HSC 308, Exam 3 Notes
HSC 308, Exam 3 Notes HSC 308
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This 10 page Study Guide was uploaded by Taylor Vermaat on Tuesday February 16, 2016. The Study Guide belongs to HSC 308 at Central Michigan University taught by Micah Zuhl in Summer 2015. Since its upload, it has received 131 views. For similar materials see Physiology of Sport and Exercise in Nursing and Health Sciences at Central Michigan University.
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Date Created: 02/16/16
1 Physiology of Sport and Exercise: Exam 3 Energy Expenditure: Almost impossible to measure energy expenditure of a contracting muscle. Measuring Energy Expenditure: Direct Calorimetry Substrate metabolism efficiency: a calorie is the basic unit of heat 30% of substrate energy ATP 70% of substrate energy heat Main Substrate for Aerobic Exercise: Utilization of OXYGEN Production of CARBON DIOXIDE Rate of O2 and CO2 exchanged in the lungs is equal to the rate of usage in the body. We can measure energy expenditure based on oxygen consumption! Because major substrates use O2 and produce CO2 we can indirectly determine substrate utilization in metabolism. Measuring Energy Expenditure: O2 and CO2 Measurements VO2: volume of O2 consumed per minute Rate of O2 consumption Volume of inspired oxygen – volume of expired O2 VCO2: volume of CO2 produced per minute Rate of CO2 production Volume of expired CO2 – volume of inspired CO2 Oxidative metabolism of fat and carbohydrate can be quantified based the amount of oxygen that we consume and carbon dioxide we produce. Can only be quantified during oxidative metabolism or aerobic metabolism. CO2 produced from pH and TCA during metabolism Substrates: 2 O2 usage during metabolism depends on the type of fuel being oxidized. Fat requires more oxygen to be consumed. More carbon atoms in molecule = more O2 needed Glucose < palmitic acid Palmitate – fat 16C Fat molecules have many carbons, oxidation provided large amounts of Acetyl CoA We need more oxygen to metabolize fats Produces CO2 from TCA Cycle Total ATP from 16C FFA Metabolism: Produce 16 CO2 Consumes 23 O2 Respiratory Exchange Ratio: RER Ratio between rates of CO2 production, O2 usage RER = VCO2/VO2 Based on this ratio we can determine what fuel we are using at rest and during exercise. 1 molecule of Palmitic Acid RER = 0.70 CHO: Glycogen/glucose molecules have less carbons and require less amount of O2 for metabolism. Produce CO2 from TCA and PDH Produce 6 CO2 Consumes 6 O2 = 1 RER for 1 molecule of glucose Measuring Energy Expenditure: RER ranges from 0.70 – 1.0 3 Aerobic metabolism 0.70 = 100% fat burning 1.0 = 100% CHO burning RER of 1? Using complete CHO Oxidation. RER of CHO and FAT: Fat produces more CO2 (16) 16 CO2 to 23 O2 CHO produced more CO2 proportional to O2 consumed! 6 CO2 to 6 O2 RER values can range between 0.70 – 1.20 measured at the lung. RQ values can only range from 0.70 – 1.0 measured at the cell a true measure of metabolism. Resting Metabolic Rate (RMR): Amount of energy used under resting conditions 1200 to 2400 kcal/day Total daily metabolic activity includes normal daily activates Normal range: 1800 to 3000 Competitive athletes: up to 10000 1. Measure VO2 and VCO2 for roughly 30 minutes. 2. Then calculate RER at rest 3. What is calorie equivalent for the RER value? Kcal = VO2 (L/mon) X RER calorie equivalent X time (minutes) Basal Metabolic Rate (BMR): Energy expenditure measured in a supine state, after 8h sleep and 12h fast. Related to fat-free mass RMR is typically higher. 4 EXAMPLE If someone’s resting VO2 is 0.30 L/min and their RER is 0.80, what is their RMR? 0.80 = 4.801 kcals/L 0.30 L/min 0.27 L X 1440 (24h) = 432 L/day Kcals = 4.801 kcals X 432 L = 2073 kcal/day Metabolic Adaptations to Endurance Training Increase fat oxidation for a given exercise intensity! CO 2omes from two locations during CHO metabolism TCA and PDH RER > 1 No longer in aerobic metabolism Lab: Reasons why measured and calculated RER values differ • High protein intake – we cannot calculate body’s use of protein in RER • The amount of muscle mass – greater heat production • Age – loss of FFM • Body temperature – increased in heat production • Psychological stress – SNS • Hormones – thyroid hormone, EPI What drives metabolism? Skeletal muscle tissue Night time feeding: Eat 20-30 minutes before bed raises RMR Based on size of meal rather than nutrient content 5 Exercise RER: Qualifying energy expenditure during submaximal exercise RER must be below 1.0 to accurately quantify exercise energy expenditure Only able to measure aerobic energy expenditure RER over 1 = no longer in aerobic metabolism! Submaximal exercise energy expenditure Collect VO2 and VCO2 during light – moderate intensity exercise Calculate RER Calculate energy expenditure Kcal = VO2 (L/min) X RER caloric equivalent X time (min) LOW INTENSITY: RER = 0.80 – 0.90 Fat oxidation is happening Low ratio of VCO2/VO2 CO2 production occurs in one place during entry into aerobic metabolism TCA Cycle Produces less CO2 than O2 consumed 16 CO2 produced, 23 O2 consumed RER = 0.70 Energy Expenditure during Submaximal Aerobic Exercise: Metabolic rate increases with exercise intensity! VO 2 Upward drift, even at low power outputs Possible due to ventilation, hormone changes, temperatures, or pH As intensity increases… O uptake kinetics at high power outputs, VO continues to increase 2 2 6 More type II (less efficient) fiber recruitment NEED HELP MEETING ATP DEMAND HIGH INTENSITY EXERCISE: RER approaches 1.0, in CHO metabolism The extra CO2 produced coming from PDH reaction Activation of PDH = ATP flux CO 2roduction occurs in 2 places during aerobic metabolism… 1. PDH reaction = CO2 production from carbohydrate metabolism 2. TCA Cycle, pyruvate entry into aerobic metabolism generates more CO2 per O2 consumed What does it mean when RER exceeds 1.0? Answer: No longer in aerobic metabolism. What is happening to the ratio VCO /V2 ? 2 Answer: Carbon Dioxide levels are increasing beyond the level of oxygen consumed. If RER exceeds 1.0, then CO2 is coming from buffering protons and not from metabolism. NON-METABOLIC CO PRODU2TION What is happening? Lactate and hydrogen are transported out of the cell through a transport protein. Fate of LACTATE AND H + Lactate circulated through body, used as energy source for heart, brain, and muscle LDH conversion to pyruvate and entry into TCA Hydrogen enter the RBC and combine with bicarbonate and is blown off as CO at the lung 2 Exercise Induced Hyperventilation: rapid ventilation to blow off CO 2 Re-breathe CO , 2lkalinic Energy Expenditure during Maximal Aerobic Exercise: 7 VO (maximal O uptake) 2max 2 Point at which O2 consumption does not increase with further increase in intensity Best single measurement of aerobic fitness Not best predictor of endurance performance Plateaus after 8 to 12 weeks of training o Performance continues to improves o More training allows athlete to compete at higher percentage of VO 2max VO 2max Untrained young men: 44-50 Untrained young women: 38-42 Absolute vs. Relative VO 2 Absolute is total consumption in L/min Max = 3 – 6 L/min Relative is oxygen consumption per kg of body weight in ml/kg/min Max = 35 – 55 ml/kg/min O2 demand > O2 consumed in early exercise Body incurs O2 deficit – time to get to steady state O2 required – O2 consumed Occurs when anaerobic pathways used for ATP production O 2eficit energy required from non-aerobic metabolism to reach steady state EPOC the VO n2eded to replenish ATP/PCr stores, converts lactate to glycogen, replenishes hemo/myoglobin, clears CO 2 Metabolic Thresholds: Lactate threshold point at which blood lactate accumulation increase markedly Lactate production rate > lactate clearance rate Interaction of aerobic and anaerobic systems Usually expressed as percentage of VO 2max 8 ~ 65 – 70% in most people What happens as exercise intensity increases? Shift to CHO metabolism – glycolysis Recruit larger muscle fibers (glycolytic systems) When NADH builds up in the cytosol = LDH reaction Threshold Summary: KNOW THIS Exercise intensity increases Increase in blood lactate o What causes this? Lactate allows glycolysis to continue Protons are generated from ATP hydrolysis Protons and La are pumped into the blood Protons cause pH to decrease! Endurance Training Adaptations: we become more efficient! Utilize greater fat% at higher intensities…30% improvement Metabolic Adaptations to Endurance Training Increased fat oxidation for a given exercise intensity. Metabolic Efficiency: 7 weeks endurance training use less muscle glycogen at a submaximal (80%) exercise intensity Why? Oxidative delivery/uptake: SV HR Cardiac Output Peripheral skeletal muscle adaptations improved oxygen extraction from the blood Oxygen consumption = cardiac output X oxygen extraction Cardiopulmonary System: Why does VO2 increase? VO2 = (cardiac output) X a – VO2diff Chronic Endurance Training 9 Ventilation and VO2 Oxygen delivery and uptake – peripheral component Increase in capillary density in skeletal muscle >15% increase 2 hrs/day for 12 days type IIA increase in capillary density Peripheral Adaptations: Type I increase in size! ~ up to 25% Shift in fiber type to type I or type IIA I IIA IIB 6 weeks of END training increase in type I fibers Mitochondria Adaptations: Increase in mitochondrial density 15% more 30 – 35% larger Why does fat oxidation improve? Greater capillary density = delivery of and extraction of oxygen Higher expression of Type I Greater mitochondria Greater enzyme activity What is the end result? More NADH, FADH delivered to the ETC through fatty acid oxidation Up to 30% increase in fat oxidation Adaptations to Aerobic Training: High-Intensity interval training (HIT): time-efficient way to induce many adaptations normally associated with endurance training Mitochondrial enzyme levels are the same after HIT versus traditional moderate-intensity endurance training. Where does metabolic hydrogen come from? ATP hydrolysis 10 Adaptations to Hydrogen Buffering: Where does metabolic hydrogen come from? ATP hydrolysis & muscle contraction and glycolysis Lactate Threshold (LT): Exercise intensity where there is an abrupt increase in either muscle or blood lactate Up to 34% greater lactate clearance in trained subjects Occurs at higher % of max/workload in trained subjects Summary of Metabolic Adaptation to Aerobic Training: Type I fibers up to 25% size increase Capillary increase >15% increase Fatty acid oxidation 30% increase Mitochondria density 15% more, 30% bigger Mitochondrial enzymes 2.5 times more Adaptations to Anaerobic Training: Review for Exam 3: Explain RER o Measuring and quantifying resting and exercise energy expenditure. o Why can we only measure energy expenditure between 0.70 and 1.0? What does an RER > 1.0 represent? Where is the CO2 coming from? What is a metabolic threshold? What is causing this to occur?
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