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Z -KIN 210 Midterm > Aerobic System > Flashcards

Aerobic System Flashcards

1
Q

NADH+H and FADH2

A

enzymes that carry H to the ETC.
- accept 2H and dump e- into ETC

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2
Q

aerobic system

A

biochemical pathways complete breakdown of glucose/glycogen, fats, some AA to make lots of energy.
energy harnessed rephorphorylates ADP to ATP
- O2 used; CO2 and H2O byproducts

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3
Q

components of aerobic pathway

A

aerobic glycolysis
krebs cycle
beta oxidation
ETC

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4
Q

aerobic glycolysis

A

HK turn glucose into G6P / PHOS turn glycogen to G6P
G6P > F6P
F6P > F1,6P via PFK
F1,6P > GA3P > 3PG (make NADH) > pyruvate
pyruvate into membrane (protein carrier) > Acetyl coA via PDH (make NADH)

(See notes for Diagram)

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5
Q

hexokinase (HK)

A

enzyme that turns glucose into G6P during aerobic glycolysis
- uses an ATP

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6
Q

phosphorylase (PHOS)

A

enzyme turn glycogen into G1P during aerobic glycolysis

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7
Q

phosphofructokinase (PFK)

A

enzyme turn F6P into F1,6P during aerobic glycolysis
- rate limiting step of glycolysis
- inhibited by: ATP and citrate
- activated by: ATP

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8
Q

pyruvate dehydrogenase (PDH)

A

enzyme convert pyruvate to Acetyl-coA once inside the mitochondrial membrane

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9
Q

formation of Acetyl-coA

A

pyruvate (CCC) decarboxylated into acetic acid (CC) (+ CO2)
PDH dehydrogenases acetic acid (CC) to make NADH+H, adds coenzyme A to make Acetyl-coA (CC)
- irreversible
- not use O2 directly, must be aerobic

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10
Q

aerobic krebs cycle

A

1: acetyl-coA (2C) + oxaloacetate (4C) = citrate via citrate synthase
2: citrate (6C) > isocitrate (6C) via aconitate
3: isocitrate (6C) > alpha-Ketoglutarate (5C) via IDH (also make CO2, NADH+H)
4: a-Ketoglutarate (5) > succinyl CoA (4C) via a-KDH (make CO2, NADH+H)
5: succinyl Co-A (4C) > succinate (4C) (ADP > ATP)
6: succinate (4C) > Furamarate (4C) (make FADH2)
7: H2O added to Furamarate > Malate (4C)
8: Malate (4C) < oxaloacetate (4C) (make NADH+H)

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11
Q

Summary of out comes of Aerobic Kreb Cycle

A

Not direct use of )2 but must be aerobic
2 ATP
6 NADH+H (3,4,8)
2 FADH2 (6)
4 CO2
Limiting enzyme = IDH

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12
Q

citrate synthase

A

Oxaloacetate + Acetyl CoA –> Citrate
- step 1 of aerobic glycolysis

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13
Q

isocitrate dehydrogenase (IDH)

A

isocitrate -> alpha-ketoglutarate, decarboxylation that generates NADH and CO2
- step 3 of aerobic glycolysis, rate limiting factor
- activated by Ca and ADP

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14
Q

alpha-ketoglutarate dehydrogenase (a-KDH)

A

enzyme that turns alpha-ketoglutarate (5C) to succinyl-CoA (4C)
- makes NADH+H and CO2
- stimulated by ADP and Ca
- step 4 of aerobic glycolysis

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15
Q

The Electron Transport Chain

A

Embedded in the inner membrane of the mitochondria

NADH+H > complex 1 > Q > complex 3 > cytochrome c > complex 4 > O2

FADH2 > Complex 2 > Q > complex 3 > cytochrome c > complex 4 > O2

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16
Q

cytochrome oxidase

A

enzyme at step 4 of ETC that is rate limiting.
- turns 1/2 O2 + 2H = H2O

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17
Q

electron transport chain (ETC) Steps

A

1: NADH+H at comp1 put e- into complex, drop H at mitochondrial matrix
1a: if FADH not NADH, drop into comp2
2a: e- shuttle down cytochromes to alt gain/lose e-
2b: e- also move along inner membrane cause p+ pumps move H from matrix to inner membrane
3: O2 accept e-; add H = H2O
4: H in intermembrane cause gradient, so sneak into matrix via ATP synthase; this energy cause ADP+P=ATP
5: ATP to intermembrane thru ATP-ADP antiporter protein, also bring in ADP
6: ATP out of mitochondria in exchange for inward ADP

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18
Q

ATP-ADP antiporter protein

A

in step 5 of ETC this antiporter protein sends ATP to intermembrane space (later leave mitochondria) and brings ADP from intermembrane to matrix

19
Q

fat metabolism

A
  • can only be metabolized aerobically
  • come from either FFA+albumin or stored triglycerides
  • brain cannot metabolize FA (too long for BBB)
20
Q

lipolysis in adipocytes

A

epinepherine stimulates hormone sensitive lipase to turn triglycerides into glycerol.
Liver then turns glycerol into glucose via gluconeogenesis

21
Q

beta oxidation

A

reaction that converts fatty acids to acetyl CoA to enter the Krebs cycle

22
Q

beta oxidation steps

A

FA enter muscle attached to albumin thru FATP
1: FA + CoA-SH = activated FA via fatty acyl-coA synthase (uses ATP)
2: FAD > FADH, go to ETC to make 1.5 ATP
3: H2O added, NAD > NADH, to to ETC make 2.5ATP
4: activated FA > acetyl coA via 3HAD, go to Krebs
5: activated FA + Coa-SH ; steps 1-4 repeated until last product is acetyl-coA

23
Q

beta oxidation of fatty acids

A

fatty acid tails are continuously broken down by coA-SH until there are none left, which results in acetyl coA itself (2C)

24
Q

3-HAD

A

3-hydroxyacyl-CoA dehydrogenase
- cleaves C off of activated FA to make acetyl-coA, which goes to the Krebs cycle (aerobic)
- rate limiting enzyme in beta oxidation

25
Q

CHO flame

A

we need CHO metabolism in the background for FA metabolism to occur.
- pyruvate (glycolysis) needed to make oxaloacetate
- oxaloacetate + acetyl-coA = Citrate (start Krebs)

26
Q

lipase

A

enzymes that breaks down triglycerides into free fatty acids (FFA)

27
Q

pyruvate carboxylase

A

enzyme that converts pyruvate (3C) to oxaloacetate (4C)

28
Q

ketone bodies

A

oxaloacetate is turned into glucose (GNG) due to low CHO available, meaning it cannot bind w pyruvate to make citrate for Krebs cycle.
Liver turns accumulated acetate fragments (acetyl-coA) into metabolites called ketones/ketone bodies.
- used as fuel for nerves, muscles, brain

29
Q

Ketosis

A

if the ketones made in the liver are not used and accumulate = ketosis
- acidic, cause affect acid-base balance
- inadequate diet (anorexia, diabetes)
- benign (anorexia) or diabetic “keto-acidosis” (toxic)

30
Q

amino acid (AA) functions

A

form body structures and enzymes
fuel source (protein metabolism)
gluconeogenic precursors
- proteins leave body via urea

31
Q

amino acid metabolism

A

amino group (N) must be removed from AA first by:
- transamination: move N to keto group, most common make amino acid “glutamate” (most common method)
- oxidative deamination: remove N entirely, excrete via urea

32
Q

amino acids entering Krebs cycle

A
  • pyruvate: alanine, glycine, cysteine, +3 more
  • acetyl coA: isoleucine
  • acetoacetate: leucine, lysine, +3 more
  • a-Ketoglutarate (via glutamate): histidine, proline +2
  • succinyl coA: isoleucine, valine, +2 more
  • fumarate: tyrosine, phenylaline
  • oxaloacetate: asparagine, aspartate
33
Q

acetyl-coA as the “crossroad”

A

acetyl co-A is the cross road for…
- made from pyruvate (glycolysis)
- made from FA spiral
- makes lipogenesis
-makes ketone bodies
- makes cholesterol, steroids
- makes/made by AA
& kick start krebs!
- excessive Acetyl coA turns into lipogenesis (fat)

34
Q

control of aerobic metabolism

A

substrate location and limitation
effect of exercise intensity
effect of exercise duration
key metabolic regulators of aerobic ATP prod.
rate limiting enzymes

35
Q

substrate location and limitations

A

adipose: triglycerides (50-100k kcal) = FFA
blood plasma: albumin+FFA, glycerol
muscle: triglycerides (2-3k kcal)=FA; glycogen (1-3k kcal)
blood plasma: liver glycogen (200-400kcal) > glucose

36
Q

effect of exercise intensity

A

at rest burn fats, at certain point in exercise change to mostly burn carbs (cross over concept)
- trainable point (more aerobically fit = burn fat longer, burn carbs later)
- still burn same amount FA but as more intense = more carbs burnt

37
Q

effect of exercise duration

A

short duration = mostly CHO
longer duration = more FA
- glycogen depleted, rely on FA

38
Q

key metabolic regulators of aerobic ATP production

A

energy state (more ADP = more respiration, want ATP)
redox state (more NAD = more respiration (want NADH)
intracellular Ca (more Ca = more respiration)

39
Q

rate limiting enzymes

A

glycolysis - phosphofructokinase
krebs cycle = isocitrate dehydrogenase
beta-oxidation = 3HAD
ETC = cytochrome oxidase

40
Q

benefits of aerobic training

A

substrates
mitochondria, oxidative enzymes
glycogen sparing
structural changes

41
Q

substrate changes from aerobic training

A
  • # of GLUT4 increase, yet GLUT4 translocation decreases
  • take up and use less glucose (slower glycogen depletion)
  • increase liver glycogen stores
  • lower RER
  • increase release of FFA from adipose
  • increase plasma FFA in submax exercise
  • increase fat storage near mitochondria
  • increase capacity to use fats
  • increase in ability to use branched AA and to make alanine (makes acetyl-coA)
42
Q

change in mitochondria and oxidative enzymes

A

increase in size and number of mitochondria
- SS adapt better w long duration
- IM adapt best from high intensity intervals
- more contractions = more changes in mitochondria
- larger mitochondria mean more pyruvate moved in
- more key enzymes available and used

43
Q

glycogen sparing from aerobic training

A

more mitochondria = spare glucose and burn more fat
- decrease GLUT4 translocation despite more [GLUT4]
- better at using fat for fuel (metabolic flexibility)

44
Q

structural changes from aerobic training

A

increase capillarization and increase substrate supply and removal of metabolic waste
- shift intermediate fibers > ST fibers
- more GLUT4 = more insulin sensitive

Z -KIN 210 Midterm (8 decks)

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