KNES360 week 3
KNES360 week 3 KNES 360
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This 6 page Class Notes was uploaded by Lindsay Burns on Friday October 2, 2015. The Class Notes belongs to KNES 360 at University of Maryland taught by Dr. Rogers in Fall 2015. Since its upload, it has received 78 views. For similar materials see Physiology of Exercise in Kinesiology at University of Maryland.
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Date Created: 10/02/15
KNES36O Lecture Week 3 91415 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 gt Contribution of Sympathetic and Parasympathetic NS to the increase in HR from rest l exercise Figure 66 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 gt Sudden Cardiac Death SCD 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 91615 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 MHR220Age Years For people gt40 MHR208 07xAge 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 91815 The Electrocardiogram ECG El l 39 al r gl ih M mhtg atlri39villy mamaum Finami m m F raw U E llf i l Eatmy m m FR Emma 39igfiznflmgulggnr E193 ap lamali m l 39lpi 39iirEFI39I39EHQUIEIJ 1 Hemi39nrim llun I was HDE i i i I I i fl attiul lglr 11ml r 4 LL 1 JJ l 1 E23 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 systoleljsystole o Systole Contraction phase during which the chambers expel bood 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 QRSIIIQRS 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 lntensity 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 lncrease 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 gt Most important tubes for blood redistribution o ARTERIOLES Change in resistance Vasodilation SNS Vasoconstriction PNS Autoregulation Local tissues Cell signals Decrease oxygen and increase carbon dioxide 0 Increase lactate lncrease nitrogen oxide gt Importance of blood ow to active skeletal muscle 0 Mechanisms to increase blood ow to active skeletal muscles lncrease SNS activity lncrease Autoregulation of local blood ow