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ExPhys 4140 Exam 1 Study Guide

by: Gabby Notetaker

ExPhys 4140 Exam 1 Study Guide EXPH 4140

Marketplace > Ohio University > Health Sciences > EXPH 4140 > ExPhys 4140 Exam 1 Study Guide
Gabby Notetaker

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These notes cover Energy Systems Part 1,2, and 3-- including Glycolysis, glycogenolysis, cori cycle, Krebs, Oxidative phosphorylation, lipolysis, and how exercise affects those systems. These notes...
Physiology of Exercise
Study Guide
Energy, Hormones, exercise, Systems
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This 10 page Study Guide was uploaded by Gabby Notetaker on Tuesday September 27, 2016. The Study Guide belongs to EXPH 4140 at Ohio University taught by Loucks/Kushnick in Fall 2014. Since its upload, it has received 8 views. For similar materials see Physiology of Exercise in Health Sciences at Ohio University.


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Date Created: 09/27/16
Physiology of Exercise- Introduction & Homeostasis: 1. The First exercise physiology lab in the United States was the Harvard Fatigue Lab, and the director was D.B. Dill (1927-47 when it closed) 2. Negative feedback (utilized most) occurs when the response reverses the initial disturbance in homeostasis to keep levels relatively constant. Positive feedback is when the control system response works to increases the initial stimulus. It is designed to push levels out of normal range. 3. Example of control system important to exercise would be a. Regulation of blood pressure: increase blood pressure, baroreceptors sense in carotid arteries and aorta, message sent to medulla, stimulates heart, response is decreased blood pumped out. b. Regulation of blood glucose: eat, blood glucose levels rise, pancreas is both sensor and effector, pancreas secretes insulin, cellular uptake of glucose 4. Exercise physiology is the study of how the body adapts physiologically to acute stress (single bout) exercise or chronic training (bouts over time). 5. Homeostasis is the maintenance of a constant or unchanging “normal” internal environment (during resting conditions). Steady state is a constant internal environment but not necessarily “normal”. It is a balance achieved between demands placed on the body and the response to those demands. Energy Systems Part 1 - CREATINE KINASE regulates the production of ATP from phosphocreatine + ADP. (ADP stimulates, ATP inhibits) - GLYCOGENOLYSIS (break down glycogen): o Glycogen ----> G1P (PHOSPHORYLASE) o G1P ----> G6P o G6P -----> glucose o PHOSPHORYLASE stimulated by increased epinephrine (cAMP), increased Ca++, ADP, and Pi while inhibited by ATP. - GLYCOLYSIS (break down of glucose): o Fructose 6-P -----> fructose 1,6 –bisP (PHOSPHOFRUCTOKINASE)  Phosphofructokinase (PFK) stimulated by ADP, AMP, increased pH (more basic)  Inhibited by ATP, PC, citrate 1. Glycogenolysis is the breakdown of glycogen into glucose (G1P) to be used by muscles and is regulated by phosphorylase. Gluconeogenesis is the formation glucose, especially in the liver, from amino acids, lactate, and glycerol (all non-carb sources). 2. CORI CYCLE: a. Glycogen in skeletal muscles  glucose (phosphorylase)  pyruvate  lactic acid. The lactic acid goes into blood and is taken up by the liver, where it transforms from lactic acid  pyruvate  G6P form of glucose. G6P will either become stored liver glycogen, or travel into blood back to skeletal muscles to be stored as skeletal muscle glycogen. 3. Rate limiting enzyme of glycolysis is phosphofructokinase. 4. The energy released from the breakdown of the high-energy phosphates ATP and PC can sustain all out exercise for about: 10-14 seconds 5. Enzymes increase the rate of chemical reactions by decreasing the energy of activation Energy Systems PART 2 KREBS - Citrate is the 6C molecule formed from 4C (oxaloacetate) + 2C (acetyl CoA). - Acetyl CoA can be made by (1) AA (2) pyruvate -3C molecule that releases CO2 to create acetyl CoA and (3) FA - 1 Turn of CAC = 3 NADH, 2 FADH, 1 ATP (Via GTP), BUT TWO TURNS PER GLUCOSE. - RATE LIMITING ENZYME OF KREBS CYCLE = o Isocitrate -----> a-ketoglutarate (ISOCITRATE DEHYDROGENASE) o Stimulated by increased O2, ADP, Pi, AMP, or isocitrate o Inhibited by decreased O2, ATP, and NADH OXIDATIVE PHOSPHORYLATION - NADH = 2.5 ATP - FADH = 1.5 ATP - CYTOCHROME OXIDASE (the 4 enzyme in the membrane) =rate limiting enzyme. NADH drops off to #1, and FADH drops off to #2. Both go to #3, then cytochrome oxidase. - Stimulators= ADP, Pi…. Inhibitors= ATP - Aerobic tally from the breakdown of 1 glucose = 32 ATP o 7 from glycolysis (2 ATP, 2 NADH x 2.5) o 5 from pyruvate  acetyl CoA (2 NADH) o 20 from Krebs (2 GTP, 6 NADH x 2.5, 2 FADH x 1.5) - Aerobic tally from the breakdown of 1 glycogen = 33 ATP - Aerobic respiration efficiency = 34%, 66% of energy released as heat LIPOLYSIS - Breakdown of triglycerides into glycerol & FFA (enzyme= hormone sensitive lipase) - Beta-oxidation = process by which FFA are broken down by enzymes into acetic acid (2C), which is converted to acetyl CoA. o Rate limiting step is TRANSLOCATION of FFA from cytosol into mitochondria. Translocation inhibited by MALONYL-COA (an intermediate in FA synthesis) o Fatty acid in cytosol binds CoA to form fatty acyl-CoA o Fatty acyl-CoA transformed to acyl-carnitine by transferase 1 in membrane, releasing Co enzyme A back into cytosol. o Acyl carnitine has carnatine taken off and CoA put back on by transferase 2 in the mitochondria, releasing carnitine into mito matrix so that it can go back across the membrane into the cytosol to transport more FA. - Break down of fatty acids occurs in turns of breaking off 2C at a time. Each 2c used for acetyl CoA. EACH 2C turn releases a net of 14 ATP. o First cycle + activation = 13 ATP (14-1) o However many cycles after = n x 14 ATP o Last cycle + remaining 2C = 24 ATP rather than 28 (14 x 2) - Glycogen requires 15% less oxygen for catabolism than fats do, but do not release as much ATP as fats do. - Deamination: process by which the amino group (NH2) is removed from the amino acid so it can be oxidized for energy or recycled.  from contractile tissue when used for energy. Protein very small store of energy (2%-15%) o Proteins  glucose = alanine cycle - Predominance of one energy source depends on rate of ATP utilization - Work intensity determines rate of ATP utilization - OXIDATIVE CAPACTIY= measure of muscle’s max capacity to use oxygen. - The oxidative capacity of muscle fibers depends on their oxidative enzyme levels, fiber-type composition (fast  lactate, slow  pyruvate), how they have been trained, and oxygen availability. 1. The energy used in a short (0-3 sec), powerful event, such as shot put, would be the almost immediate/very rapid use of ATP and Phosphocreatine. This energy is stored in the cytosol and uses a single enzyme. The energy used for a long (>2min), endurance oriented event, such as a 6 km race, would be slower but prolonged use of stored glycogen and glucose in muscle and liver, lipids from muscle, blood and adipose cells, and amino acids from muscle, blood, and liver. Endurance energy will need oxygen to create ATP. Enzymes in the cytosol and mitochondria will act on fuel sources from the cytosol, blood, liver, and adipose tissue. 2. The liver supports the provision of energy to the tissues of the body by its primary job of forming glucose through gluconeogenesis. It forms glucose from lactate (cori cycle), amino acids (alanine cycle), and glycerol from broken down triglycerides. This newly formed glucose is released into the blood during exercise. 3. What are the capacities and powers of the three energy systems? a. ATP-PCr and glycolytic systems produce small amounts of ATP anaerobically and are the major energy contributors in the early minutes of high-intensity exercise. b. The oxidative system uses oxygen and produces more energy than the anaerobic systems (oxidative capacity= measure of muscles max capacity to use oxygen) c. Carb oxidation involves glycolysis, Krebs, and ETC to produce 33 ATP per glycogen d. Fat oxidation involves B-oxidation of FFA, Krebs, and ETC to produce more ATP than carb e. Protein contributes little to energy production, oxidation is complex since AA contain nitrogen that cannot be oxidized. f. The oxidative capacity of muscle fibers depends on their oxidative enzyme levels, fiber-type composition (fast  lactate, slow  pyruvate), how they have been trained, and oxygen availability. 4. During B-oxidation, the first thing that has to happen is triglycerides get broken down into glycerol and FFA by hormone sensitive lipase. B-oxidation is the breakdown of FFA by enzymes into acetic acid, which is then converted to acetyl CoA. The rate limiting step is the translocation of the FFA into the mitochondria. A CoA binds to the FFA forming Fatty acyl-coA. Transferase 1 then replaces the Coenzyme A with a carnitine to form acyl-carnitine. Acyl- carnitine is able to travel across the membrane. Once acyl-carnitine is in the mitochondria, transferase 2 removes the Carnitine and replaces it with coenzyme A. The fatty acyl-CoA is now ready to be broken down in turns of 2C, producing a net worth of 14 ATP per turn. These 2C acyl groups form acetyl-CoA (2C) and then progress through Krebs and ETS to produce ATP. 5. The difference between the amount of oxygen required to oxidize fat compared to carbs is that fat requires ~15% more oxygen. However, fat does produce more ATP. At the beginning of a work out when oxygen saturation is near resting levels and readily available, fat is utilized more because it produces more ATP with the original oxygen levels. As exercise progresses, oxygen becomes scarce, requiring exercise systems to transfer over to utilizing more carbohydrates, since carbs require less oxygen to make ATP. 6. In aerobic metabolism, oxygen is the final electron acceptor to form water within the ETC and maintain the Hydrogen ion gradient for ATP production. Energy Systems PART 3 - At rest, almost 100% of ATP by aerobic metabolism (low lactate) - When beginning to exercise, ATP production increases immediately, while oxygen uptake increases rapidly, but not immediately. (OXYGEN DEFICIT= lag in oxygen uptake at the beginning of exercise)  reach steady state within 1-4 min. once at steady state, ATP produced via aerobic processes. - Initial ATP production through anaerobic ATP-PC and glycolysis - Trained have lower oxygen deficit (cardiovascular/muscular adaptations allow better aerobic bioenergetics capacity), and produce less lactic acid. - RECOVERY: oxygen uptake remains elevated above rest into recovery: used to think it was oxygen debt (by A.V. Hill) : repayment for O2 deficit at onset of exercise. - EPOC = Excess Post Oxygen Consumption: reflects that only ~20% elevated O2 consumption used to “repay” O2 deficit. - EPOC: o Rapid :  resynthesis of stored PC  Replenish muscle (Mb) and blood (Hb) O2 stores o Slow:  Elevated heart rate and breathing = increased energy need  Elevated body temperature = increased metabolic rate  Elevated epi and norepi = increase metabolic rate  Conversion of lactic acid to glucose (gluconeogenesis) o EPOC greater after higher intensity exercise due to higher body temp, more PC depleted, greater blood lactic acid, more epi and norepi in blood - REMOVAL OF LACTIC ACID o Classic theory: majority of lactic converted to glucose in liver o Recent theory:  70% of lactic acid is oxidized and used as a substrate by heart and skeletal muscle  20% converted to glucose  10% converted to AA o Lactic acid removed more rapidly with light exercise recovery at ~30- 40% VO2 max - MAX OXYGEN UPTAKE o VO2 max = maximal capacity for oxygen consumption by the body during maximal exertion o VO2 increases linearly until Vo2 max reached (no further increase with increasing work rate) o VO2 max is physiological ceiling for delivery of O2to muscle o Affected by genetics and training o Physiological factors influencing VO2 max= maximum ability of cardiorespiratory system to deliver oxygen to muscle AND ability of muscles to use oxygen and produce ATP aerobically o It is a good indicator of cardiorespiratory endurance and aerobic fitness o Can differ according to sex, body size, and age o Expressed relative to body weight in ml of O2 consumed per kg body weight per min (ml/kg*min) - LACTATE THRESHOLD o The point at which blood lactic acid rises systematically during incremental exercise  Appears at ~50-60% Vo2 max in untrained subjects  At higher work rates (65%-80%) VO2 max in trained subjects  Also called ANAEROBIC THRESHOLD  FROM LAB (point where the amount of lactate being produced is now more than the amount being cleared) o Explanations for the Lactate threshold  Low muscle oxygen (hypoxia)  Accelerated glycolysis – NADH produced faster than it is shuttled into mitochondria AND excess NADH in cytoplasm converts pyruvic acid to lactic acid  Recruitment of fast-twitch muscle fibers  LDH isozyme in fast fibers promotes lactic acid formation  Reduced rate of lactate removal from the blood - FIBER TYPES o Type I = slow twitch, slow-oxidative - produce pyruvate  High mito  High resistance to fatigue  Low ATPase activity  High efficiency  aerobic  ENDURANCE o Type IIa = Intermediate fibers, fast- oxidative glycolytic fibers  High/mod mito  High/mod resistance to fatigue  Combo of aerobic and anaerobic  High ATPase activity  Moderate efficiency o Type IIx = fast-twitch fibers, fast-glycolytic  produce lactate  Low mito  Will fatigue quick  Highest ATPase activity  Low efficiency  Anaerobic - PYRUVIC acid is converted to lactic acid if NAD+ is low. (requires 1 NADH to transform pyruvate lactate) - Pyruvic acid lactic acid by LDH (lactate dehydrogenase) - RER = estimation of fuel utilization during exercise (respiratory exchange ratio) - RER = VCO2/ VO2, carbs=1 ; fats = 0.7 ; 0.85 = 50/50 - During steady state exercise, VCO2 and VO2 reflective of oxygen consumption and Co2 production at the CELLULAR level - Metabolic responses to short-term, intense exercise o 1 5 seconds = ATP-PC o After 5 seconds, shift to ATP via glycolysis o Anything longer than 45 seconds = ATP via ATP-PC, glycolysis, and aerobic systems  70% anaerobic / 30% aerobic @ 1 min  50% anaerobic / 50% aerobic @ 2 min - Prolonged exercise o Longer than 10 min = ATP primarily from aerobic metabolism; steady state oxygen uptake can generally be maintained o Prolonged exercise in a hot/humid environment or at high intensity  Steady state not achieved  Upward drift in oxygen uptake over time  Due to body temperature and rising epi & norepi  On a graph, line would have steeper slope for VO2 vs time in a hot & humid environment than regular - Exercise intensity and fuel selection o Fats are primary fuel during low-intensity exercise (<30% VO2 max) o Carbs are primary fuel during high-intensity exercise (>70% VO2 max) o Cross over concept: describes shift from fat to carbs as intensity increases during exercise  Due to : the recruitment of fast twitch muscle fibers that contain more glycolytic enzymes than lipolytic enzymes  Increasing blood levels of epi o INCREASED EPI, ENHANCES REGULATORY ENZYMES, = INCREASED BREAKDOWN OF GLYCOGEN o In graph of “crossover” concept, the place where both lines meet shifts to the right in trained indivudals. o INCREASED EPI STIMULATES LIPOLYSIS o INSULIN DECERASES, normally insulin inhibits lipolysis, BUT WHEN WORKING OUT, INSULIN DECREASES SO THAT INHIBITION IS REMOVED = MORE LIPOLYSIS - Sources of fuel during exercise o Carbs (muscle glycogen/blood glucose) o Fat (intramuscular triglycerides in cytoplasm (storage) and plasma FFA (from adipose tissue lipolysis) o Protein (small amount of energy production ~2%), may increase to 5- 15% late in prolonged exercise o Blood lactate - Use plasma FFA more than muscle triglycerides, and our dependence on blood glucose only increases as muscle glycogen becomes depleted (graph on page 18) - IS low intensity exercise best for burning fat? o At low exercise intensities (~20% Vo2 max)  High percentage of energy expenditure (~60% derived from fat)  However, total energy expended is low  Total fat oxidation is also low o At higher intensities (~50% VO2 max)  Lower percentage of energy (~40%) from fat  Total energy expended is higher  Total fat oxidation is also higher o Rate of fat metabolism increases from 20% vo2 max to 50, but then decreases with higher intensity after that, due to the switching to carbs (graph pg 19) Questions: 1. Blood lactate accumulates during exercise because (1) at the lactate threshold around 50-60% Vo2 max in untrained subjects and 65-80% in trained, the amount of lactate being produced is greater than the amount being removed. This is due to (2) low muscle oxygen (hypoxia) , (3) accelerated glycolysis. – NADH from aerobic pathways produced faster than it is shuttled into mitochondria, so excess NADH in cytoplasm converts pyruvic acid to lactic acid (low NAD/NADH ratio) (4) recruitment of fast-twitch muscle fibers that contain LDH (lactate deyhydrogenase to promote lactic acid formation from pyruvic acid) 2. Draw graph on page 4 of packet (axis = VO2 in L/min and time in minutes.) trained should have a steeper slope and less oxygen deficit than untrained. 3. Draw graph on page 8. As work load increases, VO2 increases linearly until it reaches VO2 max (plateau). Axis are VO2 max (L/min) and workload in increasing watts. 4. RER for carbs = 1.0, RER for fat = 0.7 5. Removal of lactic acid following a bout of intense exercise is C. More rapid if the subject performs light exercise (~30% VO2 max), compared to rest 6. Lactic acid accumulation contributes to muscle fatigue during exercise and causes the muscle soreness that may occur 24-48 hours after exercising – FALSE. But not sure why. HORMONAL RESPONSE TO EXERCISE – PART 1 - Definition of Hormone: any substance secreted by one cell to regulate another cell. May be delivered by an endocrine, neuroendocrine, neurocrine, paracrine, autocrine, or even pheromonal route - Paracrine= release factor to cell adjacent - Endocrine = release factor into blood to distant target cells - Neuroendocrine= nerves release factor into blood to regulate distant target cells - Classify hormones on structure, site of synthesis/action, and physiological action - Ex: growth hormone released into blood, stimulates liver to release IGF1 (insulin growth factor 1) which then increases muscle mass. - STEROID hormones (from fat) - NONSTEROID hormones (from AA) o Derivatives of amines o Polypeptides o Glycoproteins: carbs attached to protein hormones - STEROID o Lipid soluble o Diffuse through cell membranes; receptors located within the cell o Chemical structure is derived from or similar to cholesterol o Secreted by ADRENAL CORTEX, OVARIES, TESTES o Carry out effects by altering activity of DNA to modify protein synthesis o Carrier protein in blood carries hormone to target cell, hormone diffuses across, receptor protein in cell attaches and carries hormone to nucleus, translocation of receptor and hormone into the nucleus, alter DNA, mRNA changes and results in protein synthesis, that then carries out the steroid hormone response. o FROM CHOLESTEROL  Aldosterone (mineralcorticoid)  Cortisol (glucocorticoid)  Testosterone (androgen)  Estrogen - NONSTEROID o Non-lipid soluble o Cannot diffuse through cell membranes, receptors located on the cell membrane o TWO TYPES: AA derivatives and protein or peptide hormones o MECHANISM:  Activating 2ndmessengers, such as cAMP, Ca++, inositol triphosphate (IP3), and diacylglycerol (DAG) via G proteins  Biological actions often involve regulating enzyme activity or mediating movement of calcium but could also change gene activity. o Tyrosine Kinase  Tyrosine kinase is a portion of the membrane receptor or is activated by the membrane receptor  Hormone binding to the membrane receptor activates enzymes and other cytosolic signaling proteins. o EXAMPLES:  Insulin binds to tyrosine kinase receptor, causes phosphorylation, stimulate signaling proteins to transfer GLUT4 vesicles to the membrane to aid in glucose transportation across the membrane  cAMP ex: hormone binds to receptor (such as epi) , activates G- protein, activates ADENYLATE CYCLASE, which stimulates the production of cAMP. cAMP activates protein kinase like PHOSPHORYLASE to increase glycogenolysis, or the breakdown of glycogen. o Over 24 hr cycle, both sleep-wake homeostasis and circadian rhythm regulates the hypothalamic pulse generators, which then control the pituitary and all the secretions of the pituitary.  Cortisol increases at night and highest when we first wake up when food deprived, decreases throughout day. - Receptors are specific to hormones - Each cell has 2-10,000 specific receptors - Magnitude of effect dependent on: o Concentration of hormone o Number of receptors on the cell o Affinity of the receptor for the hormone - Hypothalamus-pituitary-thyroid axis (control system) o Hypothalamus regulates Thyrotropin releasing hormone (TRH), which regulates the anterior pituitary, which regulates thyroid-stimulating hormone (TSH), which influences the thyroid to either (1) grow or (2) produce thyroxine. Thyroxine then acts on TRH as a negative feedback and inhibits the anterior pituitary from releasing more TSH. o Hypothalamus TRH  ant. Pit  TSH  thyroid grows or thyroxine thyroxine prevent TRH from stimulating ant pit. - Posterior Pituitary Gland o Secretes antidiuretic hormone (ADH), also known as vasopressin o Reduces water loss from the body to maintain plasma volume  Favors reabsorption of water from kidney tubules to capillaries o Release of hormone stimulated by increased plasma osmolarity (as we lose fluid, plasma osmolarity increases)  Due to sweat loss w/o water replacement  Increases during exercise > 60% VO2 max o


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