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Metabolism Final Exam

Terms in this set (100)

What are the differences between GLUT2 and GLUT4 in their tissue distribution and response to blood glucose and insulin?
GLUT2 - found primarily in liver - pancreatic beta cells
Has a low affinity for glucose and uptakes glucose into the cell during times of high blood glucose. The low affinity allows it to be strong indicator for high blood glucose and regulation of insulin secretion.
GLUT4 - found in adipocytes and skeletal muscle, cardiac muscle, is insulin-regulated glucose transporter
What is the end product of glycolysis in aerobic and anaerobic conditions, respectively?
Aerobic: Acetyl CoA
Anaerobic: Lactic Acid
What are the regulated steps in glycolysis? Which enzymes catalyze these steps?
Glucose ⇒ Glucose-6-phosphate (via glucokinase)
Fructose-6-phosphate ⇒ Fructose-1,6-bisphosphate (via phosphofructokinase)
Phosphophenyl pyruvate ⇒ Pyruvate (via pyruvate kinase
How are the steps in glycolysis regulated?
Glucokinase
Fructose and Glucose stimulate the dissociation of Glucokinase from GKRP where it then translocates from the nucleus to the cytosol; whereas fructose-6-kinase promotes the binding of GK to GKRP
Glucokinase and Glucose-6-Phosphatase substrate cycle: Insulin increases GK activity and decreases glucose-6-Phosphatase
Bifunctional Enzyme: Insulin increases the kinase activity of the bifunction enzyme which increases formation of fructose-2,6-bisphastate stimulating glycolysis and inhibiting gluconeogenesis. Glucagon and Epinephrine have the opposite effect
Pyruvate Kinase
Insulin and fructose 1, 6 - bisphosphate stimulates pyruvate kinase activity
Glucagon and alanine inhibit glucokinase activity
Which reaction does the pyruvate dehydrogenase (PDH) complex catalyze?
Pyruvate to Acetyl CoA
Where does the Pyruvate dehydrogenase take place in the cell? How is PDH activity regulated?
The mitochondria; Phosphorylation by Pyruvate dehydroginase kinase inactivates PDH
What are the functions of the TCA cycle in glucose oxidation?
The TCA cycle completes the oxidation cycle by taking the pyruvates generated through glycolysis (and other pathways) and completely breaking them down to CO2, H2O, and generating ATPs by oxidative phosphorylation.
Where does TCA occur?
In prokaryotic cells, the citric acid cycle occurs in the cytoplasm; in eukaryotic cells the citric acid cycle takes place in the matrix of the mitochondria.
How many ATPs are produced from glucose in aerobic and anaerobic conditions, respectively?
ATPs produced in aerobic conditions - 36-38
ATPs produced in anaerobic conditions - 2
In what physiological conditions (fed or fasted state) and in what tissues does gluconeogenesis occur?
Fasted state
liver (lactate and alanine) and kidney (lactate and glutamine)
Where does gluconeogenesis occur in the cell?
mitochondrion
What are the precursors for gluconeogenesis?
Lactate, alanine, glutamine, glycerol, propionate, oxaloacetate
Which steps in gluconeogenesis are regulated? Which enzymes catalyze these steps?
pyruvate --(pyruvate carboxylase and phosphoenolpyruvate carboxykinase)→ phosphoenolpyruvate
fructose 1,6-bisphosphate --(fructose 1,6-bisphosphatase)→ fructose 6-phosphate
glucose 6-phosphate --(glucose 6-phosphatase)→ glucose
How are the steps in gluconeogenesis regulated?
Fructose and Glucose stimulate the dissociation of Glucokinase from GKRP where it then translocates from the nucleus to the cytosol; whereas fructose-6-kinase promotes the binding of GK to GKRP
Glucokinase and Glucose-6-Phosphatase substrate cycle: Insulin increases GK activity and decreases glucose-6-Phosphatase
Bifunctional Enzyme: Insulin increases the kinase activity of the bifunction enzyme which increases formation of fructose-2,6-bisphastate stimulating glycolysis and inhibiting gluconeogenesis. Glucagon and Epinephrine have the opposite effect
Pyruvate carboxylase is positively regulated by acetyl-CoA and inhibited by ADP
PEPCK is the rate determining enzyme in gluconeogenesis which is not regulated by allosteric or covalent modifiers and only changed at the gene expression level
Phosphofructokinase is inhibited by ATP and citrate and activated by AMP, phosphofructokinase is the opposite
Pyruvate kinase is inhibited by alanine and ATP; Pyruvate
Which tissues are capable of releasing glucose to the circulation? What enzyme allows these tissues to do this?
Liver (mostly) and kidneys during prolonged starvation
Enzyme: glucose 6-phosphatase?
Role of Glycogenesis
process of glycogen synthesis, takes place during fed state as a way to store glucose
Role of glycogenolysis
process of breaking down glycogen, takes place during fasted state as a way to maintain blood glucose levels and bodily functions
In what physiological conditions (fed or fasted state) and in what tissues do glycogenesis and glycogenolysis occur? Where do they occur in the cell?
glycogenesis - fed; liver and muscle; Occurs in the cytosol
glycogenolysis - fasted; takes place in the liver and muscle (main tissue target of glucagon); Occurs in cytosol
What is the role of glycogen synthase and glycogen phosphorylase in glycogen metabolism? How are these enzymes regulated?
glycogen synthase → glycogen synthesis (converts glucose to glycogen). It is highly regulated by allosteric effectors such as glucose-6-phosphate, by phosphorylation reactions, and indirectly triggered by the hormone insulin.
glycogen phosphorylase → Glycogen phosphorylase catalyzes the rate-limiting step in glycogenolysis by releasing glucose-1-phosphate. Glycogen phosphorylase is regulated by both allosteric control (epinephrine, insulin and glucagon) and by phosphorylation (cAMP binds to and releases an active form of protein kinase A (PKA). Next, PKA phosphorylates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase b, transforming it into the active glycogen phosphorylase a).
What are the differences between glycogen metabolism in liver and muscle?
Glycogen is used on-site for muscles (no exported, because muscle has no glucose 6-phosphatase)
In what physiological conditions (fed or fasted state) and in what tissues does fatty acid and TAG synthesis occur?
Fed state, occurs primarily in liver and adipose tissue
Where does fatty acid and TAG synthesis occur in the cell?
cytosol
What are the precursors of fatty acid synthesis and TAG synthesis?
Precursors: glucose, pyruvate, lactate, acetyl-CoA
Starting molecule: acetyl-CoA
End product: palmitate (C16 saturated fatty acid)
Describe the key reaction in lipogenesis that converts acetyl CoA to malonyl CoA. What is the substrate, product, enzyme and vitamin involved, and other requirements in this reaction? (key enzyme: ACC- acetyl CoA carboxylase)
Acetyl-CoA carboxylase (ACC): initial and controlling step
Multi-enzyme protein: biotin carboxylase, biotin carboxyl carrier protein, transcarboxylase
Three enzymes together form ACC
Two steps of reaction: 1) carboxylation of biotin 2) transfer of carboxyl group
Other Requirements: bicarbonate, NADPH, Mn2+, ATP
Describe the substrate, products, and key enzymes involved in making a fatty acid (e.g., palmitate).
Starting Material: Acetyl-CoA, NADPH, ATP, Mn2+, Biotin, HCO3
End product: Palmitate
Enzymes Acetyl-CoA Carboxylase and Fatty acid sinthase complex
How many acetyl CoA molecules are needed to synthesize palmitate (16-carbons)? How many malonyl CoA? How many NADPH?
How many acetyl-CoA molecules are needed to synthesize palmitate? 1 molecule
How many malonyl-CoAs? 7 molecules
How many NADPHs? 14 molecules
What is the most important step of lipogenic regulation? How is lipogenesis regulated allosterically? Covalently? Be sure to know which hormones up & down regulate this pathway (insulin, glucagon and catecholomines).
Acetyl-CoA ==> Malonyl CoA via acetyl CoA carboxylase

1) Activators: High carb diet, insulin; Inhibitors: glucogon, caloric restriction, high fat diet
2) Allosteric: Citrate stimulates and also important for transporting acetyl CoA to cytosol; Long chain acyl-CoA inhibts
3) Covalent: Insulin activates, glucagon inhibits
4) Gene transcription: Insulin and glucose increase ACC Gene expression whereas glucagon and cAMP decrease it
How are most fatty acids stored in the body, under what conditions? Where are they stored in the body?
TAGs which are stored in adipose tissue only
Where do fatty acids present in the circulation come from (i.e. what are the sources of fatty acids)?
1) Diet via chylomicrons
2) Body stores via the FFA pool (adipose tissue in fasting stage)
3) De novo lipogenesis (mainly occurs in the liver)
Where are TAGs synthesized?
Major site: liver and adipose tissue mainly; many other tissues - In the cell: ER facing the cytosol ( May need to know more description of the process)
How are TAGs transported outside of tissues that it's synthesized in?
TAGs from the diet are packaged in lipoproteins, then secreted into blood as VLDL; TAGs from diet are packed into chylomicrons in the small intestines.
How is LPL regulated in the adipose and muscle in the fed state? In the fasted state or during exercise?
Fed State LPL is increased in adipose tissue so it can release TAGs from VLDL and store them. In fasting state LPL is increased in the muscle so it be used for energy
What happens to the fatty acids formed from LPL activity in the adipose? What about in the muscle?
1) n adipose tissue, fatty acids formed from LPL activity will be reesterified to TAGs and stored in lipid doplets
2) In muscle, fatty acids will be oxidized for energy
In what physiological conditions (fed or fasted state) and in what tissues does lipolysis occur?
Fasted, occurs in adipose tissue (lipolysis) and liver and muscle tissues (FA oxidation)
Does (aerobic) exercise stimulate lipolysis? What hormones play a role in this process?
Yes, Epinephrine?
Does a low carbohydrate diet induce lipolysis?
Yes.
What enzyme is the key enzyme for lipolysis or hydrolysis of TAG?
HSL - hormone sensitive lipase
How is lipolysis regulated by hormones (insulin, glucagons, and catecholomines)? (hint: how these hormones regulate HSL activity)
Epinephrine, catecholamines, and glucagon; inhibited by insulin
What is the difference between HSL and LPL?
1) LPL is activated by insulin; breakdown chylomicron/VLDL and involves in uptake of triglyceride into adipose tissues (Chylomicron becomes remnant and VLDL becomes IDL).
2) HSL is deactivated by insulin; breaks down triglycerides into fatty acids and glycerol during fasting under influence of increase epinephrine/cortisol or decrease insulin.
In what physiological conditions (fed or fasted state) and in what tissues does fatty acid oxidation increase? Where does fatty acid oxidation occur in the cell?
Fasted state
Fatty acid oxidation increase in adipose tissues
FA oxidation occurs in the mitochondrion
How is fatty acyl CoA transported into the mitochondria? Which enzymes are involved in this process? (Hint: CPT-1 is the key enzyme for this process)
1) CPT-1 converts acyl-CoA to acyl carnitine
2) Carnitine acylcarnitine translocase brings it into the mitochondrial membranes
3) CPT-2 converts it back to Acyl-CoA
How does malonyl CoA regulate CPT-1?
Inhibits
What is the end product of fatty acid oxidation?
Acetyl CoA is the end product of FA oxidation
Yield: 35 ATPs + 96 ATPs = 131 ATPS
Use: 2 ATPs
Net Yield: 129 ATPs
How many ATP does glycolysis/TCA cycle yield? 36-38 ATPs
Take home message: more carbons, more energy
Are odd chain fatty acids glucogenic?
Yes, odd-chain fatty acids can be oxidized to yield propionyl CoA, a precursor for succinyl CoA, which can be converted to pyruvate and enter into gluconeogenesis
In what physiological conditions (fed or fasted state) and in what tissues does ketone body synthesis occur?
Ketone body synthesis occurs in the fasted state, in the liver
Ketones are produced from what metabolic substrate? How was this substrate produced?
Ketones are produced from Acetyl CoA which is formed from glucose metabolism, fatty acid and Amino acid degradation
What is the principal driver of ketone body synthesis? Or what are the key regulators in ketone body synthesis?
Regulation: 1) increased lipolysis increases free fatty acids which increases ketone bodies 2) CPT-1 transportation of fatty acids into mitochondria for oxidation 3) Increase in acetyl CoA results in increased Ketone bodies
Can the liver utilize ketone bodies? Why or why not?
Succinyl CoA transferase is not present in the liver, so the liver can not utilize ketone bodies for energy.
What are the 4 major groups of lipoproteins? Which apoprotein is associated with each of these?
Chylomicron (largest; lowest in density due to high lipid/protein rate; highest % weight triacylglycerols), TG rich; Apo B-48
VLDL (very low density lipoprotein; 2nd highest in triacylgercols as % of weight), TG rich; Apo B-100
LDL (low density lipoprotein, highest in cholesteryl esters as % of weight) - most abundant in plasma, Cholesterol rich; Apo B-100
HDL (high density lipoprotein; highest in density due to high protein/lipid ratio) - most abundant in plasma, Cholesterol rich; Apo A-I, Apo A-II
What is the major lipid component of chylomicrons? VLDL? LDL? HDL?
Chylomicrons and VLDL: TG rich
LDL and HDL: cholesterol rich
Where are chylomicrons synthesized? What is the function of chylomicrons?
Chylomicrons are synthesized in the small intestine (enterocytes) with the function of transporting TGs from diet to liver.
What is the function of VLDL?
The liver makes VLDL to transport TGs throughout the body
Describe the process of making VLDL in the liver.
TAGs come from de novo synthesis from dietary carbs, FAs from lipoprotein remnants, and free fatty acids
What is the main function of HDL or HDL cycle?
Reverse cholesterol transport: transport chol. from peripheral tissue back to the liver, accomplished by HDL cycle
What can increase the free cholesterol pool in the cell?
1) increase uptake
2) increase synthesis
3) hydrolysis of CE increase
What is the role of adipose tissue LPL in lipoprotein metabolism?
LPL catalyzes hydrolysis of TAGs to FFA and glycerol
what happens to plasma TG levels if LPL activity is decreased?
Plasma TG levels increase if LPL activity is decreased?
What are the sources of metabolic fuels in the fed and fasted states? Where do endogenous fuels come from or which tissues contribute to endogenous fuels?
Fed: Glucose from diet
Fasted: Glycogen, triglyceride, gluconeogenesis
Endogenous fuels come from adipose tissue and muscle catabolism during the fasted state
What is the main metabolic fuel for the body in the fed state and fasted state, respectively?
Fed: Glucose
Fasted: Glycogen, triglyceride, gluconeogenesis
What are the two substrates for gluconeogenesis that come from fat metabolism? Where do these two substrates come from?
1) Glycerol (converted to glycerol-3-phosphate by glycerol kinase, then reduced to glyceraldehyde-3-phosphate by glycerol-3-phosphate dehydrogenase. 2) Propionyl CoA that comes from odd chain fatty acids. Converted to succinyl CoA
What is the brain's major metabolic fuel in the fed and fasted state?
Fed: glucose
Fasted: ketone bodies
Starvation: Lactate
What is the major metabolic fuel for skeletal muscle in the fed state? How about the fasting state?
Fed: Glucose
Fasted: Fatty Acids is preffered. Muscle can also utilize ketone bodies and amino acids
How does the muscle indirectly contribute to gluconeogenesis? What is the role of Cori or Alanine cycle? Describe the process of these two cycles.
Cori Cycle: Lactate produced from muscle and red blood cells are transported to the liver and conduct gluconeogenesis.
Alanine Cycle: Alanine is derived from transamination of pyruvate, where it is then released into circulation and brought to the liver. Next it is daminated to attain pyruvate again where it conducts in gluconeogenesis
What is the liver's preferred fuel? How are fuels metabolized in the liver? (
Preferred fuel is alpha-ketoacids orginating from amino acid metabolism
In fed state blood glucose is taken up for glycogen synthesis, de novo lipogenesis, Pentose Phosphate pathway, and storage of glycogen and triglycerides. Triglycerides are released in the fed state
In fasted state, liver is the main source of endogenous energy fuels from glycogen breakdown, gluconeogenesis and ketone body synthesis. The liver uses Amino Acids, fatty acids and glucose as fuel
What is the small intestine's preferred fuel? How about the colon?
Small intestine's preferred fuel is glutamine.
Colon's preferred and the majority of fuel is short chain fatty acids which are produced during fermentation of dietary fiber and resistant starch by microflora.
What are the four main branch points or substrates? Be able to link branch points to the different metabolic pathways.
1) Glucose-6-phosphate
Pathways that generate: Glycolysis, glycogenolysis, gluconeogenesis
Pathways that use: Glycogenesis, glycolysis, Pentose phosphate pathway
2)Pyruvate: Derived from glucose, lactate, alanine, and other gluconeogenic molecules
Can be converted to lactate, alanine, acetyl CoA or oxaloacetate
3) Acetyl CoA: Derived from glucose, fat and protein oxidation
Can be used in synthesis of ketone bodies, fatty acids or cholesterol
Can enter the TCA cycle for energy production
4) Succinyl CoA: TCA cycle intermediate from propionyl CoA from BCAA oxidation and odd chain fatty acid oxidation
Involved in TCA cycle and anaplerosis/cataplerosis
hat is the primary role of the adipose tissue? What are the two adipose tissue-derived hormones
Role: To store and release fatty acids
Hormones:
Leptin: Central target is Hypothalamus to suppress appetite and peripheral target is muscle and other tissues to stimulate fat oxidation and increase energy expenditure. Leptin is regulated by: fasting reduces leptin gene expression; feeding induces gene expression; and insulin increases gene expression
Adiponectin: Main targets are muscle and liver and its role is to stimulate fat oxidation and increase energy expenditure. Fasting decreases and insulin increases. Regulation: Same as for leptin, except in type 2 diabetes and insulin resistance, plasma adiponectin levels are decreased
In the fed state, which enzyme produced by adipose tissue hydrolyzes circulating TAGs?
Lipoprotein Lipase
In the fasted state, which enzyme breaks down TAGs into monoacylglycerol and 2 fatty acids in the cell?
Hormone-sensitive lipase - activated by epinephrine
Where is leptin secreted? What are the main tissue targets and role of leptin in fat metabolism?
Secreted from adipose tissue
Central target is the hypothalamus which will suppress appetite. Peripheral target is muscle which stimulates fat oxidation and increases energy expenditure
What is the role of AMPK? What happens to ACC activity, malonyl-CoA levels, fatty acid oxidation, and glucose uptake in muscle if AMPK activity is increased? How is AMPK activity regulated? (Which hormones activate AMPK, in what physiological conditions?)
Role: AMP activated protein kinase. Causes increase in fat oxidation.
ACC activity: phosphorylated and inactivated
Malonyl-CoA Activity: Decreases because ACC is inhibited
Fatty Acid Oxidation: Increases
Glucose Uptake in the muscle : Increases
Regulation: Activated by starvation, glucose deprivation, hypoxia, ischaemia, exercise and muscle contraction, increases in cellular cAMP levels
Activation: Activated by leptin and adiponectin action
How does a switch in fuel utilization happen during the fasting or starvation? (Be able to understand the changes in glucose utilization from 3- 4 hours after a meal to days of starvation). When does the body start to utilize fatty acids and ketone bodies?
Randle cycle is how the body switches fuels during starvation. The body knows when to switch fuels by via hormones, substrates, enzymes and transporters.
When does kidney become an important source of glucose?
Prolonged starvation
Why glucose is partially oxidized in most of glycolytic tissues in the fasting? Why is it important?
This allows glucose to be conserved by producing lactate that will be transported to liver (Cori Cycle) and converted back to glucose via gluconeogenesis
What is the Randle cycle (glucose-fatty acid cycle)?
Randle Cycle is how the body switches metabolic fuels during starvation; It is a metabolic process involving the competition of glucose and fatty acids for substrate utilization in starvation and type 2 diabetes and insulin resistance
How does glucose utilization inhibit fatty acid utilization/oxidation? How does fatty acid utilization/oxidation inhibit glucose utilization or spare glucose? (
Fasting: decreased blood glucose ⇒ decreased insulin and increased glucagon ⇒ increased mobilization of fatty acids from adipose tissue ⇒ increased utilization of free fatty acids ⇒ decreased glucose utilization
Fed: Increased blood glucose ⇒ increased insulin and decreased glucagon ⇒ suppressed mobilization of fatty acids from adipose tissue ⇒ decreased utilization of free fatty acids ⇒ increased glucose utilization
AMPK activation is an exception however and it stimulates both glucose and fatty acid oxidation
What are the major gluconeogenic substrates in the fasting?
Amino Acids
What happens to plasma concentrations of ketone bodies with prolonged starvation?
They increase exponentially, and are the main fuel
Know the differences in metabolic properties between different types of muscle fibers (mitochondria content, oxidative capacity, glycolic capacity, aerobic and anaerobic system for ATP production, resistance to fatigue)
1) Type 1 Red Fibers: high mitochondrial density, high oxidative capacity (red from hemoglobin), low glycolytic capacity, aerobic system ATP production, high resistance to fatigue
2) Type 2A Red Fibers: Intermediate mitochondrial density, high oxidative capacity (Red from hemoglobin), high glycolytic capacity, Aerobic system, intermediate resistance to fatigue
3) Type 2X White Fibers: low mitochondrial content, low oxidative capacity (white = low hemoglobin), high glycolytic capacity, Anerobic system, Low resistance to fatigue.
Know the differences between aerobic and anaerobic metabolism including the requirement of O2, and the involvement of mitochondria and metabolic pathways.
Aerobic: Moderate intensity, undertaken for a long duration, Use oxygen in a muscle's energy-generating process i.e. Marthon
Anaerobic: High intensity and short term; Oxygen cannot be transported quickly enough to skeletal muscle i.e. sprinting
How is exercise intensity defined and measured?
Intensity is measured by O2 consumption (% VO2 Max)
Low intensity (fast walk): 25 % VO2 max
Moderate-intensity (fast jog): 60 % VO2 Max
High Intensity (2 hr marathon): 80 % VO2 max
How are hormone levels (insulin, glucagon, and catecholamines) changed during exercise? How do the changes of hormone levels contribute to the availability of fuels during exercise?
Insulin Decreases: Increased lipid oxidation; decreased insulin stimulates HSL activity, which hydrolizes IMTGs and releases fatty acids within muscle cells
Glucagon Increases: increases gluconeogenesis and glycogen breakdown
Catecholamines increase: Increases lipolysis and use of IMTGs; Epinephrine stimulates HSL activity in adipose tissue; increases blood flow to muscles which increase delivery of fatty acids to muscle
What is RQ? What do different values of RQ represent? What does it mean to have an RQ of 0.70, or 1.0?
Respiratory Quotient: A way to evaluate the metabolic mixture in exercise from measures of gas exchange in the lungs
0.70 = 100 % fat oxidation
1.0 = 100 % carbohydrate oxidation
What drives lactate production during exercise?
1)Produced during anaerobic exercise and in prolonged endurance exercise when Type 2x muscle fibers are recruited to keep the same intensity
2) Produced in type 2X muscle fibers because of low oxidative capacity
3) Produced by glycolysis of glucose
What are the sources of energy fuels during aerobic exercise?
Carbohydrates and Fat
What are the sources of energy fuels during anaerobic exercise?
Creatine phosphate and carbohydrates
Where does glucose come from during aerobic exercise? How is glucose metabolized during aerobic exercise?
Comes from muscle glycogen, blood glucose uptake by GLUT 4, liver glycogen,
Complete oxidation in TCA cycle
Where does glucose come from during anaerobic exercise?
Glucose metabolized to lactate because of lack of oxygen
glucose comes from muscle glycogen and glucose uptake by the muscles
Where do fatty acids come from during aerobic exercise? How are fatty acids metabolized during aerobic exercise?
Adipose tissue and Muscle stores
Fatty acids are released by HSL which are stimulated by increased epinephrine and decreased insulin levels
Can fatty acids be used for energy during anaerobic exercise? Why or why not?
No, because it requires oxygen to be metabolized
How is creatine used for ATP synthesis during anaerobic exercise?
Creatine phosphate + ADP + H+ ⇐⇒ Creatine + ATP (enzyme: Creatine Kinase)
Does muscle use fat under anaerobic conditions?
No.
What are the determinants of fat oxidation during aerobic exercise? Or how muscle glycogen stores influence fat utilization during aerobic exercise?
High stores uses less fat
Low stores uses more fat
Why fat oxidation is increased from rest to moderate intensity exercise, but decreased in high intensity exercise?
1) Rest to moderate Activity:
epinephrine concentration increased
Insulin concentration decreased due to a fall in blood glucose
HSL activity in muscle and adipose increased in adipose by increased epinephrine and decreased insulin
Blood flow to skeletal muscle is increased, which further increase delivery of fatty acids to muscle
2)Moderate to high intensity activity:
As oxidation of carbohydrate and fat increased, more acetyl-CoA molecules are generated
Increased conversion of acetyl-CoA to Malonyl-CoA
Increased malonyl-CoA levels inhibit CPT-1 activity
Reduced transport of fatty acids into mitochondria
Decreased fatty acid oxidation
What is the major fuel that the body uses during the postexercise recovery period?
Fat
What are the metabolic processes that precede the citric acid cycle in fat oxidation?
Beta oxidation, FA oxidation
What are the benefits of endurance training? How does the skeletal muscle adapt to endurance training?
1)Constant use of a fuel mixture allowing less pronounced switch of fuel utilization during a race
2)Lactate releases is reduced during first hour of endurance
3)Higher fat utilization capacity
4)Increased Cardiac ouput
5)increased gas exchange in the lungs
6)increased capillary density in skeletal muscle
7)increased mitochondria numbers per unit mass of muscle
8)increased reliance on fat utilization
9)decreased reliance on carbohydrate utilization
10)Increased muscle glycogen
What type of diet would be most effective to restore glycogen in muscle after strenuous exercise?
High Carbohydrate
Creatine supplementation seems to be useful for what type of exercise?
Anaerobic
What is glycemic index? What is glycemic load? How are they used for the evaluation of glycemic effect of foods?
Glycemic Index is a ranking system for carbohydrates based on their immediate effect on blood glucose levels. GI is a percentage value representing the area under the blood glucose response curve. Used by area under the curve of test food divided by area under the curve of the standard food times 100
Glycemic Load: glycemic index divided by 100 multiplied by available carbohydrate content i.e carbohydrates - fiber in grams
Glycemic index is going to tell you blood glucose immediate response to a food while glycemic load will tell you how rapidly a particular carbohydrate turns into glucose in blood

Classifications: Low GI: 55 or less; medium 56-69; high: 70 or more
Low GL: 10 or less; 11-19; 20 or more
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