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This 0 page Class Notes was uploaded by Bailey Metcalf on Sunday March 27, 2016. The Class Notes belongs to 3805 at East Carolina University taught by Joseph White in Winter 2016. Since its upload, it has received 23 views. For similar materials see Exercise Physiology in Physical Education at East Carolina University.
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Date Created: 03/27/16
Chapter 2 Notes I Metabolism a The sum of the chemical reactions occurring in a living organism i The velocity of metabolic reactions is not constant and is controlled by a multitude of biochemical factors b Thermodynamics and energetics i The science that studies the principles limiting energy exchange c Bioenergetics i The science that involves the studies of energetic events in the biological world 1 Energy is not created rather it is acquired in one form and converted to another 2 The conversion process is fairly inefficient and much of the energy released is in a no usable form of heat d The rate of energy production is dependent on i Availability of substrate type of carbons using ii Enzyme activity proteins effecting rates e Exergonic i Energy released f Endergonic i Energy taken up ll Biochemical reactions and Enzymes a Activation energy is lowered and energy is needed c Change around the structure of a molecule to transfer into a different object d Negative feedback inhibits and slow downs pathway e Competitive inhibition i Glucose and not glucose ght for same area on the enzyme f Noncompetitive inhibition i Substrate and inhibitor bind in different areas but when binds can change the area of where substrate can bind lll ATP homeostasis a ATP to ADP to AMP b More its broken less energy c Cell tissue and organ systems are designed to maintain constant cellular ATP concentrations over wide ranges of use d Constancy of ATP concentration over wide variations of turnover is referred to as ATP homeostasis 1 ATP Homeostasis a Levels stay around the same during and after exercise b Cells would die if ATP levels dropped c Phosphate is the high energy when the bonds break is when the energy is released 2 Adenylate Energy Charge Adenylate AMP a b d e Formula comparing ATP and ADP to AMP levels The more atp the higher the charge Disturbance higher levels of amp triggers biochemical reactions to produce more atp Disturbance activation in biochemical reaction to produce atp to maintain charge 3 Energy systems a 039 d Food taken into body is broken down into free fatty acids glucose amino acids Can store them in fat pool glucose pool amino acid pool Glucose stored in liver and muscles glycogen break down is glycogenolysis Store 4 Table 21 Good values to know a b 000 g Atp is a metabolic sensor Muscles can store a decent amount because bigger liver stores more amount per gram High triglycerides BAD Can store fat within our muscle high in endurance athletes Adipose tissue is why we can survive a month or more without eaUng Muscle protein starved for 30 days within a week or so start cutting into muscle protein 5 Energy sources a b C All three are on but going at different rates depending on activity Anything over 2 minutes Table 31 Power creatine kinase Table 31 Speed non oxidative system sprint 400 m run i Glycolysis happens in cytosol rapid uses glucose 31 Endurance oxidative maintains a longer amount of time than the other two Relies on all adipose muscle liver glycogen to keep going Uses circulatory system heavily f Race to Acetoyl coA Carbon structure from breakdown of macronutrients Carbs much quicker than lipids and proteins gets to acetoyl coA quicker Acetoyl coA feeds into citric acid cycle in mitochondria can go to mitochondria to produce ATP 6 Immediate energy system a 3 sources for immediate energy system First thing used ATP Low in cells Activate Creatine kinase do per body weight 1 Only thing proven over and over to work 2 Allows you to perform better 3 Uses immediate system Adenylate Kinase AMP b Creatine kinase xii Can take up to brain heart skeletal muscles different isoforms 1 CK3 located on m line myosin head gives ATP really quick because it is right beside it LOCATON Best biomechanical marker of muscle ber damage zline streaming membrane damage leakage 2 CK2 heart increased after MI because of leakage into blood Can use creatine kinase to make phosphocreatine Phosphocreatine takes ATPs place Want to phosphorylate creatine to add phosphate Atp levels drop activates phosphocreatine Rest l Exercise Taken up against concentration gradient Phosphorylated uses ATP Phosph creatine and creatine much higher in cells than atp Synthesize in kidney liver taking too much shut down indigenous pathway to make creatine take in through diet goes to heart muscle brain or urine High in fish herring meat not that high in dairy Xiii 1 CREATNE BEFORE AND AFTER EXERCISE BOUT CP 70 in cell rapid drop Creatine dramatic increase 2 ATP and ADP stay kinda the same xiv Phosphocreatine resynthesis 1 2 3 4 Blood ow intact perfect recovery of PC No blood ow no recovery of PC Higher V02 Max quicker ability to resynthesize PC quicker Low V02 max recovery isn t that great 7 ONLINE LECTURE SLIDES 3647 a Adenylate Kinase AMPK i Increase in energy demand lead to break down of ATP 1 Adenylate kinase regenerate ATP 2 2 ADP molecules lead to ATP and AMP 39 AMP created cellular energy alert response increase levels of ATP 1 AMPK key enzyme as cell energy sensor 2 AMP activate AMPK shut down consuming pathways a Lead to increased rates of glycolysis beta uptake AMP fuel gage of cells 1 Function of AMPK iv Metformin 1 First line drug therapy of choice for type 2 diabetes and patients with insulin resistance 2 First used in 1995 3 169 billion spent on antidiabetes in 2010 4 Metformin increases insulin sensitivity and lowers glycogenesis 5 48 million prescription in 2010 alone in the US 6 activate AM PK enzyme v AMPK and exercise 1 Braun 2010 a 12 week of exercise vs metformin and exercise vs metformin only in prediabetic women b all 3 interventions increased insulin sensitivity c exercise only resulted in 2530 increase in insulin sensitivity compared to the other groups d exercise and metformin may stimulate the same pathwaymetformin blunting effects of exercise i Reduces V02 max vi Glycolytic System 1 Chemistry of glucose splitting 8 AMPK a 2 Pathway of 1112 successive enzymatic reactions in which glucose is broken down into pyruvate or lactate 3 One of the principle cellular pathways for ATP production 4 Occurs in the cytosol of all cell types 5 Source of carbon backbones for amino acids fatty acids nucleotides and cofactors 6 Same thing as fermentation making beerwine but makes pyruvate 7 Produce ATP 9 Phase 2 generate ATP reducing equivalentNADH a NAD carry electrons from cytosol to mitochondria to electron transport chain to produce ATP Creatin kinase gets activated that replenishes ATP levels b Adenylate kinase AMPK i AMP activate ATP producing pathways ii A low energy stress signal that activates to AMPK 1 Leads to a bunch of stuff glycolysis etc a Takes you from immediate energy systems to glycolysis to endurance iii Bridge gap 9 Glycolosis 6 carbons to 23 carbon structures 10 a b Glucose i Outside going in 1 Energy investment Glucose phosphate i Cant leave d e O39QJ Splits Dehydrogenase i NAD to NADH ii Shuttle of electrons to mitochondria 2 ATP in and get 4 out i net gain of 2 Glucose phospholorate NAD Nicotinamide Adenine Dinucleotide Electron acceptorreducing equivalent Carries electron from one reaction to another Synthesizes with precursors B3 and nicotinamide 11 12 13 14 15 0390 0390 0390 0390 Reduced NAD can travel to mitochondria via shuttle system and be used of the process of oxidative phosphorylation Glucose Uptake Insulin binds to receptor Through signal pathways glut 4 translocate to surface and pull in glucose Pulls in glucose from blood stream Glucose transporter 4 Glut 4 i Gets glucose in the cell ii Muscle contraction can stimulate as well iii Stimulated by insulin Insulin sensitivity i How effective the body is in responding to insulin Insulin Resistance i Decreased ability to respond to insulin ii Like type 1 diabetic Fate of Glucose upon entry into muscle Immediately converted into energy via process known as gycoysis and Krebs cycle Converted into polysaccharide glycogen a storage form of glucose Glycogen Enzyme bind to substrate Enzyme that breaks downs glycogen called phsophoralase Branching structure makes break down process rapidly breakdown i Glucose 1 Hexokinase ii Glucose 6P 1 phosphoglucomutase iii Glucose 1P 1 Glycogen phosphorylate and synthase iv Glycogen Lactate dehydrogenase Lactate is continuously being produced and removed In resting muscle there is 10x more lactate than pyruvate this ratio is increased may more times over contraction Removed mainly by oxidation 75 oxidation and 25 glycogenesis Lactate Metabolism Making too much pyruvate to oxidize Slow gycoysis Lactate accumulation i Results from conditions in which glycolytic rate is higher than mitochondrial rate not necessarily when oxygen is not available 16 17 18 19 20 21 22 Lactate threshold ii You don t need to produce ATP as fast with the red line Fate of lactate I Converted back into pyruvate and oxidized in the mitochondria ii Taken up by neighboring oxidative type 1 bers and oxidized iii Travels to the liver and is used to make new glucose gluconeogenesis 1 In blood stream GIucoseglycolysispyruvatelactate g Lactategluconeogenesis pyruvate glucose 0 Oxidase phosphorylation in the Electron transport chain and produce large amounts of ATP Pyruvate Acetoyl OcA citric acid cycle Flavine Adenine Dinucleotide Like NAD Terms Mobilization the breakdown of adipose and intramuscular triglycerides lipolysis breakdown of lipids circulation the transport of free fatty acids FFA from adipose to muscle uptake the entry of FFA into muscle from blood activation raising the energy level of fatty acids before catabolism F beta oxidation the production of acetylCoA from activated fatty acids and the production of reducing equivalents i in mitochondria mitochondrial oxidation Krebs cycle and the electron transport chain ATP produced by B oxidations and Kreb cycle Energy Systems ATP no oxygen i faster Glycolysis no oxygen Oxidative from carbs yes oxygen Oxidative from fat yes oxygen i Slower by generate more ATP Oxidative Phosphorylation Mitochondriaelectron transport chain b Powered by NADH FADH reducing equivalents c Called quot because it involves the phosphorylation of ADP with the help of energy liberated from the oxidation of NADH and FADH2 d Aerobic process depends on oxygen utilization in electron transport chain e ATP synthesis is catalyzed by ATP synthase f When ATP is produced it is exported out of mitochondria while importing ADP g Picture i ATP synthase is at complex 5 ATP from ADP ii NADH and FADH ow through system and loose H iii Electrons from NADH and FADH get when oxidized bc loosing electrons 1 Power gradient energy for ATP synthase to produce ATP 23 Statins Have been shown to inhibit exercise training adaptations High cholesterol no minimum requirement to prescribe Decrease muscle cells and V02 max Marker of mitochondrial content statins decrease Overall slows mortality V02 max Lipophilicget into cell Hydrophiliccant get into cell Chapter 11 Notes wmeom LO 1 Myoplasticity a The capacity of skeletal muscle for adaptive change b Altered Gene Expression i The molecular basis for adaptations that occur due to exercise training as well as detraining and chronic inactivity in skeletal muscle proteins ii Myoplasticity is predicted on the ability of the muscle bers genetic machinery to change either the quantity amount or quality speci c type of protein it expresses c Protein Synthesis and Degradation Ratio i The level of any protein in a muscle cell is governed by its rate of synthesis relative to its rate of degeneration ii When synthesis exceeds degradation protein content increases within the cell and vice versa d DNAtranscription by RNA polymerase RNA translates by ribosomes protein 2 Exercise Adaptations a Mitochondrial biogenesis b Mitochondrial proteins i Left to right get bolder and bigger ii Increase in content or amountintensity 3 Sawtooth Pattern of Exercise i the more of the enzyme the more activity 1 exercise b mRNA proceeds RNA synthesis c signal to create proteins is transient and related to each bout of exercise i every time there is a bout protein level increases d longer to train then detrain e can switch a ber from type 2 to type 1 f Exercise adaptations i During exercise cellular cells 4 Skeletal Muscle Fiber Type a Type 1 b Type 2 bigger more glycolytic aerobic endurance exercises c Endurance Training and ber type i Low and moderate intensity aerobic activities rely extensively on type 1 bers ii Type 1 ber hypertrophy in size iii Magnitude depends on intensity and duration iv Increases in CAS up to 25 have been reported d Endurance training and ber type transition i With endurance training there is a transition from type 2x to 2a as well as 2a to 1 1 More oxidative to produce high ATP levels e Heritage family study i 20 week endurance training program 1 increased type 1 ber from 43 to 47 2 decreased type 2x bers from 20 to 15 3 type 2a remained essentially unchanged 5 Effects of Endurance Training on Skeletal Muscle Mitochondria a Mitochondrial markers mitochondrial membrane proteins i CPT1 ii Rate limiting step of fatty acid oxidation to see if mitochondrial content increases iii Fats from cytosol to outer mitochondrial membrane to get oxidized in membrane is rate limiting step 6 Rat model a Fast twitch white type 2 x b Fast twitch red type 2 a c Slow twitch red type 1 7 Endurance Training and Mitochondria a Endurance training result in a greater mass or number of mitochondria b The speci c activity of mitochondria does not increase activity is the 8 More mitochondria more ef cient Review 0 Bioenergetics Laws humans are inef cient in converting energy bc lost through heat 0 Immediate 0 ATP 0 Phosphocreatine allows rigor bond to be released 0 Creatin kinase to phosphorylate ADP to ATP Nonoxidated o Glycolytic glycolysis occurs in cytosol Glucose to 2 3 Carbon glucose made into 2 pyruvates o Stored as glycogen in muscles 0 Pyruvate can go two ways Converted to lactate get pyruvate out of cytosol Converted to 2 COA By pyruvate dehydrogenase o Goes to COA to mitochondria to Krebs cycle to electron transport chain to generate ATP Oxidized o All of them are going just depends on rate of activity Creatin kinase 0 Takes Creatin and phosphorylate into phosphocreatine o Requires energy use ATP 0 When you sprint phosphocreatine allows ATP to be taken up quicker and back to ADP Adenylate Kinase Takes 2 ADP to 1 ATP and 1 AMP High levels of AMP are metabolic alert sensor Activate AMPK activates metabolic pathways that produce ATP AMPK is master regulator of body processes Glycolysis Beta oxidation Glucose uptake Pyruvate dehydrogenase convert pyruvate to acetylcoA Reducing equivalents both electron carriers carry electrons to chain to be oxidized 0 NAD producing glycolysis o FAD made in TCAKreb Cycle Carbs lipids and proteins all produce acetylcoA Lipids 0 COO 0 Beta oxidation in the mitochondria 0 Chop up carbon chain take 2 off at a time to produce 1 acetylcoA AMP factors into ATP homeostasis Graph 0 Beginning of exercise bout a lot of phosphocreatine high but not a lot creatine 0 When you exercise the myosin heads take the lost ATP creatine kinase makes creatine lower ATP levels back to create 0 After an exercise phosphocreatine is low creatine high When we exercise signals are produced that lead to mitochondrial increase MRNA proceeds protein response AMPK increase insulin sensitivity greater ability to get glucose into the cell 0 GLUT4 an enzyme Muscle contraction and insulin stimulate glut 4 Type 1 diabetes take metformin Saw tooth pattern after exercise mrna signals shot up 0 Decrease when you don t exercise 0 Protein synthesis increase and an increase in mitochondrial numbers Rate limiting step in beta oxidation 0 Getting the lipid into and through mitochondrial membrane to be broken down With exercise you can use fats at a lower energy because lots of mitochondria produced Glycolysiscytosol TCAKreb mitochondria electron transport chain 0 Beta oxidation Pyruvatelactase by lactase dehydrogenase Type 1 ber oxidative because endurance Type 2 ber glycolytic use glycolysis and phosphocreatine 0 Each bers can be trained ADK used in immediate energy system type 2 bers Phosphocreatine resynthesizes graph 0 2 lines of blood ow 0 aerobic process 0 endurance athletes resynthesize quicker bc high V02 max The rate of glycolysis dictates where pyruvate goes httpsprezi comte3jj iv6z4cha pter 2fuelfor exe rcise bioenergeticsutmcampa ignshareamputmmedi umcopy
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