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Exercise Physiology > Aerobic/Oxidative system > Flashcards

Aerobic/Oxidative system Flashcards

1
Q

aerobic/oxidative system

A

biochemical pathway that regenerates ATP through complete oxidation of macronutrients

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2
Q

diff between anaerobic and aerobic system

A

anerobic stops at glycolysis

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3
Q

how does fat enter glycolysis

A

beta oxidation first

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4
Q

aerobic system exercise description

A

low power and high capacity
power - 3-5min
capacity - hours

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5
Q

2 steady rate limiting factors

A

fluid loss and electrolyte depleting

maintaining adequate reserves of both liver glycogen for CNS and muscle glycogen to power exercise

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6
Q

what does your brain use if you dont have enough glycogen?

A

keto acids

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7
Q

why can we run for a long time with the all the increase in heat

A

because we can get rid of it

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8
Q

what do we use for aerobic processes

A

mitochondria

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9
Q

what kind of sports are fueled by aerobic energy?

A

marathons or race across america

intense exercise beyond several minutes

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10
Q

4 divisions of aerobic metabolism

A

slow glycolysis
krebs citric acid cycle
beta oxidation
electron transport chain

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11
Q

what kind of phosphorylation is ATP generated through in aerobic metabolism?

A

oxidative

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12
Q

why is it called the oxidative phosphorylation?

A

because oxygen is the ultimate acceptor of electrons

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13
Q

two locations for mitochondria within a muscle fibre

A

interfibrillar - energy for contraction

sarcolemmal - energy for transport

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14
Q

fast twitch fibre and mitochondria

A

doesn’t have much because it needs ATP a lot faster

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15
Q

slow twitch fibres and ATP rate

A

slower because we dont need it for a while

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16
Q

substrates for aerobic

A

carbs, fat, sometimes proteins

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17
Q

Carb storage

A

glycogen

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18
Q

where do you find glucose

A

around the blood stream

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19
Q

why dont we use protein for substrates for aerobic?

A

because it functions as other things

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20
Q

mitochondria DNA is only from

A

mother

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21
Q

folds of the mitochondria is for

A

more ball and stalk complexes for ETC

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22
Q

cristae

A

space between inter and outer membrane of mitochondria

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23
Q

what is formed in aerobic glycolysis and where does it go?

A

pyruvate - shuttled into mitochondrial intermembrane space via a monocarbocylate transporter (MCT)

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24
Q

Pyruvate converted into

A

acetyl - CoA by pyruvate dehydrogenase complex (three enzyme complex in the inner membrane) then released into mitochondrial matrix
produces a CO2 and NADHH
Pyruvate + NAD+CoA = acetyl CoA + Co2 + NADHH

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25
Q

does the formation of acetyl CoA utilize O2?

A

no but must be aerobic

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26
Q

where does formation of acetyl coA occur

A

mitochondrial matrix

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27
Q

products from the 2 formation of acetyl coA

A

2 NADHH
2 CO2
2 acetyl CoA

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28
Q

path of NADHH from glycolysis

A

enters the mitochondria via MALATE ASPARTATE shuttle or the GLYCEROL PHOSPHATE shuttle

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29
Q

NADHH in your heart

A

malate aspartate shuttle - hydrogens from NADHH passed to malate then passed to NAD

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30
Q

NADHH in your muscles

A

glycerol phosphate shuttle - hydrogens from NADHH passed to glycerol phosphate then passed to FAD

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31
Q

What can the accumulated lactate from anaerobic glycolysis do?

A

converted back to pyruvate via LDH h and enter mitochondrial matrix via pyruvate dehydrogenase complex (converted into acetyl coa)

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32
Q

where does NADH go?

A

ETC

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33
Q

where does the krebs cycle happen?

A

take place in the mitochondrial matrix

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34
Q

why is the krebs cycle called a cycle

A

oxaloacetate is combined with acetyl coA to form citrate is regenerated after the oxidation of acetyl coA

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35
Q

Products of the krebs sycle

A

NADH2 and FADH2

ATP/guanosine triphosphate - substrate level phosphorylation

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36
Q

rate limiting enzyme of the krebs cyle
activation?
neg fdbk?

A

isocitrate dehydrogenase
ADP, Pi, Ca
ATP

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37
Q

does the krebs cycle use O2

A

not directly but must be aerobic

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38
Q

where does the krebs cycle occur?

A

mitochondrial matrix

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39
Q

products of mitochondiial matrix (#s)

A

2 ATP
6NADH2
2 FADH2
4 CO2

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40
Q

ETC

A

electron transport chain

final metabolic pathway in aerobic metabolism

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41
Q

ETC location and structure

A

ball and stalk complex along the inner mitochondrial membrane
series of electron carriers and proton pumps (complex 1-4)

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42
Q

ETC utilizes

A

NADH2 and FADH produced in glycolysis and krebs cycle

electrons from H are used to drive the movement of H into intermembrane space

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43
Q

FADH2 vs NADH2

A

FADH 2 enters ETC at complex 2 so produced less ATP relative to NADH2

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44
Q

why do you want to pump H outside?

A

to make an electrochemical gradient to drive ATP synthesis through ATP synthase (ADP+Pi = ATP)

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45
Q

final electron acceptor of ETC

A

oxygen + 2e = oxygen + 2H = H2O

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46
Q

rate limiting enzyme of ETC

activation and negative fdbk

A

cytochrome oxidace (complex 4) catalyzes the final transfer of electron to oxygen

ADP
ATP

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47
Q

ETC and O2

A

directly utilize O2 as final electron acceptor

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48
Q

location of ETC

A

inner mitochondrial membrane

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49
Q

how many steps does NADHH goes through vs FADH2

A

3 and 2

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50
Q

what kind of athletes has more mitochondria?

A

mitochondrial miogenesis in aerobic athletes

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51
Q

theoretical ATP yield for NADH2 and actual yield

A

3 and 2.5

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52
Q

theoretical ATP yield for FADH2 and actual yield

A

2 and 1.5

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53
Q

why does the heart muscle produce more total ATP than skeletal muscle/glucose

A

heart uses malate aspartase which you get two of in glycolysis

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54
Q

muscle glucose ATP calculation

A 
glycolysis - 2ATP 
2FADH*1.5 =3 ATP 
pyruvate to acetyl coA = 2 NADH *1.5 = 5 ATP 
krebs cycle = 2ATP 
6 NADH *2.5 = 15 ATP 
2 FADH2 (1.5) = 3 ATP 
total of 30
55
Q

can fat be metabolized with out oxygen

A

no, it must go through aerobic metabolism

56
Q

fat can be obtained from 3 sources

A

intramuscular triaculglycerols (glycerol and 3 FA)
circulating triaculglycerols
mobilized from circulating free FAs (attached to albumin) mobilized from triaculglycerols in adipose tissue

57
Q

why is more oxygen required for fat oxidization?

A

fat has a higher ratio of carbon to oxygen

- more work to break down fat

58
Q

aerobic athletes and fat

A

a lot of fat in their muscles

59
Q

triaculglycerols - triglycerides

A

chains of carbons

60
Q

function of hormone sensitive lipase

A

breakdown of triacylglycerols

61
Q

function of lipoprotein lipase

A

on cell membranes - take an FA from circulating and use it

62
Q

FA in the sarcoplasm are activated using

A

activated using coenzyme A and ATP

which degrades into AMP so 2 ATP is invested to activate FA

63
Q

What happens after fat is activated

A

fatty acetyl coA shuttled into mitochondria via carnitine shuttle (intermembrane then matrix of mitochondria) to go into beta oxidation

64
Q

beta oxidation

A

cyclic series of steps that breaks off successive pair of carbon atoms from FFA, then used to make acetyl coA

65
Q

cycles of beta oxidation depends on and produces?

A

number of carbons present in FA, each produces 1FADH2 and 1 NADH
n/2-1 cycles

66
Q

16 carbon fat how many cycles?

A

7

67
Q

what does fat do after beta oxidation?

A

into the krebs cycle as acetyl coA, 1FADH, 3NADH2 and 1 ATP

68
Q

does beta oxidation need o2?

A

no but must be aerobic

69
Q

where does beta oxidation happen?

A

mitochondrial matrix

70
Q

what recycles in beta oxidation

A

acetyl coa, FADH2 and NADH

71
Q

How many ATP do we need to invest for beta oxidation and where?

A

2 in the cytoplasm

72
Q

location of carnitine

A

skeletal muscle - 95%, 20g

73
Q

carnitine function 2

A

transport of long chain FF from cytoplasm to mitochondria

helps to buffer increases in exercise induced acetyl coA

74
Q

purported benefit of carnitine supplementation

A

increased FA transport into mitochondria leading to increased FA oxidation and reduced demand on carb stores

75
Q

effectiveness of carnitine (3)

A

plasma concentration increases by 30-70%
2wks to 3m has not been demoed to increase muscle concentration - probably lost in urine
no clear evidence that supplementation enhances fat oxidation, reduces carb oxidation, glycogen breakdown or lactate accumulation , enhance performanc of increase VO2 max

76
Q

How does fat burn in the flame of carbs?

A

oxaloacetate in the kreb’s cycle is produced from pyruvate and it needs to be present for acetyl coA to enter the krebs cycle

77
Q

in the absence of carbs, energy production

A

slows - bonking/hitting the wall

78
Q

why arent proteins a significant source of energy during exercise

A

importatn structural and functional role

79
Q

How do AAs get turned into pyruvate, acetyl coA and krebs cycle intermediates

A

deamination (removal of NH2) and transamination (transfer of NH2 to another substrate)

80
Q

How many AAs are there and what numbers enter the cycle as what?

A 
6 entered at pyruvic acid 
8 at acetyl coa 
4 at alpha ketoglutarate 
4 at succinate 
2 at oxaloacetate
81
Q

gluconeogenesis (3)

A

ensures that the brain, nerves, and kidney and muslces have a source of carb to draw from
creation of glucose in the liver from non carb sources
glycerol (glycerol glucose cycle)
lactate/pyruvate (cori cycle)
alanine (felig cycle)

82
Q

ketones

A 
in the absense of glycogen, metabolism switches to the prodcution of ketone bodies 
liver converts acetyl coA into 
-acetoacetic acid 
-beta hydroxybutyric acid
-acetone
83
Q

why are ketones produced

A

sparse glucose for the brain and NS

84
Q

side effect of ketones

A

strong acids - contribute to ketoacidosis if high enough

85
Q

utilization of ketones as a fuel source

A

atheletes/ trained atheletes

86
Q

why is cars the preferred substrate for aerobic system

A

uses the least amt of o2

87
Q

glycogen vs glucose ATP

A

glycogen uses one more ATP

88
Q

aerobic system energy supply ranked in amount

A

triglycerides
muslce glycogen
liver glycogen
circulating glucose

89
Q

least fat percentage to survive

A

3.5

90
Q

why do we consume energy before and during a marathon

A

glycogen stores but we dont sore enough so we use fat, but to use fat we need carbs

91
Q

What controls the SNS

A

hypothalamas

92
Q

What SNS controls blood glucose (2)

A

insulin and glucagon through SNS, adrenal medulla then E and NE for pancreas for insulin and glucagon.

93
Q

glucagon effect on metabolism during exercise (6)

A 
decrease glucose uptake and utilization 
increase glycogen breakdown 
decrease glycogen formation 
increase gluconeogensis
decrease FFA storage and increase FFA mobilization
94
Q

E and NE effect of metabolism during exercise (4)

A

increase glycogen breakdown
decrease glycogen formation
increase gluconeogensis
FFA mobilization

95
Q

growth hormone and cortisol effect of metabolism during exercise

A 
decreased glucose uptake and utilization 
increase glycogen breakdown 
increase glycogen formation 
increased gluconeogenesis 
decreased FFAstorage 
Increased FFA mobilization 
increased AA transport and uptake 
increased protein breakdown for only cortisol
96
Q

why do growth hormone and cortisol increase glycogen formation

A

long term hormones that think that we need to be prepared for the next time this happens

97
Q

4 hormones that limit glucose uptake by things other than muscles

A

E/NE, Glucagon, cortisol, growth hormone

98
Q

sex differences in fuel utilization

A

males use more carbs than females because we use more glucose because of our different hormone profiles lets us oxidize diff substrates

99
Q

VO2 max

A

maximal oxygen consumption - highest amt of oxygen an ind can take in, transport, and utilize to produce ATP aerobically while breathing air during heavy exercise

100
Q

when does VO2max occue?

A

when oxygen uptake plateaus/increase only slightly with additional increases in exercise intensity

101
Q

what does VO2max require

A

integrated and high level responses of 5 diverse physiological support systems

102
Q

VO2max provides a _______ measure of?

A

quantitative measure of a person’s capacity for sustained aerobic ATP resynthesis
- ability to maintain intense exercise for longer than 4/5 mins

103
Q

high VO2 max decreases the risk of

A

CV disease

104
Q

Genetics and sex difference of VO2 max

A

50-80% genetically determined

males are higher

105
Q

will a high VO2 win everything?

A

not if he doesnt train properly

106
Q

two physiological things needed for high VO2

A

high cardiaxc output and good peripheral bloodflow and some to constrict

107
Q

as you age what happens to your VO2max?

A

drops

108
Q

VO2 max related to 2

A

heart size and hemoglobin concentration

109
Q

VO2max on mount everest

A

25%

110
Q

direct tests for anaerobic power/VO2max

A

incremental exercise through metabolic cart
- lab systems
- protable systems
douglas bags

111
Q

indirect submaximal tests for Aerobic power/VO2max (3)

A

YMCA cycle ergometer test
ebbeling single stage treadmill walking test
modified canadian aerobic fitness test

112
Q

indirect maximal test for VO2 max (anaerobic power)

A

bruce treadmill test - increments of intensity and see how long you go for
leger 20m shuttle test (incremental)
cooper 12 minute test (cooper)

113
Q

what do indirect VO2 tests usually look at

A

HR, age, formula

114
Q

anaerobic threshold/aerobic capacity

A

VO2 at which energy production supplements the aerobic capacity - % of VO2 max/absolute workload

115
Q

measuring aerobic capacity and its two thresholds

A

incremental test to volitional max
lactate threshold 1 (LT1) between 40-60% 2mM
lactate
lactate threshold 2 (LT2)/lactate turnpoint is above 80% threshold and possibly up to 95 4mM

116
Q

LT2 (3)

A

onset of blood lactate accumulation
good approximation of maximal lactate steady rate
above MLSS exercise will terminate

117
Q

maximum lactate steady rate (2)

A

highest workload that can be maintained overtime without a continual rise in blood lactate (lactate production=lactate clearance)
endurance exercise cannot be completed above the MLSS, but portions of the exercise can take place above this level

118
Q

criteria of MLSS

A

in a 30 min test blood lactate cannot change more than 1mM over the last 20 min of the test

119
Q

order of zone of occurance on a chart of lactate vs power

A 
100 watt 
steady over course of exercise 
250 watts 
exceed MLSS 
failure zone 
375
120
Q

4 reasons why does anaerobic system start supplementing aerobic metabolism when oxygen intake is not at VO2 max

A
  • increased recruitment of fast twitch motor units which have a greater reliance of glycolysis
  • increased SNS tone - stimulate glycogenolysis
  • blood stunt mechanism - vaso constriction to less tissue, resulting in enhanced accumulation of lactate and reduced clearance
  • hypoxia? not likely because operating at 70% VO2max
121
Q

increased intensity means

A

increased o2 consumption

122
Q

oxygen uptake during exercise

A

initailly rises exponentially before it plateaus, then remains a steady rate for the duration of the effoert

123
Q

oxygen deficit

A

difference between the o2 required during exercise and O2 supplied and utilized, occurs at onset of all activity

124
Q

The energy that cannot be supplied through aerobic metabolism at the initiation of submaximal exercise is supplied by?

A

ATPPC and anaerobic glycolytic energy systems, eventually if the intensity is submaximal the oxygen deficit is nullified once steady state VO2 is achieved

125
Q

Causes of oxygen deficit

A

central factors - O2 delivery to muscle - inability to circulatory and respiratory systems to deliver enough oxygen to meet energy demands
peripheral factors : O2 utilization by muscles - slow intracellular metabolic activation - metabolic inertia
* limited cellular utilization of O2 as a result of adjustments in both anerobic and aerobic systems, the metabolic systems simply respond at diff speeds - ca released activates the systems then ATPPC, ADP and inorganic phosphate triggers anaerbic glycolysis to work faster

126
Q

why is it beneficial to get to steady state asap?

A

so that metabolic products dont accumulate

127
Q

oxygen deficit is reduced through

A

aerobic
adequate warm up
- elevate muscle temp which increases the rate at which the metabolic processes in the cells can proceed

128
Q

what can decrease oxygen deficit

A

training

129
Q

10 metabolic adaptations to aerobic training

A

increased glycogen storage (muscle and liver)
increased mobilization and transportation of fats, which spares muslce glycogen
increased myoglobin to increase amt of o2 in muslce
increased capillarization to increase influx of substrates and removal of metabolic waste
increased size and number of mitochondria (mitochondrial biogenesis) and associate enzymes
increased beta oxidation at the same absolute and relative submaximal workload
decreased lactate accumulation at the same absolute and relative submax workload
increased MCT1 lactate transporters
increased LDHh activity
increased max oxygen consumption

130
Q

alactic power, capacity, intensity for power and intensity for capacity

A

0.1-3 (5)
8-12 (15)
explosive
all out

131
Q

lactic, capacity, intensity for power and intensity for capacity

A

15-30
45-120
all out
all out

132
Q

aerobic power, capacity, intensity for power and intensity for capacity

A

3-5min
hours
near max to max at end
submax

133
Q

energy activation for exercise

A

smooth blending with considerable overlap of one mode to another

134
Q

accepted explanation of O2 deficit

A

byproducts of additional energy use ADPP and NADHH to stimulate both aerobic and anaerobic metabolism (order of operations)

Exercise Physiology (17 decks)

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