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69 Cards in this Set

  • Front
  • Back
Mg2+ deficiency
Impairs virtually all metabolisms b/c ATP can neither be made nor utilized in adequete amounts
Muscle Work/Mechanical Work
Myosin head engaes with actin at multiple sites
Myosin head has an ATP binding site and is an ATPase
ATP binds to myosin disociates with actin and hydrolyzes
Myosin binds Ca2+ and reassociates with actin in new position
Anabolic Reactions
Synthesis of DNA and metabolites
Biosynthesis
Active Transport
Delivery of nutrients and building blocks
Heat Production
Maintance of a constant body temperature
ATP Production
Oxidation of fuels (proteins, cho, fats) to CO2
Fuels are highly reduced
e- lost during oxidation go into formaiton of ATP
ATP
High energy phosphate bonds
Release of 1st bond Gamma (7.3) - ADP
Release of 2nd bond Beta (6.6) AMP
Release of energy
Is coupled to other biological processes
Hydrolysis - ATP + H2O > ADP + pi
Synthesis - ADP + Pi > ATP + H2O
Acetyl CoA
Thioester bond
Intermediate between glycolysis and TCA
Pyruvate is converted into Acetyl CoA
Creatine Phosphate
High energy phosphate bond
Stored in muscle
Order of energy use in muscle
Creatine Phosphate - ATP stored in muscle - Glycogen
Summary of how work is fueled
Body work fueled by synthesis of ATP - Coupled to body's energy need's - coupled to food metabolism
Catabolism
Breakdown
Produce energy
Gothrough Oxidation
Oxidative Phosphorylation
Most efficient ATP production
Oxygen reduced to water
Phosphorylate ADP to make ATP
Mitochondria
ATP factory
Outer Membrane - permeadble to anions and small molecules
Inner - impereable to almost evrything; houses the ETC and ATP synthesis
Electron Transport Chain
Provides energy for proton pumping
Accepts electrons from NADH FADH2
O2 is ultimate e- acceptor convrted to water - ATP synthesized
Muscle Work/Mechanical Work
Myosin head engaes with actin at multiple sites
Myosin head has an ATP binding site and is an ATPase
ATP binds to myosin disociates with actin and hydrolyzes
Myosin binds Ca2+ and reassociates with actin in new position
Anabolic Reactions
Synthesis of DNA and metabolites
Biosynthesis
Active Transport
Delivery of nutrients and building blocks
Heat Production
Maintance of a constant body temperature
ATP Production
Oxidation of fuels (proteins, cho, fats) to CO2
Fuels are highly reduced
e- lost during oxidation go into formaiton of ATP
ATP
High energy phosphate bonds
Release of 1st bond Gamma (7.3) - ADP
Release of 2nd bond Beta (6.6) AMP
Release of energy
Is coupled to other biological processes
Hydrolysis - ATP + H2O > ADP + pi
Synthesis - ADP + Pi > ATP + H2O
Acetyl CoA
Thioester bond
Intermediate between glycolysis and TCA
Pyruvate is converted into Acetyl CoA
Creatine Phosphate
High energy phosphate bond
Stored in muscle
Order of energy use in muscle
Creatine Phosphate - ATP stored in muscle - Glycogen
Summary of how work is fueled
Body work fueled by synthesis of ATP - Coupled to body's energy need's - coupled to food metabolism
Catabolism
Breakdown
Produce energy
Gothrough Oxidation
Oxidative Phosphorylation
Most efficient ATP production
Oxygen reduced to water
Phosphorylate ADP to make ATP
Mitochondria
ATP factory
Outer Membrane - permeadble to anions and small molecules
Inner - impereable to almost evrything; houses the ETC and ATP synthesis
Electron Transport Chain
Provides energy for proton pumping
Accepts electrons from NADH FADH2
O2 is ultimate e- acceptor convrted to water - ATP synthesized
Electro Chemical Gradient
Produced by pumping H+ across the inner mitchondiral membrane
Reducing Equivalents
Fuel Oxidative Phosphorylation
Supplied by: Most TCA, then B-Oxidation, then Glycolysis which also upplies some ATP and Drives
ATP synthesis
Interconversion of energy from:
Oxidation/reduction (chemical) to
electro-chemical gradient (potential) which drives the phosphrylation of ADP which makes the high energy bond of ATP
Fuels that produce reducing equivalents
CHO, FA, AA
All produce some ATP and generate reducing equivalents (NADH, FADH2, NADPH)
How are the fuels reduced?
All are highly reduced and oxidized during metabolism
Glucose - Glycolysis
Fatty Acids - B-Oxidation
AA - TCA cycle
O2 is reduced to water
Energy Yeilds and Storage
Fat: 9 & 70
CHO: 4 & 1
Protein: 4 & 10
More in fat b/c hydrophobic and do not have to break water bonds
Energy Reserves (Stored Fuels)
MAIN storage Glycogen: Liver and Muscle by Glycogenolysis
Glucose: Body fluids
Proteins: Muscle for Gluconeogenesis
Fat: Adipose tissue mobilized as KB's
Fat
Stored as Triglycerides
Go to FA's and Glycerol
Most effeicient b/c w/o water
Main energy source
Carbohydrates
Supply largest part of dietary calories
Stored as Glycogen
Cannot exist in body w/o water
Proteins
"Last Resort" energy fuel
Degrade to AA
No specific storage protein
All proteins have a specific function
Usually stored with water
Calculate Calories for BMR
Weight (kg) X 24 kcal/kg/day

LOOK AT OTHER FORMULAS Page 9 Part 1
Requirements for Brain
Glucose used exclusively but KB are first priority just not around much except during fasting
Fatty Acids NOT used
Driving force for Energy Metabolism
20% REE
Requirements for Muscle
Fatty Acids - first priority
KB's - Used when no FA available
Glucose - Used only if no FA or KB avialable
80% REE
Has significant CHO (glycogen) reserve
Will provide brain w/fuel
RBC's
ONLY Glucose
Not oxidized - no mitochondria
Liver
Maintainer "Mother of all"
Regulates blood glucose and KB for brain
Regulates level of Glucose by storing it as Glycogen
Provides KB when glucose low
Converts glucose to fat when excess
Detoxifies drugs
Adipose Tissue
Maintainer Organ
Stores fat from blood Triglycerides
Releases fat as Free Fatty Acids
Kidney
Excretory Organ
Use ATP to secrete waste
Excretes non-volatile waste (H+ Urea, Nitrogen Ammonia)
Lungs
Excretory Organ
Excrete Volitile Waste: CO2
Role of Insulin
Promote Biosynthetic and Anablic Rxn
Counteracted by: Glucagon, epinephrine, cortisol, thyroid hormone
ccelerate the transport of glucose into muscle and synthesis of triglycerides
Inhibits glycogen breakdown in liver and triacylglycerol breakdown
Promotes synthesis of glycogen
Role of Glucagon
Promotes glycogen breakdown and glucose release in liver
Role of Epinephrine
Promotes glycogen breakdwon and glucose release in liver AND MUSCLE
Role of Thyroid Hormone
Controls BMR
Hypo- (underactive) slow metabolism
Hyper- (overactive) rapid metabolism
Effect on Na+/K+ - ATPase
Chylomicrons
Absorbed lipids are contained in this so they are miscible with blood
Fed State
Increase Blood Glucose which increases Insulin (Beta Cells_
Decreases Glucagon (Alpha Cells)
Fasted State
Decrease Blood Glucose which decrease Insulin (Beta)
Increase Glucagon (Alpha)
Liver not useing glucose instead supplying to blood
Gluconeogenesis: 65-70%
FA Breakdown: 25-35%
Prolonged Fasting
KB blood conc. increase alot
KB exclusive for Brain
Muscle Stop using KB use FA
Decrease Glucoes & Insulin
Increased Glucagon
Decrease in Urea production
Metabolic Changes in Prolonged Fasting in Muscle, Liver, and Brain
Muscle: Decrese Utilization of KB and Protein Degradation
Brain: Increase utilization of KB (exclusively)
Liver: Decrease Gluconeogenesis & Urea Production (b/c of decreased muscle protein breakdown)
Metabolic Capacity of Liver
Everything
Except KB utilization
Metabolic Capacity of Adipose
Cannot do B-Oxidation, Form KB, or Gluconeogenesis
Metabolic Capacity for Muscle
Does Not for KB, FA, or Glucose
Metabolic Capacity of Brain and RBC
Brain limited: TCA cyce, KB use
RBC does nothing but perform glycolysis for energy needs Lactae formed
Endergonic Rxn
Energy requiring rxn
Non-Spontaneous
Positive Delta G
Disfavored Rxn
Exergonic Rxn
Energy releasing rxn
Spontaneous
Negative Delta G
Favored Rxn
Gibbs Free Energy (DeltaG)
Change in free energy
Energy availble to do work where surroundings vary
Determine direction of a rxn
Standard Free Change (Delta G Not)
Measured in laboratory at pH 7 and 1M
Concentrations of substrates and products (Keq)
aA + bB > cC + dD
Keq = [C][D]/[A][B] or [Products]/[Reactants]

Keq > 1, Delta G Negative (More products formed)
keq < 1 Delta G Positive (Not much prodcut formed)
Speed of a Rxn
Depends onthe properties of the enzyme that catalyzes the rxn
Enzyme DOES NOT affect the Keq
Efficiency of Fuel Oxidation
Glucose Combustion
68% ATP Production through Glycolysis > TCA > ETS
32% Heat production which maintains Body Temp and drives rxns forward