Term
| Majority of dietary fats exist as ______________ |
|
Definition
TRIGLYCERIDES (both plant and animal)
-consist of a glycerol molecule and 3 attached fatty acyls
-glycerol loves water and keeps you hydrated |
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Term
| Difference b/t monounsaturated vs polyunsaturated, and saturated vs unsaturated |
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Definition
Monounsaturated vs Polyunsaturated: mono has 1 carbon double bond and poly has multiple double bonds (many C missing H)
-SATURATED: there are no double bonds b/t carbons so carbons have max amount of H's bonded to them thus they are fully saturated. (typically animal fats) |
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Term
| Cis vs Trans fatty acid facts!! |
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Definition
CIS: where H's are in same direction
-- found primarily in nature
TRANS: carbons and H are flipped at double bonds.
-trans are rare in nature but common in processed food.
-trans are made by artifically hydrating chains to increase shelf life and change fat texture (make more creamy) |
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Term
| Evidence why Trans fat may be bad: |
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Definition
-trans increases heart diseases: enzyme inside blood vessels break down triglycerides. Enzymes don't reccognize trans fat and thus fat accumulates on vessel wall or just continues to circulate in blood edventually settling on the walls.
-propagation of mutation in cells. Cell membranes are made of lipids. Trans fat causes lipids to not form right causing cell to malfunction, resulting in mutation. |
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Term
Difference:
Short chain triglycerides
medium chain triglycerides.
long chain triglycerides. |
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Definition
-short: fatty acyls 4-6 carbons
-Medium: fatty acyls 8-12 carbons
-Long: fatty acyls >12 carbons |
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Term
| Fat digestion and absorption facts: |
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Definition
-~90% of fat digestioin takes place in small intestine (basic pH needed).
-Enzymes need to breakdown fat need basic environment.
-Bile salt break down and emulsify the fat molecules and improve solubility in water. |
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Term
| Triglycerides are broken down into what three components? |
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Definition
1) GLYCEROL (hyrolysis and enzyme pancreatic lipase needed to do this)
-lipase is primary digestive enzyme for triglyceride breakdown
2) FFA
3) mono glycerides
*all three are absorbed into micelles (lipid droplets that absorb fat from intestine) |
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Term
| What does the micelle do? |
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Definition
-MG, FFA, and glycerol are all combined into micelle which is absorbed into intestinal wall.
-pull fat through intestine wall into lymphatic system.
-In intestine wall, micelle is both converted into FFA and broken down into its components.
--glycerol + pi --> alpha glycerol phosphate (AGP)
--Monoglyceride --(intracellular lipase)--> FFA
--Glycerol --> alpha glycerol phosphate |
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Term
| In Fat digestion and absorption, what is transported into the endoplasmic reticulum inside the cells of the intestinal wall? |
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Definition
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Term
| From inside the intestinal lumen, what is reformed from the FFA and AGP? |
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Definition
-tryglycerides
triglycerides, phopholipids, & cholesterol are all package into a molecule known as chylomicron (protein coat) |
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Term
| Chylomicrons are absorbed into the _____ and then do what? |
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Definition
-lymph vessels and not the portal vein.
-enter the general circulation (bloodstream) at the thoracic duct (upper chest/lower neck region). |
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Term
| _______________ are water soluble. |
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Definition
short, medium-chain fatty acyls.
--are not reformed into TG and enter the bloodstream at the portal vein |
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Term
| Fat circulation: What are the destinations of chylomicrons? |
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Definition
-LIVER (energy substrate and lipoproteins) (vast majority of chylomicrons do this)
-CARDIAC & SKELETAL MUSCLE (energy substrate)
-ADIPOSE TISSUE (storage and energy substrate) |
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Term
Formation of Lipoproteins:
What catalyzes the breakdown of TG in ________ into ___ and _____ at all target cells? |
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Definition
-Lipoprotein Lipase (enzyme that lives in vessel walls)
-chylomicrons
-FFA & glycerol |
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Term
Formation of Lipoproteins in the liver:
Flow chart of the breakdown of glycerol & FFA |
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Definition
Glycerol & FFA break down into three things:
1) Glyceraldehyde 3 phosphate (glycolysis)
2)triglyceride formation --> lipoprotein formation (supply peripheral tissue w/ FFA)
3)beta oxidation (TCA/ETC) |
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Term
| Lipoproteins are primarity formed in the _____ and are a combination of.... |
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Definition
-Liver
1)TRIGLYCERIDES (energy substrate and adipose tissue which is storage form of fat in body)
2)PHOSPHOLIPIDS
-required to form lipoproteins (no fat transport w/out them)
-key ingredient in blood clottin factors
-key ingredient in myelin
-supplier of phosphate radicals for certain rxns
-membrane formation
3)CHOLESTEROL
-cholic acid (important factor in bile salts which w/out the body can't digest fat)
-steroid formation (adrenal corticoids {cortisol}, testosterone, progesterone, and estrogen)
-corneum (waxy material that makes skin water proof.) |
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Term
| Lipoproteins are all encased in a ____ ____ and are the primary transaport mode of ____ to ______ ______. |
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Definition
-Protein coat
-fat and peripheral tissue |
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Term
| Classifications of Lipoproteins |
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Definition
1) Very Low density lipoprotein (VLDL)
-produced in greatest amounts
-has highest amount of triglycerides = greatest fat
2)Intermediate Density Lipoproteins (IDL)
3)Low Density Lipoproteins (LDL)
4)High Density Lipoproteins (HDL)
-Low density of fats
TGs are the lowest density compound in lipoproteins |
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Term
| ___________ ______ cataylzes ____ and ______ removal from lipoproteins |
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Definition
Lipoprotein lipase, FFA and glycerol
-Lipoprotein lipase is found in vessel wall and catalyses breakdown of TG
-released by liver--> blood stream --> target tissue |
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Term
LDL facts
Bad cholesterol |
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Definition
-LDLs are removed from the blood by liver and remaining contents are used to form new lipoproteins (VLDL --> to redistribute fat)
-Most involved in cholesterol transprot to peripheral tissues
--Artery walls insert = LDL : High artery fat cell lining of vessel; attach to walls easily
-Excessive fat in diet results in abnormally high levels of blood lipoproteins
-Atherosclerosis
--accumulation of fats and cholesterol (plaque)
--LDLs have high affinity for cells lining the blood vessels |
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Term
|
Definition
-Unique from VLDL and derivaties in content and function
--very low concentrations of lipids and cholesterol
--high concentrations of proteins
**scavenage cholesterol from blood, vessel walls and transport to liver
**Anti-oxidant, anti inflammatory, vasodilator |
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Term
| Lipoprotein Lipase is found in vessels serving the... |
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Definition
-Liver, Adipose tissue, and skeletal and cardiac muscle
-Lipase pulls fat out of lipoproteins and into target tissues |
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Term
Liver and adipose Lipoprotein Lipase are activated by ___________.
Skeletal, Cardiac muscle lipoprotein lipase is activated by _______, _______
Why the difference? |
|
Definition
-INSULIN (increased insulin turns LPL on)
-GLUCAGON (realease when bl.gl low from depleted glycogon) and EPINEPHRINE (high when exercising)
-WHY???
--Different activator in vessels to serve Sk. and Car Muscle. Pull fat into muscle to burn for energy.
-Exercise causes need for energy inside cell, glycagon (hungry/fasting) and epinephrine (when exercising) activate LPL.
-Adipose tissue storage excess fat, fed state wants to send fat to store. so the body activates LPL in adipose tissue to bring in fat from blood, in the liver to make VLDL. |
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Term
| 7 steps of lipid metabolism (to get ATP) during exercise: |
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Definition
1) MOBILIZATION
2) CIRCULATION
3) UPTAKE
4) ACTIVATION
5) TRANSLOCATION
6) BETA OXIDATION
7) MITOCHONDRIAL OXIDATION OF ENERGY
-most TG stored in adipose tissue and a few in skeletal muscle.
-can be burn during ex |
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|
Term
|
Definition
-first step in lipid metabolism
-Breakdown of adipose tissue TG into FFA and glycerol
Enzyme: HORMONE SENSITIVE LIPASE (HSL)
-Sensitive to different hormones
-Activators:
--Epinephrine, norepinephrine (quick response, stimulates HSL)
--Growth Hormone (delayed response of 10-15 minutes maintains lipolysis during prolonged exercise)
-Lipase sensitive to many H (Ep, Nore, & GH)
-Nor(ep) are the 1st H to respond. even before we exercise they stim HSL to start breaking down TG)
-GH then takes over the job of (No)epi |
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Term
|
Definition
2nd step of lipid metabolism
Majority of glycerol is transported to liver and used in gluconeogenesis
Essentially runs glycolysis backwards.
**Majority of glycerol ends up as glucose** |
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Term
|
Definition
-3rd step of lipid metabolism
-uptake of FFA
-No Carrier necessary to transport Free fatty acyls into the muscle cell (unlike CHO)
-Cell membrane is composed of lipids and thus lipid soluble (lipid membranes of cell walls make crossing easy for FFA)
- ~50% of blodo fats are removed to the muscle w/ each circulation of blood
-Blood FFA concentration has a significant effect on FFA uptake by the muscle ( once in cell, FFA must be activated) |
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Term
|
Definition
-4th step of lipid metabolism
-Fatty Acid/acyl is combined with CoA to form a fatty acyl Coa
-CoA activates FFA
-Activation occurs in cytosol (b/c of mitochondria)
-ATP cost/contribution is debated.
-2 views of atp cost:
1) 1 ATP, 2 P pulled off to provide energy and AMP
2) 2 ATP --> ADP |
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Term
| Translocaton to Mitochondria |
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Definition
5th step of lipid metabolism
-FFA-CoA is too big to get into mito so Coa is replaced with carnitine
-Fatty acyl carnitine is transferred to mitochondrial matrix via a special carrier.
-Special enzyme help with carrier: Carnitine acdyl transferese 1 & 2 (1 = outer membrane; 2 = inner membrane)
-Once in mito, processes are reveresed and FA-CoA is reformed, removing carnitine |
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Term
| BETA OXIDATION!!!! (5 steps) |
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Definition
-6th step of lipid metabolism and has 5 steps
-5 steps:
1) oxidation to remove H and create FADH2
2) Hydration (h20 added to C) sets stage for 2nd oxidation
3)Second oxidation to create NADH + H
4) Cleaving of Acetyl CoA (entrance into TCA) 2nd CoA adds on to rest of FA
5) Repeat process untill chain is consumed
-each time, chain is 2 carbons shorter
(Even # / 2) - 1 = turns through B-Ox
C-C-C-C-C-C-C-C-SCoA 8 C's
8/2 = 4 -1 = 3 turns through B-oxidation |
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Term
| Oxidation of energy intermediates |
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Definition
-7th step of Lipid metabolism
Each run through BO results in 3 energy intermediates:
1) FADH2 : sent to ETC to donate H and electrons to help make ATP
2) NADH + H : sent to ETC for same reasons as FADH2
3) Acetyl CoA (from FA-CoA) : goes into TCA
-TCA-->NADH+H, FADH2, and ATP
-2nd CoA goes back to start of B-oxidation
Each turn of B-ox:
1 NADH + H -ETC-> 3 ATP
1 FADH2 -ETC-> 2 ATP
Acetyl-CoA -TCA-> 3 NADH + H -ETC-> 9ATP
1 FADH2 -ETC-> 2 ATP
1 ATP
+____________________
Net ATP/B-ox turn: 17 ATP - (1 or 2) = 15- 16 ATP |
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Term
| What is the ATP Yield for a 16 carbon fatty acyl (palmitate)? |
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Definition
CC|CC|CC|CC|CC|CC|CC|CC|-SCOA & =0
B-Ox Turns: (16 C's/2) - 1 = 7 turns!
-after cleaving of acetylCoA and entrance into TCA : times each intermediate (NADH & FADH2) by 7.
-AcetylCoa: 8 per turn --> TCA
--NADH = 3 X 8 = 24 NADH --> 72 ATP
--FADH2: 2 FADH2 -ETC-> 16 ATP
--ATP: 1 ATP X 8 TURNS --> 8 ATP
--TOTAL FOR COA = 96 ATP VIA TCA
-NADH : 7 turns x 3 ATP/NADH = 21 ATP
-FADH2: 7 turns x 2 ATP/FADH2 = 14 ATP
-ATP INVESTED: -1 or 2 (b/c of FFA activation step 4)
*ATP Yield: Acyl Coa -> 96 ATP
NADH + H -> 21 ATP
FADH2 -> 14 ATP
---------
131 ATP - (1 or 2)
----------------
NET ATP: 129-130 ATP |
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Term
| Reason why ATP yeild of fats is higher than sugar: |
|
Definition
-Fats have so many C's that can be used in TCA and ETC
-16 C's in Palmite vs 6 C's in glucose (2 C's lost to CO2 so really 4 C's)
-Glucose: 4 Carbons
-Fatty Acyl: 16 Carbons
-4x as much atp from fatty acyl vs glucose |
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|
Term
|
Definition
-Fat provides more energy per gram of substrate than does CHO (9 kcal vs 4 kcal)
-NOTE: there is NO anaerobic energy pathway for fat
--thus liberating energy from fat requires more oxygen than carbohydrate
--Fat ~ 4.65 kcals/L O2
--CHO ~ 5.1 kcals/L O2
-Fat Disadvantages:
--no dedicated anaerobic process (like glycolysis) to yield ATP from fat stores
--more O2 needed to get ATP out of fat vs CHO b/c of this: 4.65 vs 5.1
--Fat storage of energy much greater but ATP realease per unit of O2 is lower |
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Term
| What effect does FAT's lack of anaerobic energy pathway (and thus increase need of O2 to liberate energy) have on substrate utilization during intense exercise? |
|
Definition
O2 utiliaztion:
Fat~4.65 kcals/L O2 | CHO~5.1 kcals/L O2
-Body uses CHO more when Ox at premium
-b/c fat needs so much O2, it isn't efficient
-reason why respiratory exchange ratio goes UP during VO2 max is that the subject is using CHO as energy source
-Atheletes who trained HI burn much more CHO resulting in Shortage of CHO storage.
-Low Intensity EX burns more fat molecules but not as much calories over all. Weight loss is burning more calories than you put in. |
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Term
| The idea behind fat supplementation and did it work? |
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Definition
-compared to CHO, fat digestion is relatively sow
-fat stores in the human body are relatively high
--60 kg man with 4% body fat
---2.4 kg fat * 9 kcals/g = 21,600 kcals as fat
----Enough to run from boone -> charlotte and back.
----exercise cannot be limited by fat stores.
-Cho way to go
-Cho stores in body very low (500 g or 2000 c stored)
-100 C burn a mile so mile 20 wall is usually hit
-10x more fat stores vs CHO stores
--can't make a dent in stores during most ex
-Medium-chain triglycerides (and SC) can be absorbed directly into the bloodstream.
-can provide energy substrate during low to moderate intensity exercise.
-Glycogen sparing effect?
--not always sent and during HI ex MCTG weren't even burnt.
-Performance always increased when CHO was consumed vs fat supplementation.
-MCTG will NOT improve anything. |
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Term
|
Definition
Advantages of MC TG:
-MC TG increases delivery rate of fat to workign muscle.
- |
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Term
| Can consuming MC TG increase the amount of fat burn opposed to glycogen? |
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Definition
-NO.
-glycogen sparing wasn't always seen b/c ex intensity
-HI EX didn't burn MCTG
-Most sports this isn't viable. |
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Term
| Proteins have a ____ ____ on one ende and a ________ _____ on the other. |
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Definition
| amino acid, carboxyl group |
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Term
| Some AAs ahve _____ in their functional groups which allows them to form _______ bonds. |
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Definition
sulfur, sulfur
-example is cysteine |
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Term
| Amino acids can be lined together with _______ ______. these bonds help to form the larger molecules known as _______. |
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Definition
| peptide bonds, polypeptides |
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Term
| Characteristics of proteins are determined by: |
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Definition
-types of amino acids
-sequence of amino acids
-types of bonds.
-they help determine the shape, consistency, activity, and function of the protein. |
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Term
| The number of AAs in human metabolism and what are the essential AAs? |
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Definition
-20 AAs in human metabolism
-Essentials AA can't be synthesize in body and must come from diet
-other 12 AA's are made from 8 essential.
8 Essential AA's:
-Isoleucine
-leucine
-lysine
-methionine
-phenyalanine
-threonine
-tryptophan
-valine
Infatns and growing children also have need for histidine and arginine making them have 10 essential.
-this is b/c they ahve not developed enzymes to convert essential AA's into histidine and arginine. |
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|
Term
|
Definition
Plant and Animal Sources
Animals provide "complete proteins"
-complete = all essential AA's
Plants often are incomplete (lacking the essential AAs)
Vegans:
-must be careful
-have to combine foods to get complement of essential AAs
-Grains have methionine but lack lysine
-Legumes have lysine but lack methionine |
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Term
| The quality of dietary protein depends on: |
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Definition
1) is it a complete prtein
2) what are the ratios of essential amino acids? (very important)
-Egg protein is considered to be the highest quality dietary protein b/c:
1)it has all essential AA's
2)It's ratios are most similar to the amino acid reqirements of humans
-After Egg, Fish/meat, milk, rice, soy, and nuts are the next highest quality proteins in that order |
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Term
| Protein type also affects the _____ ______. |
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Definition
Digestible Qualities.
Milk has 2 proteins:
1) Whey: digested and absorbed quickly
2) Casein: digested and absorbed slowly
-Curdles in low pH (stomach)
-Clumps up, increasing difficulty in absorption
-This has big effect on protein catabolism after exercise.
-Whey isn't the best type of protein to put in body after exercise. |
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Term
|
Definition
-transcription creates mRNA which is used at ribosomes to produce AA.
-mRNA consists of a series of 3 "base pairs" (codons) that will encode for a particular AA.
-Specific tRNA for specific codon. tRNA brings specific AA to site.
-As AA are brought to the site, they form peptide bonds.
-Eventually, a "multi-peptide" chain forms. Elongation of chain ceases when a Stop" is reached and chain is released forming a polypeptide. 3-4 different types of stop codons.
-polypeptide shape is manipulated into variety of structures by hydrogen bonds.
-multiple polypeptides are combined to form protein structures like Hb |
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|
Term
|
Definition
1) STRUCTURAL (m, organs, any soft or semihard tissue)
2) CARRIER/TRANSPORT
-Membranes
--glut 4 (glucose-> membrane)
-blood
3)ENZYMES
4) MAINTENANCE OF BLOOD VOLUME
-albumin maintains blood volume
5)ENERGY SOURCE |
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Term
|
Definition
-amino acid can affect shape and function of proteins just by replacing 1 AA.
Example: Sickle cell
-31 AA in globin proteins of Hb
-AA #6 is usaully a glutamine.
-substitution with valine results in sickle cell |
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Term
| How can heat denature proteins and how does that aid digestion? |
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Definition
breaking of disulfide bonds to change the shape of the structure
-breaking bonds causes proteins to unravel and allow us to more compeltetly digest the proteins, thus, getting more value from them. |
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Term
| Protein digestion in the stomach |
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Definition
-more digestion occurs in stomach vs CHO digestion
-pH ~ 2.5
-acidity continues denaturing process
--acidity breaks down membrane sacs that encase proteins.
-Pepsin (primary digestive enzyme)
--activated at low pH
--digests collagen
--allows access to other meat proteins
--proteins -> polypeptides -> AA (requires acidic environment) |
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Term
| Protein digestion in small intestine |
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Definition
Majority of digestion takes place in the upper small intestine
-polypeptides in SI stimulates cholecystokinin (enzyme) from SI
-CCK stimulates pancreatic digestive enzyme release
--PDE consists of: trypsin chymotrypsin, carboxypeptidase, elastase
-Peptidases
--specifically found on inner surface or in intestinal wall in lumen
Diff b/t Peptidases and PDE's:
-Peptidases: polypeptides --> AA's
-PDE's: polypeptides --> smaller poly peptides |
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Term
| How are amino acid's absorbed? |
|
Definition
-absorption is dependent on active carriers
-Carriers can be specific for certain types of AAs w/o being specific for individual AAs
-heavy supplementation of one AA may result in artifical shortages
--argenine supplementation (can't take enough to increase performance, saturates argenine carrier blocking out other AAs making artificial shortages) |
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|
Term
|
Definition
-once in blood stream, AA are transported to target tissues.
-at least 7 or more different systems for transport
-carriers pull AA out of bl st into target cels across membrane
-carriers specific for specific AA
-whole process not well understand but new knowledge everyday
-we can enhanced transport into tissue in severaly ways |
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Term
| How is AA transport/uptake enhanced? |
|
Definition
-INSULIN (same as bringing glucose into target tissue)
-GROWTH HORMONE (stims transport into skeltal muscle)
-MUSCLE CONTRACTION (insunlin like action just like process w/ CHO)
--ex helps you build M tissue by getting AA into cell
-INCREASED BLOOD [AA]
--lots more AA transport into cell to certain extent |
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Term
|
Definition
STRUCTURAL/CARRIER
-AAs are incorporated into peptides via translation
--muscle protein
--globin
--carier proteins (lots of factors and hormones in blood stream can't travel w/out carriers)
HORMONAL/NEUROTRANSMITTERS/ENZYMES
-many are derived from amino acids
ENERGY
-amino acids can be utilizied to produce
--Pyruvate
--Acetyl CoA
--TCA intermediates
--glucose in liver |
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Term
| Tyrosine is transported what tissues utilizing ___________ |
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Definition
1) Adrenal Medulla (adrenal gland)
2) Nerve endings (dop, nor(epi))
3) Brain Stem (dop)
-transported via catecholamines
(nor)epinephrine act as both NT (found in nerves throughout the body) and as hormones (adrenal medulla) |
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Term
| T/F: AAs are a major source of energy during exercise. |
|
Definition
False.
-They are used sparingly to synthesize glucose, TCA cycle substrate and intermediates (CoA main substrate for TCA)
-use more pronounced as glucose/glycogen stores deplete
-easier for body to use carbs/fat for energy as protein process is very complicated (especially early in exercise)
-Diets can decrease muscle mass b/c body needs substrates for TCA and ETC via Muscle catabolism.
-In exercise or starvation glucose and glycogen decreases and body catabolizes protein. |
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Term
| 2 Catergories of AA used in energy metabolism: |
|
Definition
1) GLUCOGENIC
-used to synthesize pyruvate or TCA intermediates
2) KETOGENIC
-used to synthesize acetyl CoA |
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Term
| AA that can be both glucogenic and ketogenic |
|
Definition
-Threonine
-phenylalanine
-tyrosine
-tryptophan
-isoleucine |
|
|
Term
| Before AAs can be catabolized, what must happend? |
|
Definition
the amino group must be removed.
-no N w/ H attach found in energy substrates
-This is usually achieved through Transamination or deamination
-Once amino group is removed, the remaining carbon "skeleton" can be used to form a variety of molecules (pyruvate, acetyl CoA) |
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Term
| How does transamination acheive? |
|
Definition
-involves the transfer of amino gorup from an AA to a "Keto Acid". occurs primarily in liver.
-Basically shoves amino group around
-Alanine + alpha ketoglutarate <---> pyruvate + glutamate
-W/ Alanine, transamination forms pyruvate
-this is important step in "glucose-alanine cycle" that occurs in the liver and helps maintain glucose supply durin endurance exercise
Alanine transfers NH3 to AKG:
-alanine-->pyruvate
-AKG --> glutamate
-pyruvate --> CoA burnt in TCA or sent to liver to make glucose. |
|
|
Term
| How does Deamination work? |
|
Definition
-the removal of the amino gorup to amonia
-amino goes to blood stream or interstatial fluid
-The amino acid glutamine undergoes a double deamination to form alpha ketoglutarate, a tca cycle intermediate.
-AKG -> TCA -> NADH+H & FADH2 |
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|
Term
| How do we get rid of ammonia diffused in blood? |
|
Definition
the UREA Cycle (Liver)!!!
-NH3 group from deamination must be dealt with.
-Ammonia is combined with CO2, ran through Urea cycle, resulting in urea.
-Most of urea filtered by kidneys and excerted in urine.
What goes in: CO2 + NH3
What comes out: Urea |
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|
Term
| What does the Glucose/alanine cycle do? |
|
Definition
-During starvation or prolonged exercise glucose is produce in two ways:
1) via gluconeogenesis, alanine is produce/catabolized from the muscle and converted into glucose in the liver
2)Glucose is made from non glucose sources (AA), the primary source being alanine.
2 Sources of alanine from muscle:
1)break down of muscle tissue (primary)
-alanine is structural AA
2) Pyruvate (which is similar structurally to alanine) is reaminated to produce alanine.
-alanine spills into blood and is taken up by liver. Liver converts alanine into pyruvate which, via gluconeogenesis, is converted into glucose. This glucose is released into the blood stream where it is taken up by muscle. |
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|
Term
| How does the glucose/alanine cycle metabolize muscle ammonia? |
|
Definition
-ammonia is produced when AA are used as energy substrates
-Ammonia stimulates phosphofructokinase (which helps in glycolysis to make more pyruvate)
-too much amonia is toxic so by producing alanine from that pyruvate the cycle consumes ammonia and removes it from body.
--This is the advantage of this cycle
--but this doesn't happen as much
Majority of alanine is from protein catabolism not pyruvate |
|
|
Term
| The Glucose/Alanine cycle accomplishes 3 things: |
|
Definition
1) RIDS THE MUSCLE OF AMMONIA
-NH3 is toxic to muscle environment and can lead to kidney failure
2)ALLOWS FOR MAINTENANCE OF BLOOD GLUCOSE LEVELS
-If running out of CHO (hitting the wall) cycle helps maintain the glucose levels via the AA
3) PROVIDES SUBSTRATE FOR GLYCOLYSIS
-this goes with glucose maintenance
-more glucose helps maintain glycolysis
-you must maintain glycolysis to maintain HI exercise |
|
|
Term
| What are the branched chain amino acids and how are they useful? |
|
Definition
3 BC AAs:
1) Leucine (keto) --> acetyl CoA
2)ISOLEUCINE (keto & gluco) --> acetyl & succinyl CoA
3)VALINE (gluco) --> succinyl CoA
They are particularyly useful as energy substrates
-*are catabolized primarily in skeletal muscle
-don't require a lengthy "cycle"
-transamination often results in alanine
--combined w/ pyruvate to make alanine
-BC AA stay in M where they can be broken down in skeletal M into TCA intermediates, pyruvate, CoA w/out pathways
-Main advantage: they can be readily used |
|
|
Term
| Does BCAA suppplementation work? Reasons? |
|
Definition
Sorta but not as good as CHO.
BCAAs is less than CHO.
CHO + BCAA = CHO.
-True if consumed in HI Ex vs nothing at all (glycogen and CHO stores spared)
-BUT, CHO supplement during Ex does better @ conserving CHO body stores and increasing ex performance
-combined with CHO, the result was same as CHO above.
Excess Branched in body isn't stored (no proteins are stored) so they are either used as energy or oxidized. > |
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Term
| How are protein requirements figured out? |
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Definition
-determeined using "nitrogen balence" studies
-the amount of protein (nitrogen) consumed is stricktly controlled
-lost nitrogen is measured in:
--urine
--feces
--sweat
--sloughed cells |
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Term
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Definition
-when N consumed = N lost we are in balance (neutral)
- + N balance (excreting less than we are consuming) means we are retaining N (anabolism-building tissue)
- -N balance means we are excreting more N than we are consuming (catabolic)
--breaking down tissue
--lots of N in urine = not enough CHO to fuel muscle contractions and to help build tissue
--tissue breakdown resutls in urea production so more N in piss |
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Term
| How much protein is required to maintain proper N balance? |
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Definition
~ .5-.55 g/kg bm/day of complete protein (active non-athletic population)
my limit is 36.30 g of protein
.83 g/kg is current RDA
-includes margin of error and errs on side of over consumption |
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Term
| Which Athletes have the highest requirements? |
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Definition
Endurance! according to Tarnopolsky
-need 1.4-1.6 g/kg versus body builders who need 1-1.3 g/kg
-Endurance get glycogen depleted --> protein burning for energy
-this protein and glycogen must be replaced. |
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Term
| How much protein is too much? |
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Definition
-consumption in excess of 4g/kg is dangerous
*exceeds the ability to excrete the excess ammonia (toxicity) -> have to go on dialysis b/c of kidney shutdown
--deamination -> N & NH3
--too much P -> increased deamination -> increase nitrogen and ammonia groups
-some research sugges that excess protein intake lowers calcium levels --> mechanism not determined yet
-reduce protein absorption rates (stays in gut)
-diarrhea (due to low absorption)
-Consumption of single AA supplements w/ meals is not advised |
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