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KIN 310 Exam 1 Review

by: Alina Levy

KIN 310 Exam 1 Review KIN 310

Alina Levy
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Physiology Basis of Conditioning
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This 14 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 28 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) à digestion à ATP (chemical energy) à Move (kinetic energy) + Heat Energy is neither created nor destroyed. The body Transforms energy from one form to another ATP ATP are formed in the cytoplasm  Energy is stored in the bonds of ATP molecules  ATP à ADP + P + Energy à ATPace  Breaking the outermost bonds contain the most energy. 80 – 100 g (about _3__ oz) of ATP – resting skeletal muscle ATP à ADP + Pi + Energy (catalyzed by ATPase) PCr + ADP à ATP + Cr (catalyzed by Creatine Kinase) (CK Most abundant and most active enzyme in skeletal muscle) Three processes/pathways to replenish ATP stores: 1. ATP PCr SYSTEM (Immediate energy system)  Sustains exercise for: 3 – 15 seconds  Adenosine triphosphate (ATP)  Phosphocreatine (PCr) (stored in cytosol) 2. FAST GLYCOLYSIS (Short-term energy system) Substrate: Carbs  Sustains exercise for: 30 seconds – 2 minutes 3. SLOW GLYCOLYSIS/AEROBIC (Long-term energy system) Substrate: Carbs and fats  Sustains exercise for: 2 minutes +  At rest, the body primarily uses FAT for ATP production (i.e. energy)  During short-duration exercise, the body primarily uses Carbohydrates for ATP production  During longer-duration exercise, the body uses Combination of Carbs and Fats for ATP production (i.e. energy) (longer than 10 minutes to use fat for energy. The 3 major macronutrients we eat are:  Fats  Carbohydrates  Proteins  We will refer to these as ‘substrates’  Substrates – something an enzyme acts on (something which is broken down) Carbohydrates: Break down to glucose which is stored as glycogen in the liver/muscles 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 4.1 calories of energy. Proteins rarely contribute to energy – unless an extreme state LONG TERM ENERGY SYSTEM: SHUTTLES AND ATP ACCOUNTING Lecture 3 Pt 1 Fat 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  Transport/Cellular Uptake  Activation  Translocation  Oxidation Step 1: Mobilization:  4 hormones can bind to a fat cell and stimulate it to mobilize a TG: Epinephrine, Norepinephrine, Cortisol, Growth Hormone à 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 o Most abundant of our plasma proteins (60%) o Produced in the liver o 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  Activation takes place in the cytosol  Activation involves the conversion of a FFA into a molecule of ‘Fatty Acyl- CoA’:Process requires the use of one ATP Step 4: Translocation  Fat is transported from cytosol into mitochondria  Enzyme: carnitine transferase (catalyses the translocation)  ‘Fatty-Acyl CoA’ is now inside the mitochondria Step 5: Beta Oxidation  ‘Cut up’ the Fatty-Acyl CoA into 2 carbon-molecules (acetyl CoA)  Acetyl CoA can then go through Krebs cycle  NAD & FAD go to the Electron Transport Chain  Every Beta Oxidation (cuts 2 carbons off the end) o 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: o ¿of carbons - 1 = 2  FAD/NAD from 1 Beta Oxidation spin: o 1 FAD, 1 NAD per spin = 5 ATP  Acetyl CoA per Fatty Acid Chain: 1 Acetyl = 12 ATP ¿of carbons o 2 =  1 Triglyceride = 3 Fatty Acid Chains o Multiply by 3 for a triglyceride: ATP Total     FOR ONE GLYCOGEN MOLECULE:  ATP used: __1__________  ATP produced: __4_______  TOTAL ATP: _3__________  NADH Produced: _2______  Fat oxidation requires more oxygen than glucose because a FFA molecule has more carbon and hydrogen Fat has more carbon and hydrogen  More acetyl CoA More Kreb’s cycles  + More NADH+H and FADH More ele2trons to be accepted at gate 4 ‘Fat burns in a Carbohydrate flame’ When liver cells convert amino acids to glucose, they start by converting the amino acids into an "intermediate"  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 "fats burn in the flame of carbohydrate."  Without carbohydrate in the diet,  fat is metabolized inefficiently. 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 normal/healthy range during exercise Pancreatic Hormones: Secretes: Insulin: when blood sugar levels get too high o Main function = Decrease blood glucose levels o ↑ blood glucose → ↑ insulin Secretes: Glucagon: when blood sugar gets too low o Main function = Increases blood glucose levels o ↓ blood glucose → ↑ glucagon Adrenal Gland Hormones: Adrenal Medulla: Secretes: Epinephrine and norepinephrine o Called ‘catecholamines’ – “Fight-or-Flight” response (↑ HR, BP) o Stimulate the breakdown of fat & glycogen Adrenal Cortex: Secretes: Cortisol o Promotes the use of fat as fuel o Using more fat for ATP à Spares blood glucose  Insulin levels go down during exercise* Regulation of Plasma Glucose Metabolism  More Epinephrine o More GLYCOGENOLYSIS (fat)  More Glucagon o More GLYCOGENOLYSIS o More GLUCONEOGENESIS à breakdown protein to energy  More Cortisol o More GLUCONEOGENESIS  Less Insulin o Less GLYCOGEN SYNTHESIS  Insulin Mechanisms: o Blocks glucagon release o Increases glycolytic enzymes o Decreases GLUCONEOGENESIS enzymes  All mechanisms would lower blood glucose  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 VO 2MAXAND LACTATE THRESHOLD Maximal Oxygen Uptake (VO 2max : “the greatest amount of oxygen a person can consume, transport, and utilize to produce ATP aerobically on a per-minute basis”  Also known as aerobic capacity  Best indicator of cardiorespiratory endurance and aerobic fitness  Increases with training  Magnitude of increase depends on baseline fitness level  Unfit people can increase their VO2 Max can improve by 50% How do we physiologically define VO 2max  Plateau *  Blood lactate  RER *  HR * VO 2maxdoesn’t always predict performance  Economy Lactate threshold  The point at which blood lactate appears to increase disproportionately above resting levels.  The point in time during exercise of increasing intensity when the rate of production exceeds the rate of clearance  Lactate accumulates in the blood when production exceeds its clearance  Lactate accumulation inhibits enzymes used in glycolysis à glycolysis slows downà energy production slows down Push LT to the right - Interval training is best way to push curve to right  LT is one of the best determinants of an athlete’s pace in endurance events:  Untrained = ~ 50% to 60% VO 2max  Elite athletes = ~ 70% to 80% VO 2max  World class elite athletes: 85-90% VO 2max ENERGY EXPENDITURE DURING EXERCISE RMR AND EPOC  Basal Metabolic Rate (BMR): energy expenditure (EE) required to sustain life  Requires 12 hours fasting  Participant remains in a reclined position  EE WITHOUT the influence of eating/muscle activity  Resting Metabolic Rate (RMR): similar to basal metabolic rate, but less stringent subject preparation  How much oxygen do we consume at rest?  3.5 ml/kg/min (1 MET)  What factors affect BMR and RMR?  Muscle mass-more muscle higher RMR  Weight  Age- older metabolic rate decreases.  Body temp- if your colder, metabolic rate goes down(survival mode)  Warmer- metabolic rate increases.  Gender- men have higher metabolic rate. VO 2oesn’t immediately drop to rest values after we stop exercising: “Excess Post- Exercise O C2nsumption” (EPOC)  EPOC: the volume of O con2umed above that normally consumed at rest Causes:  Elevated Hormones  Oxidizing lactic acid-still some left over when done exercising, need O2 to accept H+  Temperature-help us cool down, keep blood vessels dialated. Economy Effort Muscle fiber distribution (slow/fast twitch)  ↑ slow twitch fibres = ↑ economic Mechanics (wasted energy)  Better mechanics/technique = ↑ economic  Economy is a predictor of aerobic performance What happens to hormone Main Effects on Main Effects on Hormone Site of Release Plasma Glucose Fat Metabolism levels when we during Exercise during Exercise exercise? Lower insulin = less Lower insulin = storage of glucose as less storage of fat Insulin Pancreas ↓ glycogen (and more as triglycerides (↑ glucose stays in the FFA available for blood) energy) Glucagon Pancreas ↑ ↑ glycogenolysis ↑ lipolysis ↑ gluconeogenesis Catecholamin es Adrenal Medulla ↑ ↑ glycogenolysis ↑ lipolysis ↑ gluconeogenesis Cortisol Adrenal Cortex ↑ ↑protein catabolism for ↑ lipolysis gluconeogenesis Growth Pituitary ↑ X ↑ lipolysis hormone


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