Aerobic/Oxidative system Flashcards
aerobic/oxidative system
biochemical pathway that regenerates ATP through complete oxidation of macronutrients
diff between anaerobic and aerobic system
anerobic stops at glycolysis
how does fat enter glycolysis
beta oxidation first
aerobic system exercise description
low power and high capacity
power - 3-5min
capacity - hours
2 steady rate limiting factors
fluid loss and electrolyte depleting
maintaining adequate reserves of both liver glycogen for CNS and muscle glycogen to power exercise
what does your brain use if you dont have enough glycogen?
keto acids
why can we run for a long time with the all the increase in heat
because we can get rid of it
what do we use for aerobic processes
mitochondria
what kind of sports are fueled by aerobic energy?
marathons or race across america
intense exercise beyond several minutes
4 divisions of aerobic metabolism
slow glycolysis
krebs citric acid cycle
beta oxidation
electron transport chain
what kind of phosphorylation is ATP generated through in aerobic metabolism?
oxidative
why is it called the oxidative phosphorylation?
because oxygen is the ultimate acceptor of electrons
two locations for mitochondria within a muscle fibre
interfibrillar - energy for contraction
sarcolemmal - energy for transport
fast twitch fibre and mitochondria
doesn’t have much because it needs ATP a lot faster
slow twitch fibres and ATP rate
slower because we dont need it for a while
substrates for aerobic
carbs, fat, sometimes proteins
Carb storage
glycogen
where do you find glucose
around the blood stream
why dont we use protein for substrates for aerobic?
because it functions as other things
mitochondria DNA is only from
mother
folds of the mitochondria is for
more ball and stalk complexes for ETC
cristae
space between inter and outer membrane of mitochondria
what is formed in aerobic glycolysis and where does it go?
pyruvate - shuttled into mitochondrial intermembrane space via a monocarbocylate transporter (MCT)
Pyruvate converted into
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
does the formation of acetyl CoA utilize O2?
no but must be aerobic
where does formation of acetyl coA occur
mitochondrial matrix
products from the 2 formation of acetyl coA
2 NADHH
2 CO2
2 acetyl CoA
path of NADHH from glycolysis
enters the mitochondria via MALATE ASPARTATE shuttle or the GLYCEROL PHOSPHATE shuttle
NADHH in your heart
malate aspartate shuttle - hydrogens from NADHH passed to malate then passed to NAD
NADHH in your muscles
glycerol phosphate shuttle - hydrogens from NADHH passed to glycerol phosphate then passed to FAD
What can the accumulated lactate from anaerobic glycolysis do?
converted back to pyruvate via LDH h and enter mitochondrial matrix via pyruvate dehydrogenase complex (converted into acetyl coa)
where does NADH go?
ETC
where does the krebs cycle happen?
take place in the mitochondrial matrix
why is the krebs cycle called a cycle
oxaloacetate is combined with acetyl coA to form citrate is regenerated after the oxidation of acetyl coA
Products of the krebs sycle
NADH2 and FADH2
ATP/guanosine triphosphate - substrate level phosphorylation
rate limiting enzyme of the krebs cyle
activation?
neg fdbk?
isocitrate dehydrogenase
ADP, Pi, Ca
ATP
does the krebs cycle use O2
not directly but must be aerobic
where does the krebs cycle occur?
mitochondrial matrix
products of mitochondiial matrix (#s)
2 ATP
6NADH2
2 FADH2
4 CO2
ETC
electron transport chain
final metabolic pathway in aerobic metabolism
ETC location and structure
ball and stalk complex along the inner mitochondrial membrane
series of electron carriers and proton pumps (complex 1-4)
ETC utilizes
NADH2 and FADH produced in glycolysis and krebs cycle
electrons from H are used to drive the movement of H into intermembrane space
FADH2 vs NADH2
FADH 2 enters ETC at complex 2 so produced less ATP relative to NADH2
why do you want to pump H outside?
to make an electrochemical gradient to drive ATP synthesis through ATP synthase (ADP+Pi = ATP)
final electron acceptor of ETC
oxygen + 2e = oxygen + 2H = H2O
rate limiting enzyme of ETC
activation and negative fdbk
cytochrome oxidace (complex 4) catalyzes the final transfer of electron to oxygen
ADP
ATP
ETC and O2
directly utilize O2 as final electron acceptor
location of ETC
inner mitochondrial membrane
how many steps does NADHH goes through vs FADH2
3 and 2
what kind of athletes has more mitochondria?
mitochondrial miogenesis in aerobic athletes
theoretical ATP yield for NADH2 and actual yield
3 and 2.5
theoretical ATP yield for FADH2 and actual yield
2 and 1.5
why does the heart muscle produce more total ATP than skeletal muscle/glucose
heart uses malate aspartase which you get two of in glycolysis
muscle glucose ATP calculation
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
can fat be metabolized with out oxygen
no, it must go through aerobic metabolism
fat can be obtained from 3 sources
intramuscular triaculglycerols (glycerol and 3 FA)
circulating triaculglycerols
mobilized from circulating free FAs (attached to albumin) mobilized from triaculglycerols in adipose tissue
why is more oxygen required for fat oxidization?
fat has a higher ratio of carbon to oxygen
- more work to break down fat
aerobic athletes and fat
a lot of fat in their muscles
triaculglycerols - triglycerides
chains of carbons
function of hormone sensitive lipase
breakdown of triacylglycerols
function of lipoprotein lipase
on cell membranes - take an FA from circulating and use it
FA in the sarcoplasm are activated using
activated using coenzyme A and ATP
which degrades into AMP so 2 ATP is invested to activate FA
What happens after fat is activated
fatty acetyl coA shuttled into mitochondria via carnitine shuttle (intermembrane then matrix of mitochondria) to go into beta oxidation
beta oxidation
cyclic series of steps that breaks off successive pair of carbon atoms from FFA, then used to make acetyl coA
cycles of beta oxidation depends on and produces?
number of carbons present in FA, each produces 1FADH2 and 1 NADH
n/2-1 cycles
16 carbon fat how many cycles?
7
what does fat do after beta oxidation?
into the krebs cycle as acetyl coA, 1FADH, 3NADH2 and 1 ATP
does beta oxidation need o2?
no but must be aerobic
where does beta oxidation happen?
mitochondrial matrix
what recycles in beta oxidation
acetyl coa, FADH2 and NADH
How many ATP do we need to invest for beta oxidation and where?
2 in the cytoplasm
location of carnitine
skeletal muscle - 95%, 20g
carnitine function 2
transport of long chain FF from cytoplasm to mitochondria
helps to buffer increases in exercise induced acetyl coA
purported benefit of carnitine supplementation
increased FA transport into mitochondria leading to increased FA oxidation and reduced demand on carb stores
effectiveness of carnitine (3)
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
How does fat burn in the flame of carbs?
oxaloacetate in the kreb’s cycle is produced from pyruvate and it needs to be present for acetyl coA to enter the krebs cycle
in the absence of carbs, energy production
slows - bonking/hitting the wall
why arent proteins a significant source of energy during exercise
importatn structural and functional role
How do AAs get turned into pyruvate, acetyl coA and krebs cycle intermediates
deamination (removal of NH2) and transamination (transfer of NH2 to another substrate)
How many AAs are there and what numbers enter the cycle as what?
6 entered at pyruvic acid 8 at acetyl coa 4 at alpha ketoglutarate 4 at succinate 2 at oxaloacetate
gluconeogenesis (3)
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)
ketones
in the absense of glycogen, metabolism switches to the prodcution of ketone bodies liver converts acetyl coA into -acetoacetic acid -beta hydroxybutyric acid -acetone
why are ketones produced
sparse glucose for the brain and NS
side effect of ketones
strong acids - contribute to ketoacidosis if high enough
utilization of ketones as a fuel source
atheletes/ trained atheletes
why is cars the preferred substrate for aerobic system
uses the least amt of o2
glycogen vs glucose ATP
glycogen uses one more ATP
aerobic system energy supply ranked in amount
triglycerides
muslce glycogen
liver glycogen
circulating glucose
least fat percentage to survive
3.5
why do we consume energy before and during a marathon
glycogen stores but we dont sore enough so we use fat, but to use fat we need carbs
What controls the SNS
hypothalamas
What SNS controls blood glucose (2)
insulin and glucagon through SNS, adrenal medulla then E and NE for pancreas for insulin and glucagon.
glucagon effect on metabolism during exercise (6)
decrease glucose uptake and utilization increase glycogen breakdown decrease glycogen formation increase gluconeogensis decrease FFA storage and increase FFA mobilization
E and NE effect of metabolism during exercise (4)
increase glycogen breakdown
decrease glycogen formation
increase gluconeogensis
FFA mobilization
growth hormone and cortisol effect of metabolism during exercise
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
why do growth hormone and cortisol increase glycogen formation
long term hormones that think that we need to be prepared for the next time this happens
4 hormones that limit glucose uptake by things other than muscles
E/NE, Glucagon, cortisol, growth hormone
sex differences in fuel utilization
males use more carbs than females because we use more glucose because of our different hormone profiles lets us oxidize diff substrates
VO2 max
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
when does VO2max occue?
when oxygen uptake plateaus/increase only slightly with additional increases in exercise intensity
what does VO2max require
integrated and high level responses of 5 diverse physiological support systems
VO2max provides a _______ measure of?
quantitative measure of a person’s capacity for sustained aerobic ATP resynthesis
- ability to maintain intense exercise for longer than 4/5 mins
high VO2 max decreases the risk of
CV disease
Genetics and sex difference of VO2 max
50-80% genetically determined
males are higher
will a high VO2 win everything?
not if he doesnt train properly
two physiological things needed for high VO2
high cardiaxc output and good peripheral bloodflow and some to constrict
as you age what happens to your VO2max?
drops
VO2 max related to 2
heart size and hemoglobin concentration
VO2max on mount everest
25%
direct tests for anaerobic power/VO2max
incremental exercise through metabolic cart
- lab systems
- protable systems
douglas bags
indirect submaximal tests for Aerobic power/VO2max (3)
YMCA cycle ergometer test
ebbeling single stage treadmill walking test
modified canadian aerobic fitness test
indirect maximal test for VO2 max (anaerobic power)
bruce treadmill test - increments of intensity and see how long you go for
leger 20m shuttle test (incremental)
cooper 12 minute test (cooper)
what do indirect VO2 tests usually look at
HR, age, formula
anaerobic threshold/aerobic capacity
VO2 at which energy production supplements the aerobic capacity - % of VO2 max/absolute workload
measuring aerobic capacity and its two thresholds
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
LT2 (3)
onset of blood lactate accumulation
good approximation of maximal lactate steady rate
above MLSS exercise will terminate
maximum lactate steady rate (2)
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
criteria of MLSS
in a 30 min test blood lactate cannot change more than 1mM over the last 20 min of the test
order of zone of occurance on a chart of lactate vs power
100 watt steady over course of exercise 250 watts exceed MLSS failure zone 375
4 reasons why does anaerobic system start supplementing aerobic metabolism when oxygen intake is not at VO2 max
- 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
increased intensity means
increased o2 consumption
oxygen uptake during exercise
initailly rises exponentially before it plateaus, then remains a steady rate for the duration of the effoert
oxygen deficit
difference between the o2 required during exercise and O2 supplied and utilized, occurs at onset of all activity
The energy that cannot be supplied through aerobic metabolism at the initiation of submaximal exercise is supplied by?
ATPPC and anaerobic glycolytic energy systems, eventually if the intensity is submaximal the oxygen deficit is nullified once steady state VO2 is achieved
Causes of oxygen deficit
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
why is it beneficial to get to steady state asap?
so that metabolic products dont accumulate
oxygen deficit is reduced through
aerobic
adequate warm up
- elevate muscle temp which increases the rate at which the metabolic processes in the cells can proceed
what can decrease oxygen deficit
training
10 metabolic adaptations to aerobic training
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
alactic power, capacity, intensity for power and intensity for capacity
0.1-3 (5)
8-12 (15)
explosive
all out
lactic, capacity, intensity for power and intensity for capacity
15-30
45-120
all out
all out
aerobic power, capacity, intensity for power and intensity for capacity
3-5min
hours
near max to max at end
submax
energy activation for exercise
smooth blending with considerable overlap of one mode to another
accepted explanation of O2 deficit
byproducts of additional energy use ADPP and NADHH to stimulate both aerobic and anaerobic metabolism (order of operations)
