Chapter 7- Fats Flashcards
where is most fat found ? where is a small amount found ?
adipose tissue
small amount found in intramuscular triacylglycerol
how many km can you run on fat stores
13 000 km
why do you want to use fat instead of carbs
because you want to spare glycogen since fatigue is most closely related to glycogen depletion
total fat approximately how many times more than carb stores ?
50 times
what are the three sources of fat for energy ?
adipose tissue and muscle triacylglycerol
with a little bit of plasma TG from VLDL
what are fats stored as ?
TG
what enzyme breaks down fats ?
hormone sensitive lipase
what happens to the fats once they are broken down ?
some are released into the circulation for reuptake, while some are reesterified.
what happens to the glycerol from lipolysis ?
circulates in blood, taken up by liver and used for gluconeogenesis
fats are the primary source of energy in these three states
rest
low to moderate intensity
during recovery between intense activity
what does endurance training do to your fat use ?
improves it
is fat an efficient fuel for muscles ?
no, especially at high intensities
what will determine the principal source of exercise fuel
intensity of exercise
the body has large stores of fat, but seems impossible to use fat as fuel. true or false ?
true
what are the 6 rate-limiting steps of fat oxidation
lipolysis rate removal of FA from fat cells transport of fat in blood transport of FA into muscle cell transport of FA into mitochondria oxidation of FA
in what form is HSL found in adipocytes ?
inactive form converted to active form depending on hormone mediation
what hormones stimulate HSL
epinephrine (not NE)
why does epinephrine stimulate HSL
because it is produced in adrenal medulla, especially during exercise
what is the most important counter regulatory hormone to HSL activation ?
insulin
why can’t the adipocyte reuse the glycerol from lipolysis and therefore most glycerol is released into the plasma ?
because the enzyme glycerokinase which phosphorylates glycerol for reesterification is very low concentrations
what is the percentage of FA that are reesterified at rest ?
70%
during exercise, is reesterification suppressed ?
yes, meaning there is more FA available
why does FA availability increase in exercise ?
because reesterification is suppressed, and also b-receptors stimulate it (catecholamines)
are FA soluble in aqueous environment ?
no
how are FA transported in plasma ?
bound to albumin
does lipolysis still happen in exercise ?
yes, but reesterification is suppressed
how can rate of lipolysis be measured?
concentration of glycerol
what are the three things which regulate FA reesterification ?
rate of FA removal from adipocyte (need to bind to albumin)
rate of glycerol-3-phosphate production (a byproduct of glycolysis, and related to alpha-glycerol-phosphate which decreases reesterification)
what is glycerol-3-phosphate ?
a byproduct of glycolysis, and related to alpha-glycerol-phosphate which decreases reesterification
what are 3 factors affecting the binding of FA to albumin ?
blood flow (the higher, the more transportation of fatty acids) albumin concentration (responsible for transporting FA) free binding sites (only 3 binding sites)
what enzyme is needed to release FA
lipoprotein lipase
what kind of lipoproteins do TG bind to ?
VLDL and chylomicrons
what percentage of energy expenditure during prolonged exercise is taken from VLDL ? what does this mean ?
3%
this means that VLDL and chylomicrons are a source of FA, we need lipoproteins to release them but it’s a rather slow process and not a major contributor of energy
what can increase the use of lipoproteins as a source of energy
training and high fat diet
what are the two proteins involved in the transport of FA across the membrane?
plasma membrane FA binding protein (FABPpm) FA transporter (CD36)
transporters into the membrane become saturated at what concentration of FA?
1.5 mmol/FA
how does CD36 work ?
fat transporter into membrane across sarcolemma, works a bit like GLUT4, translocates to plasma membrane.
in exercise, muscle is contracting, increasing presence of CD36 at membrane, meaning an increase of FA transport into the cell
how does FABPpm work ?
located at cell membrane across sarcolemma, allows FA to enter the cell but then needs to be bound to FABPc
what does muscle contraction do to the concentration of CD36?
increases the plasma membrane CD36 and decreases the CD36 in sarcoplasm (translocation to membrane)
what does FABPc do ?
transport of FA from sarcolemma to mitochondria
what muscle fibers have a higher content of IMTG?
type I
how does the location of lipid droplets of IMTG change with exercise?
in trained muscle, lipid droplets closer to mitochondria and more grouped
what does IMTG stand for ?
intramuscular trialglycerols
does muscle contain HSL?
yes, lipolysis happens in similar manner
if lipid droplets in muscle are closer to mitochondria, what is suggested happens to most of them in terms of energy?
oxidized
in what 2 ways does IMTG vary in trained or untrained person
location and size
what are FA released from IMTG bound to until they go to mitochondria ?
FABPc
what are the two words for CAT/CPT
carnitine acyl transferase
or carnitine palmitoyl transferase
what is the first step for the transport of FA into the mitochondria ?
the binding of activated FA to carnitine
how do short chain and medium chain FA get into the mitochondrial matrix ?
they diffuse freely
how do long chain FA get into the mitochondrial matrix ?
they use the carnitine shuttle
what are the 4 things that affects b-oxidation ?
enzymes in pathway
concentration of TCA intermediates
TCA enzyme activity (many intermediates with NADH and ATP and other things promoting or inhibiting pathway)
presence of oxygen (MAJOR)
at rest, what is the overnight energy mostly consisted of ?
fat + most liver glycogen
what is the resting plasma FA
0.2-0.4 mmol/L
at rest, what happens to most fats after lipolysis?
most are re-esterified
only half of FA entering blood stream are oxidized
during exercise, how does the rate of lipolysis change ? how ?
it increases threefold due to catecholamine stimulation
how does exercise catecholamine stimulation influence reesterification ?
decreases it
how does exercise catecholamine stimulation influence blood flow to adipose tissue
increases, meaning more of circulating FA
first 15 min of exercise, describe the plasma FA concentrations
they usually decrease because the rate of FA uptake by muscle is higher than rate of FA appearance from lipolysis
after 15 min of exercise, describe the plasma FA concentrations
FA appearance from lipolysis > oxidation, so there is a greater concentration of FA in blood because we are not utilizing all of it
what does increase in plasma FA depend on?
exercise intensity
during moderate intensity exercise, how high can the concentration of plasma FA become ?
1 mmol/L
during high intensity exercise, what kind of concentration of plasma FA do we see ?
not that high or absent increase in plasma FA since rate of fat oxidation decreases
at 25% VO2max, most energy comes from _______
plasma FA
at 65% VO2max, where does the energy come from ?
plasma FA contribution declines, increased TG contribution to almost half of fat being oxidized
at 86% VO2max, where does the energy come from ?
sympathetic vasoconstriction will decrease fat oxidation but rate of lipolysis still high
why does fat oxidation decrease at higher exercise intensities
sympathetic vasoconstriction will decrease blood flow
lactate accumulation will increase rate of reesterification
explain the experiment with injection of lipid heparin
control group and group with injection of lipid heparin
lipid heparin will restore FA level with lipoprotein lipase as if you were in moderate physical activity. therefore, the lipid heparin group will have a higher FA concentration.
however, when it comes to fat oxidation, there is a very small difference. therefore, this shows there are other mechanisms controlling FA availability during exercise, other than simply FA concentration..
what are mechanisms that may control FA availability during exercise ?
limitations to transporting (eg long chain is carnitine dependent, can take time in high intensity exercise whereas medium chain oxidation is unaffected)
how does training affect lipolysis rate ?
it does not
how does training affect fat oxidation?
increase in mitochondrial density, oxidative enzymes, capillary density, CAT increase, binding proteins
how will IMTG change with training ?
percentage of energy used from glycogen will decrease after training while proportion of energy derived from fat will be larger
how will a high fat diet change fat oxidation
increase it
in the study with Burke et al 1999, what kind of diet was consumed ? what happened to RER ?
5 days high fat diet, then 1 day high CHO
baseline RER=0.9
day 5 RER= 0.82
1 day CHO RER=0.87 (still not restored to baseline RER)
therefore body adapts its metabolism to lower RER likely due to metabolic adaptations in muscle
what are the 5 factors affecting energy from different sources
exercise intensity diet duration activity level timing of food intake
what is the fastest way to alter fat metabolism during exercise ? what are the consequences ?
carb feeding
will increase insulin and therefore reduce lipolysis and cause reduction in FA availability and carnitine dependent transport
what did the Horowitz et al study do? what kind of diet was consumed? what happened ?
eat carbs 1 hr before exercise
lipolysis and fat oxidation were reduced, with plasma FA reduced too
measured via biopsy
however, when intralipid and heparin was introduced, followed by exercise, no difference in muscle glycogen before exercise but then after exercise at 70% VO2max it was seen that muscle glycogen spared in those who received intralipid
what kind of effect does carb feeding before exercise have on fat oxidation ?
reduces fat oxidation by reducing lipolysis and plasma FA(w insulin) and inhibits carnitine transport
if you label MCFA and LCFA, what will you see in the uptake of them if you are fasting?
high uptake of LCFA and MCFA
if you label MCFA and LCFA and also eat glucose, what kind of uptake of them will happen ?
MCFA uptake doesn’t change
LCFA uptake decreases bc depends on CAT transport
glucose intake inhibits uptake of which FA
LCFA
what is the classical explanation of the interaction between carb and fat metabolism? how does fat intake affect acetyl coA, pyruvate, PEP, PFK, hexokinase, G6P??
fat regulates carbs
therefore, increase in plasma FA will increase FA uptake and b-oxidation in mitochondria and breakdown to acetyl-coa
increased acetyl coA inhibits pyruvate dehydrogenase which breaks down pyruvate to acetyl coA (accumulation of phosphoenolpyruvate PEP)
increased acetyl coA will also increase citrate, which will inhibit PFK (reducing glycolysis, causing accumulation of G6P, inhibiting hexokinase and reducing muscle glucose uptake)
this also reduces Pi and AMP accumulation which usually stimulate glycogen phosphorylase
what is the caveat in the classical explanation of fat and carb interplay in metabolism?
the FFA in control group was <0.2 mmol/L
too low to provide tissues w sufficient fat substrate, so muscle glycogen breakdown may have increased in the control condition. the observed sparing of glycogen with the high FA in the experimental condition could have been biased
what compound increases muscle glycogen breakdown during exercise
nicotinic acid
what does the modern theory about fat and carb metabolism say in short ?
that it is carbs that regulate fat metabolism
increasing the rate of glycolysis ______ fat oxidation in the modern theory of fats and carbs
decreases
explain the modern theory about fat and carb metabolism that looks at malonyl coa concentration
increase in glycogenolysis means that there is going to be more acetyl coa in the mitochondria. some of this acetyl coa is converted into malonyl coa which inhibits CAT/CPT transporters and therefore the transport of FA into mitochondria is reduced, as well as the concentration of carnitine.
in the modern theory about fat and carb metabolism what are the two things that may inhibit fat oxidation ?
increase in acetyl coa converting to malonyl coa, as well as a reduction in intramuscular pH both inhibit the CAT
what is a more modern theory about fat and carb metabolism that depends on carnitine concentration?
the acetyl coa accumulated in an acceleration of glycogenolysis is bound to carnitine, meaning the free carnitine levels drop and less carnitine is availabile to transport FA into mitochondria.
what is a more modern theory about fat and carb metabolism that depends on pyruvate ?
pyruvate-derived acetyl coa competes with FA-derived coa for entrance into TCA cycle
rate of carb utilization is ___related to energy needs of working muscle, whereas rate of fat utilization is ___ regulated by energy needs of working muscle
carb use tightly related to the needs, unlike fat use, as no mechanisms closely match metabolism of FA to energy expenditure
what does fat oxidation depend on more- fat availability or energy needs of muscle ?
fat availability and rate of carb utilization
how does the digestion of fats compare to digestion of carbs in speed ?
digestion of fats slower (also slows down gastric emptying)
what fat does fish oil contain ?
LCFA omega-3
why should the intake of fat during exercise be avoided ?
because the primary roles of LCTG is in replenishing the IMTG stores after exercise, and the rate of breakdown of them during exercise is pretty low (won’t be an efficient source)
how are MCTG usually consumed as a supplement ?
they have few natural sources, aren’t stored in the body so athletes use them for energy to replace normal fat
what hormones and mechanism does fasting affect ?
increases plasma catecholamines, which stimulates lipolysis, more plasma FA and less glucose turnover
what effect does fasting have on exercise performance at <45% VO2max ?
no effect
what effect does fasting have on exercise performance at 50-100% VO2max ?
decreases endurance, in a non-reversible way (even with CHO ingestion during exercise)
in the study which looked at performance in fasting athletes, what was the caveat ?
control group had last meal 3 hours before exercise, and therefore it was an unfair comparison bc it would have affected the endurance capacity
in a fast of 12 hrs compared to a fast of 24 hrs, what kind of difference was seen in exercise performance
same decrease in performance + acidosis
what are the two reasons fasting may decrease endurance ?
depletion of liver glycogen and metabolic acidosis
what is metabolic acidosis
ketones lower pH
what did a short term high fat diet show in exercise performance if a high fat diet was eaten hours before ?
the research was inconclusive. no effect on endurance capacity or decreased endurance
what did a short term high fat diet eaten days before exercise do?
less than 2 weeks on high fat diet found that it is too short of an adaptation, will impair exercise capacity and is therefore ineffective
how long does a diet have to be to be considered long term
2 weeks or more
what is the rationale behind a high fat diet ?
adaptations for better capacity of fat oxidation: increasing oxidative enzymes, less use of liver glycogen
explain the Phinney et al long term high fat diet conditions of study
n=5
diet was 85% fat vs 65% carbs for 28 days, and exercised submaximally (62-64% Vo2max)
explain the Phinney long term high fat diet study conclusions when it comes to exercise time, resting muscle glycogen, and fat oxidation
no difference in exercise time
the HFD brought 50% less resting muscle glycogen
RER was lower in HFD (0.72) which would mean greater fat oxidation at 60% VO2Max
explain the 3 caveats in Phinney’s long term HFD study
in general, trained subjects can ride for a very long time
small sample size w large variability (one person rode for 60% longer after HFD)
intensity was low, not a competitive intensity and reduced carb stores are not limiting
explain the Helge study with HFD and HCD
after 7 weeks of endurance training w a HFD, some switched to a high carb diet. although in the ppl who switched their endurance was better, they still did worse than those who were on a high carb diet for the 7 weeks
therefore, the high carb switch did not reverse the effects, suggesting that the negative effects of HFD caused not only by lack of carb as fuel but also suboptimal adaptations to training
a study found reduced pyruvate dehydrogenase after fat adaptation. why?
increase in fat oxidation partly caused by reduction in ability to oxidize carbs
what kind of fat recommendations for pre-workout meal
fat is good bc reduces hunger before exercising, but too much can increase GI issues
therefore for snacks <4hrs before exercise choose low unsaturated fats
what is the AMDR for fats
20-35% total
what is the AMDR for fats for athletes
20-30% of total
what are the recommendations of saturated fat for general populations ?
<10% AMDR to reduce CHD risk
what are the recommendations of monounsaturated fat for general population ?
10-15% AHA 10% NCEP AMDR
what are the recommendations of polyunsaturated fat for general population?
10% AMDR
what kind of fat should be eaten post exercise
fat consumption not essential, but minimal fat intake recommended to ensure optimal digestion
how many carbons are LC TG
16-18
what is the dose limitation for LC TG and MC TG ?
30g max tolerable, more than 50g leads to GI distress
in a study by Ivy et al, LCT or MCT were ingested before moderate exercise. what happened ?
LCT increased serum TG but no effect on rate of FA oxidation.
in a study by Satabin et al, LCT or MCT was ingested before exercise w isotope tracers. what happened ?
MCT associated w rise in ketone bodies, and small amount of LCT was oxidized
why is LCT ingestion during exercise not desirable ?
slow gastric emptying and enter circulation in chylomicrons which is believed to be a negligible fuel source in ezercise
why does fasting still bring on fatigue if it increases fat availability
bc glycogen stores depleted, so even if fat oxidation increases, it’s compromised
so, is MCT supplementation helpful ?
not really
what is the supposed benefit of fish oil? is it true
increase VO2max
not true
what is the known benefit of fish oil ?
improves membrane characteristics and function
name 6 supplements claiming to increase fat oxidation
caffeine pyruvate carnitine vanadium chromium dihydroxyacetone
what is the claim of caffeine to improve fat oxidation
increases epinephrine / decreases adenosine receptors, therefore more lipolysis and more FFA uptake and oxidation and spare glycogen
what are the findings on caffeine supplementing fat ozidation
glycogen sparing is a thing but occures with a dose of 6mg/kg at more than 70% vo2max
how many mg caffeine in coke ?
46 mg
how many caffeine in red bull ?
8 mg
how much caffeine in Starbucks ?
250 mg
under what form is caffeine more effective ? what is the catch?
caffeine pills but may cause heart palpitations
what is carnitine synthesized from (2)?
methionine and lysine
what are 3 sources of carnitine ?
meat, poultry, fish
what is the effect of carnitine supplementation on fat oxidation ?
no effect, useless
so, conclusion; chronic fat diets, yay or nay?
nay
little evidence the hypothesis is true
