain: 2NADH
7|Run for your life

2.2. Krebs Cycle:

Acetyl CoA has two carbon atoms. This combines with a four-carbon compound to
produce a six-carbon compound. This is gradually converted to the four-carbon compound
again through a series of enzyme-controlled steps. These steps all take place in the matrix
of the mitochondrion, and specific enzymes control each step.
During this process, more CO2 is released and diffuses out of the mitochondrion and out of
the cell. More hydrogen’s are released and picked up by NAD and another coenzyme FAD.
This produces reduced NAD & FAD. At one point, ATP is produced.
Both the link reaction and the Krebs cycle occur twice for every glucose molecule because
glycolysis produces two pyruvate molecules.

- Acetyl Coenzyme A joins with 4C molecule

from the end of the Krebs Cycle making 6C
citric acid.
(Coenzyme A goes back to link reaction to bring
more molecules of acetate)
- Dehydrogenated - NAD comes in and takes H+
and e- makes NADH
- Decarboxylated - CO2 released
- ATP released via substrate level
phosphorylation
- Decarboxylated again - CO2 released
- Dehydrogenated again 3 times:
Twice, NAD picks up and becomes reduced
And the last FAD picks up and becomes reduced.
- 4C compound left that goes to the start of the reaction to pick up acetate.

From 2 pyruvates (one glucose)

-2 FADH
-2 CO2
-6 NADH
-2 ATP

 Oxidative Phosphorylation:
Oxidative phosphorylation is the process of generating ATP using the NADH and FADH2.
It involves two parts – electron transport chain and chemiosmosis.

The hydrogen’s picked up by the coenzymes are now split into electrons and protons.
The electrons are passed along an electron transport chain (ETC) on the inner membrane
in the mitochondrion.
8|Run for your life

As they move along the chain, the electrons lose energy. This energy is used to actively
transport hydrogen ions from the matrix of the mitochondrion, across the inner membrane
and into the space between the inner and outer membranes. This builds up a high
concentration of hydrogen ions in this space.
The hydrogen ions are allowed to diffuse back into the matrix through special channel
proteins (ATP synthase) that work as ATPase’s. The movement of the H+ ions through the
ATPase’s provides enough energy to cause ADP + Pi to make ATP.
The active transport and subsequent diffusion of H+ across the inner mitochondrial
membrane – CHEMIOSMOSIS
At the end of the chain, the electrons reunite with protons and they combine with oxygen
to produce water. Oxygen is thus required in aerobic respiration as it acts as the final
electron acceptor for the hydrogen’s removed from the respiratory substrate during
glycolysis, the link reaction and the Krebs cycle.

3.1. Electron transport chain:

Takes place on the inner membrane of the mitochondria. Oxygen must be available for ATP
synthesis.

Reduced NAD and FAD come in and give their hydrogen protons to the carriers.
The hydrogen atoms are actively pumped into the mitochondrial space, from the matrix.
-The electrons are also stripped off the NADH and are passed along the carriers to the last
one where they are pumped back into the matrix.

-The collection of hydrogen atoms in the inner-mitochondrial membrane space creates

a high concentration of the other side of the membrane.
-This causes diffusion down the electrochemical gradient.

-The hydrogen atoms diffuse down the protein in the membrane called the stalked particle.

-This causes the enzyme (ATP synthase) in the Stalked particle to turn, the energy is
transferred
-the enzyme ATPase uses this to synthesise ADP + Pi into ATP

The electrons that have been transferred to the matrix join with the hydrogen recently
diffused and with the presence of oxygen causes:
Oxygen + hydrogen + electron to join

-Releasing Water as a waste product.

9|Run for your life

Where does the 38 ATP come from?

Glycolysis produces; 2ATP 2NADH
Link Reaction produces; 2NADH
Krebs Cycle produces; 2ATP 6NADH 2 FADH2

Total 4 ATP 10NADH 2 FADH2

Each NADH produces 3ATP  total production is 30ATP from NADH

Each FADH2 produces 2ATP  total production is 4ATP from FADH2

Grand Total 4ATP + 30ATP + 4ATP = 38ATP

Chemiosmosis of H+ ions from

the mitochondrial envelope into
the matrix through ATP
Synthease proteins is what
actually generates the ATP in
respiration.
The electron transport chain
uses the process of
chemiosmosis (the diffusion
of ions across a membrane).
H+ ions are actively pumped
into the mitochondrial
envelope. This is done by the
proteins in the electron
transport chain, using the
energy stored in NADH and
FADH2.

The [H+] builds up to very high levels in the envelope. However, H+ cannot escape because it
is charged (hydrophilic) and therefore cannot move through the phospholipid bilayer in the
envelope membranes.

Special proteins called ATP Synthase do allow H+ to pass through them and escape into the
mitochondrial matrix. Whenever an H+ ion moves through the ATP Synthase protein an ADP is
phosphorylated by the ATP Synthase.
10 | R u n f o r y o u r l i f e

In summary;
1. NADH and FADH2 contain stored chemical energy
2. The energy is used to pump H+ into the mitochondrial membrane against the concentration
gradient
3. H+ trapped in one place represents a store of potential energy
4. H+ ions leave the envelope through ATP Synthase proteins.
5. The potential energy of the H+ is used to phosphorylate ATP as the H+ moves out of the
envelope

7.2.2. Anaerobic respiration:

If O2 isn’t available, oxidative phosphorylation cannot take place as there is nothing to
accept the electrons and protons at the end of the ETC. This means that reduced NAD is
not reoxidised, so the mitochondrion quickly runs out of NAD or FAD that can accept
hydrogen’s from the Krebs cycle reactions. So the Krebs cycle and the link reaction come to a
halt.
Glycolysis can still continue so long as the pyruvate produced at the end of it can be
removed and the reduced NAD can be converted back to NAD. In animals converting
pyruvate to lactate does this:
The lactate that is produced (usually in muscles) diffuses into the blood and is carried in
solution to the blood plasma to the liver. Here, liver cells convert is back to pyruvate. This
requires O2, so extra oxygen is required after exercise has finished. The extra oxygen is
known as oxygen debt. Later, when the exercise has finished and oxygen is available again,
some of the pyruvate in liver cells is oxidised through the link reaction, the Krebs cycle and
the ETC. Some of the pyruvate is reconverted to glucose in liver cells, and this may be
released into the blood or converted to glycogen and stored.

There are two types of anaerobic respiration:

1. Alcoholic fermentation:
- Glycolysis turns the glucose into pyruvate as normal
- however now the process changes:
- It’s Decarboxylated: CO2 released
- makes ethanol
- this now becomes the acceptor for NAD
- NADH comes in and becomes NAD
- releasing: CO2 and Ethanol

2. Lactic acid production:

- glycolysis happens
- glucose partially broken down to make ATP
- Pyruvate becomes acceptor for NAD
- NADH comes in and becomes NAD
- lactic acid formed from lactate as a waste product
- net yield is 2 ATP molecules per glucose molecule

Effect of lactate build up: Fate of lactate:

- The pH falls -taken to liver via blood
-enzyme activity effected -turned into pyruvate
-slows down ATP production -oxidised into water and carbon dioxide.
-enzymes function efficient at narrow pH range. -this causes oxygen uptake into increase
-lactic acid neutralises charged groups in -excess oxygen requirement called: oxygen
enzymes. debt or post-exercise oxygen consumption
-active site can no longer bond with substrate. -making energy for ATP
11 | R u n f o r y o u r l i f e

7.3. The Heart, Energy, and Exercise

7.3.1. Cardiac Output (cm3 min-1)

Major changes to cardiovascular and ventilation systems during exercise:
- Cardiac output (volume of blood pumped by the heart in a minute)
- Breathing (ventilation) rate
- Increased heart rate
- Depth of breathing
Cardiac output depends on the volume of blood ejected from left ventricle during contraction
(‘stroke volume’ in cm3) and ‘heart rate’:
Cardiac output (CO) = stroke volume (SV) x heart rate (HR)

Oxygen + haemoglobin = oxyhaemoglobin (unloads oxygen where needed)

(oxygen when leaving heart > oxygen leaving)

VO2: volume of oxygen consumed per minute (ml min-1 kg-1 of body mass)
VO2 (max): the maximal uptake of oxygen by body

VO2 (max) depends on:

- The efficiency of uptake and delivery of oxygen by lungs and cardiovascular system
- The efficient use of oxygen in the muscle fibres
- A fit person can work with more intensity longer, without needing to use anaerobic
respiration.

Stroke Volume (during exercise):

- During diastole, the heart draws blood into the atria as it relaxes – volume pumped depends
on volume returning from body.
- Greater muscle action during exercise, so more blood returned to heart in venous return.
- 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 more force.
- More blood is expelled.
- Increasing stroke volume and cardiac output.

Heart Rate (beats per minute):

Differences in resting heart rate depend on:
- Heart size (a heart has lower resting rate at a larger size because it will expel more blood with each beat so not have to beat as frequently to circulate blood)
- Differences in body size
- Genetic factors
- Fitness levels
12 | R u n f o r y o u r l i f e

Controlling heart rate:

 Heart muscle is myogenic:
o Requires no external stimuli (to contract) / no input required from nervous system,
o Brings about depolarisation of the heart cells.
 Heart rate is under control of the nervous system, and is also affected by hormonal action.
 Contraction of the cardiac muscle occurs by small changes in the electrical charge of
cardiac muscle cells:
o When cells have a slight positive charge on the outside, they are polarised.
o When this charge is reversed they are depolarised (depolarisation starts at the SAN).
 The change in polarity spreads like a wave, from cell to cell, causing the heart to contract.

Sinoatrial Node (SAN):

- Small area of specialised fibres located in the wall of the right atrium (beneath opening to
superior vena cava)
- Known as the pacemaker
- Determines heart rate
- Starts depolarisation
- Initiates heartbeat

How it happens:
- SAN generates electrical impulses that
spread across atria, causing them to
contract simultaneously.
- Impulse spreads to specialised cells
called the atrioventricular node (AVN).
- Impulse is conducted to ventricles after
0.13 second delay (delay ensures atria
have finished contracting, and ventricles
have filled with blood before
contracting).
- Signal reaches Purkyne fibres (large,
specialised muscle fibres that conduct
impulses rapidly) and connects impulses
to apex (tip) of ventricles.
o There are right and left bundles of
these fibres called bundles of His.
- Purkyne fibres continue around each
ventricle and divide into smaller
branches that penetrate the ventricular
muscle.
- These branches carry the impulses to the inner cells of the ventricles, from here they
spread through the ventricles.
- The heart is now depolarised and the contraction spreads like a wave upwards, from the
apex to the atria.
- This produces a wave of contraction which pushes blood from the ventricles through the
valves into the aorta and the pulmonary artery.

Measuring Electrical Activity – ECG:

- 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 – heart rate.
- In an ECG, electrodes are attached to a person’s chest and limbs. A change in polarisation
of the cardiac muscle causes an electrical current to be detected at the skins surface.
- ECGs are usually performed at rest and while lying down, but can be used in stress test.
- Each square represents 0.2 seconds; 300 squares pass through the machine each minute.
Time taken for one complete cardiac cycle = 300 ÷ no. of squares per beat
- Can provide information on abnormal heartbeats, areas of damage, inadequate blood flow,
and indicate elevated risk of sudden death.
13 | R u n f o r y o u r l i f e

How does it work?

- P wave: depolarisation of the atria, leading to atrial contraction (atrial systole).
- PR interval: time taken for impulses to be conducted from the SAN across the atria to the
ventricles, through the AVN
- QRS complex: wave of depolarisation resulting in contraction ventricles (ventricular
systole).
- T wave: repolarisation (recovery) of the ventricle during the heart’s relaxation phase
(diastole). Does not show atrial repolarisation as signals generated are too small.
14 | R u n f o r y o u r l i f e

Bradycardia:
- This is when the heart rate is less
than 60bpm.
- Common in fit athletes at rest.
- Sometimes a symptom in heart
problems.
- Causes include hypothermia, heart
disease, or use of medicines or
drugs.

Tachycardia:
- This is when the heart rate is
greater than 100bpm.
- Normally the result of anxiety, fear,
fever or exercise.
- Can be a symptom of coronary
heart disease, heart failure, fluid
loss, anaemia or the use of drugs and medicines.
- Relatively harmless and needs no treatment, but other forms can be life threatening.

Ischaemia:
- When the heart muscle does not receive blood due to blockage of coronary arteries
(atherosclerosis).
- This disrupts the normal electrical activity and rhythm of the heart.
- Arrhythmias arise (irregular beatings caused by electrical disturbances) and can affect a
larger area of heart muscle than that affected by the original ischaemia.

Arrhythmia:
- This is a condition of irregularity in the heart rhythm due to a defect in the heart.
- It may also be due to drugs and medicines, anxiety, potassium deficiency, or
hypothyroidism

Nervous control of heart rate:

- The cardiovascular control centre, located in the medulla of the brain, controls heart rate.
- Nerves from the autonomic nervous system (the nervous system that we have no control
over) lead from the cardiovascular control centre to the heart.

- Two nerves go from the cardiovascular control centre to the heart:

o Sympathetic nerve (accelerator): Stimulation of the SAN by this nerve causes an
increase in heart rate.
o Vagus nerve (decelerator): Impulses from the vagus nerve (parasympathetic nerve)
slow down heart rate.
15 | R u n f o r y o u r l i f e

The cardiovascular control centre detects:

- Accumulation of CO2 and lactate in the blood.
- Reduction of oxygen.
- Increase in temperature.

The sympathetic nerve: The parasympathetic nerve:

- Prepares body for action - Controls body resting and digesting
- Increases breathing - Decreases breathing
- Increases heart rate and volume - Decreased heart rate and stroke volume
- Inhibits peristalsis (muscle contraction) in the gut. - Stimulates peristalsis

To increase cardiac output:

- Skeletal muscles contract
- Stretch receptors in the muscles and tendons are stimulated.
- They send impulses to the cardiovascular control centre.
- This raises the heart rate via the sympathetic nerve (accelerator).
- There is an increase in venous return leading to a rise in stroke volume.
- The elevated heart rate and stroke volume both result in higher cardiac output.
- This means more oxygen and fuel is transported more quickly to the muscles.

 Blood pressure rises with higher cardiac output.

 To prevent blood pressure rising too high, pressure receptors in the aorta and carotid
artery send nerve impulses back to the cardiovascular control centre. Inhibitory impulses
are then sent from here to the SAN.
 This is an example of negative feedback.

Hormonal effects on heart rate:

- Fear, excitement and shock cause the release of the hormone adrenaline into the blood
from the adrenal glands located above the kidneys.
- Adrenaline has a similar effect on the heart rate as simulation by the sympathetic nerve.
- Adrenaline has a direct effect on SAN, increasing heart rate for any likely physical
demands.
- It also causes dilation of arterioles (that supply skeletal muscles), constriction of arterioles
(going to the digestive system) and other non-essential organs. This maximises blood flow
to active muscles.
- Adrenaline causes an anticipatory increase in heart rate before exercise/exertion.

7.3.2. Breathing:
Tidal volume: the volume of air we breathe in and out at each breath. Usually 0.5dm3.
Vital Capacity: the maximum volume of air we can inhale and exhale. Usually 3-4dm3.
Residual air: the air left over in the lungs, when breathing out to stop collapse.
Minute ventilation: the volume of air taken into the lungs in one minute.
Minute Ventilation = Tidal Volume x Breathing Rate (no. of breaths per minute)

You measure the lung volumes using a spirometer. A spirometer has an enclosed chamber
containing air or medical-grade oxygen, lying over water. The lid of the spirometer lifts up
and down as the volume of air inside it changes. These movements can be recorded with a
pen on a chart attached to a revolving drum.
As a person breathes in and out through the mouthpiece, the lid of the air chamber moves up
and down, producing
a trace on a chart.
By counting the
number of traces
over known period of
time, we can
calculate breaths per
minute.
16 | R u n f o r y o u r l i f e

Control of breathing:
The ventilation centre in the medulla oblongata of the brain controls breathing:
 Inhalation:
- The ventilation centre sends impulses ever 2-3 seconds to the intercostal muscles and
diaphragm muscles.
- These sets of muscles contract to cause inhalation.
- During deep inhalation, intercostal and diaphragm muscles, and neck and upper chest
muscles are brought into play.
 Exhalation:
- As lungs inflate, stretch receptors in the
bronchioles are stimulated.
- They send inhibitory impulses back to
ventilation centre and impulses to
muscles stop.
- The muscles relax stopping inhalation
and allow exhalation.
- Exhalation is caused by the elastic recoil
of lungs and gravity helping to lower the
ribs.
- Not all of the air in the lungs is exhaled
with each breath; residual air mixes with
inhaled air with each breath.
- The internal intercostal muscles only
contract during deep exhalation.

Controlling breathing rate and depth:

At rest, the most important stimulus controlling the breathing rate etc.is the conc. of dissolved
CO2 in the arterial blood via its effect on pH.
A small increase in CO2 conc. causes an increase in ventilation. This is achieved as follows:
- CO2 is dissolves in the blood plasma, making carbonic acid.
- Carbonic acid dissociates into H+ ions and hydorgencarbonate ions, thus lowering pH.
- Chemoreceptors sensitive to hydrogen (found in the ventilation centre of medulla
oblongata) detect the rise in hydrogen ion concentration.
- Impulses are sent to other parts of ventilation centre.
- Impulses are sent from ventilation centre to stimulate muscles involved in breathing.

Increasing carbon dioxide and the associated fall in pH leads to an increase in rate and depth
of breathing, through more frequent and stronger contraction of the appropriate muscles. The
more frequent and deeper breaths maintain a steep concentration gradient of carbon dioxide
between the alveolar air and the blood. This in turn ensures efficient removal of carbon dioxide
and uptake of oxygen. The opposite response occurs with a decrease in carbon dioxide. The
control of carbon dioxide levels in the blood is an
example of homeostasis operating via negative
feedback.

The constant movement of blood past the alveoli

causes a steep concentration gradient:
- There is always a steep CO2 concentration
gradient in the blood stream as it approaches
the alveoli sacs.
- There is always a steep O2 concentration
gradient in the sac, causing it to diffuse into the
bloodstream.
 17 | R u n f o r y o u r l i f e

7.3.3. Slow and Fast Twitch Muscle Fibres:

Within the striated muscle tissue, there are two types of muscle fibre: Slow Twitch and Fast
Twitch.
Fast twitch fibres are adapted for rapid contraction over a short period of time (explosive
actions generally). Slow twitch fibres are adapted for slightly less rapid contraction over
longer periods of time (continuous activity).

Slow twitch muscle fibres: Fast twitch muscle fibres:

• Use aerobic respiration to produce ATP • Use anaerobic respiration to produce ATP
• Have many mitochondria and respiratory • Have few mitochondria. ATP used is produced
enzymes to carry out the Krebs cycle and almost entirely from anaerobic glycosis (not in
oxidative phosphorylation mitochondria)
• Have large amounts of the protein myoglobin, • Very little myoglobin (light/white in colour), so
which acts as oxygen store (dark red in colour) fewer reserves of oxygen
• Relatively narrow fibres, so oxygen can diffuse
• Are relatively wide
into their centres rapidly
• Are supplied with oxygenated blood by many
• Few capillaries supplying them
capillaries
• Fatigue resistant • Rapid lactate build-up causes quick fatigue
• Low glycogen content • High glycogen content
• Low levels of creatine phosphate • High levels of creatine phosphate
• Little sarcoplasmic reticulum • Extensive sarcoplasmic reticulum
• Specialised for slower, sustained contraction • Specialised to produce rapid, intense
and can cope with long periods of exercise contractions in short bursts (e.g. eye
(e.g. maintaining posture, long-distance running) movement, sprinting)

 In mammals, these muscles fibres are not separate but are found together in all skeletal
muscles.
 The proportion of each type of these fibre seems to be genetically determined (varies
between people).
 Athletes with a high aerobic capacity usually have a higher concentration of slow twitch
fibres compared to fast twitch. Sprinters however have a smaller concentration of slow
twitch fibres.

7.3.4. Sweating and Temperature Control:

For human body cells to work properly – stable internal conditions must be maintained.
The maintenance of this is called homeostasis which is achieved by maintaining stable
conditions within the blood. This in turn affects the tissue fluid that bathes the body’s cells.

In the blood, the concentration of glucose, ions, CO2 must be kept in their narrow limits, and
water potential (determined by concentration of solutes in blood), ‘pH’ and temperature of the
blood must be tightly regulated.

Each condition that is controlled has a norm value or set point that homeostatic mechanisms
try to maintain.
Receptors detect deviations from the norm and are connected to a control mechanism
which turns effectors (muscles and glands) on or turn off to bring the condition back to the
norm.
e.g. Glucose concentration may increase/decrease above/below the norm. This information is
sent back to the control mechanism and it is changed back to the norm. This is known as
negative feedback.
18 | R u n f o r y o u r l i f e

Negative Feedback
- A communication system, effectors, and
receptors comprise homeostatic systems
o Receptors: detect whether a specific level
is too low or too high.
This information is then communicated to
the hormonal system through the nervous
system to the effectors.
o Effectors: react to counteract the change
by bringing the level back to normal.
- The mechanism that works to restore the level
back to normal is negative feedback.
- It essentially works to keep the internal environment factors in the normal range.
- However, it only works within certain limits. If the changes are too big, then the effectors
may be unable to counteract.

Thermoregulation: The control of body temperature

Our core temperature is stable at 37.5°C (0.5°C higher than oral temp).
This temperature allows enzyme-controlled reactions to occur.
o At lower temperatures, the enzyme-controlled reaction rate would be too slow.
o At higher temperatures, the enzymes would denature, and an increase of the core body
temperature can be fatal.
Temperature is controlled/maintained by the negative feedback system (in humans).
19 | R u n f o r y o u r l i f e
 20 | R u n f o r y o u r l i f e

Temperature regulation during exercise:

Methods of
Effect
energy transfer
Energy can be radiated from one object to another – through air even a
Radiation vacuum. Our bodies are usually warmer than the surrounding environment.
Therefore we can radiate heat. This can work other way: sun – person.
Conduction Energy loss by conduction involves direct contact between objects.
Air next to skin will be warmed by body. As air expands and rises, it is
Convection replaced by colder air – Then warmed by body. This is how thermal insulation
works.
Energy is needed to convert liquid water into vapour. The energy draw to
Evaporation
evaporate sweat is taken from body.
21 | R u n f o r y o u r l i f e

7.4. Exercising and Immune Systems:

Athletes engaged in heavy training are more prone to infection. A moderate amount of
exercise is the best for maintaining an excellent immune system.
Overtraining can result in ‘burnout’ symptoms that can last for weeks or months; like poor
athletic performance, chronic fatigue, and immune suppression which can lead to frequent
infections (URTIs), and increased wear and tear on joints which may need surgical repair.

Effects of exercise on immunity

 Moderate exercise increases the number of a type of lymphocyte called ‘natural killer
cells’. These cells are found in blood and lymph and provide non-specific immunity against
cells invaded by viruses and cancerous cells.

Natural Killer cells:

- These work by releasing the protein perforin which makes pores in target cell’s
membranes. These pores allow molecules such as protease to enter the host cells and
cause apoptosis (death of the cells and its contents).
- They were thought to require no activation; they are however activated by:
o Cytokines
o Interferons
- They offer non-specific protection against UTRIs and other infections.

 Vigorous exercise:
The quantity of these immune cells falls with increased vigorous exercise:
• Natural killer cells • T helper cells
• Phagocytes • B Cells
As a result, the specific immune system is depressed.
A decrease in helper T cells = decrease in amount of cytokines available to activate
lymphocytes. This reduces the amount of anti-bodies produced in the system.
An inflammatory response also occurs in muscles due to damage to muscle fibres.

Joint damage during exercise:

Repeated forces on joints can lead to wear and tear to one or more parts of the joints. Many
joint disorders are associated with overuse of these muscles – similar to those of aging.

Causes: Treatments:
- Pain - Rest R
- Inflammation - Ice I
- Restricted movement - Compression C
- Elevation E
- Anti-inflammatory drugs
- Surgical repair

Knees are more susceptible to damage. Typical problems include:

- Articular cartilage covering surface of bones wears away and bones grind together.
This causes damage that leads to inflammation and a form of arthritis.
- Patellar tendonitis (jumper’s knee) – occurs when the kneecap doesn’t glide smoothly
across the femur due to damage of the articular cartilage on the femur.
- The bursae (fluid sacs) that cushion points of contact between bones, tendons and
ligaments swell up with extra fluid and push against other tissues in the joint, leading to
inflammation and tenderness. Bursitis (‘housemaid's knee’) common in housemaids due
to repetitive kneeling.
- Sudden twisting and abrupt movements of the knee joint causes damage to ligaments.
1|Run for your life

How can medical technology help?:

 Keyhole surgery:
Joint injury can limit exercise and shorten athletic careers. Surgical operations for repair
damage caused pain, were risky, and took a long time for recovery.
Keyhole allows:
- Use of fibre optics or tiny video cameras to repair damaged joints or remove diseased
organs through small holes.
- Keyhole surgery on joints is known as arthroscopy. The process involves:
o Surgeon makes one or two small incisions (4mm long)
o Small camera and light inserted to see inside of joint
o Diagnosis is made or confirmed
o If surgery is necessary and undertaken – miniature tools are used
o Recovery is rapid; only a short hospital stay is needed - can be active in a few weeks
- Inside of most joints can be view with arthroscope.
- Damage to cruciate ligaments can be tackled effectively by keyhole surgery.
- The knee is a hinge joint held together by four ligaments (bone to bone). Two of the
ligaments found deep inside the joint (anterior and posterior cruciate ligaments) are
attached to the femur and tibia.
- Posterior cruciate ligament normally prevents the knee from being bent to far back.
Most athletic injuries result from falling onto a bent knee,
- Anterior cruciate ligament prevents knee from being bent too forward.
- A popping or snapping can be herd when cruciate is torn.
- Repeated damage to a joint can affect cartilage and shorten career.

 Prosthesis:
- Prosthesis is an artificial body part used by an individual with a disability in order to regain
normal function (e.g. enabling them to walk) or appearance.
- Adaptable body parts – e.g. dynamic response prosthetic foot that changes shape when
under body weight. This puts a spring in the foot and allows sturdy footing.
- Prosthetic feet may/may not have artificial joints and in some cases foot might not be
required at all – a flipper or a pedal binder for cycling maybe used.
- Some prosthesis used to replace joints that have not responded to medical therapy (e.g.
with arthritis).
Replacing hip or knee joints with artificial joints is a successful use of prosthesis. To do this:
- An incision is made and the patella is moved out of the way
- Ends of femur and tibia trimmed, and care is taken so as not to damage the ligaments
- Underneath of patella trimmed so that an artificial piece may be fitted
- Bone cement is used to attach metals (stainless steel or titanium) to end of femur
Metal, ceramic or polyethylene is used to attach to tibia and patella
- A fit person will recover within a few months
- Contact sports should be avoided after joint replacement

Taking enough exercise:

Regular physical activity can be advantageous:
- Increases arterial vasodilation, lowers blood pressure, reduces risk of coronary heart
disease, cardiovascular disease, and stroke.
- Increases levels of blood HDLs (transport cholesterol to liver to be broken down) and
reduces LDLs (associated with development of atherosclerosis in CHD and stoke).
- Balance of energy input and output helps to maintain healthy weight; decreasing the risk of
obesity by increasing metabolic rate during, and for a temporary time after, exercise.
This helps us to use respiratory substrates such as glucose and fatty acids, reducing the
amount of adipose tissue.
- Increased sensitivity of liver and muscle cells to insulin improves blood glucose
recognition & reduces likelihood of developing type II diabetes (insulin dependent diabetes).
- Increases bone density and delays and reduces it loss during old age.
- Reduces risk of some cancers.
- Improves mental well-being.
2|Run for your life

Obese people also have high risk of CVDs. There are two obesity indicators:
- BMI (Body Mass Index) = Body mass (kg) / Height (m) (a normal adult has BMI of 18-25)
- Waist to Hip Ratio = Waist (cm) / Hip (cm)

However, people who exercise very frequently or who push their bodies to the limit also run
the risk of causing damage to the body.
 Joints may become abnormally worn, e.g. knee joints damaged by over strenuous
running activity.
 Very strenuous exercise taken over long periods of time can cause the immune
system to become less effective. Athletes put themselves under a lot of competitive
stress and train very hard may be more likely to suffer infections than others.
 Studies show correlation between athletes and frequent infection in upper respiratory
tract.
 Moderate levels of exercise reduce risk, but high levels decrease activity of
lymphocytes and therefore the ability of the immune system to destroy viruses and
pathogens. Amount of an antibody called IgA which is especially important in
preventing infection of the upper respiratory tract, is also reduced by strenuous
exercise, especially if this takes place over long periods of time.

7.4.1. Performance-enhancing substances:

Professional athletes train hard to improve their performance in competition. Some have
been tempted to take a short-cut by taking performance-enhancing drugs. For example,
steroids that increase protein synthesis in cells and so can increase muscle size and strength.
The use of drugs is called doping and this isn’t a recent problem; found throughout history.

Many performance-enhancing drugs are now banned – professional athletes face severe
penalties if they’re found to have used them. This process is coordinated by the World Anti-
Doping Agency (WADA) which prevents performance enhancing drug abuse like:
- Blood doping (taking extra blood or red blood cells).
- Artificially enhancing the uptake, or transport and delivery of oxygen using drugs or
haemoglobin products.
- Gene doping/non-medical use of cells, genes or gene expression that may affect
athletic performance.
- Athletes with medical conditions requiring prescription of inhibited drugs need
permission to use them.
- Human growth hormone, insulin, testosterone, and erythropoietin (EPO) are on the
list of prohibited substances.

There are very strong arguments for preventing the use of performance-enhancing
substances in sport, these include:
- Risk to athlete’s health – potential development of serious health problems
- Competitive advantages are unfair
- Using such drugs kills the spirit of sports.

Hormones
- Hormones are chemical messengers, released directly into the blood from the endocrine
glands.
- Unlike exocrine glands (sweat and salivary glands), endocrine glands have no ducts.
- Most hormones are produced in an inactive form or are packaged within secretory
vesicles (by the Golgi apparatus) to ensure that the cells in the endocrine glands are not
damaged. Vesicles fuse with cell surface membrane, releasing contents by exocytosis.
 3|Run for your life

Gland Hormone Function

 Growth Hormone
 Stimulates growth
Pituitary  Follicle stimulating
 Controls testes and ovaries
gland hormone
 Causes reabsorption of water in kidneys
 Antidiuretic hormone
Thyroid
 Thyroxine Raises basal metabolic rate
gland
Adrenal Raises basal metabolic rate, dilates blood vessels, prepares body
 Adrenaline
gland for action
Pancreas  Insulin Lowers blood glucose level
Promotes development of ovaries and female secondary sexual
Ovary  Oestrogen
characteristics
Testis  Testosterone Promotes development of male secondary sexual characteristics

Each hormone affects only specific target cells, modifying their activity.
- Hormones are carried around the body via the blood stream.
- They either enter the target cell, or bind to complementary receptor molecules on the
outside of the cell membrane (producing a second message that activates enzymes
inside the cell).
- Each hormone brings about characteristic responses by effect on enzymes.
- Others act on the cell by indirect or direct control of transcription.

How hormones affect cells:

 Peptide hormones:
- Protein chains of 10-300 amino acids.
- Relatively small, but not able to pass through cell membrane easily
because they are charged.
- Instead they bind to a receptor molecule on cell membrane,
activating a molecule in the cell cytoplasm (second messenger).
- Second messenger brings about chemical changes in cell; directly,
or indirectly by affecting gene transcription.
- e.g. EPO, human growth hormone, and insulin.

 Steroid hormones:
- Formed from lipids and have complex ring structures.
- They pass through the cell membrane and bind directly to a receptor
molecule in cytoplasm.
4|Run for your life

- Once activated, the hormone-receptor complex (functions as a transcription factor)

brings about characteristic responses resulting from its effect on transcription.
- The transcription factor switches enzyme synthesis on or off.

Transcription factor:
- Transcription is initiated by an enzyme
called RNA polymerase and a cluster of
associated protein transcription factors –
the result is a ‘transcription initiation
complex.’
- Genes are switched on by successful
formation and binding of transcription
initiation complex to the promoter
region.
- Genes remain switched off by failure of the
transcription initiation complex to form and
attach to the promoter region.
- This is due to the absence of a
transcription factor or action or of repressor molecules.

Hormones used to enhance performance – performance enhancing substances:

 Erythropoietin (EPO) (banned):
- EPO is a peptide hormone produced naturally by the kidneys. It stimulates the formation
of new RBCs in bone marrow. Taking synthetic EPO increases the rate at which red
blood cells are made and so can increase the oxygen-carrying capacity of the blood.
- EPO can be produced using DNA technology; and is used to treat anaemia.
- Since it is a natural substance it is difficult to test if EPO is raised or not.
- If EPO levels are too high (too many RBCs produced) there is an increased risk of
thrombosis, possibly leading to a heart attack and stroke.

 Testosterone (banned):
Steroid hormone made from cholesterol in the adrenal glands and testis. It is one of a
group of male hormones known as androgens (‘andro’ meaning man/male in Greek).
- Causes development of male sex organs and during adolescence, the male secondary
characteristics like hair, skeletal and muscular changes, and deepening of the voice.
- Binds to androgen receptors.
- Modify gene expression to alter development of cell – increases anabolic reactions like
protein synthesis in muscle cells.
- Athletes and body builders abuse this – inject anabolic steroids (longer lasting
synthetic, chemically modified testosterone) to increase muscle development.
o Anabolic steroids were originally developed for treatment of muscle wasting diseases
and osteoporosis. They are a banned class C drug, and can easily be detected in
urine.
o Over use of anabolic steroids causes:
- High blood pressure - Kidney failure
- Liver damage - Heart disease
- Changes in menstrual cycle in - Increase aggression in both men
women and women
- Decreased sperm production and
impotency in men

 Creatine (not banned):

- An amino acid derived compound that is considered as a nutrition supplement
- Naturally found in meat and fish
- Increases amount of creatine phosphate (CP) found in muscles and decreases recovery
time – increased CP storage increases performance during high-intensity, repeated,
short-duration exercise.
1|Run for your life

- Can cause diarrhoea, vomiting, nausea, high blood pressure, kidney damage, and
muscle cramps.

Ethical issues of performance-enhancing substances:

Against:
 Some performance-enhancing drugs are illegal
 Competitions are unfair if some people take drugs – they gain an advantage rather than
through training or hard work
 There are serious health risks such as high blood pressure or heart problems
 Athletes may not be fully informed of the health risks
For:
 It is up to each individual – athletes have the right to make their own decisions about drugs
and whether they are worth the risk
 Drug-free sport isn’t fair – different access to training facilities, coaches, equipment etc.
 Hard to detect every drug so it’s hard to develop the technology
 No ban on nutritional substances such as vitamins