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Year 13 - Biology > C17 - Metabolism and Exercise > Flashcards

C17 - Metabolism and Exercise Flashcards

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1
Q

What are the immediate, short term effects of exercise? (7)

A

Increase in heart rate

Vasodilation of arterioles in skeletal muscles

Increase in blood flow to active muscles

Increase in stroke volume

Reduced blood flow to digestive system

Vasodilation of arterioles supplying the skin surface

Increased breathing rate and depth

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2
Q

What causes the heart rate to increase after short term exercise?

A

There’s an increase in the secretion of adrenaline and the sympathetic nervous system is stimulated.

Before exercise, HR increases in anticipation - the anticipatory response.
This is due to the release of neurotransmitters: adrenaline and noradrenaline.

After this, HR increases proportional to exercise intensity.

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3
Q

What causes vasodilation of arterioles in skeletal muscles after short term exercise?

A

The secretion of nitric acid by arteriolar endothelium in response to the fall in O2 levels.

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4
Q

What causes an increased blood flow to active muscles after short term exercise?

A

Dilation of arterioles supplying oxygenated blood to active muscles.

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5
Q

What causes an increase in stroke volume after short term exercise?

A

More blood is being returned to the left atrium of the heart, filling the ventricle in diastole with more blood so more is pumped out during systole.

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6
Q

Why is there reduced blood flow to the digestive system after short term exercise?

A

There’s a finite volume of blood within the body.

More blood is diverted to active muscles so less flows to the digestive system.

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7
Q

What causes vasodilation of arterioles supplying the skin surface after short term exercise?

A

Adrenaline is secreted, causing the arterioles to receive more blood. Heat is lost via radiation.

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8
Q

What causes increased breathing rate and depth after short term exercise?

A

Increased ventilation brings more air into the alveoli.
This increases the concentration gradient, increasing the amount of gas exchange.

Increase in blood acidity is detected by chemoreceptors which sends impulses to the respiratory centre in the medulla of the brain.
This leads to the increase in rate and extent of contractions of the diaphragm and intercostal muscles.

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9
Q

What 3 systems are affected by long term exercise?

A

Circulatory

Respiratory

Skeletal

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10
Q

How does the circulatory system change after long term exercise?

A

Increased VO2 max

Increased heart size

Decreased resting heart rate

Increased stroke volume

Decreased heart rate recovery time

Increased number of red blood cells

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11
Q

How does the respiratory system change long term exercise?

A

Increased maximum breathing rate

Increased tidal volume

Increased vital capacity

Increased density of capillaries in the lungs

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12
Q

How does the circulatory system change after long term exercise?

A

Increase in cross-sectional area of slow-twitch muscle fibres

Increase in number and size of mitochondria in muscle fibres

Increased capillary network surrounding muscle fibres

Increased efficiency in lipid metabolism in muscle fibres

Increased myoglobin and glycogen stores

Increased vascularisation of muscles

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13
Q

What is aerobic fitness?

A

How efficiently oxygen is used by the body e.g. the amount taken up, transported via blood, pumped by the heart and how well muscles use the oxygen for energy.

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14
Q

What affects aerobic fitness?

A 
Age
Gender
Participation
Smoking
Quality of nutrition
Use of stimulants
Alcohol consumption
Depression
Motivation
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15
Q

What are the health benefits of improved aerobic fitness?

A

Strengthening of skeletal muscles

Improved circulatory system efficiency

Reduced blood pressure

Improved mental health

Reduced risk of diabetes

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16
Q

What are the FITT factors influencing aerobic fitness?

A

Frequency of exercise

Intensity of exercise

Time (duration)

Type of exercise

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17
Q

What is VO2 max?

A

The maximum rate at which oxygen can be taken in, transported and utilised. (Measured in dm3min-1)

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18
Q

How can VO2 max be tested?

A

An individual is put through a graded exercise test.
Before an exercise test, a risk assessment is undertaken.
During the test, exercise intensity increases. Ventilation and oxygen & CO2 concentration of inhaled and exhaled air is measured.

VO2 max is reached when O2 consumption remains at a steady state, regardless of increased workload.

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19
Q

What’s oxygen deficit?

A

The difference between the oxygen demand of the active muscles and the oxygen they actually receive.

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20
Q

What is produced in anaerobic respiration?

A

Lactate.

This could result in the lactate pathway and glycolysis stopping due to a decrease in pH.

Lactate is removed from muscles and broken down in liver cells. Its breakdown requires a supply of oxygen.

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21
Q

What does EPOC stand for?

A

Excessive post-exercise oxygen consumption

Oxygen debt

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22
Q

What’s EPOC?

A

Excessive post-exercise oxygen consumption. (Oxygen debt).

It’s the increased volume of oxygen consumed following vigorous exercise. It’s used to restore the body’s resting state.

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23
Q

What is the oxygen from EPOC (excessive post-exercise oxygen consumption) required for? (8)

A

Re-oxygenating haemoglobin

Re-oxygenating myoglobin

Balancing hormones

Replenishing glycogen stores in muscles

Carrying out any necessary cell repair

Regenerating ATP

Converting lactate into glucose or glycogen

Meeting the demands of the increased metabolic rate as a result of thermogenesis in brown adipose tissue (from the increase in body temperature due to exercise) and the increased heart rate remaining immediately after exercise.

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24
Q

How is EPOC (excessive post-exercise oxygen consumption) calculated?

A

By calculating the difference between the total volume of oxygen consumed during the recovery period and the total volume of oxygen that would be consumed over the same period when the body is at rest.

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25
Q

How does EPOC (excessive post-exercise oxygen consumption) differ amongst people?

A

It’s usually highest after exercise. It increases with exercise intensity and duration, however is lower in aerobically fit people.

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26
Q

What’s carbohydrate loading?

A

A strategy to increase the amount of glycogen stored in muscles, his improving athletic performance. This allows muscles to work longer (but not faster or harder).

Glycogen can then be hydrolysed rapidly, releasing energy faster.

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27
Q

What are the 3 stages of carbohydrate loading?

A

Carbodepletion - carb intake is reduced in favour of protein and fat.

Carb loading

After the event, the athlete recovers by consuming carbs and proteins.

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28
Q

What does EPO stand for?

A

Erythropoietin

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29
Q

What’s EPO (erythropoietin)?

A

A hormone secreted by the kidneys that increases the rate of production of red blood cells in response to falling levels of oxygen in the tissues.

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30
Q

What does erythropoietin do?

A

It’s a hormone secreted by the kidneys that increases the rate of production of red blood cells in response to falling levels of oxygen in the tissues.

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31
Q

What does RhEPO stand for?

A

Recombinant human erythropoietin

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32
Q

What does RhEPO (recombinant human erythropoietin) do?

A

It enables the artificial increase of red blood cell levels, by stimulating erythrocyte production.

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33
Q

How does RhEPO act as a athletic performance enhancer?

A

It enables the artificial increase of red blood cell levels, by stimulating erythrocyte production.

34
Q

What’s blood doping?

A

A method of raising red blood cell levels.

(Approx 1dm3) Blood is removed several months before an event (so the athletes body can naturally replenish blood by secreting extra erythropoietin)

The removed erythrocytes are separated from the plasma and stored before being reintroduced to the athletes blood.

35
Q

How is blood doping used as an athletic performance enhancer?

A

As a method of raising red blood cell levels.

(Approx 1dm3) Blood is removed several months before an event (so the athletes body can naturally replenish blood by secreting extra erythropoietin)

The removed erythrocytes are separated from the plasma and stored before being reintroduced to the athletes blood.

36
Q

How is steroid enhancement an athletic performance enhancer?

A

Steroids are non polar and lipid soluble so can diffuse through cell membranes.

They stimulate anabolic reactions e.g. Protein synthesis, and promote tissue growth and repair.

37
Q

What do steroids do?

A

Stimulate anabolic reactions e.g. protein synthesis and promote tissue growth and repair.

38
Q

What are the 2 main respiratory pigments?

A

Haemoglobin - can bind to 4 O2 molecules. Used to transport O2. Located within erythrocytes.

Myoglobin - can bind to 1 O2 molecule. Used to store O2. Located within skeletal muscle cells.

39
Q

How do haemoglobin and myoglobin differ?

A

Haemoglobin:

  • can bind to 4 O2 molecules
  • used to transport O2
  • located within erythrocytes

Myoglobin:

  • can bind to 1 O2 molecule
  • used to store O2
  • located within skeletal muscle cells
40
Q

How does haemoglobin carry oxygen?

A

Present in erythrocytes, it binds to oxygen in the pulmonary capillaries near alveoli to form oxyhaemoglobin.
This then travels in the blood to where needed.

The oxygen then dissociates in repairing tissues and is used as the final electron acceptor in the production of ATP by oxidative phosphorylation.

41
Q

How does myoglobin carry oxygen?

A

It binds to one oxygen molecule.

Oxymyoglobin acts as an oxygen reserve, only releasing oxygen when oxygen levels in skeletal muscles becomes very low.

It has a greater oxygen affinity than haemoglobin.

42
Q

What does an oxygen dissociation curve show?

A

The relationship between the partial pressure of oxygen and saturation of the respiratory pigment.

Calculated by:
V (gas) / V (total) = P (gas) / P (total)

43
Q

What is the dissociation curve for adult haemoglobin?

Why?

A

It’s an S shaped sigmodial curve.

When first oxygen molecule attaches to Hb, it causes a conformational change in the haem group in one of the four subunits.

This causes the binding sites of the 3 remaining subunits to change, making it easier for oxygen to bind.

This is called cooperative binding.

44
Q

How does affinity for oxygen for haemoglobin change with regards to O2 partial pressure?

A

At very low partial pressures, affinity of Hb for oxygen is low - it’s difficult for oxygen to combine with the first haem group.

Affinity increases after the first oxygen is added so the rest will bind more easily.

45
Q

What is the oxygen dissociation curve for fetal haemoglobin?

A

A S shaped curve shifted to the left of the curve for adult haemoglobin.

This is because it has a greater affinity for oxygen than HbA. Oxygen will bind more readily with HbF because two of the subunits in HbF differ to those within HbA.

46
Q

Why is the oxygen dissociation curve for fetal haemoglobin to the left of the curve for adult haemoglobin?

A

Fetal haemoglobin affinity for oxygen than HbA. Oxygen will bind more readily with HbF because two of the subunits in HbF differ to those within HbA.

47
Q

What is the oxygen dissociation curve for myoglobin?

A

A curve which increases greatly at low partial pressures then plateaus as pO2 increases.
(Looks like an ln(x) curve)

48
Q

Why does myoglobin have a curved oxygen dissociation graph?

A

It has a higher affinity for oxygen than haemoglobin so will only release its oxygen at low partial pressures of oxygen.

At any partial pressure of oxygen, there will be a higher oxygen saturation level for myoglobin then HbA.

49
Q

Why is it important for myoglobin to release its oxygen only at very low partial pressures of oxygen?

A

It enables myoglobin to act as an oxygen store.

When skeletal muscles work hard, oxygen demand may be greater than oxygen supply.
Oxymyoglobin will then dissociate to release oxygen and enable aerobic respiration to continue for a longer period of time.

50
Q

What (3) factors affect the dissociation of oxygen from haemoglobin?

A

Carbon dioxide

pH

Temperature

51
Q

How is CO2 transported in the blood?

A

In aqueous solution in plasma (5%)

Combined with the amine group of the 4 polypeptide chains in haemoglobin as carbaminohaemoglobin (10%)

As hydrogen carbonate ions dissolved in plasma (85%)

52
Q

Why does CO2 affect the dissociation of oxygen from haemoglobin?

A

CO2 diffuses into the red blood cells.

The zinc-containing enzyme ‘carbonic anhydrase’ catalyses the reaction between CO2 and water, forming H2CO3 which dissociates to form HCO3- and H+.

The H+ ions in the erythrocyte cytosol with the haemoglobin to form haemoglobonic acid.
The haemoglobin acts as a buffer and ‘mops up’ additional hydrogen ions.

The formation of haemoglobonic acid causes the oxyhaemoglobin to release its bound oxygen, which will diffuse out of the red blood cell.
(Bohr effect)

53
Q

Why would Cl- ions diffuse into the erythrocyte?

A

Because of an increase in H+ ions in the red blood cell due to the production of hydrogen carbonate (from the diffusion of CO2 into the cell).

54
Q

What happens when CO2 diffuses into erythrocytes?

A

The zinc-containing enzyme ‘carbonic anhydrase’ catalyses the reaction between CO2 and water, forming H2CO3 which dissociates to form HCO3- and H+.

The H+ ions in the erythrocyte cytosol with the haemoglobin to form haemoglobonic acid.
The haemoglobin acts as a buffer and ‘mops up’ additional hydrogen ions.

The formation of haemoglobonic acid causes the oxyhaemoglobin to release its bound oxygen, which will diffuse out of the red blood cell.

55
Q

What is the Bohr effect?

A

When the presence of carbon dioxide helps the release of oxygen from haemoglobin.

This is because an increase in CO2 shifts the curve to the right.

56
Q

How does pH affect the oxygen dissociation of haemoglobin?

A

A decrease in pH shifts the dissociation curve to the right (due to the formation of haemoglobonic acid) while a increase in pH causes a shift to the left.

57
Q

How does temperature affect the dissociation of oxygen from haemoglobin?

A

Hyperthermia shifts the curve to the right, as increasing temperature will weaken the association between oxygen molecules and the haem group. This will disrupt hydrogen and ionic bonds in the haemoglobin structure.

The higher the temperature, the less saturated the haemoglobin is with oxygen.

Hypothermia shifts the curve to the left.

58
Q

What are the three types of muscle?

A

Cardiac muscle - this is myogenic and found in the walls of the heart.

Smooth muscle - found in blood vessels and walls of the digestive tract, ureter, urethra, bladder and uterus. It’s an involuntary muscle and neurogenic as it is controlled by the autonomic nervous system.

Skeletal muscle - found attached to the skeleton by tendons and is used to generate movement. It’s voluntary muscle and neurogenic as it is controlled by the motor cortex in the brain.

59
Q

What features make up the structure of skeletal muscle? (7)

A

Nucleus (multinucleated)

Myofibrils (containing myosin and actin)

Mitochondria

Blood vessels

Sarcolemma

Transverse tubules

Sarcoplasmic reticulum

60
Q

How do myofibrils appear under an electron microscope?

Why?

A

Striated (stripy)

Due to the presence of overlapping strands of a contractile protein (myosin) and strands of smaller proteins (actin).

61
Q

What’s a sarcomere?

A

A structural unit of a myofibril in striated muscle, consisting of a dark band and the nearer half of each adjacent pale band.

62
Q

What’s sarcoplasm?

A

The cytoplasm of striated muscle cells.

This surrounds the myofibrils and contains a system of membranes - the sarcoplasmic reticulum.

63
Q

What’s a myofibril?

A

Any of the elongated contractile threads found in striated muscle cells, consisting of anisotropic and isotopic bands.

64
Q

What is the anisotopic band (A band) within skeletal muscles?

A

Sections/bands along the myofibrils made up of actin and myosin filaments.

It’s a dark region in the sarcomere where the actin and myosin overlap.

In the centre of the A band in a relaxed muscle is a lighter region called the H zone, consisting of myosin filaments only.

65
Q

What does the anisotropic band of myofibrils look like?

A

It’s a dark region in the sarcomere where the actin and myosin filaments overlap.

In the centre of the A band in a relaxed muscle is a lighter region called the H zone, consisting of myosin filaments only.

66
Q

What is the H zone?

A

The lighter region of the anisotropic band of myofibrils consisting of myosin filaments only.

67
Q

What is the isotropic band (I band) within skeletal muscles?

A

Sections/bands along the myofibrils made up of actin filaments only.

It possesses a central line called the Z line.

The z line marks the end of one sarcomere and the start of the next.

68
Q

What is the Z line?

A

A central line which marks the end of one sarcomere and the start of he next.

69
Q

What are the two proteins within muscle fibres?

A

Actin (associated with tropomyosin and troponin)

Myosin

70
Q

What is the structure of actin (protein in muscle fibres)?

A

A long, globular protein forming thin filaments.
These link together to form long chains which situate side by side and are twisted around each other, anchored by Z lines.

Tropomyosin (long, thin molecule) lies in the groove between the two actin chains.

Troponin (globular protein) binds to actin at regular intervals.

71
Q

How are tropomyosin and troponin incorporated into the structure of actin?

A

Actin is a long, globular protein forming thin filaments.
These link together to form long chains which situate side by side and are twisted around each other, anchored by Z lines.

Tropomyosin (long, thin molecule) lies in the groove between the two actin chains.

Troponin (globular protein) binds to actin at regular intervals.

72
Q

What’s the structure of myosin (protein within muscle fibres)?

A

It’s a fibrous protein which forms thick filaments that situate side by side.

They comprise of a long rod-shaped fibre with a head at the end.

73
Q

What are the features present at a neuromuscular junction? (11)

A

Myelin sheath

Nerve axon

Mitochondrion

Sarcoplasm

Muscle nucleus

Synaptic vesicles containing acetylcholine

Presynaptic membrane

Synaptic cleft

Postsynaptic membrane

‘A’ band of myofibril

‘I’ band of myofibril

74
Q

What is a neuromuscular junction?

A

Where a motor neurone meets a muscle cell.

75
Q

What occurs at a neuromuscular junction?

A

When a nerve impulse is received at the junction, it triggers the release of the neurotransmitter ‘acetylcholine’ which diffuses across the gap and binds with receptors on the sarcolemma at the motor end-plate.

This causes depolarisation of the sarcolemma and results in skeletal muscle cells contacting.

76
Q

Why do skeletal muscles contract?

A

As a result of actin and myosin filaments sliding over each other - sliding filament theory.

As the muscle fibre contracts, the myosin filaments pull the actin filaments towards the centre of the sarcomere, causing the sarcomere to shorten.
As each sarcomere shortens, the overall muscle length of the fibre reduces.

77
Q

What’s the sliding filament theory?

A

Skeletal muscle contraction as a result of actin and myosin filaments sliding over each other.

As the muscle fibre contracts, the myosin filaments pull the actin filaments towards the centre of the sarcomere, causing the sarcomere to shorten.
As each sarcomere shortens, the overall muscle length of the fibre reduces.

78
Q

What is the (brief) sequence of events in muscle contraction?

A

The neuromuscular junction is the place where the motor neuron forms a synapse with a muscle cell.

A nerve impulse, in a motor neuron, arrives at the neuromuscular junction.

This causes the release of acetyl choline from the terminal of the motor neuron.

The acetyl choline diffuses across the synaptic cleft and binds to specific receptors in the muscle cell membrane.

This initiates an action potential in the muscle cell membrane (sarcolemma).

The impulse spreads through the T tubule system in the muscle fibres, causing Ca2+ to be released from the sarcoplasmic reticulum.

Ca2+ binds to troponin which changes shape causing tropomyosin to move from the myosin binding sites on the actin filaments.

Myosin filaments can now attach to actin forming cross bridges. Myosin is able to bind to actin due to the removal of ADP from the myosin head.

Binding causes the myosin head to change shape – the ‘power stroke’, which pulls on the actin filament.

ATP then attaches to the myosin head, breaking the cross bridge and returning the myosin head back to its original shape.

ATP is hydrolysed again to form ADP, allowing another cross bridge to form, resulting in another power stroke.

The process of cross bridges breaking and reforming continues as long as Ca2+ and ATP are present.

As a result the actin and myosin filaments move past each other causing the muscle fibre to contract.

When the nerve impulse to the muscle stops, Ca2+ is pumped back into the sarcoplasmic reticulum.

No more cross bridges can form and the muscle relaxes.

79
Q

What is the (detailed) sequence of events in muscle contraction?

A

1) A nerve impulse reaches the neuromuscular junction.
2) Synaptic vesicles in the motor neurone fuse with the end-plate membrane and release the neurotransmitter ‘acetylcholine’.
3) The neurotransmitter binds to the sarcolemma (muscle membrane) and depolarises it.
4) The neurotransmitter is hydrolysed by enzymes.
5) An action potential is generated which passes down the T-tubules of the sarcolemma.
6) The action potential passes from the T-tubules to the sarcoplasmic reticulum, causing the release of calcium ions into the sarcoplasm.
7) Calcium ions bind to troponin, causing it to change shape.
8) The troponin moves the tropomyosin so that it no longer blocks the myosin binding site on the actin filament.
9) Myosin heads are usually attached to ADP. The calcium ions activate an enzyme called myosin kinase, which releases the ADP so the myosin head is free to bind. The myosin heads attach to the actin filament, forming ‘cross-bridges’.
10) The myosin head tilts, pulling the actin filaments over the stationary myosin filaments towards the centre of the sarcomere, known as the ‘power stroke’.
11) ATP attaches to the myosin head causing it to detach from the actin filament.
12) Hydrolysis of ATP releases energy to move the myosin head outwards from the centre of the sarcomere, re-setting the myosin head. The myosin head acts as enzyme ‘ATPase’.
13) The myosin heads reattach, forming new cross-bridges to the actin at binding sites adjacent to the ones previously occupied.
14) Once the nerve impulse stops, calcium ions are reabsorbed.
15) Troponin reverts back to its original shape.
16) Tropomyosin blocks the attachment of the myosin head to the actin filament to prevent further muscle contraction.
17) Calcium ions are actively pumped into the cisternae of the sarcoplasmic reticulum and T-tubule system for use in further muscle contraction.
18) To reset the sarcomere, the filaments will be pulled back to their original position by the action of an antagonistic muscle.

80
Q

What’s a tendon?

A

A flexible but inelastic cord of strong fibrous collagen tissue attaching a muscle to a bone.

81
Q

What’s a ligament?

A

A short band of tough, flexible fibrous connective tissue which connects two bones or cartilages or holds together a joint.

The tissue that connects two bones to form a joint.

82
Q

What’s cartilage?

A

Firm, flexible connective tissue between joints, being replaced by bone during growth.

Year 13 - Biology (18 decks)

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