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Biology > topic 7 > Flashcards

topic 7 Flashcards

1
Q

muscle fibre

A

a single cell
can be several cm in length
several nuclei - multinuleate

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2
Q

antagonistic pairs

A

skeletal muscles work in these
this means pair of muscle which pull in opposite directions
muscles can only pull so at least 2 muscles are needed to move a bone
- extensor: a muscle that contracts to cause extension of a joint
- flexor. the corresponding muscle that contracts to reverse movement.

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3
Q

tendon

A

joins muscle to bone enabling the muscles to power joint movement

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4
Q

ligament

A
  • joins muscle to bone
  • strong and flexible
    bones are held in position by ligaments that control and restrict the amount of movement in the joint
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5
Q

cartilage

A

absorbs synoviral fluid
acts as a shock absorber
protects the bones from becoming damaged

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6
Q

fibrous capsule

A

encloses the joints

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7
Q

synoviral membrane

A

creates synoviral fluid

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8
Q

synoviral fluid

A

acts as a lubricant. joints are separated by a cavity filled with it enabling them to move freely.

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9
Q

myofibrils

A

muscle fibres contain numerous myofibrils

which are made up of contractile units called sarcomeres

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10
Q

sacromeres

A

make up myofibrils
made of 2 types of protein molecules
- thin filaments: made of actin (light band)
- thick filaments: made of myosin (dark band)
contraction is brought about by co-ordinated sliding of filaments with sacromeres when the muscle contracts actin moves between the myosin shortening the length of sacromere.

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11
Q

what protein molecules in actin associated with

A
  • troponin

- tropomyosin

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12
Q

how does the nerve impulse trigger the contraction of muscle

A

when a nerve impulse arrives at a neuromuscular junction calcium ions Ca2+ are released from the sarcoplasmic recticulum.
the Ca2+ diffuses through the sarcoplasm
this initiates the movement to the protein filament leading to muscle contraction

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13
Q

stages in the sliding filament theory (7)

A
  1. Ca2+ attaches to the troponin molecules causing them to move
  2. as a result tropomyosin shifts exposing myosin binding sites
  3. myosin heads bind with these sites forming cross bridges
  4. when myosin head binds to actin. ADP and Pi on head are released
  5. myosin changes shape, causing myosin head to nod forward. resulting in relative movement of filament attached action moves over the myosin
  6. an ATP molecule binds to the myosin head. causes the myosin head to detach from the actin
  7. ATPase on myosin head hydrolyses ATP forming ADP + Pi.
  8. this hydrolysis changes shape of myosin head returns to upright position able to bind again to actin
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14
Q

what happens when the muscle is no longer being stimulated by nerve impulses

A

the muscles relaxes
Ca2+ are actively pumped out of the muscle sarcoplasm, using ATP.
troponin and tropomyosin move back blocking the myosin binding site on the actin.

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15
Q

sacroplasmic reticulum

A

specialised type of endoplasmic reticulum: a system of membrane bound sacs around the myofibrils

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16
Q

sarcoplasm

A

specialised type of cytoplasm which surrounds actin and myosin in the sacromere

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17
Q

how does ATP release energy

A

ATP(aq) —-> ADP(aq) + hydrated Pi + energy
ATP in water is at a higher energy level than ADP and PI
ATP in water has chemical potential energy
a small amount of energy is required to break the bond holding phosphate to ATP. once removed Pi becomes hydrated.
a lot of energy is released as bond form between water and phosphate
it requires energy to separate Pi from water to make ATP

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18
Q

overall equation for aerobic respiration

A

C6H12O6 + 6 O2 —–> 6 CO2 + 6H2O + energy

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19
Q

glycolysis (4 steps)

A

first step in respiration

  1. 2 Pi are added to the glucose from 2ATP molecules increasing glucose reactivity
  2. glucose splits into 2 phosphorylated 3 carbon compounds
  3. each intermediate is oxidised producing 3 carbon pyruvate. 2 H are removed and are taken up by co enzyme NAD producing reduced coenzyme NADH
  4. Pi from intermediate compound transfers to ADP creating ATP along with the energy produced when glucose goes to pyruvate as it is at a higher energy level.
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20
Q

reactants and products of glycolysis

A

glucose ———–> 2 intermediate phosphorlated 3 carbons
2 ATP ———–> 2 ADP

2 intermediate ————-> 2 pyruvate + 4 Hydrogens
4ADP + 2 Pi (from pyruvate) —–> 4ATP
4H + 2NAD —–> 2 NADH

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21
Q

summary and net yield of glycolysis

A 
net yield of: 
- 2 ATPs
- 2 pairs of H = 4 Hydrogens 
- 2 3 carbon pyruvate 
2H + coenzyme NAD ---> reduced coenzyme NAD 
- 2 NADH / reduced coeNAD
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22
Q

what happens to pyruvate in the link reaction

A

pyruvate is
- de carbozylated (Co2 released as a waste product)
- de hydrogenated (2 Hydrogens are removed and taken up by coenzyme NAD
resulting in 2 carbon molecule which combines with coenzyme A to form acetyl co enzyme A (acetyl CoA)

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23
Q

equation for the link reaction

A

pyruvate + NAD + CoA –> Acetyl CoA + reduced NADH + CO2

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24
Q

where does the link reaction occur

A

mitochondrial matrix

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25
Q

what are the 4 important types of reaction that occurs in the krebs cycle

A
  • phosphorylation reactions. which add a phosphate e.g ADP + pi —> ATP
  • decarboxylation reactions, which break off CO2
  • dehydrogenation. (redox reaction) molecule which gains H is reduced
    molecule that loses H is oxidised
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26
Q

what happens in the Krebs cycle

A
  • each 2c acetyl CoA combine with 4 carbon compound creating 6 carbon compound
  • in a circular pathway the original 4 carbon compound are recreated
  • 2 steps involve decarboxylation
  • 4 steps involve dehydrogenation
  • 1 step involves substrate level phosphorylation with direct synthesis of ATP
    hydrogen produce turn FAD / NAD into reduced NAD / FAD
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27
Q

net yield of Krebs cycle

A 
2 acetyl CoA go in 
produces 
- 2 ATP 
- 6 reduced NAD / NADH 
- 2 reduced FAD
- 2 CO2 
- reformation of the 4 carbon intermediate
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28
Q

where does the krebs cycle occur

A

mitochondrial matrix

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29
Q

stages in the electron transport chain (6)

A
  1. reduced Co enzyme carries 2H+ and 2e- to electron transport chain on inner mitochondrial membrane
  2. e- pass from 1 electron carrier to the next in a series of redox reactions
  3. H+ move inter membrane space creating high H+ conc.
  4. H+ diffuses back into mitochondrial matrix down electron chemical gradient
  5. H+ diffusion allows ATP synthases to catalyse ATP synthesis.
  6. e- and H+ recombine to form H which combines with O2 to create water.
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30
Q

chemiosmotic theory (4)

A
  1. energy is released as electron pass down electron transport chain
  2. this energy is used to move H+ from matrix into intermembrane space creating an electrochemical gradient making intermembrane space more positive than matrix
  3. H+ diffuses down electrochemical gradient through protein channels with ATP synthase causing a conformational change enabling the ADP and Pi to bind with active site
  4. within matrix H+ and e- recombine and combine with oxygen to form water. oxygen acting as the final carrier of the electron transport chain
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31
Q

number of ATP molecules made per glucose molecule

A

1 glucose molecule produces a net yield of 38 ATP

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32
Q

how many ATP can be made from reduced NAD / reduced FAD

A

each reduced NAD results in 3 ATP

each reduced FAD results in 2 ATP

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33
Q

oxidative phosphorylation

A

happens in the electron transport chain

ATP formed as a result of the transfer of electrons from reduced NAD / FAD to O2 by a series of electron carriers

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34
Q

what is the percentage of total potential chemical energy stored in glucose is turned into ATP

A

1 mol of glucose releases 2880 KJ
only 1163 KJ of energy is released from the ATP made from 1 mole of glucose
40%
assuming that 38 molecules of ATP are produced per molecule

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35
Q

how is respiration controlled by ATP

A
  • ATP inhibits enzymes involved in glycolysis
  • the phosphorylation of glucose
  • the enzyme responsible can exist in 2 different forms
  • in the presence of ATP enzyme has a shape that makes it inactive
  • as ATP is broken down, the enzyme is converted back to the active form and catalysis phosphorylation of glucose
    end point inhibition
    then end products inhibits early step in the metabolic pathway controlling processes.
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36
Q

anaerobic respiration

A

it is possible to oxidise the reduced NAD created during glycolysis in absence of oxygen
- pyruvate produced at the end of glycolysis is reduced to lactate and oxisides form of NAD is regerated
continue to break down glycose to make a small amount of ATP

net yield: 2 ATP per glucose 2% efficiency

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37
Q

how is lactate removed

A

lactate is converted back to pyruvate
it is oxidised directly to CO2 and H2O via Krebs cycle releasing energy to synthesis ATP
as a result O2 uptake is greater than normal in recovery period

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38
Q

oxygen debt

A

excess oxygen requirement which is needed to fuel oxidation of lactate

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39
Q

ATP / Pc system. supplying instant energy

A

creatine phosphate —> creatine + Pi
ADP + Pi —> ATP
creatine phosphate (Pc) is hydrolysed to release energy
energy used to regenerate ATP from ADP and Pi provided by Pc
Pc is broken down as soon as exercise begins triggered by formation of ADP
does not require oxygen and provides 6 - 10 seconds of intense exercise. later Pc is regenerated from ATP

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40
Q

what are the 3 energy systems

A
  1. aerobic respiration
  2. ATP / Pc system
  3. anaerobic respiration
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41
Q

aerobic capacity

A

the ability to taken in, transport and use oxygen

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42
Q 
V O2 
V O2 (max)
A

VO2 - at rest we consume about 0.2 -0.3 litres of CO2 per minute
VO2 max. 3-6 litres per min during max aerobic exercise
dependent on the efficiency of uptake and delivery of oxygen by the lungs and cardiovascular system and the efficient use of oxygen in the muscle fibres.

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43
Q

cardiac output

A

the volume of blood pumped by the hear in 1 minute
at rest 5 dm3 per min
cardiac output depends on stroke volume (the volume of blood ejected from the left ventricle) and heart rate

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44
Q

adequate oxygen supply is maintained by

A
  • increasing cardiac output
  • faster rate of breathing
  • deeper breathing
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45
Q

equation for cardiac output

A 
cardiac output (Co) =
stroke volume (SV)  X   heart rate (HR)
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46
Q

stroke volume

A

the volume of blood pumped out of the left ventricle each time the ventricle contracts measured in cm3

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47
Q

venous return

A

the flow of blood back to the heart

the volume of blood returning to the heart from the body

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48
Q

what happens to the stoke volume and cardiac output during exercise

A

during diastole heart fills with a larger volume of blood
the hear muscle is stretched to a greater extent, causing it to contract with a greater force and so more blood is expelled
increasing the stroke volume and cardiac output.

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49
Q

hear rate

definition of resting heart rate

A

the rate at which the heart beats in beats per minute (6pm)
- resting heart rate is 60 - 100 bpm
- females 72 bpm - males 70 bpm
a fit person rate is 65 bpm

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50
Q

what factors cause differences in heart rate

A

heart size due to body size and genetic factors

a larger hear will have lower resting heart rate as it expels more blood so does not have to beat as frequently.

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51
Q

the heart is myogenic

A

myogentic means it does not need external nervous stimulation to function
the heart muscle can contract without external nervous system

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52
Q

charges on cardiac muscle cells

A

when polarised cells have a slight +ve on the outside
when depolarised they have a slight -ve on the outside
a change in polarity spreads like a wave from cell to cell causing cells to contract

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53
Q

steps in hear muscle contraction (3)

A
  1. SAN generates electrical impulse which spreads across the atria causing them to contract
  2. impulse travels to AVN. slight delay through non conducting cells ensuring atrias finish contacting
  3. signal reaches the purkyne fibres conduct impulse to the ventricular muscle depolarising at the apex ventricular cells and going upwards causing contraction moving up ventricles pushing the blood into the aorta and pulmonary artery
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54
Q

what is the SAN

A

sinoatrial node
small area of specialised muscle fibres located in the wall of the right atrium
also known as the pacemaker
generates the electrical impulse

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55
Q

what is the AVN

A

atrioventricular node

located below the SAN

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56
Q

non conducting layer in heart wall

A

located between atria and ventricles
allows for a delay of 0.13 seconds which ensures that the atrias have finished contracting and that the ventricles have filled before they contract

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57
Q

purkyne fibres

A

large specialised muscle fibres that conduct the impulse from the AVN to the apex.
there are right and left bundles of fibres collectively known as the bundle of His

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58
Q

bundle of His

A

the collective name for the left and right bundles of purkyne fibres

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59
Q

what is an ECG

A

electrocardiogram

a graphical record of the electrical activity during the cardiac cycle

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60
Q

QRS complex

A

the wave of depolarisation resulting in contraction of the ventricles
ventricular systole

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61
Q

the P wave

A

atrial systole

depolarisation of the atria leading to atrial contraction

62
Q

PR interval

A

the time taken for impulse to be conducted from the SAN across the atria to the ventricles through the AVN

63
Q

T wave

A

repolarisation (recovery) of the ventricles during the hear’ts relaxation phase
disatole

64
Q

why does the ECG not show atrial repolarisation

A

because the signals generated are small and are hidden by the QRS complex

65
Q

how do you work out heart rate from an ECG

A

number of large squares between QRS complexes x length in seconds of 1 large squares = time for one beat
60 / time for one beat = heart rate

66
Q

non conducting P wave ECG pattern

A

where the p waves is not followed by an QRS complex

showing there is a break in conduction system of heart

67
Q

ventricular fibrillation

A

irregular stimulation of the ventricles make them contract in a week and uncoordinated manner
ECG is basically a mess

68
Q

how is the heart rate under nervous control

A

heart rate is under control of the cardiovascular control centre located in the medulla oblongata region of the brain. there are 2 nerves going from the cardiovascular centre to the sinoatrial node of the heart

69
Q

what are the 2 nerves going from the cardiovascular control centre to the heart

A
  • a sympathetic nerve (accelerator)
    this raises the heart rate. increases venous return, which leads to a rise in stroke volume, resulting in higher cardiac output, thus transporting oxygen and fuel more quickly
  • vagus nerve, parasympathetic. (decelerator)
    does the opposite
70
Q

the cardiovascular control centre

A

located in the medulla oblongata

controls the heart rate via nervous system

71
Q

what can the cardiovascular control centre detect

A
  • the accumulation of CO2 and lactate in the blood, increased oxygen and increased temperature
  • sent impulses from sensory receptors in muscles detecting mechanical activity in muscles.
72
Q

when cardiac output increases what happens to blood pressure
what is the role of pressure receptors

A

blood pressure also rises
to prevent is from rising too high pressure receptors in the aorta and the carotid artery send impulses back to the cardiovascular control centre which stimulates inhibitory nerve impulses to be sen to the sinoatrial node slowing heart rate and lowing blood pressure. Negative feedback.

73
Q

stretch receptors

A

located in muscles and tendons send impulses to the cardiovascular control centre when skeletal muscles and tendons contract

74
Q

the autonomic nervous system is split into 2 different types of nerves

A
  • sympathetic nerves
    stimulation prepares the body system for action (fight or flight response)
  • parasympathetic nerves
    stimulation controls the body’s system of resting and digesting
75
Q

what is the effect of the parasympathetic NS

A

decreases breathing rate (intercostal muscles)
decreases heart rate and stroke volume
stimulates peristalsis in the gut

76
Q

what is the effect of the sympathetic NS

A

increases breathing rate (intercostal muscles)
increase heart rate and stroke volume
inhibits peristalsis in gut

77
Q

peristalsis

A

muscle contraction in the gut wall that move food through the gut (digestion)

78
Q

adrenaline affect on heart rate

A

adrenaline is a hormone produced by the adrenal glands located above the kidneys
direct affect on SAN increasing heart rate to prepare the body for fight / flight.

79
Q

adrenaline affect on the body

A

causes dilation of the arteries supply skeletal muscles
constricts arteries going to the digestive and other non essential organs, this maximises blood flow to the active muscles
increases heart rate.

80
Q

tidal volume

A

volume of air we breathing in and out at each breath

usually around 0.5dm3

81
Q

vital capacity

A

maximum volume of air a person can inhale and exhale for most it is 3-4 dm3

82
Q

residual air

A

the air remaining in the lungs after exhalation mixes with the air inhaled with each breath
not all of the air is exhaled

83
Q

minute ventilation

A 
the volume of air taken into the lungs in one minute 
tidal volume (dm3)   X   number of breaths (min-1)
84
Q

what happens during inhalation

A

ventilation centre sends nerve impulses every 2-3 seconds to external intercostal and diaphragm muscles which contract causing inhalation
during deep inhalation, not only are the external intercostal and diaphragm muscles stimulated but upper chest and neck muscles are also stimulated

85
Q

what happens during exhalation

A

stretch receptors in bronchioles stimulated which send inhibitory impulses to ventilation centre
impulses to muscles stops and muscles relax
elastic recoil of the lungs and with the help of gravity lowers the ribs

86
Q

the medulla oblongata contains

A
  • cardiovascular control centre. controls heart rate

- ventilation centre. controls breathing q

87
Q

ventilation centre receives impulses from

A
  • motor cortex which controls movement
  • chemoreceptors in medulla oblongata, aorta and carotid artery detect changes in CO2, pH and temperature of blood.
  • stretch receptors in muscles, tendons and bronchioles.
88
Q

what happens to breathin when CO2 in the blood increases

A
  • CO2 dissolves in blood making carbonic acid H2CO3 which dissociates to H+
    CO2 + H2O –> H2CO3 –> H+ + HCO3-
  • chemoreceptors sensitive to H+ / pH located in ventrilation centre of the medulla oblongata detect H+ concentration increase / pH decrease
  • impulses are sent from the ventilation centre stimulating breathing muscles. increasing rate and depth of breathing
89
Q

how does more frequent and deeper breaths increase oxygen in the blood

A

maintains a steep gradient of CO2 between alveolar air and blood and uptake of oxygen into the blood

90
Q

the control of CO2 levels in the blood is an example of ________ operating via __________

A

the control of CO2 levels in blood is example of homeostasis operating via negative feedback.

91
Q

myoglobin

A

protein similar to haemoglobin
it has a high affinity for O2 and only releases it when the concentration of 2 in cell falls very low
it therefore acts as an oxygen store within muscle cells
found in larger quantities in slow twitch fibres

92
Q

what are the 2 types of muscle fibres

A
  • fast twitch fibres

- slow twitch fibres

93
Q

key features of slow twitch fibres

A
  • specialised for slower sustained contractions can cope with long periods of exercise
  • carry out a larger amount of aerobic respiration
  • lots of mitochondria and high concentration of respiratory enzymes
  • large amounts of dark red pigment myobglobin making muscle red-pink
  • associated with numerous capillaries to ensure good O2 supply
94
Q

features of fast twitch fibres

A
  • produce rapid, intense contractions
  • ATP used for contractions comes from anaerobic glycolysis
  • few mitochondria
  • little myoglobin small reserve of O2
  • few associated capillaries
  • reliance on anaerobic respiration means there is a rapid build up of lactate
  • so fatigue easily
95
Q

differences between slow and fast twitch fibres (6)

A

S- slow F- fast

  • S is red because it has lots of myoglobin F is white because it has few myoglobin
  • S has lots of mitochondria. F has few
  • S little sarcoplasmic recticulum where as F has extensive sarcoplasmic reticulum
  • S has low glycogen content. F has high glycogen content
  • S has numerous cappilaries. F has few capillaries
  • S is fatigue resistant and F fatigues quickly
96
Q

why do fast twitch fibres need more sarcoplasmic reticulum

A

because calcium ions released from SR initiate muscle contraction; more sarcoplasmic reticulum allows rapid, repeated contraction of the muscle.

97
Q

how does slow twitch fibres regenerate ATP

A

regenerates ATP via aerobic respiration

98
Q

how does fast twitch fibres regenerate ATP

A

regenerates ATP via anaerobic glycolysis reactions

99
Q

homeostasis

A

the maintenance of a stable internal environment

100
Q

how is homeostasis achieved in the body

A

maintaining stable conditions within the blood which in turn gives rise to tissue fluid that bathes the body’s cells

101
Q

Homeostasis

norm value / set point

A

condition controlled by homeostasis has a norm value / set point usually the optimum for the condition

102
Q

homeostatic control mechanism

A

the mechanism trying to maintain a condition at a set point

103
Q

negative feedback

A

type of homeostasis
when a change from norm occurs effectors move it back to the norm value
output results in control mechanism that inhibits further change

104
Q

control of glycolysis

A

type of negative feedback
glucose is converted to pyruvate in a series of enzyme controlled reactions producing ATP and reduced NAD
when ATP rises it binds to enzyme that catalysis glycolysis preventing the formation of enzyme substrate complex inhibiting further glycolysis.

105
Q

what is the enzyme which ATP binds to preventing glycolysis

A

phosphofluctokinase
in its active form it has the correct shape to form enzyme substrate complex
when it binds with ATP it becomes unactive as it changes shape so enzyme- substrate complex cannot form.

106
Q

allosteric enzymes

A

enzymes that are controlled by a substance binding to the enzyme causing it to change shape preventing enzyme substrate complex forming

107
Q

how is testosterone concentration controlled by negative feedback

A

testosterone concentration change detected by hypothalamus
a decrease causes gonadotrophin releasing hormone to be produced by the hypothalamus
this stimulates the pituirity gland to release hormones that stimulate the testes to synthesise testosterone

108
Q

how is population size controlled by negative feedback

A

for a given species, an environment will support a particular size population which is the norm.
if population increases above this norm competition, predation or other density dependent factors causes the population size to fall, returning it to the norm

109
Q

positive feedback

A

when the output from the control centre moves the condition further from the set point

110
Q

child birth is an example of

A

positive feedback.
the pressure of the baby on uterus detected nerve messages to the hypothalamus causes the hormone oxytocin to be released, which makes contractions on the uterus speed up and become more intense.
this puts more pressure on uterus which caused the release more oxytocin

111
Q

the blood clotting cascade is an example of

A

positive feedback
blood vessel wall becomes damaged
platlets stick to exposed collagen and to each other
platelets release chemicals that attract more platlets
these platelets continue to collect and release more chemicals until a clot forms

112
Q

thermoregulation

A

the control of body temperature

type of negative feedback

113
Q

what controls body temperature

A

hypothalamus
receptors detect changes in blood temperature
the hypothalamus turns on effectors necessary to return temperature to norm.
thermoreceptors in skin

114
Q

the heat loss centre in the hypothalamus

A

control of reducing body temperature to norm

stimulates: sweat glands to secrete sweat
inhibits:
- contraction of arterioles in skin (dilating capillaries in the skin
- hair erector muscles relax
- liver (reduces metabolic rate
- skeletal muscles relax.

115
Q

heat gain centre

A 
controls the processes that increases heat gain to normal temperature 
stimulates: 
- arterioles in the skin to constrict 
- hair erector muscles to contract 
- liver to raise metabolic rate
- skeletal muscles to contract in shivering 
inhibits 
- sweat glands
116
Q

how does shivering increase body temperature

A

uncontrolled contraction of muscles and can increase heat production x6
shivering transfers energy to muscle tissue which helps maintain body temperature

117
Q

how does sweat reduce body temperature

A

released on the skin via the sweat duct
it evaporates tacking heat energy from the skin
sweat glands are stimulated by nerves from hypothalamus

118
Q

how do hairs on the surface of the skin control body temperature

A

when raised in cold weather by contraction of the erector muscles. reflex
the aim to trap air that insulates the body

119
Q

vasoconstriction

A

in colder conditions the muscles in the arterioles wall contract.
causing the arterioles to constrict reducing blood supply to the surface capillaries
blood diverted through shunt vessel which dilates to allow more blood.
blood flows further from the skin surface so less energy is lost.

120
Q

vasodilation

A

in warm conditions the shunt vessel constricts and muscles in wall of the arterioles relax
blood flows through the arterioles making them dilate. more blood flows closer to the surface so more energy is lost

121
Q

4 ways of energy transfer

A
  • radiation. our bodies are usually warmer than surrounding environment so we radiate heat through the air
  • conduction. direct contact between two objects.
  • convection. by trapping a layer of still air next to the skin using fur/ hair reduces the convection insulating
  • evaporation. energy is needed to convert liquid to vapour. energy required to evaporate sweat is drawn from the body cooling it. this does not work in high humidity
122
Q

what are the different types of knee injury (4)

A
  • arthritis, cartilage covering surfaces of the bone wares away so that the bones grind causing damage
  • patellor tendonitis. knee cap does not glide smoothly across femur
  • bursitis. Bursae cushion contract between bones, tendons and ligaments sweel and push against tissue in joints causing inflammation
  • damage to ligament caused by sudden twisting.
123
Q

what are the advantages of keyhole surgery

A 
used to confirm diagnosis 
short recovery as only small incision made 
less bleeding and pain 
lowered risk of infection 
less of a dangerous operation 
shorter hospital stay. less expensive
124
Q

arragnement of muscle fibres within muscles

A
  1. tendons at each end connect muscle to bone
  2. muscle is made up of bundles of muscle fibres up to 2cm across. bound together by connective tissue
  3. each muscle fibreis a single muscle cell
  4. each muscle fibrire may be several cm long but less than 0.1 mm in diameter
  5. inside muscle fibre is cytoplasm containing organelles. contain numerous myofibrils each composed of repeated contractile units called sacromere.
125
Q

cruciate ligaments

A

found deep inside the joint and are attached to the end of the femur and to the top of the tibia

126
Q

prosterior cruciate ligaments

A

prevents knee from bending too far back

127
Q

anterior cruciate ligaments

A

prevents the knee from being bent to far forwards

128
Q

2 factors that may be involved in the relationship between illness and exercise

A
  • increased exposure to pathogens

- suppressed immunity with hard exercise

129
Q

moderate exercise effect on immune system

A

increases the number and activity of a type of lymphocyte called natural killer cells which are found in blood and lymph.

130
Q

lymphocytes

A

provide non specific immunity against cells invaded by viruses and cancer cells
do not use specific antigen recognition
natural killers activated by cytokines and interfron
release protein perforin which makes pores in cell membrane causing apoptosis.

131
Q

what is the effect of vigour exercise on immune system

A

immune cells number and activity fall. this includes
- natural killer cells
- phagocytes
- B cells
- T helper cells
specific immune system depressed decrease in T helper cells reduces amounts of cytokines to activate lymphocytes reducing quantity of antibody produced.
inflammation in muscles due to damage reduce availability of non specific immune response

132
Q

what hormones are secreted in physical exercise and psychological stress

A
  • adrenaline
  • cortisol
    these hormones also suppress the immune system
133
Q

what are the advantages of physical activity (7)

A
  1. increases atrial vasodilation lowers blood pressure reduces risk of CHD and stroke
  2. increase blood HDLs reduce LDL associated with development of atherosclerosis
  3. helps maintain healthy weight balance energy input = energy output
  4. increases sensitivity of muscle cells to insulin improving blood glucose regulation decreasing type 2 diabetes
  5. increases bone density delaying onset of bone wasting
  6. reduces risks of some cancer
  7. improves mental well being.
134
Q

type 2 diabetes

A

body does not produce enough insulin and body cells do not respond to insulin that is produced, so blood sugar levels cannot be controlled
decreased absorption of glucose from blood, cells break down fatty acids and proteins instead leading to weight loss.

135
Q

the piturity gland

A

in the brain
produces hormone:
- growth hormone - simulates growth
- follicle stimulating hormone. controls testes and ovaries.
- anti-diuretic hormone. causes reabsorbtion of water in kidneys.

136
Q

thyroid gland

A

near the trachea

produces hormone thyroxine which raises basal metabolic rate

137
Q

adrenal gland

A

produces adrenaline which raises basal metabolic rate, dilates blood vessels and prepares body for action

138
Q

pancreas

A

produces insulin which lowers blood glucose concentration

139
Q

ovaries

testis

A

produces oestrogen which promotes the development of ovaries and female secondary sexual characteristics
produces testosterone which promotes development of male secondary sexual characteristics

140
Q

peptide hormones

A

protein chains not able to pass through cell membrane because of charge
- instead bind to receptor on the cell membrane which activates another molecule in the cytoplasm,
- the functional second messenger brings about chemical changes in cell directly or indirectly by affecting gene transcription.
EPO, human growth hormone and insulin

141
Q

steroid hormones

A

formed form lipids have complex ring structure
pass through the cell membrane and bind directly to a receptor molecule in cytoplasm
hormone receptor complex brings about characteristic response resulting from its effect on transcription . transcription factor.

142
Q

transcription factors

A

in order for transcription to be iniated RNA polymerase and a cluster of associated protein transcroptoion factors form transcription initiation complex which binds to the promoter region.
most transcroption factors produced by cells in an inactive form which re converted into active form by hormones, gorwth gactors and other regulatory molecules. remains switched off until complex attaches.

143
Q

erythropoietin (EPO)

A

peptide hormone produced in kidneys
stimulates formation of new red blood cells in bone marrow
produced using DNA technology to treat anaemia
natural substance can be hard to detect
too many red blood cells increases risk of thrombosin leading to heart attack and stroke
increase blood oxygen carrying capacity enhancing oxygen delivery improving aerobic capacity.

144
Q

protein repressor molecules

A

attach to promoter region blocks the attachment sites for transcription initiation complexes to bind
alternatively attach to transcription factors preventing them from forming complex. may be inactive transcription factor activator molecules stimulated binding of complex.

145
Q

thrombosis

A

blood clots in arteries or veins.

146
Q

testosterone as used to enhance performance

A 
steroid hormone (made from cholesterol) produced by testes in males and by adrenal glands in both males and females. causes the development of male sexual organs secondary male sexual characteristics. aggression is linked to testosterone.
it binds androgen receptors. they modify gene expression to alter development of the cell. increase anabolic reactions, such as protein synthesis in muscle cells, increasing the size and strength of the muscle. 
as testosterone is broken down quickly. synthetic anabolic steroids are used.
147
Q

dangers of synthetic anabolic steroids / testosterone

A

cause high blood pressure, liver damage, changes in the menstrual cycle, decreased sperm production and impotence in men, kidney failure and heart disease.
they can increase aggression in both men and women.
in women the androgenic side effects are not always desirable.

148
Q

testing and classification of synthetic anabolic steroids

A 
class C drug. world anti doping code has banned the use. illegal in human and animal sport (e.g horse and dog racing)
can be detected relatively easily in urine samples use mass spec. however, as the substances occur naturally it is difficult to set a level above which and athlete is doping. 
when athlete takes anabolic steroid the ration of testosterone to epitstosterone increases.
149
Q

creatine

A

this is a performance enhancing drug but is no banned. considered to be a nutrition supplement
many athletes take dietary supplements containing cretaine. found naturally in meat and fish. it is also synthesised in the body from glycine and arginine.
increase amounts of creatine phosphate (CP) in muscles. increased CP storage improves performance during repeated, short duration, high intensity exercise.

150
Q

side effects of creatine

A

diarrhoea, nausea, vomiting, high blood pressure, kidney damage and muscle cramps

151
Q

should performance enhancing drugs be banned

A
  • unhealthy and against ethics of sport. aims to protect the health athletes and ensure that there is fair competition.
  • athletes have the right to decide whether they take the drug or not, deciding for themselves if the potential benefits out way the risks to their health.
  • frequently don’t make a properly informed decision, lacking information about the possible health consequences.
  • drug use is acceptable on the grounds that there is already inequality of competition due to the differences in time available for training and in resources.

Biology (13 decks)

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