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KIN321 Week 2 Class Notes (8/29-9/2)

by: askcch

KIN321 Week 2 Class Notes (8/29-9/2) 321

Marketplace > University of Miami > Kinesiology > 321 > KIN321 Week 2 Class Notes 8 29 9 2
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These notes cover Lecture 3 ATP, CP, and Glycolysis and Lecture 4 Lipid Metabolism
Introduction to Systemic Exercise Physiology
Dr. Kevin Jacobs
Class Notes
Kinesiology, Systemetic, Physiology
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This 5 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 8 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     lass   Notes   Week   2   8/29­9/2)  ________________________________________________________________________________  From    reviou  ection    ­ Bioenergetiand   alorimetry  ­ Digesti & Absorption  ________________________________________________________________________________  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  ■ 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             ____________________________________________________________________________   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:  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   ○ 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 2peak as  long as exercise energy expenditure is the same  ■ “Fat burning zone” is not necessary/valid  ■ ^ energy expenditure (cal burned) = ^ fat burned afterwards                       


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