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KNES360: exam 1 study guide

by: Lindsay Burns

KNES360: exam 1 study guide KNES 360

Marketplace > University of Maryland > Kinesiology > KNES 360 > KNES360 exam 1 study guide
Lindsay Burns
GPA 3.5
Physiology of Exercise
Dr. Rogers

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I have highlighted important information mention on the gear mechanism slides in turquoise and important equations in yellow!! TYPO: My notes say TPR increases with workload but TPR DECREASES w...
Physiology of Exercise
Dr. Rogers
Study Guide
50 ?




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This 16 page Study Guide was uploaded by Lindsay Burns on Saturday October 3, 2015. The Study Guide belongs to KNES 360 at University of Maryland taught by Dr. Rogers in Fall 2015. Since its upload, it has received 246 views. For similar materials see Physiology of Exercise in Kinesiology at University of Maryland.


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Date Created: 10/03/15
KNES36O Exam 1 Study Guide Introduction History gt Hippocrates Proved that disease was a natural process 0 Signs and symptoms of disease are caused by natural reactions of the body gt Krough 1st to discover diffusion of oxygen 0 Muscle contraction o Skeletal muscle during contractions 0 Muscle biochemistry gt Astrand 1st exercise physiologist to develop a devise for exercise testing 0 Karolinska institute gt DB Dill 1st dedicated to exercise physiology lab facility 0 Harvard fatigue lab 0 During WWII helped with soldiers not fatigue gt Hill and Meyerhof 0 Muscle biochemistry Glycolysis 0 High intensity short duration l good at producing ATP The Cardiovascular system and exercise gt 4 major tubes 0 Arteries veins arterioles and capillaries gt Functions of the cardiovascular system 0 Transports oxygenated blood to tissues 0 Delivers metabolic substrates to the cells Amino Acids Glucose Triglycerides Fatty acids 0 Removes metabolic endproducts C02 Urea Ammonia Lactic acid 0 Regulates pH to control acidosisalkalosis o Transports hormones to cells to regulate metabolic pathways and cardiovascular functions Hormones o Epinephrine Norepinephrine Contraction of heart Insulin Glucose uptake and blood redistribution in skeletal muscle 0 Maintain uid volume o Absorbs heat and redistributes blood to periphery skeletal muscle Ability to exercise in heat Mitral and Aortic Valves gt Valves and main functions 0 Tricuspids 0 Pulmonary o Mitral o Aortic Aid unidirectional ow gt Chordae Tendineae and papillary muscles 0 Facilitate the opening and closing of valves Important in ejecting blood and keep blood ow in one direction gt Stenosis Narrowing gt Prolapse Retraction of valve l opposite direction 0 Allows blood to move backwards Disrupts unidirectional ow gt Heart size factors 0 Body size 0 Genetics 0 Exercise training status 0 Presence of disease Ex COPD Hypertrophy of right side of heart Circulation gt Blood volume from rest l exercise doesn t change 0 Unless exercising for prolonged time in the heat gt Venous return low pressure 0 Blood ow coming back to the heart 0 Site of most blood at rest gt Arterial ow High pressure gt To measure status of CV system during exercise 0 Graded exercise test Stress test 0 CV response to exercise 0 Measure arterial side 0 See heart rate responses and arterial pressure Blood pressure gt Normal response to exercise 0 Systolic pressure increases 0 Diastolic pressure remains about the same 0 Coronary arteries vasodilate 2030 To facilitate increase in blood ow 0 Pulmonary artery Carries blood to lungs to get oxygenated 0 Pulmonary vein Brings oxygenated blood back to the right side of the heart right atrium gt Left side of the heart 0 Bigger left ventricle and walls Contracts pushes blood to aorta To entire body 0 High pressure side of circulatory system gt Coronary artery disease CAD o Blockages or plaque buildup l reduces opening to the artery l reduces blood ow reducing ability to vasodilate gt Why are there cardiac tubes 0 Cardiac muscle is so thick that oxygen substrates and hormones cannot diffuse through the tissue gt Angiograms 0 Thread plastic tube from femoral artery or more recently through small vessel in the wrist l to the heart 0 Infuse dye in vessels so it can show up in the pictures 0 Used to invasively detect if coronary arteries are open or blocked o Performed when one possesses Chest pain Shortness of breath The Intrinsic conduction system CS gt Syncytium o All the cardiac cells have the ability to contract in unison gt Electrical cells 0 Generate electrical impulses gt Contractile cells 0 8085 Contract as unit Shorten Generate force Myosin Thick lament o Actin Thin lament gt Structures of CS 0000 0 SA node Electrical ces Right Atria Made of P ces Pacemaker cells Spontaneously generate impulse Velocity 3ftsec 0 AV node Electrical ces Between right atria and ventricle Velocity 3ftsec 0 Bundle branches Electrical cells Right and left bundle branches along the inner ventricular septum Transmit impulse down ventricles Velocity 1ftsec o Purkinje bers Electrical cells Impulse to each cardiac cell Hearts ability to act in unison Velocity 13ftsec gt Cardiac muscle a syncytium o Myofibrils actin and myosin Help cardiac muscle contraction 0 Z line Z line Sarcomere o TTubule Carries impulse from sarcomere to cell 0 Mitochondria Power house of cell 0 Sarcoplasmic reticulum Stores calcium l muscle contraction gt o Intrinsic conduction system 0 lntercalated disks Extrinsic Control of the Heart gt Extrinsic Control ANS 0 Balance between SNS and PSN the two branches of the ANS that bring about extrinsic control of cardiac activity Heart rate and strength of contraction of left ventricle o Sympathetic Nervous System SNS Increases heart rate and ventricle contractility o Parasympathetic Nervous System PNS o Endocrine system Catecholamines gt Responses to changes in the cardiovascular system 1 o Baroreceptor response to stretch and pressure In the walls of internal carotid artery aorta and femoral artery Information to the cardiovascular control center about uid in the tubes 0 Chemoreceptors In the carotid body Information to the cardiovascular control center response to chemicals Regulates pH 0 Sympathetic nerve bers Stimulatory Cardiac accelerator nerves Input to SA node AV node right and left ventricles interventricular septum and adrenal gland Increases heart rate and ventricular contractility Increases as a result of rest exercise 0 Parasympathetic nerve bers Vagus nerve Inhibitory Input to SA node and AV node and little to atria Increase in heart rate Decrease as a result of rest exercise 0 Endocrine System 0 Increase in Catecholomines Epinephrine and Norepinephrine From adrenal medulla Increase heart rate and contractility Norepinephrine also comes directly from sympathetic nerve endings Increase much greater than increase in Epinephrine o X axis Maximal oxygen uptakeV02max Restmaximal exercise Rest25 low intensity exercise 0 5075 moderate exercise majority of exercise 0 100 maximal exercise 0 Y axis Heart ratebpm o Predominately PNS control of heart rate until about 30 oxygen uptake 0 Once about 50 oxygen uptake or a heart about 100bpm SNS takes over 0 Medications affecting PNS or SNS Beta blockers may cause an abnormal Heart rate or blood pressure response 0 Cardiac arrest within one hour of symptoms Seen often in high school and college athletes 60 football and basketball athletes o Etiology Hypertrophic cardiomyopathy HCM Abnormally enlarged heart Asymmetrical and disorganized arrangement of cardiac cells Inherited only lt1 of the population 0 Only detected by ECG Heart Rate and the Cardiac Cycle gt Resting Heart Rate RHR o 6080 bpm 0 Increase with age 0 Decrease with increased cardiovascular tness 0 Effected by environmental factors High altitude High temperature gt Maximum Heart Rate MHR 0 Highest HR value one can achieve in an allout effort to the point of exhaustion o Remains constant from day to day 0 Changes slightly year to year Age decreases MHR 1bpmyear 0 Estimate MHR For people lt40 For people gt40 gt Peak Heart Rate PHR 0 Maximum HR in particular mode EX Test on treadmill ergometer and cycle ergometer Your HR reached 190 on treadmill and 185 on the cycle ergometer 190 would be you MHR and 185 would be a PHR because it is your highest HR achieved on that particular mode The Electrocardiogram ECG El 39 lr sa 39 ri pirih i magma rmins Elrrg ijvzlli i l Fliti er jii lli tall n I ll Warn D giuIJrLIE zun v am at m FR Swimmm 39iil39ilnrl izular 93 mlaiqul39m hmplmi 39iarummsuIar 1 HENEurim39llun I WMquot H i t i i I g i l antlul39lglr LEW gt 1 box 1mm 04 sec gt In a normal healthy heart the ST segment is even with the base line x axis 0 If depressed or elevated more than a block or two indicates myocardial ischemia Reduction of blood ow and decrease in oxygen delivery to the cardiac muscle gt Depolarization 0 Movement of sodium into the cells 0 Contraction gt Repolarization o Pumping sodium outside of the cells 0 Prep for next contraction gt The Cardiac Cycle 0 Events that occur between two consecutive heart beats systoesystole o Systole Contraction phase during which the chambers expel blood QRS complex T wave 0 38 of cycle duration Left ventricle l aorta Right ventricle l pulmonary artery 0 Diastole Relaxation phase during which the chambers ll with blood T wave QRS complex 0 62 of cycle duration Most blood owing through coronary arteries to the heart occurs during diastole gt The Cardiac Cycle During Exercise 0 Cardiac cycle shortens QRSDQRS o Systole and diastole both shorten Systole shortens 25 Diastole shortens 75 gt Wiggers diagram Figure 68 gt Graded exercise Test GXT or Stress Test 0 Intensity gradually increases until subject gets tired or until something abnormal is detected 0 Look at the following in response to exercise HR BP ECG RPE 0 Important because many problems don t show up until stress is put on the heart gt Basic Structure of Blood Vessels o Vein Artery Arteriole Capillary Have endothelium 0 Inner smooth muscle lining Protects inside 0 Resists the formation of clots Basement membrane 0 Provides structure 0 Artery Primary resistance vessel 0 Capillary Smallest vessel Just big enough for a RBC Primary exchange vessel Ability to open and close 0 From rest exercise most are open 0 Allows more blood ow 0 Veins Low pressure Contain valves 0 Arterioles Increase blood ow to active skeletal muscle gt Blood volume distribution at rest 0 Blood volume from rest exercise doesn t change but the distribution of blood does Greater cardiovascular tness allows more efficient distribution to active skeletal muscles 64 veins 13 arteries 9 pulmonary 7 heart 7 arterioles and capillaries 0 00000 0 ARTERIOLES Change in resistance Vasodilation SNS Vasoconstriction PNS Auto regulation 0 Local tissues Cell signals Decrease oxygen and increase carbon dioxide 0 Increase lactate Increase nitrogen oxide gt Importance of blood ow to active skeletal muscle F Increase SNS activity Increase Auto regulation of local blood ow The composition of Total blood Volume TBV gt Men 56 Lmin gt Women 45 Lmin o Differ due to mass 0 Does not change much from rest exercise 0 Higher in endurance trained athletes gt Hematocrit O O 0 Norm 4045 Women 38 42 If exceeds 60 blood is too viscous and cannot ow readHy Blood Contains Plasma 55 0 90 water 0 7 plasma proteins 0 3 other Formed elements 45 0 gt99 RBC 0 lt1 WBCplatelets Hematocrit 45 formed elements 100 TBV Men have higher oxygen carrying capacity and larger pump Increases in response to greater endurance training and higher altitude gt RBC ReInfusion O gt EPO 0 Freeze blood so when reinfuse the blood one has greater amount of RBC s Increases TBV 10 Hormone produced by the kidneys During exercise training and high altitude gt Cardiac performance 0 Stroke volume SV amp Cardiac output Q increase 0 V02max n Viscosity of uid Increases resistance L length of tube r radius 0 Relatively small changes in r make huge changes in resistance O As pressure increases blood ow increases As resistance increases blood ow decreases Need mechanisms to return blood to right side of heart F o 1 Ventilatory pump o 2 Muscle pump 0 1 amp 2 increase venous return 0 3 Valves in large veins l Prevent BF from going backwards 4 Vasoconstriction increase SNS 0 Signi cant increase SNS activity rest exercise 0 Increase HR amp contractility Hemodynamics gt Stroke Volume SV Difference between enddiastolic EDV and end systolic volume ESV 0 After exercise diastolic is greater and systolic less and SV increases gt Ejection fraction EF 0 Fraction of blood ejected when the heart contracts I SV x 100 EDV o lncreases with exercise in normal person 0 Greater ejection of blood to aorta 0 Heart disease decreases EF Congestive heart failure CHF 0 Less capacity to contract vigorously Cardiac bers stretched Coronary artery disease CAD Heart attack patients gt Cardiovascular quotBig Picturequot 0 lntrinsic and extrinsic control mechanisms 0 Systolic and diastolic phases of cardiac cycle shorten when one goes from rest exercise 0 All 4 cardiovascular tubes are important for redistribution during exercise 0 Capacity to vasodialate from arterioles in active skeletal muscle critical aerobic exercise 0 4 major hemodynamic variables change from rest exercise Module 2 gt Cardiac Output Q 0 Q HR x SV Q Lbeatmin HR bpm SV mLbeat gt How is Q measured 0 1 Cardiac catheterization At rest o 2 Doppler Ultrasound method Noninvasive o 3 C02 Rebreathing Directly related to blood ow Most common method Rebreathing o Anesthesia bag N2 02 Exchangedinlungs Breath out in bag Content samples in machine Non invasive way to measure cardiac output Resting Q values for endurance athletes and sedentary control subjects are the same 0 Depends on size of individual Larger the person larger the heart larger blood volume the gt cardiac output Q If HR is slower there is more time for the ventricle to ll with blood 0 Greater diastolic 0 Greater SV 0 Greater period of diastole Blood Flow at rest Blood Flow during exercise Visceral Organs 45 10 Heart 5 no change rate 34x 5 Bone 5 1 Brain 15 dec Absolute inc 4 lntegumentary 5 520 Muscles active 20 7085 o Vasoconstriction to visceral organs 0 Vasodilation in active skeletal muscle gt Fick Principle a arterial v mixed venous gt Frank Starling mechanism important response to exercise 0 Greater stretch greater contraction gt Most basic relationship in cardiovascular exercise physiology 0 Relationship between HR and work rate gt Maximum heart rate has little effect from endurance training but from age o Noninvasive way of accessing SV 0 Echocardiogram Measure end diastolic blood volume Systolic volume Size of chambers Thickness of walls Volumes in end diastole Just after contraction systolic o SV EDV ESV o SV increases signi cantly during exercise 50 V02max then SV levels off Linear then levels off 0 Q linear 0 HR linear gt Well trained endurance athletes o Bigger heart 0 Larger left ventricle Size of chamber Thickness of walls 0 Greater TBV o SV may not level off until about 8590 V02max o 1 Venous return Enhanced by 0 Ventilartory pump 0 Muscle pump Unidirectional valve Vasoconstriction o 2 Ventricular distensibility o 3 Ventricular contractility o 4 Aortic pressure Inhibiting factor Resist ventricular uptake Aortic pressure increases as SV decreases FrankStarling Mechanism CFC and Q gt Congestive Heart Failure CHF 0 Cardiac bers are so stretched there is little overlap between actin and myosin Decreased force of contraction 0 Most people s SV increases then levels off at 50 V02max o Untrained After SV levels off it may decrease a little 0 Trained Levels off 0 Elite Increases signi cantly 1 Bigger heart left ventricles 2 Greater TBV 1015 increase Greater Frank Starling mechanism gt Coronary Artery Disease CAD o Might not show up until a stress test is performed 0 Low 20 s normal healthy individuals 0 Mid 30 s highly trained endurance athletes gt Changes in av 02 difference with acute exercise 0 Can be measured across Whole body a muscle the heart catheterization performed by Cardiologist What39s the Deal During Acute Aerobic Exercise gt Arterial blood stays about the same gt Mixed venous blood decreases substantially gt av 02 difference increases 0 18 is the highest 0 Greater in endurance trained athletes gt Blood Pressure response to acute exercise 0 Norm SBP increases 812 mmHg per MET Submax 190220 DBP same no major change 0 13 because diastole lasts a long period 0 Vasculature is signi cantly less than in legs 0 Muscle mass is less l less tubes smaller tubes Increased resistance Greater BP gt Blood pressure response to resistance exercise 0 Shoots way up Comes right back Doesn t last long Not primary mode for hypertensive patients Monitor BP Adjust exercise prescription per person s conditions Pressure Flow and Resistance in the CVS gt Total Peripheral Resistance TPF o What is it Total resistance in the peripheral vascular system 0 Where is it Primarily in the arterioles Arterioles have the greatest capacity to vasodilate and vasoconstrictimportant in shunting blood to active skeletal muscle 0 How do we measure TPR Very difficult to do in humans 0 Millions and millions of tubes Arterioles are so small Estimate TPR Measuring MAP is easy to do 0 Rest and at exercise 0 Taking BP DBP 13 SBPDBP Measure Q is very easy to do 0 C02 Rebreathing What is the TPR response to acute exercise 0 TPR is relatively high at rest 0 Most blood is going to visceral organs TPR decreases from rest l exercise 0 Because of the vasodilation in active skeletal muscle 0 Hypertension 0 Very high TPR 0 Don t have the ability to vasodilate as well their TPR may not decrease with increased work 0 Aerobic activity decreases TPR gt Cardiovascular Variables In relation to work load 0 HR Increases SV Increases then levels off Q Increases BP SBP Increases a lot DBP Stays about the same 0 If signi cant increases in DBP corresponds with myocardial ischemia 0 MAP Goes up Not as much as SBP TPR Increases V02 Increases av 02 difference Increases OOO gt Factors the Affect Arterial Blood Pressure During Exercise 0 MAP Q X TPR 0 Signi cant increases in SBP Heart not working as an effective pump What increases SBP Inc in Blood volume 0 Doesn t happen in graded exercise test Inc in Blood viscosity 0 Blood doping 0 EP0 0 RBC reinfusion TPR no impact 0 Contributes to increased blood ow Inc in HR 0 Greatest effect Inc in SV gt What is the RatePressure Product RPP 0 Product of HR and SBP 0 Major increase from rest l exercise 0 Greater peripheral resistance with arm exercise verses Ieg exercise Arterioles are smaller Fewer Resistance is greater 0 Why is RPP important Very high correlation between RPP and MV02 MV02 Myocardial Oxygen consumption If RPP does not increase Heart is not getting enough blood ow and oxygen 0 Increase in HR Inc in contractility Inc in SBP all induces an increase in MV02 gt Cardiovascular drift 0 Gradual decrease in stroke volume and systemic and pulmonary arterial pressures and an increase in heart rate 0 Occurs with steadystate prolonged exercise or exercise in a hot environment


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