Unit 5 (Run for your life)

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  • Created by: Chako
  • Created on: 26-03-13 13:03

Joints and movement

- Muscles bring about movement at a joint

- Muscles shorten, pulling on the bone and so moving the joint

- Muscles can only pull; they cannot push, so they're normally found in pairs

- Pairs of muscles which pull in opposite directions are called antagonistic pairs  

- Extensors
contract to extend/straighten a joint

- Flexors: contract to flex/bend a joint

- Ball and socket joints: found in shoulders and hips and give very free movement

- Hinge joints: found in fingers and knees and are much more restrictive

- Saddle joints: found in wrists

- Pivot joints: found in elbows

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Joints and movement

Joint structure

- Cartilage: lines joints to allow them to articulate smoothly and it is elastic, a good shock absorber, absorbs synovial fluid and prevents erosion of bones

- Pad of cartilage: additional protection

- Synovial fluid: a liquid lubricant that fills the joint cavity and ensures easy, friction-free movement in the most mobile joints

- Tendons: connects muscle to bone; made up almost entirely of white fibrous tissue, making them strong but relatively inelastic

- Ligaments: attach bone to bone, holding them in the correct alignment; elastic to allow bones of a joint to move when necessary

- Synovial membrane: secretes synovial fluid

- Fibrous capsule: encloses joints

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A typical synovial joint

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- Striated muscles: involved in locomotion and under the control of the voluntary nervous system; contract rapidly but fatigue quickly

- Muscles are made of bundles of muscle fibres bound together by connective tissue

- Muscle fibres: single muscle cells surrounded by a cell surface membrane

- Each muscle cell has several nuclei and is striped

- Inside the muscle fibre is the cytoplasm containing mitochondria and other organelles found in a cell

- Muscle fibres also contain myofibrils

- Myofibrils contain repeated, contractile units called sarcomeres

- Actin and Myosin are proteins that make up the sarcomere

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Other types of muscles

- Smooth muscle (involuntary muscle): not striped and under the control of the involuntary nervous system.

  • Found in the gut where it's involved in moving the food along   
  • Also found in blood vessels 
  •  Contracts and fatigues slowly 

- Cardiac muscle: found exclusively in the heart

  • It is striated
  •  Fibres are joined by criss-cross connections
  • Contracts spontaneously and doesn't fatigue
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The Sarcomere

Actin filamentsthinner filaments made of the protein Actin

Myosin filamentsthicker filaments made of the protein Myosin

There is a light band on the sarcomere where actin filaments appear on their own

- There is a dark band where both actin and myosin filaments appear

- There is an intermediate-coloured band where only myosin filaments appear

During contraction, I-band and H-zone get smaller and sarcomere shortens

- The A-band remains the same size

When fully contracted, H-zone disappears

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Relaxed muscle

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Contracted muscle

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The Sliding Filament Theory

- Myosin filaments have flexible heads that can:

  • Change their orientation
  • Bind to actin
  • Hydrolyse ATP (using ATPase)

- Actin filaments are associated with two other proteins; tropinin and tropomyosin

- Troponin and tropomyosin control the binding of the myosin heads to the actin filaments

- Sarcoplasmic reticulum: specialised endoplasmic reticulum which can store and release calcium ions

- Sarcoplasm: cytoplasm inside a muscle cell

- Neuromuscular junction: specialised synapse between neurones and muscle cells

- When a nerve impulse arrives at a neuromuscular junction, calcium ions are released from the sarcoplasmic reticulum, which attach to the troponin, causing it to move together with the threads of tropomyosin

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The Sliding Filament Theory

The following events then take place:

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The Sliding Filament Theory

The myosin binding sites are normally blocked by tropomyosin, so the myosin head can't bind. The calcium ions that are released after a nerve impulse arrives at the neuromuscular junction attach to the troponin and cause it to move together with the threads of tropomyosin, which enables the following steps to occur:

1) Myosin binding sites on the actin are exposed so myosin forms cross-bridges with the actin filament

2) The myosin heads release the ADP and Pi and change shape as a result; this is the power stroke

3) ATP binds to the myosin head, causing it to detach from the actin

4) Myosin head returns to upright position

...and the cycle begins again from step 1

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Fast-twitch and slow-twitch muscle fibres

Fast-twitch muscle fibres

  • Rapid, intense contractions in short bursts
  • Few mitochondria; ATP comes from anaerobic respiration (glycolysis)
  • Little myoglobin, making it paler
  • Few capillaries
  • Fatigues easily
  • High glycogen
  • High levels of creatine phosphate

Slow-twitch muscle fibres

  • Slower, sustained contraction; can cope with long periods of exercise
  • Many mitochondria; ATP comes from aerobic respiration (electron transport chain)
  • Lots of myoglobin to store oxygen, making it darker
  • Many capillaries to supply oxygen
  • Fatigues slowly
  • Low glycogen
  • Low levels of creatine phosphate
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Two different ways living organisms respire:

  • Aerobic respiration; using oxygen
  • Anaerobic respiration; without oxygen

Aerobic respiration

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- Energy released per mole of ATP hydrolysed ~ 34 kJ

- Energy is required to add a 3rd phosphate bond to ADP to create ATP

- This bond can be broken by hydrolysis, which is catalysed by ATPase; this releases energy, which can be used in energy-requiring processes taking place within a cell

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Breakdown of glucose in glycolysis


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Breakdown of glucose in glycolysis

- Glycolysis takes place in the cytoplasm of cells

- 2ATP is used at the beginning of glycolysis to phosphorylate glucose; this increases its reactivity and enables it to be split (glucose on its own is too stable)

- 4 ATP is produced at the end, making the net gain of ATP = 2ATP

- 2H atoms are removed from the 3C sugars and are taken up by NAD, forming reduced NAD

- One glucose molecule eventually forms 2 pyruvate molecules at the end of glycolysis

The following are formed at the end of glycolysis:

  • 2 pyruvate molecules (which go to the link reaction)
  • 2 ATP molecules (2 input, 4 output, so overall is 2ATP)
  • 2 reduced NAD molecules (which go to the electron transport chain)

- No carbon dioxide is produced in glycolysis



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Anaerobic respiration

- Glycolysis does not need oxygen; for it to continue, it needs a constant supply of NAD

- In aerobic respiration, NAD comes from the electron transport chain

- In anaerobic respiration, the pyruvate from glycolysis is reduced to form lactate; this oxidises the reduced NAD to NAD

- Lactate forms lactic acid in solution, which lowers the pH

- This can inhibit enzymes; if it builds up, it can cause muscle cramps

- Once anaerobic respiration resumes, most of the lactate is converted back to pyruvate; it is oxidised via Kreb's cycle to carbon dioxide and water

- The extra oxygen required for this process = oxygen debt

- NAD and FAD: coenzymes and hydrogen acceptors

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Krebs cycle

Preparation for Krebs cycle (link reaction)

- Each pyruvate molecule from glycolysis enters the mitochondrial matrix where it is converted an acetyl (2C) group

- This involves the loss of carbon dioxide (decarboxylation) and hydrogen (dehydrogenation)

- The acetyl group is carried by coenzyme A as acetyl coenzyme A

Krebs cycle

- The 2C compound combines with a 4C compound to form the 6C compound citric acid

- This 6C compound goes through a cyclical series of reactions during which the 6C is broken down in a number of stages to give the original 4C compound

- Two further molecules of carbon dioxide are removed (waste product)

- The 4C compound then combines with more acetyl coA and the cycle turns again

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Krebs cycle

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Krebs cycle

- Each molecule of the acetylcoenzyme A is used to generate:

1) Three molecules of reduced NAD

2) One molecule of reduced FAD

3) One molecule of ATP by substrate-level phosphorylation

4) Eleven molecules of ATP (as 1 NAD = 3 ATP and 1 FAD = 2 ATP)

5) Two molecule of carbon dioxide

- For each glucose molecule entering glycolysis, two acetyl groups are formed, so the Krebs cycle will turn twice (i.e. producing 2ATP by substrate-level phosphorylation, 6 reduced NAD etc.)

- Substrate-level phosphorylation: when energy from the formation of ATP comes from the substrates

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How much ATP is produced

- Glycolysis produces 2ATP and 2 reduced NAD

- Link reaction produces 2 reduced NAD

- Krebs Cycle produces 2ATP, 6 reduced NAD and 2 reduced FAD

Total: 4ATP, 10 reduced NAD and 2 reduced FAD


- Each reduced NAD produces 3ATP so 3 x 10 = 30ATP

- Each reduced FAD produces 2ATP so 2 x 2 = 4ATP

Grand total: 4ATP + 30ATP + 4ATP = 38ATP

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The electron transport chain

Chemiosmotic theory

1) Energy is released as electrons pass along the electron transport chain and it is used to move hydrogen ions (from the H atoms released in glycolysis, the link reaction, Krebs cycle) from the matrix, across the inner mitochondriol membrane, and into the intermembrane space

2) Steep electrochemical gradient created across inner membrane; large difference between concentration of hydrogen ions across membrane and large electrical difference, so intermembrane space more positive than matrix

3) Hydrogen ions diffuse into the matrix down the electrochemical gradient through hollow protein channels in stalked particles. As they pass through the channel, ATP synthesis is catalysed by ATPase located on each stalked particle

4) Hydrogen ions cause a change in shape in enzyme's active site, so ADP can bind

5) Within the matrix, hydrogen ions and electrons recombine to form hydrogen atoms; the atoms then combine with oxygen to form water

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The electron transport chain

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- Oxygen acts as the final electron acceptor in the electron transport chain and it is reduced (OILRIG). If the supply of oxygen stops, the electron transport chain stops and ATP synthesis also stops

Q) Why is the synthesis of ATP via the electron transport chain termed "oxidative phosphorlyation"?

Ans) Redox reactions occur as electrons pass along the electron transport chain and the final electron acceptor is oxygen (the "oxidative" part). The electron transport chain results in phosphate being added to ADP to form ATP (the "phosphorylation" part).

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The ATP/PC system

- Creatine phosphate (phosphocreatine or PC): a substance stored in muscles which can be hydrolysed very quickly to release energy.

- Energy used to make ATP from ADP + Pi from the PC itself

- PC breakdown begins as soon as exercise starts (triggered by the formation of ADP)

- Summary of reaction: creatine phosphate + ADP à ATP + creatine


- The reactions do not require oxygen and provide energy for about 6-10 seconds of intense exercise

- The ATP/PC system is relied upon for regeneration of ATP during bursts of intense activity

- Creatine phosphate stores can be regenerated from ATP when the body is at rest

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Control of heart rate

- The heart is myogenic; it can contract without external nervous stimulation

- Depolarisation starts at the sinoatrial node (SAN), which is a small area of specialised muscle fibres located in the wall of the right atrium; the SAN is our internal pacemaker

1) Electrical impulses from SAN spread across atria walls, causing contraction (atrial systole)

2) Impulses pass to ventricles via AVN after a short delay (0.13 seconds) to allow time for the atria to finish contracting

3) Impulses pass down the Purkyne fibres (left and right fibres collectively called bundle of His) to the heart apex

4) Impulses spread up through ventricle walls causing contraction from the apex upwards. Blood is then squeezed into the arteries (ventricular systole)

- After systole, the cardiac muscle relaxes for a period called the diastole, which is when the blood returning from the veins fills the atria.

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What does an ECG trace show us?

- P wave: depolarisation of the atria, leading to atrial systole

- PR interval: time taken for impulses to be conducted from SAN to the ventricles through the AVN

- QRS complex: depolarisation of ventricles, leading to ventricular systole

- T wave: repolarisation (recovery) of ventricles; ventricular diastole

- Distance between 1 QRS complex and another and time shows us the heart rate/beats min-1

300 squares pass through the ECG per minute so each medium sized square = 0.2 s (each 1/2 cm = 0.2 s)

- Time for one complete cardiac cycle: (number of squares between QRS complexes x 0.2) ÷ 60

- The ECG doesn't show atrial repolarisation because the signals generated are small and hidden by the QRS complex

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ECG trace

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What does an ECG trace show us?

- Bradycardia: heart rate of less than 60 bpm

- Tachycardia: heart rate of more than 100 bpm

- Arrhythmia: irregular beatings of the heart caused by electrical disturbances

- An ECG can provide information about: 

  • abnormal heartbeats
  • areas of damage
  • inadequate blood flow
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Peak performance

- Aerobic capacity: the ability to take in, transport and use oxygen; the peak performance you can work at

- VO2volume of oxygen consumed per minute (0.2-0.3 litres at rest)

VO2 max: volume of oxygen consumed during maximal aerobic exercise (3-6 litres per minute, units: ml min -1 kg-1)

- Cardiac output: volume of blood pumped in one minute (units: dm3 min -1)

Cardiac output = stroke volume x heart rate

- Ventilation rate: the rate at which someone breathes

Ventilation rate = tidal volume x number of breaths per minute

- Stroke volume: volume of blood leaving the left ventricle

- Venous return: when more blood returns to the heart due to more exercise and greater muscle action

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Cardiac output, stroke volume and heart rate

Effect of exercise on cardiac output and stroke volume

- During exercise, there is greater muscle contraction so more blood returns to the heart (increased venous return)

- In diastole during exercise, the heart fills with a larger volume of blood

- The heart muscle is stretched to a greater extent, increasing stroke volume and cardiac output

Size of heart and heart rate

- A larger heart usually has a lower resting heart rate; this is because it will expel more blood with one beat so it doesn't have to beat as frequently to keep the circulation of the blood constant

- Endurance training produces a lower resting heart rate because it thickens the muscle cell walls which increases the size of the heart

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Regulation of cardiac output

- Cardiac output = stroke volume x heart rate

- Heart rate can be affected by hormones and nervous control

- The cardiovascular control centre in the medulla controls the sinoatrial node via nerves (sympathetic nerve and parasympathetic/vagus nerve)

- Sympathetic nerve:

  • Speeds up heart rate
  • Runs from the accelerator centre (in the medulla) to the SAN

- Parasympathetic/vagus nerve:

  • Slows down heart rate
  • Runs from the inhibitory centre (in the medulla) to the SAN
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How does the cardiovascular control centre respond

- When muscles are active, they respire more quickly and cause several changes to the blood, such as decreased oxygen concentration, increased carbon dioxide concentration, decreased pH (carbon dioxide dissolves to form carbonic acid) and increased temperature

- The main chemoreceptors (receptor cells that can detect chemical changes) are found in:

  • The walls of the aorta (aortic body), monitoring the blood as it leaves the heart
  • The walls of the carotid arteries (carotid bodies), monitoring blood to the head and brain

- After detecting an increase in hydrogen ions (drop in pH due to carbonic acid being formed), the chemoreceptors send nerve impulses to the cardiovascular centre indicating that more respiration is taking place, and the cardiovascular centre responds by increasing the heart rate

- A similar job is performed by temperature receptors and stretch receptors in the muscles, which also detect increased muscle activity

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Lung volumes

- Ventilation rate: rate at which someone breathes

Ventilation rate = breathing rate x tidal volume

- Tidal volume: the volume of air breathed in or out of the lungs per breath

- Vital capacity: the maximum volume of air that can be forcibly exhaled after a maximal intake of air

- Lung volumes can be measured using a spirometer

- The ventilation centre is also found in the medulla

 - During exercise, the ventilation rate increases; this increases the rate and depth of breathing

- The ventilation rate increases so that:

  • Oxygen can diffuse from the air to the blood faster
  • Carbon dioxide can diffuse from the blood to the air faster
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How does the ventilation centre control breathing

- An important stimulus controlling breathing rate and depth is the concentration of dissolved carbon dioxide in the arterial blood

- A small increase in carbon dioxide concentration causes a large increase in ventilation

- Carbon dioxide dissolves in blood plasma, making carbonic acid which dissociates into hydrogen ions, lowering the pH

- Chemoreceptors sensitive to hydrogen ions are located in the ventilation centre, carotid artery and aorta

- Impulses are sent from the ventilation centre to stimulate the muscles involved in breathing

- The chemoreceptors in the carotid artery and aorta are stimulated by changes in pH of the blood (the chemoreceptors monitor the blood before it reaches the brain and send impulses to the ventilation centre)

- Ventilation also increases in response to impulses from stretch receptors located in muscles and tendons in the same way

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What happens during inhalation and exhalation?


- The ventilation centre sends nerve impulses every 2-3 seconds to the external intercostal muscles and diaphragm muscles

- Both sets of muscles contract, causing inhalation

- During deep inhalation, the neck and upper chest muscles are also used


- As the lungs inflate, stretch receptors in bronchioles are stimulated

- The stretch receptors send inhibitory impulses back to the ventilation centre, causing the muscles to relax, which stops inhalation and lets exhalation begin

- Exhalation is caused by elastic recoil of lungs and by gravity helping to lower ribs

- Intercostal muscles contract during deep exhalation

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- Homeostasis: maintenance of a stable internal environment

- Each condition that is controlled in the body (e.g. blood glucose level, body temperature, water potential etc) has a set point that homeostatic mechanisms are trying to maintain

- Receptors are used to detect changes from the set point

- These receptors are connected to a control mechanism which turns effectors on or off to bring conditions back to the set point

Temperature control

- Thermoregulation: control of body temperature

- Body temperature = 37 degrees celsius; this enzyme-controlled reactions to occur at a reasonable rate (too low = reactions too slow and too high = enzymes denature)

- In humans, thermoregulation is maintained by a negative feedback system

- This system involves receptors located in the hypothalamus to detect changes

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        Heat loss centre                                              Heat gain centre

Stimulates:                                                  Stimulates: 

- Sweat glands to secrete sweat                     - Contraction of arterioles;

Inhibits:                                                          vasoconstriction

- Contraction of arterioles in skin;                    - Hair erector muscles to contract

vasodilation                                                   - Liver to raise metabolic rate     

- Hair erector muscles relaxing;                      - Skeletal muscles to contract

hairs lie flat as a result                                      causing shivering  

- Liver reducing metabolic rate                        Inhibits:

- Skeletal muscles relaxing; no shivering        - Sweat glands 

as a result

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Temperature control: sweat and hairs


- Sweat released via the sweat ducts evaporates taking energy from the skin

- Sweat glands are stimulated by nerves from the hypothalamus


- They are raised in cold weather by contractions of the erector muscles (we have no control over this reflex)

- This traps a layer of air that insulates the body

- Due to our shortage of hair compared to other mammals and birds, we wear clothes for further insulation

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Temperature control: skin

When cold:

- Energy is lost from the blood flowing through the surface capillaries by radiation

- In cold conditions, muscles in the arteriole walls contract causing the arterioles to constrict

- This reduces the blood supply to the surface capillaries

- Blood is diverted through the shunt vessel which dilates as more blood goes through it

- Blood flows further from the skin surface so less energy is lost

- This is vasoconstriction

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Temperature control: skin

When warm:

- Constriction of the arterioles and shunt vessels is controlled by the hypothalamus

- In warm conditions, the shunt vessels constrict and muscles in the walls of the arterioles relax

- Blood flows through the arterioles, making them dilate

- Blood flows closer to the surface of the skin so more energy is lost

- This is known as vasodilaton

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How energy is transferred to and from the body


- Sweat evaporation increases energy loss

- Evaporation from moist surfaces of the lungs increases energy loss

- Arteriole vasoconstriction decreases blood flow to skin, reducing energy loss by conduction, convection and radiation

- Arteriole vasodilation increases blood flow to skin, increasing energy loss by conduction, convection and radiation

- Hairs raised by contraction of erector muscles reduces energy loss by conduction, convection and radiation

- Voluntary muscle contractions and involuntary shivering release energy, raising body temperature

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Methods of energy transfer


- Energy can be radiated from one object to another through air or vacuum as electromagnetic radiation

- Our bodies are usually warmer than the surrounding environment so we radiate energy


- Energy loss by conduction involves direct contact between objects and energy transfer from one to the other


- Air lying next to the skin will be warmed by the body

- As the air expands and rises, it wil be replaced by cooler air which is then warmed by the body

- The energy loss by bulk movement of air is called convection

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Excessive exercise and immune suppression

- Athletes engaged in heavy training programmes seem more prone to infection than normal

- Upper respiratory tract infections (sore throat and flu-like symptoms) are most common

- Two main factors can contribute to higher infection rates:

  • Increased exposure to pathogens 
  • Suppressed immunity with hard exercise

- There is a "U-shaped" relationship between risk of infection and amount of exercise

- A moderate level of exercise improves health and well-being but overtraining can result in the opposite effect

- This phenomenon is known as "burn-out"

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Effects of exercise on immunity

- Components of the non-specific and specific immune system are affected by both moderate and excessive exercise

Moderate exercise

- Increases the number of a lymphocyte called natural killer cells (found in the blood and lymph)

- Natural killer cells:

  • are not like B and T cells because they do not use specific antigen recognition
  • provide non-specific immunity against cells invaded by viruses and cancerous cells
  • are activated by cytokines and interferons and they target cells that are non-self
  • release the protein perforin which makes pores in the targeted cell membrane
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Effects of exercise on immunity

Vigorous exercise

- After vigorous exercise, the number of some cells in the immune system falls such as:

  • Natural killercells
  • Phagocytes
  • B cells
  • T helper cells

- The decrease in T helper cells reduces the amount of cytokines available to activate lymphocytes

- This then reduces the amount of antibodies being produced

- Physical exercise and psychological stress cause secretion of hormones such as adrenaline and cortisol; both these hormones are known to suppress the immune system

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Positive effects of exercise

- Increased basal metabolic rate (BMR)

- Decreased blood pressure

- Increased HDL and decreased LDL

- Maintaining a healthy BMI

- Decreased risk of diabetes

- Increased bone density

- Improved well-being

- Less stress

- Decreased risk of CHD

- Moderate exercise increases levels of natural killer cells

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Negative effects of exercise (over-training)

- Decreased levels of natural killer cells, phagocytes cells; this decreases immune response

- Increased muscle inflammation

- Muscle tears and sprains

- Increased adrenaline and cortisol levels, which decreases immune response

- Increased stress

- Damaged cartilage

- Tendinitis

- Ligament damage

- Swollen bursae

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How joints are damaged by exercise

- The high forces that sports generate on athletes' joints can cause joint injuries

- Repeated forces on such joints of the knee can lead to wear and tear in the joint

- Examples of knee injuries:

  • The articular cartilage covering the surfaces of the bones wears away and the bones grind on each other, causing damage
  • Patellar tendonitis occurs when the kneecap (patella) does not glide smoothly across the femur due to damage of the articular cartilage on the femur
  • Fluid sacs swell up with extra fluid causing them to push against other tissues in the joint causing inflammation
  • Sudden twisting or abrupt movement of the knee often result in damage to the ligament
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How can medical technology help?

Keyhole surgery

- Allows doctors to conduct surgery with the minimum possible damage to the patient

- The surgeon makes a small incision and uses a fibre-optic camera to view the damaged area

- The surgeon also makes a second incision to insert a number of small, remote-operated tools to repair the damage

- Because the incisions are small and only the damaged area is targeted, the patient recovers quickly and there is less chance of infection

- Unfortunately, the procedure requires a high degree of training, expensive equipment and can only be used on certain types of surgery


- An artificial body part used by someone with a disability to enable him or her to regain near to normal function (participation in sports, jobs etc.)

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- Hormones: chemical messengers that are released directly into the blood from endocrine glands

- Most are produced either in an inactive form or packaged within secretory vesicles by the Golgi apparatus 

- The vesicles fuse with the cell surface membrane, releasing their content by exocytosis

Glands and hormones

Pituitary gland secretes:

  • Growth hormones that stimulate growth
  • Follicle-stimulating hormone that causes the maturation of an egg
  • Antidiuretic hormone that causes reabsorption of water in kidneys

Thyroid gland secretes:

  • Thyroxine which raises basal metabolic rate
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Adrenal gland secretes:

  • Adrenaline which raises BMR, dilates blood vessels and prepares body for fight or flight

Pancreas secretes:

  • Insulin which lowers blood glucose concentration
  • Glucagon which increases blood glucose concentration

Ovaries secrete:

  • Oestrogen which promotes the development of ovaries and female secondary sexual characteristics

Testes secrete:

  • Testosterone which promotes the development of male secondary sexual characteristics
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- Each hormone affects only specific target cells, modifying their activity

- Hormones are carried around by the blood stream

- They can either enter the target cells or they bind to complementary receptor molecules on the outside of the cell membranes

How hormones affect cells

- Peptide hormones are protein chains; they are relatively small molecules but they cannot pass through cell membranes easily because they are charged

- Instead, they bind to a receptor on the cell membrane

- This receptor activates another molecule in the cytoplasm called a second messenger; this brings about chemical changes in the cell by affecting gene transcription

- Steroid hormones are formed from lipids and have complex ring structures

- The hormone-receptor complex functions as a transcription factor, switching enzyme synthesis on or off

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How transcription factors work

- Genes can be switched on or off

- Genes are switched on by transcription factors binding to the promoter regions of DNA right before the gene

- RNA polymerase binding site is then revealed, which allows RNA polymerase to bind to DNA; this is called the transcription-initiation complex

- The gene opens and transcription begins 

- Genes are switched off by inhibitor/repressor molecules binding to the promoter region, which stops the gene from being transcribed

- The transcription-initiation complex is not formed 

- The gene is switched off and not transcribed within the cell

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How can drugs affect your gene

- Some drugs such as anabolic steroids are closely related to natural steroid hormones

- They can pass directly through cell membranes and be carried into the nucleus bound to a receptor molecule

- These hormone/receptor complexes act as transcription factors; they bind to the promoter region of a gene allowing RNA polymerase to start transcription

- As a result, more protein synthesis takes place in the cells

- E.g. testosterone increases protein synthesis in muscle cells, increasing the size and strength of the muscle tissue

- Peptide hormones don't enter cells directly; they bind with receptors on the cell surface membrane

- This starts a process that results in the activation of a transcription factor within the nucleus

- For example, erythropoietin (EPO) stimulates the production of red blood cells, meaning the blood can carry more oxygen which is an advantage for an athlete

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Hormones used to enhance performance

Erythropoietin (EPO):

- is a peptide hormone produced naturally by the kidneys

- stimulates the formation of new red blood cells in the bone marrow

- can be made using DNA technology and is used to treat anaemia

- in large amounts can make the body produce too many red blood cells and can cause heart attacks and strokes


- is a steroid hormone produced in the testes by males and in the adrenal glands by males and females

- is in a group of male hormones called androgens

- causes the development of male sexual organs

- binds to androgen receptors

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Hormones used to enhance performance


- is not banned; it is considered to be a nutrition supplement

- is derived from amino acids

- is naturally found in meat and fish

- once ingested is absorbed, unchanged and carried into the blood to tissues

- is also synthesised in the body from the amino acids glycine and arginine

- has some side effects such as:

  • diarrhoea
  • nausea
  • vomiting
  • high blood pressure
  • kidney damage
  • muscle cramps
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Should athletes use performance-enhancing drugs?

- They cause side effects

-  They are illegal and athletes may be banned from competing if caught

- Coaches may pressure athletes to use them 

- Unfair disadvantage on those not taking them

- Funds can be used to manufacture other drugs

- Athletes have the right to exercise autonomy; they may choose to achieve their best performance and also have a duty to any sponsor they may have

- Athletes would be capable of performing at a higher level

- Performance-enhancing drugs could be a potential revenue source

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Ethical positions relating to the use of performan

Ethical absolutists: see things as very clear cut and would take one of two positions:

1) It is never acceptable for athletes to use performance-enhancing drugs (even if they are legal)

2) It is always acceptable for athletes to use any substance available to them to compete for effectively, even if there are associated risks to their health


Ethical relativists: realise that people and circumstances may be different for example:

  • It is wrong for athletes to use performance-enhancing substances, but there may be some cases and circumstances where it is acceptable
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