Study guide for exam 1
Study guide for exam 1 KIN 545
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This 45 page Study Guide was uploaded by Alec Greenspoon on Saturday February 28, 2015. The Study Guide belongs to KIN 545 at University of Miami taught by Dr. Smith in Spring2015. Since its upload, it has received 342 views. For similar materials see Special sport populations in Kinesiology at University of Miami.
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Date Created: 02/28/15
545 Exam 1 1122015 81100 AM Introduction Samson office hours 114 M and W 11415 Hypertension o Classifications 0 Essential hypertension used to be thought of as necessary 0 No medical cause 0 Risks include heart failure stroke myocardial infarction etc O systolic diastolic pulse pressure 0 Increase in pulse pressure is a sign of arterial stiffness o 10 point difference between sides can indicate peripheral artery disease should have 90 of BP in legs when compared to arms leading killer is diabetes hypertension known as the silent killer high BP heart must work harder to eject stroke volume 0 Become thicker stiffer enflamed and ventricular hypertrophy bad Ejection fraction will diminish Congestive heart failure blood pools in atrialungs and makes breathing difficult Endurance exercise can combat development of heart failure directly 0 Increases ventricular chamber size instead of thickness eccentric hypertrophy Increased venous return Increased ejection fraction and increased stroke volume 0 O O O 0 BP can be lowered up to eight hours after 20 minutes endurance or resistance training 0 Hypertensive individuals respond better to exercise Drug treatments and classifications Hypertension paradox NEJM HBP rx algorithm 11615 0 Exercise hypertension 0 Systolic above 250 0 Stage 1 1 drug 0 Stage 2 2 drugs 0 Increase in vegal tone from exercise contributes to decrease in BP 0 Response within 1 week 0 Plants more potassium 0 Frequency of exercise is important for acute and chronic effects of BP lowering o Lowered for at least 8 hours afterwards o Poiseuille s Law 0 Velocity of blood flow is related to pressure and directly proportional to the fourth power of the vessel s radius Radius is most important factor for blood flow 0 SNS9 vasoconstriction o Catecholamines angiotensinII 0 Beta blockers stop SNS signal calcium channels constrictors prevent vasoconstriction ACE and ARBs work on angiotensin II o Postexercise 0 Increase in NO adenosine decrease in NE which leads to a decrease in SNS tone and a decrease on baroreceptor sensitivity 0 Every pound of fat blood must travel an extra mile 0 Endothelial function 0 Ability of NO to be released by cells potent vasodilator o Sheer stress activates the production of NO from eNOS o Arterioles constrict and dilate the most 0 Stopcocks of our circulation o Vasodilators adenosine K C02 lactate Determinants of hypertension see slide disease defined Beta blocker ends in olol 0 Beta receptors in heart 0 Beta blocker competes with catecholamines for receptor resulting in decrease in SV and HR 0 Kidney has beta 1 receptors as well will activate rennin system and decrease angiotensin II High BP leads to thickening of heart wall bad hypertrophy 0 Also from heavy weight lifting Exercise increases lumen diameter of arteries Vitamin D low levels are a risk factor for high BP 0 People who are deficient Indoors Sedentary African American Elderly Medications 0 Beta blockers Compete with catecholamines for beta 1 receptors on heart which would normally increase HR Renin angiotensin system a End in oo o ACE inhibitors Prevents conversion from angiotensin 1 to angiotensin 2 a No aldosterone production so decrease fluid volume decrease BP End in pril o ARBs Prevent production of aldosterone End in zar o Diuretics Increase fluid excretion by blocking sodiumpotassium pumps Commonly end in ide Most are not potassium sparing work in kidney to inhibit aldosterone n Causes low potassium levels muscle weakness a May have risk of hypotension with exercise 0 Calcium channel blockers Work on smooth muscle of the arteries n Weaken arterial walls to cause dilation n End in ine 0 Know if meds effect cardiac output or peripheral resistance see slide 12315 0 Salt stress 0 Why are there discrepancies 0 Surgical procedure for high BP 0 Percutaneous renal denervation Diminishes SNS activity Also improves glucose metabolism 0 NE Journal BP treatment algorithm see slide 0 Stage 1 Step 1 lifestyle modification Step 2 single drug treatment Step 3 add second drug of different class Step 4 add third drug of different class 0 Stage 2 Step 1 two drug regimen Step 2 add third drug of different class Step 3 add fourth drug of different class Step 4 evaluate for secondary hypertension 0 Staples of DASH eating plan 0 Lower sodium lower dairy increase fruits and veggies increase whole grains limit sugar and red meat 0 BP numbers 0 Immediate medical referral o Contraindicated to exercise even with medical clearance resting systolic over 200 or diastolic greater than 100 0 BP stop test indicator systolic over 220 and diastolic over 105 OR if systolic drops by 10mmHG with increasing intensity Clinical setting systolic over 250 or diastolic over 120 0 Fat cells shrink and release adiponectin 0 Causes vasodilation and is antiinflammatory o In hypertensive individuals 0 1kg decrease in body weight will cause systolic to fall by 16mmHG and diastolic by 13mmHG o Squeezing handles increases BP 0 Mean arterial pressure needs to be at least 60 to maintain blood perfusion to the brain 0 Hyperinsulinemia causes sodium reabsorption in the kidneys 2215 Fight or flight 0 Increase SNS activity 0 Catecholamines Alarm n Increase BP and HR n Increased sweat rate and airway diameter a Dilated pupils n Increased AMPK and glycogenolysis n Decreases insulin 0 Cortisol Increases hepatic glucose output Immune suppressant and antiinflammatory Antiinsulin Increases muscle breakdown catabolic o 9 without modern fights these contribute to insulin resistance and cardiometabolic disease 0 Sugar not used and is stored around the liver 0 Increased risk of diabetes 0 Effects would be even worse with inactivity and high carb diet Cardiometabolic disease 0 Steps of coronary artery disease how each of the following contributes 0 High BP Blood sugar Choleterol Inflammation Fibrinogen Endothelial function HDLs 0 Average BMI of patients is overweight o 60 of all deaths in the modern world 0 Endothelial cells line the lumen o Plaque formation begins between endothelial cell and smooth muscle lining the artery LDLs and VLDLs main problem 0 Glucose free radicals inflammation and high BP damage arteries 0 Dyslipidemia High TGs low HDLs small LDLs n Decreasing CHO is best way to lower TGs a High TGs block leptin mess with set points 0 Plaque formation 1 damage to endothelial layer 2 LDL entry I 3 LDL gets oxidized 0 Fat soluble antioxidants will help prevent oxidation carotenoidsvitamins A and E 3 Inflammatory response a Adhesion molecules increase along artery wall 4 Macrophages engulf the LDLs and become foam cells n Initiate positive feedback scenario 0 Produce ROS o Recruit more WBCs 5 Platelets produce PDGF n contributes to atherosclerotic lesions 0 ENOS and superoxide combine to form peroxynitrite Potent free radical ENOS no longer causes vasodilationpositive effects OOOOOO o HDLs have protein A that binds to foam cells and collects cholesterol shuttles it back to liver 0 Once plaque ruptures can have thrombus death 0 How to combat plaque formation Aerobic exercise a Antiinflammatory n Decreases BP n Increases HDL cholesterol n Increases ENOS Weight loss a Higher levels of adiponectin antiinflammatory a Lower BP Antioxidant diet a Decrease radical stress a Lower inflammation Low processed CHO diet a Decrease TGschange LDL profile a Decrease blood sugar Omega 3s a Reduce inflammation n Improve vasodilation n Lowers blood clotting when in place of omega 65 2414 Topics Cholesterol transport in the body Steps of coronary artery disease ABCa1 Why are T65 and HDL usually inverse Focus on total cholesterol minus HDL Describe what metabolic syndrome consists of Findings of diabetes prevention program Finnish study Why is statin therapy the drug used to treat cholesterol 0 How and why does it work through inflammation Metabolic syndrome and dyslipidemia triad High TGs Small dense LDLs Low HDLs 0 Patients with metabolic syndrome respond to lifestyle change see blue slide for metabolic syndrome causes Alcohol is grain toxin detoxified in the liver 0 Acetylaldehyde from alcohol is turned into fat in the liver and stored around the liver Fructose goes straight to liver 0 Does not raise insulin levels 0 Fructose is sweeter Desensitize individual to sweet taste 0 Has own transporter GLUTS Uses facilitated diffusion o Glucose is cotransported and taken up quicker Deposited all over the body 0 ATP needed to phosphorylate sugar 0 High level of TG synthesis Make palmitic acid bad Surge in T65 low HDLs Whole grain 0 Fiber rich bran coat protects us from high level of fructose inside the grain TGs gt 150 leads to leptin resistance and set point dysregulation Creeping obesity 0 Gain weight gradually each year Insulin leads to increase in pyruvate dehydrogenase activity 0 Increased acetyl CoA turned into malonyl and then fatty acid FAs attach to glycerol forming TGs 0 High TGs are indicative of insulin resistance Visceral fat storage 0 Alzheimers linked to high T65 and insulin resistance 0 Fat gets oxidized and leads to inflammation 0 Does not produce leptin good thing No set point easier to lose Fat cells producetrigger more cortisol Aldosterone promotes reabsorption of sodium raising blood volume and BP 0 Insulin also increases sodium reabsorption Metabolic syndrome need 35 0 High BP systolic over 135 High TG over 150 HDL below 40 Fasting blood glucose above 109 Abdominal obesity Waist greater than 35 in women and 40quot in men Finnish study 0 45 leads to 2400 risk of type 2 diabetes mellitus Diabetes prevention program 0 10 decrease in BW leads to 60 reduction in diabetes risk Diabetes dialysis amputation blindness High caloric expenditure is most effective AMI acute myocardial infarction Acute coronary syndrome Peripheral vascular disease 0 Claudication pain from exercising increases with exercise Systolic heart failure 0 Heart is too weak to overcome aortic pressure 0 Too filled Diastolic heart failure 0 Inadequate filling of the heart 0 End diastolic volume is not sufficient Inadequate filling of the ventricle Muscle is always stronger in lengthened position Brain attacks 0000 o Strokes Exercise most effective Cholesterol 0 Make LDLs in liver Deposit in arterial walls 0 HDLs pick up LDLs and bring them back to the liver 0 Has several good functions 2615 0 Majority of synthesized TGs come from sugar 0 Apo a HDL 0 Reverse cholesterol transport cardio protective o Abo b VLDLs that become LDLs non HDLs 0 Small dense particles are the worst 0 Used for delivery of T65 and cholesterol throughout the body 0 Protein is more dense than lipid density refers to protein content 0 Lipo protein lipase LPL High LPLs better at putting TGs into muscle cells 0 Apo C2 activates LPL o APO E o Statins weaker membranes 0 Increased risk during exercise 0 CoQ inside mitochondria is major antioxidant o Apo B remnants o Recycled by the liver LRP receptors 0 Arterial wall macrophages take up the oxidized LDLs and become foam cells Inflammation increases adhesion molecules for macrophages to bind to artery 0 Mg mgdL o 1mg increase in HDL 2 reduced risk in men and 3 reduced risk in women 0 HDL sucks cholesterol directly out of the foam cell Reduces adhesion molecules 0 HDLs increased via Exercise Low glycemic index diet low carb Decreased android fat pattern Not smoking Niacin nuts beans mushrooms 0 CETP cholesterol ester transfer peptide 0 Exchanges 0 LMOB lean metabolic obesity o LCAT o Infusion of cholesterol inside the HDL 2915 Purpose and benefit of using nonHDL cholesterol Major finding of Jupiter trial support for lifestyle modification ARIC study key wellness programming guidelines 0 LCAT o Esterifies free cholesterol on HDL s surface 0 SR Bl receptors help collect more cholesterol HDL and T65 have inverse relationship 0 CETP o More TGs put into blood stream 0 Sugar increases activity Lifestyle and low sugar diet are most effective for lowering T65 and HDLs o Transports cholesterol from HDLs to VLDLs transports TGs from VLDLs to HDLs or into circulation 0 Cholesterol in liver 0 Used to increase bile production Emulsifier of fats frees fat soluble vitamins o Bigger HDL is more protective o Smaller LDL more dangerous 0 5 reduction in size 50 increase in uptake by arterial wall plaque formation 0 ApoA HDLs o ApoB lipid carriers 0 Vitamin D has short halflife 0 Could be supplemented along with CleO 0 VLCD very low carb diet 0 Muscle has higher level of LPL o More energy extraction from lipids 0 Train low compete high theory 0 Insulin resistance 0 Higher Rq oxidizing more carbs low fat oxidation 0 Pima Indians are extra susceptible o Jupiter trial Statins reduced risk of mortalitycardiovascular incidents Mainly effective through lowering inflammation Lifestyle modification is most effective for reducing inflammation Plant based diet also very effective in lowering inflammation Elevated T65 is risk factor for CVD and pancreatitis Insulin resistance high TG levels Omega3 FAs have the ability to lower TGs does not raise HDLs much 0 Benefits of nonHDL cholesterol 0 Total cholesterol minus HDLs All ApoB particles VLDLs LDLs TGs Can be taken in fed state fast not needed Hospitalized patients are rarely fasting Measures the cholesterol content of all arthrogenic lipoproteins Elevates ApoB small dense LDLs Normal LDLs but high cholesterol number suggests small dense LDL particles More accurate for metabolic syndrome patients Less reliance on LDL number 0 NonHDL typical therapeutic targets 0 Add 30 to recommended LDL target 0 Elevated CRP elevated inflammation 0 Disease Zone study 0 Exercise decreased sepsis fever and inflammation after E Coli injection 0 IL6 from muscle during exercise 0 Antiinflammatory o Cascadecluster on slide 0 Elevated inflammation 0 More likely in sedentary individuals 21315 Exercise leads to collateral circulation 0 Add new vessels to go around blockages alternative routes for blood flow UL for cholesterol is 300mgday 0 Being removed from recommendations 0 SOFAS solid fats and added sugars Mech for cleaning up cholesterol 0 HDLs o Lipoprotein lipase o Circulating nonHDL cholesterol binds to LPL Takes cholesterol out of arteries 0 Cholesterol from diet makes little difference in terms of bad cholesterol in blood Smoking 0 100 increases risk of CAD and ZOO400 increased risk of sudden death TZDM o fasting glucose gt 126mg 0 Post prandial glucose level more important 0 A1c gt 7 glucose is damaging blood vessels 0 Lifestyle mods are most effective treatment Obesity 0 Poly cystic ovarian syndrome 0 Irregularity 0 Increased risk of diabetes from weight gain several cancers 0 Higher testosterone levels 0 Enzyme in fat cells 17beta hydroxy steroid dehydrogenase 17BHSD o In fat cells and makes testosterone o Abdominal fat produces IL6 cortisol and PAI1 0 Greater risk of clotting Physical activity 0 Reduces oxygen demand 0 Improved endothelial function 0 Lowers nonHDL cholesterol 0 Decreased platelet aggregation 0 Increased LPL activity 0 Vacuum that clears blood of cholesterol Recommend 5 tennis ball servings of fruits and veggies 0 Fresh with skin Microalbumineria 0 Normally there shouldn t be albumin in the urine 0 Increased risk of heart disease and stroke Poly pill o Metformin o Lowers glucose by 13 0 Aspirin 0 Lower inflammation 0 Statin 0 Lower cholesterol 0 Ace inhibitor 0 Lower BP ACSM recommendations to be active 0 150 minutes of moderate o 75 minutes of vigorous exercise 0 for exercise benefits double both ARIC study 4 things to decrease risk by 40 0 Don t smoke 0 BMI under 30 0 Eat 5 fresh vegetables and fruits o Vigorous exercise gt 150 minutesweek 21615 Know 0 APOB o APOA o CRP o A1C o SRB o LPL o ABCA1 o LCAT o CETP MTOR not part of protection against IR injury Stress testing exercise and heart disease 0 Systolic vs diastolic HF 0 Heart murmur o Dilated vs hypertrophic cardiomyopathy o Hypertrophic thickening of walls smaller chambers o Dilated heart becomes frail and overstretched Can be caused form high EDV o Vagal vs sympathetic tone and inotropic vs chronotropic Stress test EKG is only 40 predictive Preload force generated by the heart Afterload pressure in the aorta LV or pulmonary artery RV that the heart has to overcome o Increases with hypertension 0 Can lead to hypertrophic cardiomyopathy Pulmonary disease can lead to RV hypertrophy Systemic circulation low 02 dilates low C02 constricts Pulmonary circulation low 02 causes constriction low C02 causes dilation o COPD patients increase right side hypertrophy 0 Resistance training increases left side hypertrophy 21815 CVD o Atrial systole 0 Early vent systole 0 Late vent systole 0 Early vent diastole 0 Late vent diastole o EKG o QRS complex indicates ventricular depolarization Sodium moved into heart potassium out Significant Q wave indicates heart attack Red line across screen is aorta pressure Yellow line is atrial pressure Blue line is ventricular pressure Green is EKG 1 and 52 are heartbeats Murmur results from AV valves not closing in sync OOOOOO T wave is ventricular repolarization potassium coming out 0 ST depression signifies ischemia Pressure differences drive openingclosing of valves Sodium channels open wave of depolarization Papillary muscle prevents valve from relapsing o Mitral valve on left Not optimal filling diastolic heart failure Preload gt afterload rapid ejection Efflux of potassium causes repolarization 0 High potassium level outside the heart heart won t repolarize o Sodiumpotassium ATPase recycles the potassium o Ischemic heart cannot generate enough ATP No energy to drive sodiumpotassium pump 0 Premature ventricular contraction PVC is very large on EKG 5060 of ventricular blood volume should eject SA node generates its own action potential 0 100bpm if not innervated at all Greater vagal innervation parasympathetic AV node automaticity is 4060 bpm o P wave would be missing if AV node is pacing heart Athletes with increased vagal tone increase the delay to allow further filling of the ventricle Mechanism of slowing down heart is increased permeability of potassium 0 Greater repolarization so further from threshold Plateau is caused by equal conentrations of sodium and potassium Inotropic increased contractility Cronotropic increases heart rate Atropene is parasympathetic blocker o Inhibits ACH Slow response vs fast response cells 0 Slow response have automaticity Vasodilators 0 Systemic C02 is vasodilator 02 is vasoconstrictor 0 Pulmonary C02 is vasoconstrictor 02 is vasodilator o COPD will lead to right ventricular hypertrophy 0 High C02 in lungs causes vasoconstriction 22015 Heart failure main points to study 0 Bainbridge reflex and tachycardia o Reactive oxygen species and its effect on nitric oxide 0 PVD and bradycardia 0 Problem with aerobic exercise 0 Treppe phenomenon w regard to arrhythmia 0 True sensitivity of cardiovascular testing 0 Abnormal chronotropic response to aerobic exercise 0 HR response to ventilatory threshold 0 Post testing BP and HR 0 DBP changes related to ischemia 0 Thallium stress test nonexercise o V02 peak instead of V02 max 0 Why is upper body ergometry used often in cardiorehab patients Vagas nerve PNS increases potassium permeability o Takes it further away from threshold 0 Athletes have greater vagal tone Sympathetic NS increases permeability to sodium 0 Increases HR 0 Postitive chronotropic and inotropic effects Heart failure patients have high resting HR and low max HR 0 Limited capacity for exercise Central command 0 Greatest control over HR during exercise 0 On way down the spinal cord stimulates HR receptors to raise HR 0 Abnormal chronotropic response because central command is in charge of that EKG o Weakened heart doesn t have enough output to supply brain along with working muscles which are vasodilating o Shunts blood to brain thus taking blood away from working muscles and causing ischemic pain Carotid artery palpation o Baroreceptors are over sensitive from peripheral vascular disease 0 End up with bradycardia Slow HR Sign of conductance blockage in heart or significant PVD Magnesium is cofactor for ATPase 0 Important for energy production Vasodilation from low oxygen increased C02 High level of free radicals and inflammation 0 NO inhibits calcium release thus preventing vasocontriction Reacts with radicals to form peroxy nitrate n Less NO available to cause vasodilation Anthocyanins from blue and purple fruits are great for vasodilation o Nitric oxide supplements can cause decreased sensitivity to NO not good Lateral leads I AVL V5 and V6 Inferior II III and AVF AVR right Septal V1 and V1 Anterior V3 Elevated ST segment is probably acute myocardial infarction Premature atrial beat 0 Early P waves not significant Right ventricular hypertrophy 0 Big QRS across V1 decreases from V1V4 height 0 Common in COPD patients Irritable focus 0 Muscle cell not getting enough oxygen Not enough energy for NaK ATPase pump Fires early less dopolarization heart is now being paced by nonpacemaker Entire heart depolarizes from PVC premature ventricular contraction n Several in a row are dangerous n More calcium left over from early firing stronger ensuing contraction o Treppe phenomenon 0 High heart rate greater contractility o More calcium left over from previous beat stronger contractions o PVCs are strong 0 Results in less end diastolic volume faster HR Dangerous heart quivering and not pumping properly 0 Significant Q wave would indicate infart somewhere in the heart ECG testing 0 True sensitivity is only 4050 0 Limited exercise capacity heart disease patients 0 1 MET discrepancy becomes a big deal 0 Sub max testing not used in these patients Unable to achieve 80 of max HR expected 0 Abnormal chronotropic responseweakened heart and sign of advanced heart failure 0 Inability to reassert vagal tone Talkless point during exercise 0 Healthy people have negative deflection in HR 0 Heart disease patients have positive deflection in HR Absolute stop test indicator 0 Systolic BP fails to rise during exercise or decreases o Diastolic increase greater than 10 compared to resting level Sign of ischemia 3 minutes post exercise BP should be less than it was at 1 min 0 suggests ischemic abnormality if not lack of vagal tone 22315 Stress testing and CVD o EKG stress testing only 4050 effective in determining disease Heart disease Inability to achieve 80 of maximal HR BP does not drop between 13 min after exercise should be less at 3 than it was at 1 HR continues to increase after talkless point 92 of HR max use METs instead of HR Systolic drops due to increase in intensity stop test and call 911 HR does not rise with increased demand Diastolic BP increases more than 10 indicative of myocardial ischemia V02 max vs V02 peak V02 peak is always less than V02 max Heart failure patients Able to hit V02 peak on treadmill bc skeletal muscle system plays major role will not reach V02 max Limited cardiac output so rely more on muscular endurance Bruce and Balke protocol Able to determine functional capacity with stress test Balke has linear increase Bruce test is stepbystep increase Ideal stressV02 max test should not exceed 12 minutes Patients should be pushed to reach around 2 on angina scale minor ischemia Promote agiogenesis in the heartcardiac adaptations Reach 20 on Borg scale Reach 85 of max HR if possible Thallium binds to potassium channels Shows areas of the heart that are repolarizing correctly by binding to those areas Nonbinded areas are cold areasquot and indicate a blockage Adenosine will cause vasodilation Beneficial because it does not require exercise Indicators of CHD Upper body ergometry Common because less muscle is involved can get to max easier in CVD patients Lowers V02 peak by about 30 Doesn t burn as many calories so not as beneficial in terms of rehabprevention Won t have benefits from weight loss like treadmill or cycling Safety Low risk of death 01 Risk of acute heart attack increases slights 04 Overall not really dangerous Group training sessions are beneficial Improvements in CHD patients Reduced ratepressure product delays onset of angina allowing greater intensity and duration of exercise Heart under less stress Combine resistance training with aerobic training Keep intensity around 60 for longer duration of time will require less blood flow to respiratory muscles Light resistance unilateral Focus on muscular endurance 2 daysweek Home based training was effective high retention rate Cardiac transplantation No longer have parasympatheticsympathetic influences on the heart Takes about 510 minutes for HR to come up Catecholamines need to come from adrenal gland takes more time Improves longevity Frankstarling curve Central venous pressure pressure filling the heart Diastolic heart failure would be lower on curve Heart failure increases edema Increased capillary pressure on back side of circuit blood forced into other areas Valve diseases Stenosis Narrowing of valve limiting venous return AV valves don t open fully Insufficiency Valve closes improperly causing backflow into atrial chambers 22515 Prolapse Enlarged valve leaflets bulge back into the atrium blocking venous return through the atrium Heart has to work harder with increased volumevenous return Try to work up to total of 2000 caloriesweek not tested on EKG stuff Not really benefit of monitoring EKG during rehab in Canada Congestive heart failure Blood backs up on left side of heart into lungs pulmonary veins Increase pressure in veins Blood in capillaries encounters resistance from veins and has no choice but to shoot out into interstitial spaces around the lungs More likely systolic bit diastolic could contribute COPD C02 build up in lungs Vasoconstrictor in the lungs Increases pulmonary pressure Right ventricle needs to work harder Diabesity People stop eating lose wieght rapidly Not sustainable lowers BMR and weight is gained back rapidly For sustained weight loss should not decrease calories by more than 300day Must maintain weight loss for at least 2 years to sustain it over lifetime Grehlin makes you hungry and lowers BMR Leptin makes you feel full Need to improve insulin sensitivity for weight loss 23 of Americans are overweight CHOs ONLY provide energy stored around the waist Having obese friend is 171 increase in risk of obesity sibling is only 42 increased risk Insulin binds to muscle liver and adipocytes Can be insulin resistant in each area or several 22715 Inactivity muscles are resistant to insulin so they bind more to fat cells Fat cells can convert precursors into cortisol Body should be mainly muscle Not burning fat increased risk of obesity FAO fatty acid oxidation Lean people are better at oxidizing lipids Pima Indians are really bad fat burners only store carbs Visceral fat does not produce leptin does not have set point Allows fat to be lostgained more easily Intermittent fasting improves glucose uptake Obese people do not burn fat as well Lower levels of aerobic enzymes Exercise can be beneficial to weight loss beyond calories hormone sensitivity Microbiota does not seem to help with weight loss Infectobesity virues Twins with higher BMI have exposure to virus antibodies 1 Body shape index 2 Replacing saturated fat w CH0 3 TNF alpha on HSL of SCAT and LPL of VAT 4 Indications for bariatric surgery and two most common procedures 5 Pumping syndrome Diabesity Calories in vs calories out only effective for people with functioning set points Potato and grain based deserts cause the most weight gain Diet high in saturated fat and cholesterol is probably low in antioxidants vitamins etc can t blame directly on sat fat or cholesterol Also high in dairy and meat Harvard heart study Replace sat fat with any form of CHO no net change in markers for CVD Starchy carbs are most common TLC diet Decrease saturated fat below 7 of diet Will compensate by adding more sugar fat freelow fat All unsaturated fats are essential can t be made in the body Excess carbs are made into saturated fat Hormone sensitive lipase HSL turns TGs into FFAs and glycerol in subcutaneous fats Inflammation causes increase in HSL Good thing Would decrease subcutaneous fat LPL is fat vacuum Shift from subcutaneous to visceral fat storage Body shape index More accurate and more predictive than waist circumference and BMI in predicting mortality ABSI WC BMIA23XHeightA12 Competencies 1122015 81100 AM Hypertension 1 11575 every 20 pt increase in SBP and 10 point increase in DBP doubles risk of CV events 2 Beta blockers CO side ends in olo ARBs block angiotensin II to aldosterone conversion ACE inhibitors block angiotensin converting enzyme diuretics end in ide most are not potassium sparing increase urine output and calcium channel blockers end in ine 3 African Americans are more susceptible to hypertension don t respond well to ARBs and ACE inhibitors 4 MAP SBP DBP x 23 5 Stage 1 BPgt 14090 stage 2 BPgt 160100 Stage 1 try lifestyle mods first then drug Stage 2 start with two drugs and lifestyle mods 6 More studies are trying to suggest that sodium changes lt2300mg decrease BP depends on the length of the study acute changes may not have long term effectstudy did not follow patients for long enough 7 Sodium should consume lt 2300mg most consume about 354g Potassium gt 4700mg 8 Salt reduction increased fiber low dairy increase whole grains limit red meat and sugar 9 Estimate of myocardial oxygen demand Systolic BP x HR want it to be less than 11000 10 DBPSBP Pulse pressure greater than 60 indicates arterial stiffness Indicates elasticity of the arteries 11 Maximal graded exercise test BP peaks around 200 Some will reach 250 exercise hypertension 12 Exercise increases vagul tone greater renal clearance of norepi increased release of vasodilators increase gaba inhibitory neurons Cardiometabolic 1 Why use the term Cardiometabolic Disease Cardiometabolic disease is a group of risks that can lead to cardiovascular diseases and TZDM Better term because incorporates all the components vascular amp metabolic Metabolic syndrome Dyslipidemia Cardiometabolic diseasee 60 of all deaths in developed world 80 cardiac rehab patients are obese 2 Describe the role of inflammation oxidative stress and cholesterol in the pathogenesis of CAD CAD Atherosclerosis 1 Endothelial Wall of blood vessel becomes damaged High BP AGlucose AFree radicals oxidants stress AInflammatory cytokines A Cholesterol smoking diabetes 2 When arterial wall is damaged LDLC small cholesterol can get into the wall of the artery LDLs becomes oxidized behind endothelial wall rancid 3 White blood cells cause inflammation of endothelial wall Increased adhesion molecules on arterial wall become sticky Macrophages are sent to consume the LCLC 4 Macrophages consume LCLC and become enlarged Foam Cells embedded in vessel wall 5 W accumulation of Foam Cells9 platelets amp fibrinogen block off the Foam Cells in arterial wall forms Plaque 6 Plaque reduces blood flow in vessel aneurysm Can rupture amp create blood clot HDLs Bind to Foam Cell collects the LDLC out of the Foam cell plaque and bring it back to the liver HDL gt 60 9 subtract a CMD risk factor Must AHDLC and lower LDLC 3 Define Metabolic Syndrome If you have 35 risk factors Metabolic Syndrome 1 High BP SBP gt 135 mmhg 2 High TGs gt150 mgdL 3 Low HDL lt40 mgdL 4 Fasting Blood glucose gt or equal to 109 mg 5 Abdominal Fat waist gt 35 female 40quot male 4 What is the Dyslipidemia Triad High TGs Low HDLs Small dense LDLs more dangerous 5 Why is there good and badquot LDL cholesterol Small dense LDLs are more dangerous atherosclerotic than normal LDLC 6 Know the role of cholesterol in the body LDLs small dangerous Get inside arterial wall amp form plaque HDLs cardioprotective Transports LDLC from vessels to liver for elimination Cholesterol for cell membrane make bile salts for digestion and make steroids and Vitamin D 7 Be able to describe the ATP III and the relationship with LDL cutpoints ATP III Adult Treatment Panel III On detection evaluation treatment of high cholesterol Established LDL cutpoints and goals for people with CVD risk factors LDL lt100 optimal 160189 high gt 190 very high TC lt200 desirable gt240 high HDL lt40 low gt60 high 8 What are the roles of APOB APOC and APOE NonHDL Lipoproteins LDLs APOB nonHDL Originate from small intestines or liver Chylomicron or VLDL Used for delivery of T65 and Cholesterol Carries APO C2C3 amp E APOC2 In APOB Activates LPL Lipoprotein Lipase Harvests fat Increases with endurance exercise Remodeling of APOB starts when this occurs APOE In APOB Essential for catabolism of TGs within the particle and for the remodeling process of APOB APOB 9 gets transformed into smaller and smaller Cholesterol rich remnants amp remodeled further by hepatic lipase 9 What is the function of LPL LPL Lipoprotein Lipase Binds to nonHDL activated by APOC2 Harvests fat takes it out of the cell 10 Describe the fate of APOB Remnants APOB Remnants 1 Recycled by liver in the LDLreceptor related protein LRP or the LDL receptors 2 Peripheral cells can take up the APOB via LDL receptors and used for cholesterol content or be taken up by arterial wall macrophages further oxidized foam cells 9 plaque 3 Gummed up or Oxidized by sugars Less ability to be taken up by HDL and greater chance of becoming plaque 11 What are the APOA carriers and describe their cardioprotective abilities HDLs do reverse cholesterol output Every 1mg increase in HDL leads to a 2 decreased risk in men and 3 decreased risk in women Protection 1 Reverse cholesterol transport via APO A1 they take the Cholesterol out of the foam cell 2 decreased monocyte adhesion 3 improved endothelial function increase NO HDLs increase via 1 exercise 2 low glycemic index diet 3decreased android fat pattern 4 not smoking Antioxidant properties trigger for atherogenesis APOA1 HDL 9 secreted by liver and intestines into plasma and removes cholesterol from cells forming nascent HDL 12 What are the functions of ABCA1 SRBl CETP and LCAT in the cholesterol transport pathway ABCA1 Upregulated by Cholesterol in macrophages Transfers cholesterol from inside the macrophage and places it in the macrophage cell membrane for HDL to come pick it up LCAT Esterfies free cholesterol on nascent HDL surface amp moves it to the HDLs core forming mature HDL3 lipoprotein SRBl Receptors in HDL3 membrane that cause HDL3 to collect more Cholesterol and become HDL2 The bigger the HDL2 the more protective CETP In plasma Induces a 11 exchange of cholesterol from HDLs for TGs Results in more TGs in HDL particle and more cholesterol in APOB particles transports Cholesterol from HDLs to VLDLs in the liver Eventually LDLs Transports TGs from from HDLs to VLDLs in the liver 9LDLs circulation Also transports TGs from VLDLS to HDLs or circulation Less HDLs causes more TGs to leave from the liver Inverse relationship between T65 and HDLs when HDLs decrease TGs increase HMG CoA Reductase inhibitors reduce the LDL when less cholesterol is needed to be delivered HDLs will increase to return to homeostasis High TGHDL ratio predicts insulin resistance 13 A 5 smaller LDL diameter can lead to a increases in the rate of arterial wall uptake 5 smaller LDL diameter M increase in the rate of uptake by the arterial wall 14 Be able to describe why a high sugar diet especially fructose can lead to dyslipidemia Fructose no insulin response goes straight to the liver It is sweeter than glucose has it s own transporter Glut5 across the small intestine Fructose has no insulin response it goes straight to the liver metabolized and turned to fat This leads to ATGs and thus decreased HDLs which can lead to dyslipidemia 15 How may regular exercise and a low carbohydrate diet be effective at combatting dyslipidemia Physical Activity Improved myocardial oxygen demand Decreased platelet aggregation and break down of fibrinogen AEndothelial function decreased obesity amp arrhythmia Combats dyslipidemia Decreases TGs Increases HDLs Improved glucose sensitivity Low carbohydrate diet Less fructoseglucose lower TGs 16 What is the liver overloadquot theory described in class and how does it contribute to Dyslipidemia Obesity Inflammation Diabetes and Hypertension Physical Inactivity amp Stress causes Cortisol production along with Afructose amp Alcohol consumption leads to increased glucose output by liver Inactivity9 leads to muscle lipid accumulation insulin resistance9 increased insulin production by pancreas due to Aglucose output by liver This Causes A fatty acids TGs decreased fatty acid oxidation9dyslipidemia Visceral Fat storage inflammationobesity Obesity9diabetes Sodium retention hypertension 17 What is the mechanism of action for Metformin Metformin9 decreases blood glucose levels Decrease liver glucose output Increased insulin sensitivity Slows glucose absorption after meal 18 What is the mechanism of action and potential adverse effects of Statin medications Statins9 Lowers cholesterol Lowering cholesterol possibly make cell membranes weak reduce CoQ10 and reduce Vitamin D 19 Be able to describe how physical inactivity leads to altered fuel partitioning and hyperlipidemia Physical inactivity mitochondrial impairments insulin resistance increased insulin production9 Increased fatty acid synthesis reduced fatty acid oxidation 20 What is a weakness with conventional cardiac rehabilitation programs Conventional cardiac rehabilitation does not focus on caloric expenditure even though 80 of cardiac rehab patients are overweight Weight loss leads to favorable cardiovascularmetabolic components High caloric expenditure is more effective than conventional cardiac rehathann 21 How might a metabolic cart predict insulin resistance and risk of the metabolic syndrome Metabolic cart electronically measures body s metabolism through the amount of heat produced when body is at rest 22 Define TlDM T2 DM and Type 15 DM M9insulin dependent pancrease produces little or no insulin M9 Insulin resistant pancreas produces extra insulin to compensate Fasting glucose gt126mg HBAlC gt 7 T15DM9 combo of T2DM ampT1DM Diabetes Prevention Study Lifestyle changes are more effective than metformin 23 What are the blood markers defining diabetes fasting and glucose challenge methods Fasting glucose gt126mg PreDM lOOlZSmgOo HBAlC gt7 24 What is the significance of A1C What are the desired levels of A1C for prediabetic and diabetic patients Hemoglobin A1C A1C measures blood glucose control If A1C levels are high blood glucose levels are high Desired Level below 7 25 What healthcare cost savings is expected per 1 decrease in A1C in diabetic patents varies 26 Define Central and Nephrogenic Diabetes Insipidus NOT ON TEST 27 A decrease in body weight of 710 reduces the risk of T2DM by 00 710 decrease in BW 60 reduction in the risk of T2Dm 28 What is PVD and claudication M9 Peripheral vascular disease narrowingocclusionblocking of arteries with plaque PAD usually in legs Claudication crampingpain in leg induced by exercise caused by obstruction of arteries in leg 29 What is the possible significance of Interarm BP variation and Ankle Brachial Index Having a difference gt10mmHg in SBP between arms is a symptom of increased CVD risk Having AnkleBrachial Index Ankle BP arm BP of lt or 09 9 peripheral artery disease 30 Know precisely when medical referral is required prior to exercise and exercise testing Any signssymptoms MC Male 45yr Female 55 w 2 or more RFs MC CAD Risk Factors 1 Coronary eventdeath 55yr or earlier in male 1st degree relative or 65yr old female 1St degree relative 2 Smoking 3 BP 14090 measured on 2 separate occasions 4 LDLs gt 130 OR HDLlt40 OR TCL gt200 or if on statin 5 Fasting glucose gt or equal to 100 mgd 6 BMI gt 30 Waist gt 40quot males and gt35quot females 7 Sedentary 8 HDL gt 60 9 subtract one risk factor 31 What is POCS and what are the risk associations with Metabolic Syndrome Polycystic Ovary Syndrome Endocrine system disorder Irregular menstrual periods Excess androgens male hormones Testosterone production 17B HSD in fat cells Increased risk of CVD with weight gain Makes metabolic syndrome worse 32 What is the major implications of the Jupiter Trial Lowering cholesterol helps to indirectly reduces heart diseaseCV mortality by reduced inflammation 33 Define CRP CPeptide A1C HOMA and Microalbuminuria CRP Creactive protein Marker of inflammation in the body produced by the liver CPeptide Marker of how much insulin is being produced AlC Hemoglobin A1C Marker of glucose stress HOMA Homeostatic model assessment Assess insulin resistance Microalbuminuria elevated levels of albumin in Urine 34 What are the risk values with hsCRP CDC Risks amp hsCRP lt1 mgL 9 Low risk 13 mgL average risk gt3 mgL High risk 35 What is a carotid IMT scan and why is it used Carotid IMT San Carotid Intima Media Thickness Scan Used to evaluate atherosclerosis 9 scans to see plaque thickness on arterial wall 36 What is the relationship between smoking and cardiometabiolic disease statistically Smokers have a 100 increased risk of CAD ZOO400 increased risk of sudden death increased adhesion molecules fibrinogen risk of arrhythmia myocardial oxygen demand Environmental smoke increases risk of CAD by 35 37 How would obesity increase the risk of blood clotting Abdominal fat leads to ACortisol output9AGlucose output more arterial wall damage ultimately lead to plaqueblood clot Physical inactivity abdominal fat macrophage infiltration of visceral fat chronic systemic inflammation9insulin resistance atherosclerosis9 diseases 38 Be able to provide solid exercise and dietary recommendations to be used as an effective therapy for cardiometabolic disease Diet 5 Tennisballsized vegetable serving per day Fruits vegetables whole grains Limit SoFAS solid fats and added sugar Don t smoke 300mins Moderate intensity exercise 46 METs 4060 VOZmax or 150mins of Vigorous exercise 6 METs per week 39 What is the polypill PoyPil pill w multiple medicines to treat cardiometabolic disease Metformin lowers blood glucose Aspirin lowers inflammation Statins9 lower cholesterol ACEinhibitor lower blood pressure 40 Be able to describe the medical ABC squot of primary and secondary CAD prevention 1 Aerobic exercise lowers BP antiinflammatory Increased HDLC Increased ENOS activity 2 Weight loss Higher levels of adiponectin antiinflammatory Lower BP 3 Antioxidant Diet Decreased free radical stress Lower inflammation 4 Lower CHO diet processed lower blood sugar less endothelial damage 5 Omega3 lowers inflammation vasodHaHon lowers blood clotting 41 Statistically what did the ARIC study show 1 Don t smoke 2 BMI under 30 3 Eat 5 servings fruitsvegetables 4Vigorous exercise gt 150 minutes per week ARIC study suggests that taking these 4 steps for 4 years can reduce risk of CVD by 40 CVD and Stress testing 1 Atrial systole early vent systole late vent systole early vent diastole late vent diastole 2 SA node atria AV node bundle of HIS Purkinje fibers ventricles 3 Intrinsic 100110 extrinsic responds to messengers in order to accelerate the heart prior to exercise adjusts to the intensity of exercise 4 Stimulation of sympathetic nerve centers release epi and norepi causing chronotropic and inotropic effects also vasoconstriction Stimulation of parasympathetic nerve centers release ACH which acts to reduce heart rate stimulation of vagus nerves 5 BP 11575 ESV 50mL EDV 120mL SV 70mL CO 525Lmin EF58 o 6 Increased capillary pressure decreased plasma proteins increased capillary permeability lymph blockage heart failure 7 Systolic heart failure left ventricle cannot pump with enough force to push sufficient blood into circulation Diastolic heart failure left ventricle filling is abnormal and is accompanied by elevated filling pressures 8 Stroke volume increases in response to increased volume of blood filling the heart stretches the ventricle causing cardiac muscle to contract more forcefully 9 10 Blood backs up on left side of the heart into the pulmonary veins increased pressure in veins blood in capillaries encounters resistance from veins and has no choice but to shoot out into interstitial spaces around the lungs causing congestion 11 12 Failure to decrease HR by 12bpm in 1 minute following exercise inability to reassert vagul tone 13 4050 14 Achieve 85 of max HR and 20 on Borg scale 15 Unable to accelerate HR 16 Inability to achieve 80 of HR BP does not drop 13 min after exercise 17 V02 peak is always less than V02 max heart failure patients only hit V02 peak muscle contributions 18 Stenosis narrowing of valve insufficiency valve closes improperly causing back flow prolapse enlarged valve leaflets protrude into atria heart must work harder 19 Thallium binds to potassium channels shows blockage via cold spotsquot 20 Lowers V02 peak by about 30 less strenuous 21 Inpatient minimize deconditioning due to bed rest early outpatient improve exercise performance and reduce CVD risk factors maintenance 22 Don t monitor ECG during rehab 23 Light resistance unilateral focus on muscular endurance 24 25 No longer have sympatheticparasympathetic influences on the heart takes 510 minutes for HR to increase prior to exercise Diabetes and Obesity 1 Not everyone has functioning set point therefore calories inout and exercise will not be as effective in determining weight loss Also certain groups of people Pima Indians are really bad at burning fat and therefore have an increased risk for obesity and diabetes 2 Must maintain weight loss for at least 2 years in order to prevent risk of regain 3 Exercise can increase sensitivity to insulin intermittent fasting can improve glucose uptake decrease saturated fats and sugars eat whole grain carbs 4 5 Percentage of FFA uptake oxidized during basal and exercise was significantly reduced in obese subjects and obese subjects following weight reduction compared to lean individuals makes it difficult to maintain healthy body weighteffects of weight loss 6 Saturated fats and sugars both end up as the same thing in the body visceral fat and items with decreased fat often have increased sugar 7 Pulmonary disease nonalcoholic fatty liver disease gall bladder disease osteoarthritis skin gout phlebitis cancer severe pancreatitis coronary heart disease cataracts stroke idiopathic intracranial hpyertension 8 Indicated for morbidly obese BMI40 and class 2 BMI 3539 with comorbidities RouxenY bypass jejunum attached to proximal stomach bypassing distal stomach duodenum and small part ofjejunum Gastric banding is a simpler procedure performed laparoscopically and restricts the amount of food than can be consumed Banding has fewer complications and a greater percentage of weight loss is fat Complications of bariatric surgery vomiting up to 6 months past surgery dumping syndrome sweating dizziness and fatigue after ingesting sugar BlZ deficiency iron deficiency and gallstones Weight regain can occur and FatMax is decreased following surgery Other complications include skin rashesinfections 9 Can be tolerated longer so individual will burn more calories even though they are working at a lower intensity Also will burn more fat working aerobic system 10 Risk levels Microalbuminuria 20200 micrograms Cpeptide gt 21ngdL CRP gt 10mgdL AIC gt 5 suggests glucose stress fibrinogen gt34 gL supine abdominal height gt 12 measures visceral fat recovery HR distal pulse and ectopic fat index 11 Monitor decrease with weight loss also lose FFM 12 13 Set during adolescence and remains constant throughout adulthood 14 Gynoid fat stored in hips buttocks and thighs Android central adiposity more dangerous due to more visceral fat 15 Eat breakfast eat for nutrient density avoid processed carbssugar adequate hydration high fiber 2535 CHO 45 replacing fat w protein will increase TEF shoot for approx 500 kcal deficitday 16 First place fat is stored will be the last place it is lost from 17 Average body shape index more accurate and predictive than weist circumference and BMI in predicting mortality ABSI WCBMI 23 x height12 18 Intermittent fasting improves glucose uptake 19 Following glucose challenge lt 140 normal 140199 prediabetic 200 indicates diabetes Fasting BG lt 100 normal 100125 prediabetic 126 indicates diabetes 20 Acute postprandial rise in glucose is toxic and negatively effects endothelial cells circulation and promotes oxidative stress Since we are awake more than we sleep most of the day we have postprandial glucose levels 21 A1c greater than 5 suggest glucose stress 22 90 of DM patients are type 2 10 type 1 Type 1 DM has auto antibodies occur suddenly insulin low or absent Type 2 DM usually occurs with abdominal obesity and develops gradually insulin levels progress form high to low Symptoms are weight loss hunger thirst frequent urination and blurred vision Dietary management is essential for both oral hypoglycemics only effective in type 2 insulin required for all type 1 and 40 of type 2 23 Autonomic neuropathy impaired thermoregulation and likelihood of hypoglycemia use of RPE due to altered cardiac responses Peripheral neuropathy aquatics and nonweight baring exercise avoid trauma to feet Nephropathy avoid vasalva and exercise increases in BP heavy RT Retinopathy avoid vasalva HIT overhead lifting activities that lower or jar the head keep BP lt 170 24 Low fat vegan diets are at least as effective as more conventional diabetes diets for weight reduction and glycemic control and are significantly better for lipid management 25 Biguanides reduces hepatic glucose output by 13 probably via increasing AMPK may also increase cellular sensitivity to glucose systematically Injectable incretin GLPl GIP mimetics DPP4 inhibitors by inhibiting DPP4 it increases incretin levels which inhibit glucagon increase insulin secretion and decrease gastric emptying Meglitines and sulfonylureas act on ATP dependent pancreatic K channels leading to reduced hyperpolarization and easier depolarization which opens voltage gated Ca channels to secrete more proinsulin SGLTZ inhibitors new oral class of meds in phase II studies inhibiting PCT reabsorption of glucose 26 Researches believe focus should be on postprandial glucose lt 140 at 2 hours ADA is just 180 anytime postprandial 27 1 in 3 children expected to develop diabetes spend 176 of GDP on healthcare and its rising savings through prevention Paper discussion 1122015 81100 AM Grape powder 0 Rats given physiologically equivalent amount of grape powder equal to handful of grapes for humans 0 Glutathione peroxidase is antioxidant 0 Measured MDA final product of lipid peroxidation 0 MBA lower in grape diet hydrolyzene didn t do much Medicine not as effective as photochemical rich diet Adenosine and prostacyclin 0 Thought exercise would especially benefit hypertensive individuals due to increased adenosine which causes vasodilation o Prostacyclin comes from omega 3s 0 Both hypertensive and normotensive individuals responded equally o Hypertensive individuals don t have as much circulating adenosine or prostacyclin 0 Can be increased via exercise Central mechanisms 0 Nuclei tract in medulla oblongata o GABA is inhibitory glutamate is excitatory sympathetic 0 Substance P raised blood pressure 0 AS BP rises neuro kinen 1 receptor starts to down regulate o More GABA at end of exercise inhibitory 0 During exercise BP rises and we try to prevent peak in BP by inhibition Inhibition lasts even after exercise and thus decreases BP Workplace hypertension 0 Workout for 20 minutes 8 hrs of lower BP Heart rate recovery 0 What is relationship bt HRR and CV mortality 0 Impaired HRR causes an increase in CV mortality 0 What HRR is bad 0 12 beats in 305 or less 26 beats in a minute 0 Trouble reasserting vegal tone parasympathetic nervous system 0 What was the ex rx 0 Moderate exercise 0 Then vigorous exercise 0 Cycling because it reduces physical stress o How did HRR improve 0 Went from 12 to 17 in 305 from 26 to 335 in a minute 0 Heart rate reserve is very important 0 Narrow range is bad 0 Endurance exercise should improve heart rate recovery and increase heart rate reserve via reduced resting heart rate IR injury myocardium o What is IR injury ischemia reperfusion o Myocardial stunting 0 Blood flow is cut off then reperfuses the heart Releases a lot of metabolites that increase oxygen flow All blood that was blocked is immediately perfused in n Causes oxidative stress Exercise can provide oxidative protection 0 What model is used in this research 0 Rat model 0 Name redundant mechs of exercise cardioprotection 0 Higher levels of GPX super oxide dismutase elevated levels of heat shock proteins protect proteins that are in the process of being built by the ribosome Heat denatures proteins 0 What are the implications 0 Exercise is cardioprotective reductions of plaque Rowing vs football heart changes 0 How was ventricular function measured 0 Diastolic filling and ejection fraction Endurance athletes had increases in left diastolic volume while resistance athletes had no increase 0 Diastolic heart failure Decreased end diastolic volume so less stroke volume 0 What were the differences before the season began 0 Training was not regulated endurance athletes participated in endurance activities and strength athletes participated in weight lifting and football drills like the study 0 There were also minor differences in systolic BP 0 No major differences before the group o How did endurance athletes change their heart morphology and heart function 0 After the endurance program endurance athletes had reduced resting heart rates and diastolic blood pressure Additionally endurance athletes experienced significant increases in left atrial volume as well as increases in left ventricle structure end diastolic volume end systolic volume and mass Left ventricle ejection fraction had no significant changes while resting cardiac output dropped significantly Right ventricle size also increased as a result of the program 0 Increased left ventricle mass due to chamber size 0 How did resistance athletes 0 Reduction in left ventricle diastolic function 0 At the conclusion of the strength program systolic blood pressure was elevated while other resting measures remained constant In contrast to the endurance group both left ventricle wall thickness and the interventricular septal thickness increased significantly In addition left ventricle mass and relative wall thickness also increased while ejection fraction volume and cardiac output were unchanged 0 Concentric hypertrophy thickening of heart wall bad 0 How does this pertain to athletes heart 0 Strongly refuted the notion 0 Training makes heart structure that way not born with it Audio 1122015 81100 AM 11415 Hypertension o Consume too much sodium about 3500mg sodium or 9g of salt 0 Should be gt2300 mg sodium or 6g of salt 0 Sodium to potassium ratio important 0 DASH diet 0 Doesn t mention sugar 0 Half of Americans need less than 1500mg 0 African Americans diabetics and hypertensive o Vasoconstriction leads to stiffening of arteries 0 From chronically elevated angiotensin 2 levels 0 African Americans don t respond as well to ace inhibitors and ARBs 0 Low dose diuretic is first treatment for prehypertensive individuals 0 Exercise and weight loss is most important for dealing with blood pressure 0 1kg of weight loss 12mmHg drop in systolic and diastolic BP 0 Whole grain is as effective as meds at lowering BP 30 reduction 0 Should eat 3 servings a day 0 Brown rice decreases diabetes risk white rice increases 2615 Plant based diet for heart disease prevention Esselstyn o What is best evidence that Western diet contributes to heart disease food born illness 0 Autopsy of young American soldiers showed signs of coronary artery disease 80 same aged Vietnamese soldiers did not 0 Young Americans with accidental death also had clogged arteries 0 Only 18 cases of prostate cancer deaths in Japan 0 Most controversial statement 0 Olive oil and anything with a face contributes to plaque formation 0 Stopped angina after 36 weeks of plant based diet 0 Endothelial cells regained capacity to produce NO and improved circulation What is the mechanism of plant based diet and how long does it take 0 10 days to a couple weeks Shear stress activates ENOS o Decreases calcium release and causes vasodilation Radical and NO form peroxynitrite which contributes to oxidative damage Arugula and beets have high nitric oxide content Everyone exposed to Western diet had increased disease rates
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