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KIN321 Week 3&4 Class Notes (9/5-9/13)

by: askcch

KIN321 Week 3&4 Class Notes (9/5-9/13) 321

Marketplace > University of Miami > Kinesiology > 321 > KIN321 Week 3 4 Class Notes 9 5 9 13
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About this Document

These notes cover Lecture 5 Amino Acid Metabolism & Exercise Metabolism and Lecture 6 Neural-Endocrine Control of Metabolism
Introduction to Systemic Exercise Physiology
Dr. Kevin Jacobs
Class Notes
Kinesiology, Systemetic, Physiology
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This 7 page Class Notes was uploaded by askcch on Wednesday September 21, 2016. The Class Notes belongs to 321 at University of Miami taught by Dr. Kevin Jacobs in Fall 2016. Since its upload, it has received 3 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   Class     otes     eek   3&4    9/5­9/13)  ________________________________________________________________________________  From    reviou   ection    ­ ATP    and   lycolysis  ­ LipiMetabolism  ________________________________________________________________________________  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  ● 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  ■ Each gram of CHO stored with 3g H O → 2ompounds 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   ○ 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          ________________________________________________________________________________   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)  ○ 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:  ○ 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   


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