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3/3 and 3/5 notes

by: Alec Greenspoon

3/3 and 3/5 notes KIN 421

Marketplace > University of Miami > Physics 2 > KIN 421 > 3 3 and 3 5 notes
Alec Greenspoon
GPA 3.65
advanced systemic physiology
Dr. Perry

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About this Document

All notes from lecture and discussion
advanced systemic physiology
Dr. Perry
Class Notes
25 ?




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This 7 page Class Notes was uploaded by Alec Greenspoon on Sunday March 15, 2015. The Class Notes belongs to KIN 421 at University of Miami taught by Dr. Perry in Fall. Since its upload, it has received 165 views. For similar materials see advanced systemic physiology in Physics 2 at University of Miami.


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Date Created: 03/15/15
33 amp 35 03032015 3315 Prostaglandins Different types 0 Cytoprotective COX 1 PGE and PGF gastric protection Inhibition causes an upset stomach and decrease in platelet aggregation o In ammatory COX 2 PGI prostacyclin Involved with regulating sodium and water cause sodium to be secreted Inhibition causes clotting sodium retention increased BP Lipoxygenase enzymes 0 Form leukotrienes 0 Inhibition will cause vasodilation less in ammation less free radicals Thrombroxanes cause platelets to become sticky increases aggregation and clotting involved with COX1 Know main drugs and which group they are in COX1 vs COX2 Nonselectivel work on both sides some work more towards one side 0 Slide goes from mainly COX1 to mainly COX2 beginning with aspirin Know which drug to take with current medical conditions hypertension CVD risk upset stomach etc Single action drugs 0 Block COX1 andor COX2 but not lipoxygenase enzymes Dual action inhibit COX enzymes and lipoxygenase enzymes Prevent cleavage of arachidonic acid 0 Block phospholipase A2 Higher dosage more antiin ammatory Cox 3 inhibitors 0 Inhibits conversion of prostaglandins to brain prostaglandins Promotes feeling of well being Works more on pain and fever No effect on lipoxygenase pathwayactivity Does not reduce in ammations GI distress or platelet activity Acetaminophen Tylenol n Too much can be toxic to liver 0 Makes liver work harderincreases enzymes Increased temp with exercise 0 Friction from contracting muscles causes temp to go up but does not effect set point 0 Brain realizes temp wants to go beyond set point 0 Uses mechanisms to reduce temp sweating vasodilation How do prostaglandins effect temp Increases temp of hypothalamus increases set point 0 Allows temp to climb fever Glucocorticoids synthetic OOOO 0 Work higher up the cascade more effective 0 Have higher potential adverse effects bone loss muscle loss increased BP edema etc Kidneys potential for acute renal failure Vasoconstriction to the kidneys increased sympathetic tone with exercise P65 and local kidney substrates cause vasodilation to prevent decrease in glomerular ltration rate from exercise and ensuing vasoconstriction o COX1 inhibitors will work against kidney P65 and cause constriction 0 Could cause kidney failure especially in the heathumid environment Myoglobin will leak into bloodstream from intense exercise and cause kidney issues ultimately failure and death 3515 Energy systems 0 Energy capacity to perform work Several forms of energy chemical light nuclear etc see slide Muscle contraction electromechanical energy Phosphate group furthest from parent molecule is highest in energy 0 Last P on ATP has more energy than last on ADP AMP Power depends on rate that ATP can be supplied Phosphagens see slide 0 ATP and phosphocreatine PCr o PCr lasts up to 305 0 Break down PCr yields energy and free P Free P liberated and added to ADP in order to make ATP PCr broken down rapidly to keep ATP synthesis going 0 Limiting factor is PCr Once gone no more free P to add to ADP o Breakdown of ATP during recovery yields a free P Added to Cr to make PCr ADP Difficult to increase PCr stores with training Bigger musce stores more substrates ATP and PCr 0 Weight lifters Related to size of the muscle rather than training adaptations Sprinters are better at increasing enzymes that break down the phosphagens 0 Less related to increased stores different mech from resistance training athletes Data on creatine monohydrate o Allows you to train harder doesn t necessarily increase speedmuscle mass directly 0 Enzymes that break down ATP are highest in sprinters 23 fold higher in type 2 compared to type 1 PCr breakdown increases hydrogen phosphate 0 Combine with H ions to form H2PO4 Associated with peripheral fatigue In CHF and diabetics PCr is more quickly turned over higher ATP consumption 0 Rates of resynthesis are slower Short term negative effects of PCr 0 Increase ionic bulk thus changing ionic balance Draws extra water into the cell thus diluting electrolytes n Increased cramping Anaerobic Glycolysis No molecular 02 involved 6 carbon sugar becomes two 3 C sugars IOYruvate Net of two ATP produced Niacin involved with NADH Glycogen is branched stored in muscle 2ncl messenger of aglycogen phosphorylase is cAMP o activates protein kinase Glycogenolysis refers to rst two steps of glycogen breakdown in muscle 0 Glycogen l glucose6P 0 see steps for muscle glycogen breakdown on diagram lnsulin gets glucose into the cell Costs one mole of ATP to phosphorylate glucose into glucose6P 0 Adding P traps it into the muscle can no longer break out into bloodstream G6P F6P o PFK converts F6P into fructose 16 bisphosphate Accumulation of H ions inhibits PFK 0 Breaking SH thiol bond yields a lot of energy 0 NAD reduced to NADH 0 Type II bers are higher glycogen bers more NAD shuttles Pay attention to functional group on top aldehyde to carboxcylic acid Anemic runners have mutation that creates 23 instead of 13 bisphosphoglycerate helps with unloading oxygen 0 Not al NADH will go to the electron transport chain 0 Used to convert pyruvate into lactate Too much lactic acid destroys enzymesinhibits conversion Begins to break down immediately with exercise becomes predominant system in 20305 0 400m sprinters rely heavily on this 0 Summary 0 Will always prefer to breakdown muscle glycogen then use glucose from blood stream 0 One mole of ATP is spent for every mole of glucose phosphorylated 0 Net ATP is closer to 3 than 2 2 when using glucose from the bloodstream o All reactions are cyclical Know where NAD comes from which step Fate of lactic acid 0 Taken up by muscle and oxidized Taken up by liver and converted into glycogen via Cori cycle Lactic acid accumulation stimulates testosterone Don t worry about hybrids Lactate accumulation does not mean lactate production 0 Could be due to less clearing of lactate lf mitochondria is full of other substrates no where to put pyruvate 0 Will have higher lactic acid levels 0 More fast twitch more lactate Lactate threshold 0 Point where lactate levels shoot up dramatically 0 Most highly correlated with performance 0 Delaying onset jump in production makes u fastermore efficient 40mgdL is break point onset of blood lactate accumulation 0 build up of end products 0 acid breaks down enzymes


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