KIN 310 Exam 1 Review Guide
KIN 310 Exam 1 Review Guide KIN 310
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This 11 page Study Guide was uploaded by Alina Levy on Wednesday December 9, 2015. The Study Guide belongs to KIN 310 at Michigan State University taught by in Fall 2014. Since its upload, it has received 30 views. For similar materials see Physiology Basis of Conditioning in Kinesiology at Michigan State University.
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Date Created: 12/09/15
Bioenergenics Lecture 2 Pt 1 What s the energy source in the Human Body Food chemical energy 9 digestion 9 ATP chemical energy 9 Move kinetic energy Heat Energy is neither created nor destroyed The body Transforms energy from one form to another ATP are formed in the cytoplasm Energy is stored in the bonds of ATP molecules ATP 9 ADP P Energy 9 ATPace Breaking the outermost bonds contain the most energy 80 100 g about 3 oz ofATP resting skeletal muscle ATP 9 ADP Pi Energy catalyzed by ATPasel PCr ADP 9 ATP Cr catalyzed by Creatine Kinase CK Most abundant and most active enzyme in skeletal muscle Three processes pathways to replenish ATP stores 1 000 ATP PCr SYSTEM Immediate energy system 0 Sustains exercise for 3 15 seconds 0 Adenosine triphosphate ATP 0 Phosphocreatine PCr stored in cytosol FAST GLYCOLYSIS Shortterm energy system Substrate Carbs 0 Sustains exercise for 30 seconds 2 minutes SLOW GLYCOLYSISAEROBIC Longterm energy system Substrate Carbs and fats 0 Sustains exercise for 2 minutes At rest the body primarily uses FAT for ATP production ie energy During shortduration exercise the body primarily uses Carbohydrates for ATP production During longerduration exercise the body uses Combination of Carbs and Fats for ATP production ie energy longer than 10 minutes to use fat for energy Percent capacity of energy systems 1 00 o Shortterm energy system glycolysls 1 Longterm energy system aerobic Immediat e 2 3339 1 l l 10 30 2 5 min Exercise duration The 3 major macronutrients we eat are 0 Fats 0 Carbohydrates 0 Proteins 0 We will refer to these as substrates 0 Substrates something an enzyme acts on something which is broken down Carbohydrates Break down to glucose which is stored as glycogen in the livermuscles FAT Triglyceride Glycerol molecule has 3 fatty acids attached to it When the fatty acids are broken off it produces energy Protein 1 g protein provides 41 calories of energy Proteins rarely contribute to energy unless an extreme state CHO glycogen TABLE 21 Body Stores of Fuels and Energy Glucose6phosphate M Carbohydrates Glycolysis J Liver glycogen 110 451 Muscle glycogen 500 2050 Pyrwic acid Glucose in body fluids 15 62 Fat Acety 30A Subcutaneous and visceral 7800 73320 Intramuscular 161 1513 Total 7961 74833 Note These estimates are based on a body weight of 65 kg 143 l with 12 body fat LONG TERM ENERGY SYSTEM SHUTTLES AND ATP ACCOUNTING Lecture 3 Pt 1 ATP L CO2 1 molecule of GLUCOSE I ATP ADP Glucose 6 Phosphate Fructose 6 phosphate ATP 9 ADP Fructose 1 3 diphosphate DHAP Phosphoglyceraldehyde Phosphoglyceraldehyde 15 Diphosphoglycerate 13 Diphosphoglycerate m 02 A H A Hd H A H20 e39d ed e gt Electron transport chain Metabolism Lecture 4 pt 1 Where is fat stored Adiposytes What is the storage form of fat Triglyceride TG Triglyceride 1 glycerol 3 fatty acids 5 steps of Fat Metabolism MTATO Mobilization Iransport Cellular Uptake 0 Activation Translocation Qxidation Step 1 Mobilization 4 hormones can bind to a fat cell and stimulate it to mobilize a TG Epinephrine Norepinephrine Cortisol Growth Hormone 9 all act to increase the activity of HSL Hormone Sensitive Lipase HSL Enzyme Step 2 Transportation FFA s are carried in the blood by albumin 0 Most abundant of our plasma proteins 60 o Produced in the liver 0 When it gets to the muscle albumin will release into the muscle where it is used for Uptake Pulling fatty acids out of the blood and into the muscle Regulated by SFABP Sarcolemmal Fatty Acid Binding Protein Muscle cells take up 50 of Free Fatty Acid in the circulation Total amount of fat taken up increases during exercise Step 3 Activation 0 Activation takes place in the cytosol Activation involves the conversion of a FFA into a molecule of Fatty AcylCoA Process requires the use of one ATP Step 4 Translocation Fat is transported from cytosol into mitochondria Enzyme carnitine transferase catalyses the translocation FattyAcyl CoA is now inside the mitochondria Step 5 Beta Oxidation Cut up the FattyAcyl CoA into 2 carbonmolecules acetyl CoA Acetyl CoA can then go through Krebs cycle NAD amp FAD go to the Electron Transport Chain Every Beta Oxidation cuts 2 carbons off the end 0 1 X Acl CoA o 1 X NADH H o 1 X FAD Activation 1 ATP per Fatty Acid Chain Cycles Spins per 1 Fatty Acid Chain of carbons f39 1 FAD NAD from 1 Beta Oxidation spin 0 1 FAD 1 NAD per spin 5 ATP Acetyl CoA per Fatty Acid Chain 1 Acetyl 12 ATP of carbons 2 1 Triglyceride 3 Fatty Acid Chains 0 Multiply by 3 for a triglyceride ATP Total FAST GLYCOLYSIS ATP COL39NT Glucose ATP COUNT Glycogg 0 ATP Glucose Glycogen l ATP Mm Phosphorylasc 1 ADP Glucose 6 Phosphate 0 1 Fructose6 Phosphate 0 ATP ADP Phosphofructokinasc Rate Limiting 2 F ructose 16 Diphosphate 1 2 Phosphoglyceraldehyde DHAP 1 I I NAD Phosphoglyceraldehyde 2 NADH Dehydrogenase NAD Phosphoglyceraldehyde 1 NADH Phosphoglyceraldehyde DH 2 13 Diphosphogl cerate 13 DPG 13 Diphosphoglycerate 13 DPG 1 ADP Phosphoglycerate Kinase Phosphoglycerate Kinase ADP ATP ATP 0 3Phosphoglycerate 3P6 3Phosphoglycerate 3P6 1 0 2Phosphoglycerate 2P0 2Phosphoglycerate 2P0 1 0 Phosphoenolpymvate PEP Phosphoenolpyruvate PEP 1 ADP ADP ruvate Kmase ruvate Kmase ATP Py Py ATP 2 Pyruvate Pyruvate 3 ruvate DH Lactate DH OR Lactate D OR Pyruvate DH NAD N ADH NADH NADH NADH N AD N AD Lactate AcetylCoA Lactate AcetylCoA Slow Glycolysis Slow Glycolysis Enzymes you need to know FOR ONE GLYCOGEN MOLECULE ATP used 1 0 ATP produced 4 TOTALATP3 NADH Produced 2 Oxaloacctatc NAD Malate NADH H Dehydrogenase Malatc Puma rate A Succinate Dehydrogt nase FAD FADH Succingtc SuccinylCOA Synthesase JDI i39l39I ATP 3 SuccinvlCOA KREBS CYCLE P 39ruvatc Pyruvate Dehydrogcnase NAD NADH H Acetyl CoA I Citrate Cis Aconitatc lsocitratc NAD NADH H lsocitrate Dehydrogenase xglosuccingtc a Kctoglutamtc aKetoglutarate NAD Dehydrogenase NADH H Fat oxidation requires more oxygen than glucose because a FFA molecule has more carbon and hydrogen Fat has more carbon and hydrogen 9 More acetyl CoA 9More Kreb s cycles 9 More NADHH and FADHz 9More electrons to be accepted at gate 4 Fat burns in a Carbohydrate ame When liver cells convert amino acids to glucose they start by converting the amino acids into an quotintermediate chemical compound This intermediate is the starting material for building glucose This intermediate is also the starting material for the metabolism of fat Therefore liver cells cannot metabolize fat if they must produce glucose Biochemists phrase this as quotfats burn in the ame of carbohydratequot Without carbohydrate in the diet fat is metabolized inef ciently Endocrine Control of Metabolism Lecture 4 Pt 2 Includes all tissues glands that secrete hormones o Hormones travel in blood to specific target cells Bind to receptors and control cellular activity Hormone receptors Upregulation an increase in available receptors Downregulation a decrease in available receptors Homeostasis of glucose levels Maintain blood glucose within a normalhealthy range during exercise Secretes Insulin when blood sugar levels get too high 0 Main function Decrease blood glucose levels 0 T blood glucose gt T insulin Secretes Glucagon when blood sugar gets too low 0 Main function Increases blood glucose levels 0 l blood glucose gt T glucagon Adrenal Medulla Secretes Epinephrine and norepinephrine o Called catecholamines FightorFlight response T HR BP 0 Stimulate the breakdown of fat amp glycogen Adrenal Cortex Secretes Cortisol o Promotes the use of fat as fuel 0 Using more fat for ATP 9 Spares Insulin levels go down during exercise GLYCOGEN SYNTHESIS blood glucose Glycogen is formed from glucose and stored GLUCONEOGENESIS Production of glucose from nonCHO forms GLYCO LYSIS Breakdown of glucose glycogen GLYCOGENOLYSIS Glycogen is broken down for energy production gulation of Plasma Glucose Metabolism More Epinephrine o More GLYCOGENOLYSIS fat More Glucagon o More GLYCOGENOLYSIS o More GLUCONEOGENESIS 9 breakdown protein to energy More Cortisol o More GLUCONEOGENESIS Less Insulin 0 Less GLYCOGEN SYNTHESIS Insulin Mechanisms 0 Blocks glucagon release 0 Increases glycolytic enzymes 0 Decreases GLUCONEOGENESIS enzymes I All mechanisms would lower blood glucose I Insulin decreases during exercise Glucose and Acute Exercise Short explosive events Rapid release of catecholamines Leads to a sharp increase in blood glucose levels far above normal level Long endurance events Slower more graded release of hormones Slower increase in blood glucose levels ENERGY EXPENDITURE Lecture 5 V02MAx AND LACTATE THRESHOLD Maximal Oxygen Uptake V02max the greatest amount of oxygg a person can consume transport and utilize to produce ATP aerobically on a perminute basisquot III Also known as aerobic capacity III Best indicator of cardiorespiratory endurance and aerobic fitness III Increases with training III Magnitude of increase depends on baseline fitness level I Unfit people can increase their V02 Max can improve by 50 How do we physiologically define V02max III Plateau III Blood lactate El RER El HR VOZmax doesn t always predict performance III Economy Lactate threshold III The point at which blood lactate appears to increase disproportionately above resting levels III The point in time during exercise of increasing intensity when the rate of production exceeds the rate of clearance III Lactate accumulates in the blood when production exceeds its clearance III Lactate accumulation inhibits enzymes used in glycolysis 9 glycolysis slows down energy production slows down Push LT to the right Interval training is best way to push curve to right III LT is one of the best determinants of an athlete s pace in endurance events III Untrained 50 to 60 VOZmaX III Elite athletes 70 to 80 VOZmaX III World class elite athletes 8590 VOZmaX ENERGY EXPENDITURE DURING EXERCISE RMR AND EPOC III Basal Metabolic Rate BMR energy expenditure EE required to sustain life III Requires 12 hours fasting III Participant remains in a reclined position III EE WITHOUT the in uence of eating muscle activity III Resting Metabolic Rate RMR similar to basal metabolic rate but less stringent subject preparation III How much oxygen do we consume at rest III 35 mlkgmin 1 MET III What factors affect BMR and RMR III Muscle massmore muscle higher RMR III Weight El Age older metabolic rate decreases III Body temp if your colder metabolic rate goes downsurvival mode I Warmer metabolic rate increases El Gender men have higher metabolic rate V02 doesn t immediately drop to rest values after we stop exercising Excess PostExercise 0 Consumption EPOC III EPOC the volume of 02 consumed above that normally consumed at rest Causes III Elevated Hormones III Oxidizing lactic acidstill some left over when done exercising need 02 to accept H III Temperaturehelp us cool down keep blood vessels dialated Economy Effort Muscle fiber distribution slowfast twitch III T slow twitch fibres T economic Mechanics wasted energy III Better mechanicstechnique T economic III Economy is a predictor of aerobic performance What happens to Main Effects on Fat Main Effects on Plasma Hormone Site of Release hormone levels Metabolism during Glucose during ExerCISe when we exerc15e ExerCISe Lower insulin less Lower insulin less storage of glucose as storage of fat as Insunn Pancreas l glycogen and more triglycerides T FFA glucose stays in the blood available for energy Glucagon Pancreas T T glyCOgenmySlS T lipolysis T gluconeogeneSIS Catecholamines Adrenal Medulla T T glycogenolysis T lipolysis T gluconeogenesis Cortisol Adrenal Cortex T Tprotein catabolism for T lipolysis gluconeogenesis GrOWth Pituitary T X T lipolysis hormone
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