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research methods > exercise physiology midterm 1 > Flashcards

exercise physiology midterm 1 Flashcards

1
Q

catabolism

A

breakdown of molecules

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2
Q

anabolism

A

synthesis (bringing together) of molecules

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3
Q

bioenergetics

A

converts food into useable energy

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4
Q

ATP

A

adenosine triphosphate

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5
Q

main unit of energy

A

ATP `

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6
Q

ATP storage

A

normal storage (80-100g)
- this ends up equalling 160-200 units of ATP (not very much as all)

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7
Q

regular ATP consumtion

A

25kg

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8
Q

enzymes

A

specific protein molecules that catalyze reactions
- speeds up reactions by cuasing lower energy of activation

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9
Q

enzymes under complex control

A
  1. competitive inhibition
  2. non-competitive inhibition
  3. feedback inhibition
  4. enzyme affinity
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10
Q

competitive inhibition

A

some molecules “compete” for binding sites

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11
Q

non-competitive inhibition

A

molecules can bind to another part of an enzyme resulting in an inhibition at the site for another molecule

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12
Q

feedback inhibition

A

end products of reactions can inhibit or controls the action of the enzyme that helped produce it
- end product formed in reaction actually gets enzymes to slow down or stop making new products altogether

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13
Q

enzyme affinity

A

how likely the enzyme is to catalyze the reaction

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14
Q

kinase

A

transfers phosphate group (phosphorylation)

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15
Q

phosphorylase

A

addition of a Pi molecule

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16
Q

phosphatase

A

remove phosphate group

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17
Q

dehydrigenase

A

remove H+ atoms

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18
Q

oxidase

A

catalyze oxidation-reduction reactions involving O2

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19
Q

catalyze

A

cause or accelerate a reaction

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20
Q

isomerase

A

rearrangement of the stucture of a molecule

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21
Q

main nutrients in exercise metabolism

A

carbohydrates
- glucose
- glycogen
-muscle and liver
lipids
- FAs
- TGs (triglycerides
proteins
- ammino acids

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22
Q

factors affecting energy production

A
  • total energy demand
  • rate of demand
    - coupled glycolysis
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23
Q

glycolysis

A

breakdown of glucose to pyruvate

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23
Q

glycogenolysis

A

breakdown of glycogen to glucose

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24
Q

gluconeogenesis

A

formation of glucose from a non-CHO source
- i.e. protein and fat

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24
Q

two phases of glycoslysis

A
  1. energy investment phase
  2. energy generation phase
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25
Q

NAD

A

nicotinamide adenin dinucleotide

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26
Q

FAD

A

flavin adenine dinucleotide

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27
Q

oxidation reaction

A

loss of electronsres

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28
Q

reduction reaction

A

gain of electrons

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29
Q

glycogen —> glucose 1-phosphate

A

glycogen phosphorylase (GP)

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30
Q

glucose —> glucose 6-phosphate

A

hexokinase (HK)
(- 1 ATP)

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31
Q

fructose 6-phsophate —–> fructose 1,6-biphasphate

A

phosphofructokinase (PFK)
(- 1 ATP)

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32
Q

glyceraldehyde 3-phosphate —> 1,3-biphosphoglycerate

A

glyceraldehyde-3-phosphate dehydrogenase (G3PDH)
(produces NADH)

33
Q

1,3-diphosphoglycerate —-> 3 phosphoglycerate

A

phosphoglycerate kinase (PGK)
(+ 1 ATP )

34
Q

phosphoenolpyruvate (PEP) —> pyruvate

A

pyruvate kinase (PK)
( +1 ATP)

35
Q

sources of CHO during exercise

A
  • muscle glycogen (primary source for higher intensity)
  • blood glucose (primary source during low-intensity)
36
Q

products of krebs cycle

A

3 NADH
1 FADH
1 ATP

37
Q

enzymes involved in forming an NADH + H+

A
  • isocitrate dehydrogenase (IDH)
  • alpha-ketoglutarate dehydrogenase (αKDH)
  • malate dehydrogenase (MDH)
38
Q

enzymes involved in fomring a FADH2

A

succinate dehydrogenase (SDH)

39
Q

enzyme involved in direct ATP production

A

succinyl-CoAsynthetase

40
Q

citrate synthase

A

forms citrate form oxaloacetate and acetyl CoA

41
Q

overall production of ATP using krebs

A

20

42
Q

steriod hormone

A
  • fat derived
    help to solubolize the hormone
43
Q

blood hormone concentration determined by:

A

rate of secretion
rate of metabolism
quantity of transport protein
changes in plasma volume

44
Q

downregulation

A

decrease receptor number in response to high hormone

45
Q

upregulation

A

increase in receptor number in response to low hormone

46
Q

sources of TG

A
  • adipocytes (adipose tissue cells)
  • intramuscular TG
  • blood lipoproteins
47
Q

stages of lipid catablism (fat metabolism)

A
  1. mobilization
  2. transport
  3. uptake
  4. activation
  5. beta-oxidation
  6. mitochondrial oxidation
48
Q

HSL (mobilization)

A

hormone sensitive lipase (adipose, muscle)

49
Q

LPL (mobilization)

A

lipoprotein lipase (vascular wall)

50
Q

EPOC (stands for)

A

excess post-exercise oxygen consumption

51
Q

lipolysis

A

process of breaking down TG into glycerol and 3 FFA using lipase

52
Q

trained vs untrained

A

TR subjects have lower O2 deficit

53
Q

EPOC purpose

A

how much O2 is needed to restore body to resting metabolic state

54
Q

factors effecting EPOC

A

resynthesis of PRc
lactate conversion to glucose
restoration of muscle blood oxygen
elevated temp
increased HR and breathing
increased hormones

55
Q

interval exercise

A

= rapid recovery

56
Q

lactate as a fuel source (2)

A

converts lactate to acetyl CoA for the Krebs cycle
or
converted to glucose in the liver (Cori cycle)

57
Q

cori cycle

A

lactate —> glucose through glyconeogenesis

58
Q

lactate threshold / aerobic threshold

A

point where lactate begins to accumulate

59
Q

OBLA (stands for)

A

onset of blood lactate threshold

60
Q

RER

A

respiratory exchange Ratio

61
Q

what is RER

A

ratio of CO2 produced in comparison with O2 consumed
VCO2/VO2

62
Q

RER assumptions

A

no protein contribution
steady state conditions

63
Q

blood hormone concentration depends on

A
  1. ratee of secretion
  2. rate of metabolism
  3. quantity of transport proteins
  4. change in plasma volume
    • exercise decreases plasma volume and increases hormones
64
Q

magentiude of hormone receptor interation depends on

A

hormone
number of receptors on the cell
affinity if the receptordown

65
Q

regulation

A

decrease recptor number in response to high hormone

66
Q

upregulation

A

increase recptor number in response to low hormone

67
Q

steriod hormone action

A
  • enter cell
  • binds to receptor protein
  • binds to hormone response element on DNA, regulates gene transcription
    -protein synthesis
  • change in protein synthesis is cellular response
67
Q

insulin receptor action

A
  1. binds to alpha-subunit
  2. beta-subunit phosphorylates others, allowsing the unsulin response protien to be activated
  3. phosphorylated insulin repsonse protien activates glycogen synthase
  4. glycogen synthase
  5. converts glucose to glycogen
68
Q

estrogen

A

female sex hormone
- increased reliance on fat as a fuel source

69
Q

progesterone

A

important for reproduction

70
Q

testosterone

A

leads to high muscle -mass to fat-mass ratio
released during exercise, may be involved ni stimulating protien synthetic reposnse with training

71
Q

growth hormones

A

effect all tissues
secretion controlled by hypothalamus

72
Q

leptin

A

controls appetite
- increases insulin senstivity and FA oxidation

73
Q

adiponectin

A

increase insulin sensitivity and FA oxidation

74
Q

increased fat mass

A
  • increased leptin, decrease adeponextin
  • causes inflamation
75
Q

insulin

A

released form beta cells in pancrease
increases nutrient uptake
decreases lipolysis

76
Q

glucagon

A

released from alpha cells in pancrease
opposite effect of insulin:
- increase nutrient release
- increase liver glycogenolysis and FA release

77
Q

epinephrine

A

adrenal medulla
- increases muscle glycogenolysis
- increases lipolysis (muscle adipose)

78
Q

norepinephrine

A

SNS fibres and adrenal medulla
- increase lipolysis
increase cardiorespiratory function

79
Q

roles of cortisol

A

slow acting
decrease low-intensity
increase high intensity
supported by growth hormones

80
Q

epinephrinea nd norepinephrine

A

fast acting
maintians blood glucose
increase during exercise

research methods (13 decks)

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