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KIN321 Exam 1 Review

by: askcch

KIN321 Exam 1 Review 321

Marketplace > University of Miami > Kinesiology > 321 > KIN321 Exam 1 Review
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These notes cover what's on the first exam on 9/15
Introduction to Systemic Exercise Physiology
Dr. Kevin Jacobs
Study Guide
Kinesiology, Systemetic, Physiology
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This 18 page Study Guide was uploaded by askcch on Wednesday September 21, 2016. The Study Guide belongs to 321 at University of Miami taught by Dr. Kevin Jacobs in Fall 2016. Since its upload, it has received 5 views. For similar materials see Introduction to Systemic Exercise Physiology in Kinesiology at University of Miami.


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Date Created: 09/21/16
  KIN321  Exam1Review    Lecture 1 Bioenergetics and Calorimetry   ● Thermodynamics = study of energy exchange in physical science.   ○ 1800s ➙ ability to predict work output of steam engines.   ● Bioenergetics = study of the exchange of energy in the biological world.  ● 1st Law of Thermodynamics ➙ Energy can be neither created nor destroyed,  but only converted from one form to another.  ● 2nd Law of Thermodynamics ➙ The exchange of energy is imperfect and  some energy will escape.   ○ Loss of heat  ● ATP is used for many functions including:   ○ Chemical work ➙ driving reactions that are not spontaneous  ○ Transport ➙ movement of substances against concentration gradients  (Na+ - K+ pump)  ○ Mechanical work ➙ “crossbridge cycling”   ● [ATP] changes very little even during intense exercise.   ● Metabolism is sum of all energy transformations within an organism.   ○ Impossible to measure ➙ ∴ metabolism is the rate of heat production.  ● Calorimetry is measurement of heat to determine metabolic rate.  ○ Direct calorimetry involves the measurement of heat production.   ■ Bomb Calorimeter determines caloric content of food   ■ Room Calorimeter determines heat production (closed room  measuring temp change)  ○ Indirect calorimetry involves the measurement of oxygen consumption    1          ● Caloric Equivalents of Food    ○ Protein’s energy density is lower inside the body than outside the body  because human can’t use nitrogen (in proteins) as energy   ○ Protein is a building block for muscle, hence if using protein as fuel it  breaks them down   ○ Carb is prefered energy source during exercise as it gives more kcal/L of  O2 consumption  ● V co2/V O2 ratio (R ratio)  ○ Range 0.7~1.0  ○ This number is determined because of the structures of protein and fat            2        Lecture 2 Digestion & Absorption   ● Functions of food  1. Energy   2. Growth & Development  3. Regulation of metabolism (how the body uses fuels)  ● Carbohydrates   ○ Not good optimal energy to be stored because of low caloric  density   ○ Monosaccharides, Disaccharides,  Oligosaccharides/Polysaccharides   ■ Only fructose, glucose, and galactose can be absorbed  ■ Mono and Disaccharides are “simple sugar”  ● Lipids   ○ Simple: Triglycerides,   ○ Compound: Phospholipids, Lipoproteins, Chylomicrons (how  triglycerides appear in blood)  ○ Derived (body can produce): Cholesterol   ○ No double bond = saturated (tend to be solid in room temperature  e.g. butter)  ○ One double bond = monounsaturated   ○ More double bond = polyunsaturated   ○ Trans fat→ “partially hydrogenated” as code name  ■ ^ shelf life  ■ Bad, increases LDL-C and lowers HDL-C    3        ● Protein  ○ Combination of up to 20 dierent amino acids via peptide bonds.   ■ C, H, amino group (Nitrogen), carboxylic acid group, and side  chain.  ● Why GI function is important to exercise?  ○ Dehydration, Hyperthermia, and CHO depletions are common  causes of fatigue during prolonged exercise  ● Small intestine: absorbs macro nutrients, water, and electrolytes   ○ Glucose and Amino Acids absorbed go into the Liver before they  enter the circulation   ● Large intestine: absorbs water and electrolytes ONLY  ● Gastric Emptying:  ○ Stomach is a holding tank-> only a small amounts of alcohol and  vitamin B12 is absorbed here  ○ Stomach’s elasticity (rebound eect) pushes food into small  intestine, therefore, gastric emptying poses limiting factor for  absorption   ○ how to measure gastric emptying?   ■ ingest uid with dye, put tube into the stomach through GI to  extract samples to see how much does the dye go away   ● Gastric emptying is controlled to ensure delivery of water and  solute at rate slightly less than intestine’s absorptive capacity   ● Factors inuencing gastric emptying:   ○ Volume ➙ ↑ V = ↑ emptying rate.   ○ Energy content ➙ ↑ energy = ↓ emptying rate.     4        ■ < 6-8% CHO, 6-8 g CH O/L 2ecommended.   ○ Osmolality ➙ ↑ osmolality = ↓ emptying rate.   ■ Glucose polymers   ○ Exercise ➙ > 70-75% VO2max ↓ emptying rate.   ○ Dehydration ➙ ↓ emptying rate.   ○ Optimal uid/CHO replacement ➙ 30-60 g CHO/hour in a  6-8% solution ingested at a rate of 600-1200 ml/hour.  ● 1.4g of CHO/min is the max avg rate for CHO to be absorbed  ○ So don’t take more than ~70g of CHO per hour  ● Intestinal Digestion:  ○ The majority of CHO digestion happens in the small intestine   ○ The majority of FAT digestion happens in the small intestine   ■ Bile breaks down large fat droplets into smaller pieces for  pancreatic lipase to further break down (breaks fat into FA,  diacytlglycerols, and monoacytlglycerols)  ○ The majority of PROTEIN digestion happens in the stomach  ■ and it also extend into the intestinal epithelial cells  ● Intestinal Absorption:  ○ Small intestine divided into:  ■ Duodenum  ■ Jejunum  ■ Ileum  ● Surface area of small intestine is increased up to 600 fold by:  ○ Circular folds (x3)  ○ Villi (x10)    5        ○ Brush border (x3)  ● The time from ingestion to blood appearance for:  ○ glucose ~15min  ○ fat ~2-4hrs  CHO:  ● Glucose and galactose are actively transported by sodium- and  glucose-linked transporter molecule (SGLT-1)  ○ SGLT-1: glucose, galactose, sodium, and water (like GLUT-4)  ● Fructose moves by facilitated GLUT-5 transporter   ● goes into the liver  LIPIDS:  ● ingested long chained fat turns into chylomicrons in the epithelial cells,  then into the lymph system, then into bloods   PROTEINS:   ● active transport, go into the liver  H 2:  ● Water always moves to where it has more particles, to dilute the uid  ● Majority are absorbed in the small intestine (85%)  ● Water absorption can occur passively via osmosis or actively via SGLT-1.   ○ SGLT-1 mediated water absorption may account for up to 70% of  total water absorption.      6        Lecture 3 ATP, CP, and Glycolysis  ● 3 major ATP generating methods:   ○ Creatine Phosphate (v. rapid)  ○ Glycolysis (rapid)  ○ Oxidative Phosphorylation (slow)  ● Benet of low resting ATP: to maintain metabolic sensitivity   ● Slow Glycolysis   ○ All the pyruvate can be oxidized in the mitochondria   ■ Doesn’t need to produce lactate  ○ Rate of NAD regeneration is enough from shuttle   ● Rapid Glycolysis  ○ Rate of pyruvate production > pyruvate oxidation  ○ Rate of NAD regeneration via mitochondrial shuttle is insucient   ○ Therefore, lactate is produced to recycle o the rate-limiting  factors  ■ RBC all the time, take in glucose spit out lactate  ■ Type IIB bers across a wide range of exercise intensities   ● ∵ low mitochondrial density ∴rate of pyruvate  production > oxidation early  ■ Type I bers only at max intensity because of high  mitochondrial density  ■ Lactate can be oxidized at the production site, or be sent  through blood to another site (heart mainly) to be oxidized.  Or → liver (gluconeogenesis) → glucose    7        ■ Lactate can be seen as a glucose (CHO)/Energy group to be  donated from one muscle to another  ■ The CORI cycle: Muscle produce pyruvate/lactate → liver take  them to make glucose → muscle for fuel   ● Lactate threshold test → the lactate threshold indicates the intensity at  which one can withhold for a prolonged period of time  ● Lactate is more metabolically ecient* ∵only 1 step Lactate → Pyruvate  ∴Body oxidizes it more than glucose when it becomes more prevalent   ● Intracellular lactate shuttle: NADH shuttle to produce NAD   + ○ Pyruvate/Lactate Carrier (MCT) is found on the mitochondrial  membrane   ○ LDH found inside the mitochondria turns lactate and NAD into  + pyruvate and NADH  ○ This shuttle substrates into mitochondria for ATP production  (while the other two shuttle NADH in)  ○ This shuttle adds on to the other two shuttles when lactate level is  really high   ■ E.g. during rapid glycolysis and recover period  ● Lactate causes fatigue by leading to lactate acidosis?  + ○ Lactate actually consumes H to buer muscle acidosis             8        Lecture 4 Lipid Metabolism    ● Lipid mobilization is dependent on:  1. Rate of lipolysis  2. Rate of re-esterication   3. Rate of fatty acid export via circulation   ○ Fatty acid is either re-esteried or enter the circulation   ○ Glycerol always goes to the blood → liver  ■ Therefore glycerol level in blood is a good lipolysis rate indicator   ● At times of stress, you always mobilize energy  ○ Epi → Lipolysis  ○ Insulin (storage) → Lipolysis inhibitor   ● Proportion of fatty acid re-esteried is high during   ○ rest (body doesn’t need much fuel)  ○ high intensity exercise (reduced blood ow to adipose tissue &  increased need for glucose)  ○ FA → circulation is 30-50% during rest, but 65-80% during  low/moderate exercise, 10-30% during high intensity exercise  ■ Railroad switch, provide immediate supply of FA for energy   ● FA are transported in the plasma in association with protein albumin → thre  high anity FA binding sites  ● Lipid uptake is likely facilitated transport instead of passive diusion because  of Saturated Kinetic, which the plasma FFA Uptake level plateaus with  increasing FFA concentration in blood  ○ Only that many transporters can work simultaneously at a time  ● Three key fatty acid transporters identied:    9        1. Sarcolemmal FABP → membrane bound (low rate, working 24/7) (at  sarcolemma)  2. FAT/CD36 → translocated from sarcoplasm (move when needed,  recruited after meal, during or after exercise) (at sarcolemma)  3. Cytosolic FABP (moves fat within the cytosol)  ● Abundance of fatty acid transporters increase with:  1. Endurance training (pushing ability to oxidize fat)  2. High fat/low CHO diets  ● FA in the sarcoplasm have two potential fates:  ○ Prior to either fates, FAs are activated using ATP and forms fatty-acyl  CoA  1. Esterication into intramuscular triglyceride (IMTG)  a. IMTG is important for exercise recovery   2. Transport into mitochondria for oxidation   ● Fatty acids must enter mitochondrial matrix to undergo oxidation   ○ Short- and medium-chain fatty-acyl CoA enter via specic carrier  protein → little or no regulation   ○ Long-chain fatty-acyl CoA enter via carnitine and carnitine acyl  transferase enzymes (CAT1 and CAT2)   ■ CAT1 takes CoA o, puts on carnitine  ■ CAT2 reverses the process, takes carnitine o, put on CoA from  the matrix  ■ ∴ CAT is the rate-limiting enzyme of long chain fat oxidation   ● High intensity exercise inhibits CAT1  ● Carnitine-decient patients have reduced capacity to oxidize  lipids   ● Beta oxidation     10        ○ Creates Acetyl-CoA → TCA cycle; FADH , NADH → Elec2ron Transport  Chain  + ○ Promoters = low Acetyl-CoA, low NADH/NAD   ■ Low intensity exercise   ■ CHO depletion  ○ Inhibitors = high Acetyl-CoA, high NADH/NAD   + ■ High exercise intensity   ■ CHO supplementation   ● Metabolism during recovery   ○ Need to rebuild glycogen storage   ○ Thus increased fat oxidation as fuel  ○ Low RER values during recovery from exercise = heavy reliance on fat as  a fuel source  ○ Although CHO is primary energy source during moderate to high  intensity exercise, lipid oxidation is substantial during recovery  ○ Lipid oxidation is the same during recovery from 45 and 65% VO 2peakas  long as exercise energy expenditure is the same  ■ “Fat burning zone” is not necessary/valid  ■ ^ energy expenditure (cal burned) = ^ fat burned afterwards              11        Lecture 5 Amino Acid Metabolism & Exercise Metabolism   ● Nitrogen is metabolically useless; we can’t use it as fuel   ● Use of amino acids as fuel sources limited to fasting and prolonged exercise  (depletion of CHO)  ● Nitrogen can be removed from amino acids by one of two ways:  ○ Oxidative deamination  + ■ Occurs ONLY in the mitochondria of the LIVER and involves NAD as an  oxidizing agent  ○ Transamination   ■ Occurs in many tissues (including muscles) and involves the transfer of  nitrogen  ○ They all compounds the nitrogens to get rid of it through the Urea Cycle  ■ When ppl consume excess protein, Nitrogen content goes up in the  urea  ■ High protein diet → increased urea amount & frequency → loss of  water weight  ● Most amino acids carbon skeletons are converted to either:  1. Pyruvate  2. Acetyl-CoA  3. TCA cycle intermediates   ○ BCAAs are preferentially oxidized  ■ Use of BCAA as a fuel source begins with transamination to glutamate  ● Gluconeogenesis   ○ ONLY IN LIVER (& small portion in kidney)  ○ Pyruvate → Alanine → Gluconeogenesis  ○ Enzymes for conversion: Alanine/Lactate → Pyruvate → Pyruvate  Carboxylase → PEPCK → F1, 6BP (reverse PFK) → G6P → Glucose      12        ● Regulation of CHO metabolism     ● Regulation of Lipid metabolism    ● Endogenous fuel stores  ○ Fat is a very ecient form of energy storage   ■ 9 kcal/g for fat vs. 4 kcal/g for CHO    13        ■ Each gram of CHO stored with 3g H O → comp2unds storage  ineciently   ○ CHO is a more ecient source of energy during exercise   ○ AA contributes 15% of energy fasting/prolonged exercise, 5% when fed  ● Substrate partitioning during exercise   ○ Exercise intensity is primary factor, all others are secondary   ○ Duration  ○ Fuel availability → Diet and exercise duration  ○ Gender (During prolonged moderate exercise, female tend to use more fat  than male)  ○ Ambient temperature   ● Why does relative contribution of lipids decrease with increasing intensity?  ○ Higher necessary ATP re-synthesis rates  ○ CHO metabolism regulates lipid metabolism → inc. glycolytic ux likely  decreases long-chain FA transport into mitochondria (inhibits CAT enzymes)  ○ Inc. recruitment of fast twitch bers  ○ Decreased FFA availability → reduced adipose blood ow and lactate  ● Exercise duration     14        ○ Inc. exercise duration results in:  ■ Inc. reliance on plasma sources of fuel (glucose and FA) and dec.  reliance on intramuscular fuel sources (glycogen, IMTG)  ■ Inc. reliance on lipids and dec. reliance on CHO  ○ Approx. depletion times of CHO during moderate exercise  ■ Muscle glycogen: 60-90 min  ■ Liver glycogen: 80-120 min  ● Ingestion of CHO during exercise spares liver glycogen (glucose absorbed goes  right into circulation and to muscles) → protect blood glucose level → support  longer exercise, and higher race pace/intensity   ● Training adaptations   ○ Endurance training → adaptations that favor greater reliance on lipids at the  same absolute intensity  ■ Inc. capillary density  ■ Inc. expression of sarcolemmal FA transporters  ■ Inc. mitochondrial density  ● Higher activities of beta-oxidative enzymes  ● Higher activities of TCA cycle enzymes  ○ However, pattern of use at the same relative intensity is unaltered by  endurance training   ■ CHO needs are not reduced by such training and instead are likely  increased due to:  ● Improved ability to sustain higher exercise intensities  ● Improved ability to sustain longer exercise durations   ∴ People think CHO doesn’t matter that much in a trained state is wrong        15        Lecture 6 Neural-Endocrine Control of Metabolism  ● Hormones - chemical messengers that act either locally (acetylcholine, Nepi) or  generally (Epi, Nepi, insulin, glucagon, etc.)  ○ Polypeptide hormones interact with receptors on cell surface  ○ Steroid hormones move through cell membrane and interact with cell  nucleus   ○ Hormones generally have three eects:  ■ Alter permeability of cell membrane to metabolites or ions  ■ Activate an enzyme or second messenger (Epi → cAMP → HSL →  Lipolysis)  ■ Activate genetic apparatus to manufacture intracellular proteins  (Steroid Hormones)  ● Insulin  ○ Translocates GLUT-4 to cell membrane to increase glucose storage into the  cell  ● Cyclic AMP  ○ Increase 1) Glycogenolysis 2) Lipolysis 3) Hormone release  ● Hormone regulation and action  ○ Endocrine Glands:  ■ Hypothalamus and pituitary glands (growth hormone)  ● Hypothalamus controls activity of the anterior and posterior  pituitary glands; it also receives neural input and is sensitive to  blood metabolite concentrations (esp glucose, some lactate)  ● Growth hormone is essential for normal growth (protein  synthesis and bone growth)  ○ It increases during acute exercise   ○ Mobilizes fatty acids from adipose tissue (secondary to Epi)    16        ○ Aids in the maintenance of blood glucose by increasing  gluconeogenesis and reducing uptake by adipose tissue   ■ THyroid and parathyroid glands  ■ Adrenal glands (Cortisol/Catecholamines i.e. Epi, Nepi)  ● Adrenal medulla secretes Epi and Nepi  ○ Promotes lipolysis, liver and muscle glycogenolysis (glucose  breakdown)  ○ ^VO 2maxintensity ^CATs (positive linear correlation due to  sympathetic signals)  ● Adrenal cortex secretes   ○ Aldosterone → maintain plasma Na /K and regulates BP  ○ Cortisol → promotes lipolysis, protein catabolism, and  gluconeogenesis  ■ Pancreas   ● Secretes digestive enzymes and bicarbonate into small intestine  ● Insulin → promotes the storage of glucose, amino acids, and fats  ● Glucagon → promotes the mobilization of glucose from the liver  and FA from adipose tissue   ■ Testes and ovaries (Testosterone/Estrogen)   ● Estrogen may promote lipolysis BUT progesterone seems to have  anti-estrogen eects on metabolism   ● Estrogen spikes late follicular phase → higher rate of lipolysis,  countered by spike of progesterone during mid luteal phase of  the menstrual cycle   ● Hormone potency is a function of:  ○ Concentration (High [epi]=0.003mg/5L blood)  ○ Receptor density (^receptor ^potency)  ○ Durability and half-life  ● Hormone eects:    17        ○ Metabolism  ■ Supply or mobilization  ■ Use  ○ Fluid Balance  ○ Blood pressure  ○ Muscle repair and hypertrophy   ● Eect of acute and chronic exercise on Insulin, Glucagon, and Epi  ○ Insulin  ■ Acute: Reduction in [insulin] from rest to exercise  ● Increasing time since last meal  ● Epi-induced inhibition of insulin secretion  ● Increased importance of contraction for glucose uptake (Insulin  not needed for GLUT-4 anymore since muscle contraction can do  the trick)  ■ Chronic: Reduction in [insulin] at rest following training   ● Training-induced increase in insulin sensitivity   ○ Glucagon (not important for exercise, important during starvation)  ○ Epinephrine   ■ Acute: Increase in [epi] from rest to exercise  ● Sympathetic stimulation of the adrenal medulla that is  proportional to the intensity of exercise  ■ Chronic: Lower [epi] during at the same absolute intensity, but similar  [epi] at the same relative intensity following training   ● Catecholamine (CAT) release scales to relative exercise intensity  whether the subject is untrained or trained      18 


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