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This 16 page Class Notes was uploaded by Ericka Pacocha on Sunday October 11, 2015. The Class Notes belongs to SPMD202 at Eastern Michigan University taught by WilliamArmstrong in Fall. Since its upload, it has received 27 views. For similar materials see /class/221469/spmd202-eastern-michigan-university in Sports Medicine at Eastern Michigan University.
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Date Created: 10/11/15
Cardiodynamics Movements amp forces generated during cardiac contractions CARDIAC CYCLE Systole Diastole 5mm Cardiac cycle 0 Contractions of the heart are carefully timed to assure the correct pressure relationships Atrial systole and ventricular systole do not occur simultaneously and Atrial diastole and ventricular diastole differ in duration 5mm Atria act as primer pumps for ventricles 0 Delay of gt110 sec between passage of cardiac impulse from the atria to the ventricles 7075 of the blood flows passively into the ventricles 5mm Phases of the Cardiac Cycle 0 Atrial systole 100 msec rest 0 Ventricular systole 270 msec rest 0 Ventricular diastole last 430 msec of cycle 5mm EndDiastolic Volume EDV amt of blood in each ventricle at the end of ventricular diastole the beginning of ventricular systole EndSystolic Volume ESV amt of blood remaining in each ventricle at the end of ventricular systole the start of ventricular diastole 5mm Stroke Volume SV 0 amt of blood pumped out of each ventricle during a single beat EDVESVSV Ejection Fraction 0 Percentage of EDV represented by SV 5mm Cardiac Output 0 The amount of blood pumped by each ventricle in 1 min CO SV x HR mlmin mlbeat beatmin Difference between resting amp maximal CO is cardiac reserve 5mm Factors Controlling S V SV EDVESV EDV filling time venous return ESV preload contractility afterload 5mm Factors Affecting EDV Filling time depends on HR increased HR decreases filling time 0 3 Principle Mechanisms that Increase Venous Return 1 Venoconstriction 2 Muscle pump 3 Respiratory pump 5mm Factors Affecting ES V Preload degree of stretching experienced during ventricular diastole Lengthtension relationship applies FrankStarling Principle 1VIechanism more in more out gtEDV gtContraction 5mm Factors Affecting ES V Contractility the amount of force produced by each contraction Changes in contractility caused by 1 Autonomic stimulation 2 Hormones 3 Changes in ion concentration 5mm Factors Affecting ES V Afterloadthe amount of tension the contracting ventricle must produce to force open the semilunar valve and eject blood T afterload D T isovolumetric contraction 3 1 duration of ventricular ejection 2 T ESV amp i sv 5mm Factors Affecting HR 0 Autonomic NS 0 Hormones 0 Changes in ion concentration 0 Changes in body temperature 5mm Metabolism The sum of all biochemical processes under way in the human body at any moment SPMD 202 Metabolism Adenosine Triphosphate ATP is the basic energy source in the human body All food is ultimately broken down to ATP SPMD 202 Metabolism Carbohydrates Ilplds and promlns 02 CATABOLISM oxargonic ADP Pi ANABOLISM endergonic Synthesized Building block end products precursors Metabolism 3 Bioenergy Systems Phosphagen ATPCP Glycolytic Lactic Acid Oxidative Aerobic Metabolism 5mm Metabolism Catabolism breaks down organic substrates releasing energy that can be used to synthesize ATP or other high energy compounds About 40 efficient 5mm Metabolism Anabolism 0 Cells synthesize new organic components for three reasons 1 To perform structural maintenance and repazrs 2 To support growth 3 To produce secretions 5mm Metabolism Cells tend to conserve the materials needed for anabolism and breaks down the rest CHO Fats Proteins 5mm Carbohydrate Metabolism CGHIZOG 6 02 a 6 C02 6 H20 glucose oxygen carbon water dioxide net gain of 38 or 36 molecules of ATP 5mm Carbohydrate Metabolism Glycolysis Anaerobic energy production does not require oxygen breakdown of glucose to pyruvate occurs within the cytoplasm 5mm Glycolysis Requires 0 glucose 0 appropriate cytoplasmic enzymes 0 ATP and ADP inorganic phosphates Pi 0 NAD nicotinamide adenine dinucleotide 5mm Glycolysis Net reaction CBHIZO6 2 NAD 2 ADP 2 Pi gt 2 pyruvate 2 NADH 2 ATP 5mm Glycolysis Phosphorylation 3 R OH ATP lt gt R O P O ADPH 0 5mm Glycolysis Q39YCDQEquot CYTOSOL 2235 NADH amp NAD H 2 pyruvate lactate Mitochondrial ATP Production Double Layer Membrane outer layer is permeable to pyruvate inner membrane contains a carrier protein that moves pyruvate into the mitochondrial matrix 5mm Mitochondrial ATP Production Pyruvate F Coenzyme A COz J K NADH AcetylCoA 5mm Mitochondrial ATP Production Tricarboxylic Acid TCA Cycle 0 AKA citric acid cycle or Krebs cycle CH3CoA 3 NAD FAD GDP 12 H20 gt CoA 2 02 2 NADH FADHZ 2 H GTP 5mm Mitochondrial ATP Production Oxidative Phosphorylation 0 produces over 90 of ATP used by cells 0 involves oxidationredu ction Oxidation lose electron Reduction gain electron the reduced molecule gains energy at the expense of the oxidized molecule 2 Hz 02 gt 2 H20 5mm Mitochondrial ATP Production 2x Pyruvate 3C CoA gt Acetyl CoA 2C COz Acetyl CoA 2C Oxaloacetate 4C gt Citrate 6C CoA 2 H20 2 C 2 2 NAD 2 NADH FAD FADHZ GDP GTP ATP 5mm Mitochondrial ATP Production 0 Thus far we have only net how many ATP 4 The rest are produced via the electron transport ch ain synmm Electron Transport Chain NADH 3 ATP ATP NADHVQ Reducmse Coenzyme Q ltI FADH12 ATP ATP cymchmme Reductzse Cytochrome C ATP Cytochrome Oxidzse 1 02 smnzuz SUMNIARY GLYCOLYSIS 2 ATP 2 NADHx3 3 6ATP TCA CYCLE amp 2 GTP 3 2 ATP ELECTRON s NADH x 3 3 24 ATP TRANSPORT 2 FADHz x 2 3 M 38 ATP synmm Lipid Metabolism Adipose triacylglycerols triglycerides are broken down and released as free fatty acids FFA and glycerol 0 FFA are taken up by the cells and broken down into Acetyl CoA Oxidation 5mm Lipid Metabolism Oxidation FFA molecules are broken down into 2C fragments 0 each step generates molecules of acetyl CoA NADH and FADHz 5mm Lipid Metabolism Acetyl CoA TCA Cycle or Ketone Bodies acetoacetic acid hydroxybutaric acid acetone smnzuz Lipid Metabolism Fats burn in the ame of carbohydrates I Acetyl CoA enters TCA cycle only if fat and CHO degradation are appropriately balanced I That is entry of acetyl CoA into the TCA cycle depends upon availability of oxaloacetate for the formation of citrate I The concentration of oxaloacetate is lowered if CHO is not available Oxaloacetate is normally formed by pyruvate 5mm Lipid Metabolism I In fasting and diabetes oxaloacetate is consumed to form glucose and acetyl CoA is converted to ketone bodies 5mm Lipid Metabolism Ketone Bodies I converted to acetyl CoA in the tissues esp muscle and enter the TCA cycle I can be used directly for energy in the heart and kidney 5mm Lipid Metabolism BOxidation 2C NADH X 3 3 3 ATP FADH2 X 2 2 ATP TCA Cycle 12 ATP FFA CoA 1 ATP 16 ATP 18C FFA X 9 3 144 ATP 5mm Lipid Metabolism Glycerol 0 can be converted to glucose via glyceraldehyde3phosphate G3P and enter glycolysis 0 Conversely glucose can be converted to glycerol and join FFAs to triacylglycerols lipogenesis 5mm Protein Metabolism 0 Proteins can also be used for energy in the case of starvation and excessive endurance training 0 Amino acids are either 7 ketngznic converted to acetyl CoA 7 glucugenic converted to pyruvate 7 or both 5mm
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