Aerobic System Flashcards
NADH+H and FADH2
enzymes that carry H to the ETC.
- accept 2H and dump e- into ETC
aerobic system
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
components of aerobic pathway
aerobic glycolysis
krebs cycle
beta oxidation
ETC
aerobic glycolysis
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)
hexokinase (HK)
enzyme that turns glucose into G6P during aerobic glycolysis
- uses an ATP
phosphorylase (PHOS)
enzyme turn glycogen into G1P during aerobic glycolysis
phosphofructokinase (PFK)
enzyme turn F6P into F1,6P during aerobic glycolysis
- rate limiting step of glycolysis
- inhibited by: ATP and citrate
- activated by: ATP
pyruvate dehydrogenase (PDH)
enzyme convert pyruvate to Acetyl-coA once inside the mitochondrial membrane
formation of Acetyl-coA
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
aerobic krebs cycle
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)
Summary of out comes of Aerobic Kreb Cycle
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
citrate synthase
Oxaloacetate + Acetyl CoA –> Citrate
- step 1 of aerobic glycolysis
isocitrate dehydrogenase (IDH)
isocitrate -> alpha-ketoglutarate, decarboxylation that generates NADH and CO2
- step 3 of aerobic glycolysis, rate limiting factor
- activated by Ca and ADP
alpha-ketoglutarate dehydrogenase (a-KDH)
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
The Electron Transport Chain
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
cytochrome oxidase
enzyme at step 4 of ETC that is rate limiting.
- turns 1/2 O2 + 2H = H2O
electron transport chain (ETC) Steps
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
ATP-ADP antiporter protein
in step 5 of ETC this antiporter protein sends ATP to intermembrane space (later leave mitochondria) and brings ADP from intermembrane to matrix
fat metabolism
- can only be metabolized aerobically
- come from either FFA+albumin or stored triglycerides
- brain cannot metabolize FA (too long for BBB)
lipolysis in adipocytes
epinepherine stimulates hormone sensitive lipase to turn triglycerides into glycerol.
Liver then turns glycerol into glucose via gluconeogenesis
beta oxidation
reaction that converts fatty acids to acetyl CoA to enter the Krebs cycle
beta oxidation steps
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
beta oxidation of fatty acids
fatty acid tails are continuously broken down by coA-SH until there are none left, which results in acetyl coA itself (2C)
3-HAD
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
CHO flame
we need CHO metabolism in the background for FA metabolism to occur.
- pyruvate (glycolysis) needed to make oxaloacetate
- oxaloacetate + acetyl-coA = Citrate (start Krebs)
lipase
enzymes that breaks down triglycerides into free fatty acids (FFA)
pyruvate carboxylase
enzyme that converts pyruvate (3C) to oxaloacetate (4C)
ketone bodies
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
Ketosis
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)
amino acid (AA) functions
form body structures and enzymes
fuel source (protein metabolism)
gluconeogenic precursors
- proteins leave body via urea
amino acid metabolism
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
amino acids entering Krebs cycle
- 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
acetyl-coA as the “crossroad”
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)
control of aerobic metabolism
substrate location and limitation
effect of exercise intensity
effect of exercise duration
key metabolic regulators of aerobic ATP prod.
rate limiting enzymes
substrate location and limitations
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
effect of exercise intensity
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
effect of exercise duration
short duration = mostly CHO
longer duration = more FA
- glycogen depleted, rely on FA
key metabolic regulators of aerobic ATP production
energy state (more ADP = more respiration, want ATP)
redox state (more NAD = more respiration (want NADH)
intracellular Ca (more Ca = more respiration)
rate limiting enzymes
glycolysis - phosphofructokinase
krebs cycle = isocitrate dehydrogenase
beta-oxidation = 3HAD
ETC = cytochrome oxidase
benefits of aerobic training
substrates
mitochondria, oxidative enzymes
glycogen sparing
structural changes
substrate changes from aerobic training
- # 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)
change in mitochondria and oxidative enzymes
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
glycogen sparing from aerobic training
more mitochondria = spare glucose and burn more fat
- decrease GLUT4 translocation despite more [GLUT4]
- better at using fat for fuel (metabolic flexibility)
structural changes from aerobic training
increase capillarization and increase substrate supply and removal of metabolic waste
- shift intermediate fibers > ST fibers
- more GLUT4 = more insulin sensitive
