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Mock paper 2 > 17 Metabolism and exercise > Flashcards

17 Metabolism and exercise Flashcards

1
Q

how many minutes per week should a healthy adult be active?

A

150 mins (at least 10 mins per day)

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2
Q

why does heart rate increase immediately with exercise?

A

incr. in adrenaline secretion
incr. in stimulation of the sympathetic NS
incr. anticipatory response –> release of NT (e.g. adrenaline and noradrenaline)

–> increases proportional to exercise until plateau/max h.r. reached

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3
Q

how does vasodilation of arterioles in skeletal muscles occur?

A

secretion of nitric oxide by arteriolar endothelium

in response to fall in O(2) levels

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4
Q

why does stroke volume increase with exercise?

A

more blood returns to left atrium

∴ larger volume of blood filling ventricle in diastole

∴ greater volume of blood pumped out in systole

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5
Q

why does breathing rate + tidal volume increase with exercise?

A

more air into alveoli –> incr. in concentration gradient ∴ O(2) can diffuse into the blood more easily

∴ incr. rate of aerobic respiration ∴ more CO(2) produced ∴ more H(2)CO(3) produced

incr. in blood acidity detected by chemoreceptors - sends impulses to respiratory centre in medulla
incr. in rate and extent of contractions of diaphragm and intercostal muscles

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6
Q

what are the long term effects of exercise on the circulatory system?

A

incr. VO2 max
incr. heart size (hypertrophy of cardiac muscle –> incr. in wall thickness)
decr. resting h.r.
incr. stroke volume
decr. recovery time

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7
Q

what are the long term effects of exercise on the respiratory system?

A

incr. max b.r.
incr. tidal volume
incr. vital capacity
incr. capillary density –> decr. b.r. at rest

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8
Q

what are the long term effects of exercise on the skeletal system?

A

incr. in cross-sectional area of slow twitch muscle fibres
incr. in size/number of mitochondria in muscle fibres
incr. capillary network surrounding muscle fibres
incr. efficiency of lipid metabolism
incr. Mb and glycogen stores

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9
Q

what is the definition of aerobic fitness?

A

a measure of the ability of the heart and lungs to respond to the demands of aerobic exercise

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10
Q

what are three indicators of aerobic fitness?

A

efficiency of GES/CVS

extent of aerobic respiration without fatigue

efficiency of respiration

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11
Q

how is aerobic fitness achieved?

A

20 mins of exercise

3 x per week

increasing in intensity to 50-55% of VO2 max

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12
Q

give four factors that affect aerobic fitness

A

age

gender

smoking

malnutrition

motivation

programme

alcohol consumption

stimulants

depression

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13
Q

give four health benefits of regular aerobic exercise

A

strengthened skeletal muscle

improved circulatory efficiency

reduced blood pressure

improved mental health

reduced risk of diabetes

stimulate bone growth

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14
Q

how can aerobic exercise be improved?

A

increase:

  • Frequency
  • Intensity
  • Type
  • Time (i.e. duration)
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15
Q

how is aerobic fitness measured?

A

decr. resting h.r.
decr. recovery time
incr. VO2 max

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16
Q

how does a successful training programme bring improved aerobic fitness?

A

successful training = stressor

body adapts

progressive overload –> prevents plateau

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17
Q

what is the definition of VO2 max?

A

the maximum rate at which oxygen can be taken in, transported and utilised, as measured by/during incremental exercise

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18
Q

what units is VO2 max measured in?

A

absolute rate = dm^3 min-1

relative rate = ml kg-1 min-1

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19
Q

what is the function of the Bruce treadmill test?

A

to check the development of general endurance

can check nerve impulses from SAN if coronary heart disease is suspected

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20
Q

how is VO2 max calculated for men and women?

A

men: VO2 max = 14.8 - (1.379 x T(1)) + (0.451 x T(2)) - (0.012 x T(3))
women: VO2 max = 4.38 x T - 3.9

{where T = minutes on treadmill}

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21
Q

what is directly measured in the Bruce treadmill test?

A

ventilation rate

oxygen concentration of inhaled air

CO(2) concentration of exhaled air

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22
Q

when is VO2 max reached?

A

when O(2) consumption remains steady despite increased workload

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23
Q

what is excessive post-exercise oxygen consumption (EPOC)?

A

the increased volume of oxygen consumed following vigorous exercise

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24
Q

how is EPOC calculated?

A

oxygen consumed during recovery period - total oxygen consumed

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25
Q

why is oxygen required after exercise?

A

reoxygenate Hb and Mb

balance hormones

replenish glycogen stores in skeletal muscles

carry out cell repairs

regenerate ATP

convert lactate to glucose/glycogen

meet demands of incr. metabolic rate

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26
Q

what are the advantages of high intensity interval training?

A

incr. resting metabolic rate

improved VO2 max

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27
Q

how does erythropoietin enhance athletic performance?

A

recombinant human erythropoietin (RhEPO)

EPO normally secreted from cells in renal cortex of kidneys

incr. erythrocyte production in bone marrow
incr. RBC count

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28
Q

how is RhEPO produce?

A

GE bacteria

detectable ∴ random tests given

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29
Q

what are the advantages of RhEPO and blood doping?

A

incr. RBC count
incr. Hb concentration
incr. oxygen-carrying capability of the blood
incr. VO2 max
incr. performance

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30
Q

what are the disadvantages of RhEPO?

A

unethical

illegal

can cause severe cardiovascular problems

can lead to renal failure

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31
Q

how does blood doping enhance athletic performance?

A

remove ~ 1 dm^3 several months before competition

extra EPO secreted naturally

RBC count increases to normal

blood reintroduced a few days before the competition

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32
Q

what are the disadvantages of blood doping?

A

unethical

illegal

dangerous
- incr. blood viscosity –> clotting/pulmonary embolism

difficult to detect

33
Q

how do steroids enhance athletic performance?

A

stimulate anabolic reactions

cause transcription of specific genes

artificial anabolic steroids can be used to increase muscle mass

34
Q

what are the advantages of steroids?

A

incr. muscle size and strength

more aggressive

35
Q

what are the disadvantages of steroids?

A

unethical

can cause liver damage

decr. natural testosterone production
decr. immune response

36
Q

how does carbohydrate loading enhance athletic performance?

A

incr. stored glycogen in skeletal muscles (more a. glucose)

carbodepletion - CBH intake reduced

carbloading - high CBH diet for days before competition –> incr. a. glucose

37
Q

what is the advantage of carbohydrate loading?

A

more a. glucose ∴ more aerobic respiration ∴ can work for longer

38
Q

what are the disadvantages of carbohydrate loading?

A

weight gain

digestive issues + bloating

39
Q

around how many molecules of haemoglobin (Hb) are there per RBC?

A

~ 280 million

40
Q

how many O(2) molecules can each Hb molecule transport?

A

4

{accounts for 98% of O(2) in blood)

41
Q

what is the prosthetic group of a Hb molecule?

A

haem (Fe2+)

binds cooperatively (allosteric conformational change makes it easier for the next O(2) to bind)

42
Q

what is the definition of a respiratory pigment?

A

a specialised molecule that is capable of binding reversibly with oxygen

43
Q

what is the function of Hb?

A

to transport O(2) as oxyHb to all respiring cells, where is acts as the final e- acceptor in the eTC

44
Q

what is association?

A

the binding uptake of O(2) by Hb to form oxyHb

45
Q

what is dissociation?

A

the ability of oxyHb to release O(2) from haem groups

46
Q

what is the oxygen dissociation curve (ODC)?

A

a graph that shows the relationship between the partial pressure of oxygen (PO(2)) and % saturation of Hb

47
Q

how is PO(2) calculated?

A

volume of gas/total volume = pressure of gas/total pressure

48
Q

what is the oxygen binding capacity?

A

1.34 cm^3 of O(2) per g-1 of Hb

49
Q

what is the appearance of the ODC for adult Hb (aHb)?

A

{sigmoidal curve - coop binding}

at high PO(2), little/no change in % saturation of Hb (i.e. plateau)

∴ O(2) is still taken up by Hb in capillaries

steep part = active skeletal muscles

∴ small changes in PO(2) –> large change in % saturation

50
Q

what is the appearance of the ODC for foetal Hb (fHb)?

A

fHb has higher affinity for O(2) than aHb

∴ at any PO(2), fHb has higher % saturation than aHb

∴ fHb can obtain (O(2)) from maternal Hb via placenta

51
Q

what is the quaternary structure of fHb?

A

2 alpha and two gamma p.p.c.

haem prosthetic groups

52
Q

what is the quaternary structure of myoglobin (Mb)?

A

1 a. helix p.p.c.

1 haem prosthetic group

53
Q

when does Mb release O(2)?

A

at low PO(2)

~ 0.5 kPa

54
Q

why can Mb not bind cooperatively?

A

only 1 prosthetic group

Mb + O(2) MbO(2)

55
Q

what is the appearance of the ODC for Mb?

A

a hyperbolic curve

56
Q

what are the three ways in which CO(2) is transported in the blood?

A

dissolved in the blood plasma (5%)

reacts with terminal amine groups in haem p.p.c. to form carbaminohaemoglobin (10%)

reacts with water to form carbonic acid (85%)

57
Q

which enzyme is required to turn CO(2) and H(2)O into carbonic acid (H(2)CO(3))?

A

carbonic anhydrase

can also catalyse the reverse reaction

58
Q

how does the reaction between CO(2) and H(2)O in the blood decrease blood pH?

A

dissociation of H(2)CO(3) into H+ and HCO(3)-

H+ combines with Hb to form haemoglobinic acid (H.Hb)

59
Q

what is the Bohr shift?

A

an decrease in blood pH due to the presence of CO(2) causes more O(2) to dissociate from Hb in erythrocytes

respiring tissues require more oxygen for more aerobic respiration to produce more ATP

more CO(2) is produced ∴ less Hb can combine with O(2) ∴ it is released more easily

60
Q

what does the Bohr shift look like on a graph?

A

shift of ODC to right at same PO(2)

61
Q

what happens to the HCO(3)- ions produced? what is their effect?

A

diffuse out of RBCs into plasma

Cl- diffuse in to balance change in charge

62
Q

how is CO(2) reformed from H(2)CO(3) in the lungs and exhaled?

A

carbonic anhydrase catalyses the reverse reaction

releasing CO(2) and H(2)O

CO(2) diffuses down concentration gradient into the alveolar space and is exhaled

63
Q

give three features of cardiac muscle

A

striated

myogenic

has intercalated discs

64
Q

what is the purpose of intercalated discs?

A

cells membranes fuse and form gap junctions

free diffusion of ions for action potential movement

65
Q

give three types of cardiac muscle

A

walls of atria

walls of ventricles

specialised conductive and excitatory muscle fibres

66
Q

give three features of smooth muscle

A

tires easily

not under conscious control

has circular and longitundinal bundles for peristalsis

67
Q

how is smooth muscle used in the iris?

A

circular bundles: contraction –> constriction of pupil

radial bundles: contraction –> dilation of pupil

68
Q

give three features of skeletal muscle

A

multinucleated

striated

under conscious control of motor cortex

69
Q

muscle –> ……… –> sarcomere

A

muscle

muscle bundle

fascicle

muscle fibre (cell)

myofibril

sarcomere

70
Q

name the three proteins that make up actin

A

troponin (globular)

tropomyosin (‘string’)

G-actin (where myosin binds)

71
Q

what enzyme can a myosin head function as?

A

ATPase

72
Q

sliding filament theory: outline the formation of the cross bridge

A

myosin head has ADP + P(i) bound to it

E from hydrolysis of ATP activates myosin to ‘cocked’ position

Ca2+ released from sarcoplasmic reticulum and bind to tropomyosin

troponin undergoes allostery causing tropomyosin to move and expose mysosin binding sites on G-actin

myosin binds, forming cross bridge

P(i) released –> bridge strengthened

73
Q

sliding filament theory: outline the power stroke

A

ADP is released from myosin head

head pivots and slides actin filament towards centre of sarcomere

74
Q

sliding filament theory: outline the cross bridge detachment

A

another ATP binds to the myosin head

cross bridge weakens and myosin detaches

75
Q

sliding filament theory: outline the reactivation of the myosin head

A

ATP is hydrolysed by myosin kinase

E released activates myosin head to ‘cocked’ position

76
Q

why is Ca2+ required in muscle contraction?

A

causes troponin to undergo an allosteric change

which moves tropomyosin

exposing actin binding sites for the myosin heads

77
Q

how is a nerve impulse converted into a muscle contraction?

A

a.p. arrives at synaptic end bulb of axon

synaptic transmission of ACh (see chap. 26)

ACh binds to receptors on motor end plate, opening Na+ channels

t tubules carry Na+ to centre of muscle fibre, spreading a.p. through the muscle

Ca2+ released and spread to actin filaments

78
Q

outline the differences between slow and fast-twitch muscle fibres

A

slow:

  • ATP production in aerobic respiration
  • lots of mitochondria for KC and OP
  • high Mb conc.
  • small diameter
  • high capillary density

fast:

  • anaerobic respiration
  • few mitochondria
  • low Mb conc.
  • large diameter
  • low capillary density

Mock paper 2 (9 decks)

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