Lecture exam 2 (Aerobic metabolism) Flashcards
pyruvate enters the mitochondria of the cell for this
aerobic metabolism
aerobic demands are less than
80% max intensity
T/F: body perfers aerobic oxidative metabolism
T
This must be in sufficient concentration to have pyruvate enter the mitochondria
O2
during aerobic metabolism you use this to produce this
O2
CO2
acetic acid is an example of a
2 carbon acid
acetyl-CoA =
acetic acid + coenzyme A
484-884 rule
when we calculate ATP production we assum all pyruvate is coverted to acetyl CoA and none goes to oxaloacetate (directly)
These are the intermediate steps between glycolysis and kerbs cycle
PDH
PC
This always proceeds aerobic metabolism
anaerobic metabolism
T/F: aerobic metabolism occurs inside the sarcoplasm
F, mitochondria
Kreb’s cycle goes from here to here
citrate to citrate
2 other names for kreb’s cycle
citric acid cycle
tricarboxylic acid cycle
aerobic pathways is only used in presence of this
O2
Citrate is formed by the combination of these to intermediates by this enzyme
Acetyl-CoA
Oxaloacetate
Citrate synthase
Citrate has this many carbons
6
After citrate is reacted with aconatase this is prduced
isocitrate
isocitrate is converted to this by this enzyme
alpha-ketogluterate isocitrate dehydrogenase (IDH)
This is the rate limiting enzyme of krebs cycle
isocitrate dehydrogenase (IDH)
AKG has this many carbons
5
What happens during the IDH step other than conversion
NAD is reduced to NADH+H+
CO2 is released
This enzyme has the lowest turnover ratio in krebs cycle
IDH
Alpha-ketogluterate is converted to this by this
succinyl coenzyme A
alpha-ketogluterate dehydrogenase
succinyl coA has this man carbons
4
what happens during the AKGDH step other than coversion
NAD is reduced to NADH+H+
CO2 is released
Succinyl CoA is converted to this by this
succinate
succinyl coenzyme A synthetase
what happens during the succinyl coenzyme A synthetase step other than conversion
1 ATP is produced
Succinate is converted to this by this
fumerate succinate dehydrogenase (SDH)
What is a functional use for SDH concentration
Muscle typing, oxidative muscles have more
what happens during the SDH step other than conversion
FAD is reduced to FADH2
fumerate is converted to this by this
malate unnamed enzyme (don't need to know)
malate is converted to this by this
oxaloacetate malate dehydrogenase (MDH)
what happens durin the MDH step other than conversion
NAD is reduced to NADH+H+
These are all the 4 carbon compounds in krebs
Malate
Fumerate
Succinate
succinyl CoA
From glycolysis to the end of krebs cycle 1 molecule of blood glucose will net
4 ATP
10 NADH+H+
2 FADH2
From pyruvate two end of krebs cycle will net
1 ATP
4 NADH+H+
1 FADH2
From acetyl-CoA to end of krebs cycle will net
1 ATP
3 NADH+H+
1 FADH2
T/F: electron transport system is anaerobic
F, aerobic
the ETS is this type of phosporylation
oxidative
This is another way to describe the electron transport chain
hydrogen transport system
The passage of electrons/hydrogen are all examples of this type of reaction
oxidation reduction
ETS: First electron acceptor
flavoprotein
flavoprotein is made by this substance
Vit. B2 or riboflavin
NADH+H+ enters the ETS at this stage
flavoprotein
Flavoprotein reduces
Coenzyme Q
FADH2 enters the ETS at this stage
Coenzyme Q
Coenzyme Q is a derivative of
Vit E
Coenzyme Q reduces
cytochrome b
cytochrome b reduces
cytochrome C
Cytochrome C reduces
cytochrome a
cytochrome a reduces
cytochrome asub3
1/2 O2 is reduced to H2O at the end of this step
cytochrome a to cytocrome asub3
ATP is produced at these steps of the ETS
flavoprotein to coenzyme Q
cytochrome b to cytochrome c
cytochrome a to cytochrome asub3
Theoretical yield model of the ETS is
3 ATP from the whole system
Oxidation of NADH+H+ in the ETS generates this much ATP
3
Oxidation of FADH2 in the ETS generates this much ATP
2
These are iron containing molecules similar to hemo/myo-globin
cytochromes
Oxygen is called this
the final election acceptor
the more oxygen consumed increases this
ATP production over time
Each molecule of blood glucose converted to CO2 and H2O produces a net of this much ATP
38 ATP
4 feedback systems associated with carb metabolism
pasteur effect
high concentrations of ATP inhibit citrate synthase
end of exercise high concentrations of ATP inhibits G3PDH
LDH, PK, PFK are inhibitied by increase in ATP concentraion
kreb’s cycle processes are inhibited by a lack of oxidated NAD, that causes the cellular concentrations of ATP to go down with a concomitant increase in cellular concentration of ADP. And ADP stimulates PFK
Pasteur effect
This is a stop gap procedure
pasteur effect
define stop gap procedure
doesn’t cure, but help us get through (delay) effects of a problem
Pasteur effect is initiated when this occurs
ETS is backing up not allowing NADH+H+ to be oxidized
As a result of the pasteur effect this increases, and causes this
anaerobic ATP production
fatigue through accumulation of lactate
% intensity that can be ran at without fatiguing due to accumulation of lactate, or without running out of oxygen to use as final electron acceptor (approx 80% max)
anaerobic threshold
What do we need to do at the end of exercise
store intermediates as carbs so they can be used in the future
When high concentrations of ATP that inhibit citrate synthase occur our bodies do this
store acetic acid as fat
When citrate synthase is inhibited due to high concentrations of ATP we start to back up at this step, resulting in this
PDH
acetic acid builds up in the mitochondrea
1 cycle of the krebs cycle produces this much ATP
12
Acetic acid being stored as fats explain this
how carbohydrates that we eat are stored as fat (one mechanism)
At the end of exercise high concentrations of ATP inhibit G3PDH resulting in this
G3P and DHAP build up in the cell and are eventually stored as fats
LDH, PK, PFK are inhibited by increased ATP concentrations which then favors the production of this
glycogen from glucose
Fatty-acits are utilized through this type of metabolism
aerobic
aerobic metabolism of fatty acids is know as
beta oxidation of fatty acids
This provides very little ATP per unit time
Beta oxidation of fatty acids
One benefit of beta-oxidation of fatty acids
inexhaustable storage capacity of fat
R-value associated with beta-oxidation of fatty acids
0.7
FA are stored in this form
triglycerides
triglyceride =
glycerol backbone = 3 FA
This breaks down triglycerides to its constituents
lipase
fatty acids are
long carbon (mostly even #) chains
N =
of carbons in a fatty acid chain
energy cost to prepare one FA for Beta-oxidation
1 ATP to AMP +P2
First reduction agent formed from BO
1 FADH2
Second reduction agent formed from BO
1 NADH+H+
Final substance fromed from BO
1 acetyl-CoA
ATP does not get used here in BO of FA
to add CoA to the carbon chain in the cycle
Each cycle cleaves this many carbons form the fatty acid
2
When determining the amount of ATP produced from burning a FA know these 2 things
# of cycles # of acetyl-CoA produced
of cycles of BO of FA =
(N/2)-1
Each cycle of BO of FA produces this much ATP from production of reduction agents
5 ATP
of acetyl-CoA produced in BO of FA =
(N/2)
Each acetyl-CoA produced during BO of FA produces this much ATP when burned to CO2 and H2O
12
Enter net and gross equations into calculator for BO of FA
okay
