1/65
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
When are fats the primary energy source?
at rest and low-mod intensity exercise
What are fats?
carbon, hydrogen and oxygen
9 kcals/g
What are the classifications of fats?
TGs: 3 fatty acids + glycerol, most common dietary lipid
Phospholipids: glycerol + 2 FAs + phosphate group, cell membranes, water and fat soluble
sterols - cholesterol
Where are TGs stored?
adipose tissue, muscle tissue and liver
When will someone rely more on muscle TG’s?
during exercise because it’s immediately available
How do TG’s provide protection?
add cushioning
insulator (thermal/electrical)
myelin sheath - sheath on nerves
What vitamins are stored/carried in fats?
A, E, D, K
fats are necessary for absorption of certain nutrients (bioavailability)
What are the functions of fats/TG’s?
energy source
energy reserve
provides protection
vitamin carrier
satiety in diet
What are the different lengths of fatty acid chains and why is it important?
The longer the chain, the more ATP can be produced
short-chain fatty acid (SCFA): 2-4 carbons
medium-chain fatty acid (MCFA): 6-10 carbons
long-chain fatty acid (LCFA): 12+
What are saturated and unsaturated fats?
saturated: no double bonds, saturated with hydrogens, solid at room temp
unsaturated: mono- (1 carbon double bond) and poly- (2+ carbon double bonds), liquid at room temp
What are phospholipids and their functions?
glycerol backbone, 2 FAs + phosphate
function: cell membrane, transporters
What is the recommended intake of fats?
fat: 20-35% of total calories
saturated: 5-6%
trans: <1%
What is HDL cholesterol?
good cholesterol
high density lipoproteins
higher protein content
cholesterol from blood stream delivers to liver
What is LDL cholesterol?
low-density lipoproteins
bad cholesterol
delivers cholesterol to cells
can accumulate in arterial walls, trigger inflammatory response, fibrous cap can then rupture
What is VLDL cholesterol?
very low-density lipoproteins
lipoprotein lipase digests some of the TG forming intermediate density lipoprotein (IDL)
IDL then converted to HDL or LDL in liver
Where is fat mobilized from during exercise?
muscle
adipose tissue
blood lipoproteins
exogeneous
What limites the amount and source fat is utilized from?
fitness leve, type of exercise, I + D, avaible fat reserves in muscle, ability to mobilize and transport FA’s (limited if dehydrated, cold and low on CHO), composition of pre-event meal, availability of CHO
What does c-AMP PK do?
activates HSL
What activates lipolysis?
exercise
~0.2 - 0.4 mmol/L at rest
increases 10-20 fold during exercise
I + D
rate of lipolysis (during exercise) exceeds need for FAs for oxidation by muscles
What is the rate limiting step in fat metabolism (lipolysis)?
HSL bc it can be inhibited by various factors
What is the fate of glycerol after lipolysis?
goes to liver
gluconeogenesis or re-esterified with FAs to make TGs
What happens to FFAs when TGs breakdown?
blood (passive or active)
then bound to albumin and transported to working muscles
re-esterification
intracellular recycling
extracellular recycling
When is re-esterification high?
at rest and recovery
What factors affect re-esterification?
albumin not available - malnutrition or blood loss
blood flow through tissue is low - cold, dehydrated, etc
transport sites of albumin are full
high lactate levels - decrease FFA mobilization to increase re-esterification
What is re-esterification and when is it low and high?
reutilization of the FFAs by fat cells through a futile cycle
high during rest and recovery
low during exercise
What is the difference between lipolysis and beta oxidation?
lipolysis is break down of TGs into FAs and glycerol
oxidation: metabolism of fat to make ATP in presences of O2, electron transport chain, oxidizes FAs in Acetyl-CoA
What are the 4 factors that hormonal responses during lipolysis depend on?
intensity, duration, fitness level, nutritional statue
What are catecholamines and which ones are the strongest stimulators for lipolysis?
hormones and neurotransmitters
epinephrine and norepinephrine
stimulate breakdown of stored fat and CHO
blood levels increase dramatically within seconds
What other hormones influence lipolysis?
GH (growth hormone), cortisol, TSH (thyroid stimulating hormone)
What does insulin do in lipolysis?
strongest inhibitor
decreases phosphorylation of HSL (by inhibiting cAMP)
What is the strongest regulator of lipolysis?
BG
increase BG = suppresses lipolysis (independent of insulin)
What affects how much fat is stored in muscle?
muscle fiber type (type 1 stores more fat bc energy system)
nutritional status
type PA performed
What is the process of fat oxidation?
FAs bound to albumin, transported to muscle, FABP transports FA’s into muscle
Once in cytoplasm
re-esterified and stored as TG
transported to mitochondria
used by mitochondria, first activated by acyl-CoA (outside mitochondria)
Activated FA transported across mitochondria with CPT1 and CPT2
What is CPT1?
brings fatty acid across outer membrane of mitochondria
What is CPT2?
brings fatty acids across inner membrane mitochondria
What are 2 different ways increasing BG inhibits fat use?
increase in BG = increase in insulin and inhibits HSL (lipolysis)
increase BG = elevated malonyl-CoA that inhibits CPT1 (fat oxidation)
What is carnitine?
conditionally essential
does not affect fat oxidation
What does maximizing fat oxidation do?
helps prevent fatigue and improve performance
glycogen stores are limited
What are some limitations of fat oxidation?
lipolysis and mobilization of FA’s from adipose tissue
transportation of FA’s within muscle and to the muscle
uptake of FA’s across muscle membrane
lipolysis/fat mobilization FA’s from intramuscular triacylglycerol pools
regulation FA movement across mitochondrial membrane
When does most fat use occur?
untrained people max is 60-65% VO2max vs trained people 45-50% VO2max
Is there a way to enhance fat mobilization during exercise?
eat enough carbs
Do high fat diets work to improve performance?
no
but increased mobilization and oxidation of fat and may spare MG
What are the benefits of caffeine?
CNS stimulation: alters perception of effort, improve neural activation of muscle
affect sk. muscle by altering enzymes/systems regulating CHO breakdown
altered metabolism
increase epinephrine = increase fat mobilization (lipolysis), decrease CHO use
lacks support
What is caffeine’s effect on performance?
moderate does 3-9mg/kg 1 hr prior = enhanced endurance performance
TTE protocols show greatest impact
direct caffeine different than drink
response differs based on use
Why does caffein work to improve performance?
not one physiological mechanism
primary effect on CNS
What is carnitine?
“fat burner”
required to transport FA’s into mitochondria
What should fat consumption look like after exercise?
normal dietary recommendations
20-35% fat
focus on unsaturated
CHO and pro predominate
Is a single high-fat meal prior to exercise beneficial?
not beneficial
GI distress (bloating, diarrhea, stomach cramping)
fullness
Why is fat considered a calorie-dense nutrient?
it has the highest concentration of calories per gram of any macronutrient
What are trans fats and why should they be avoided?
hydrogenation: addition of H to unsaturated fats take on saturated properties
increase risk for heart disease, diabetes and metabolic syndrome
What are sources of saturated fats?
animal products
What is total cholesterol?
HDL+LDL+TG
Why is HDL considered the “good” cholesterol and how can we increase it?
removes other cholesterol from blood stream and reduces risk of heart disease and stroke by working against plaque buildup in arteries
aerobic exercise regularly, choose healthier fats (mono and polyunsaturated fats), include high fiber foods
Why is LDL considered “bad” cholesterol?
carries cholesterol to cells
collects in walls of blood vessels causing plaque buildup leading to narrowing of arteries
increases risk of heart disease, stroke and peripheral artery disease
What are the steps of fat metabolism (lipolysis)?
exercise starts: release epinephrine, binds to cell membrane
epinephrine stimulates production of phospo-HSL (active form)
final FA split off by MGL
glycerol not used is released into blood (marker of lipolysis) - substrate for hepatic gluconeogenesis
What are the four sources of fat for energy metabolism?
muscle TGs
adipose tissue
blood lipoprotein/fat in blood
exogenous
What factors do the amount and source of fat depend on?
fitness level
available fat reserves in muscle
intensity
duration
What are the steps of fat metabolism during exercise?
epinephrine stimulates lipolysis and breakdown TGs
transport FAs out of adipocyte to blood, to muscle and then transported in muscle to mitochondria
if TG is in muscle it goes directly to mitochondria
then starts Krebs cycle
What is the role of epinephrine and insulin in lipolysis?
epinephrine: stimulates HSL/lipolysis - HSL breaks off FA from TG
insulin: inhibits HSL/lipolysis - stopes HSL break odd of FA from TG
What is the role of albumen in fat metabolism?
protein that transports free fatty acids in the blood
What are two possible fates of FFAs after they are cleaved off of glycerol?
blood: then bound to albumin and transported to working muscles
re-esterification: intracellular recycling, extracellular recycling
How/why does the rate of appearance (Ra) of glycerol and FFAs change in the blood as we go from rest to exercise? How might RER change and why?
within 20 minutes of exercise, huge jump of glycerol and continues to increase, end of exercise it drops
more fat we use the lower RER is but RER goes up
Why is insulin a strong inhibitor of lipolysis and why does this “make sense”?
it prevents FFAs from cleaving off of glycerol
it makes sense because it maintains blood glucose because glycerol can be converted to glucose and that would raise blood glucose levels
How could you demonstrate that a training program increases and individual’s fat use as an energy source?
do baseline test and measure RER, train them for X amount of weeks and then test them at same workload and if RER decreases that demonstrates an increase in fat use
When might an individuals fat use be hindered and why?
anything that limits blood flow and O2 delivery bc it limits the aerobic system relying more on glycolysis so less fat use and more carb use
Ho can exercise training improve fat use?
more mitochondria
bigger mitochondria
increase aerobic pathway enzymes