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HSC 308, Exam 4 Notes

by: Taylor Vermaat

HSC 308, Exam 4 Notes HSC 308

Taylor Vermaat
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These notes go over what will be covered on exam four.
Physiology of Sport and Exercise
Micah Zuhl
Study Guide
Physiology of Sport and Exercise
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This 13 page Study Guide was uploaded by Taylor Vermaat on Tuesday February 16, 2016. The Study Guide belongs to HSC 308 at Central Michigan University taught by Micah Zuhl in Summer 2015. Since its upload, it has received 35 views. For similar materials see Physiology of Sport and Exercise in Nursing and Health Sciences at Central Michigan University.

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Date Created: 02/16/16
Vermaat 1 Physiology of Sport and Exercise: Exam 4 Lecture 8  The Cardiovascular System and Its Control Exercise for health of heart and skeletal muscle rather than weight management. Weight management is done by a restriction of calorie intake. Cardiovascular System: Major Function Delivers O2 Removes CO2 and waste Transports hormones Organization of Cardiovascular System The pump  heart  Capable of adjusting work to meet metabolic demands of body  Very fatigue resistant  Able to generate own electrical impulse  Made up of Type I muscle fibers and LOTS of mitochondria o Location: mediastinal cavity between R/L lung, behind body of sternum and in front of spinal cord o Valves are attached to the papillary muscle by chordae tendineae  Separated into four quadrants… o Interventricular Septum o Fibrous Skeleton  Separates atria and ventricles  Electrical signal cannot penetrate  Three layers of the heart wall o Pericardium  10-30 mL of fluid that decreases friction around heart  Pericarditis  swelling and irritation of the pericardium, the sac like membrane that surrounds heart  Anchors heart o Myocardium  Contracts to eject blood  Think muscular layer  Cardiac tissue o Endocardium  Smooth, thin layer  Lines heart chambers Vermaat 2  Allows blood to flow smoothly Blood flow through the heart: Right atrium  tricuspid  R. ventricle  pulmonary semilunar valve  pulmonary artery  lungs  pulmonary veins  L. atria  mitral  L. ventricle  aortic semilunar  aorta Right heart = pulmonary circulation Left heart = systemic circulation Myocardial Blood Supply Circulation R. Coronary: supplies R. atrium and ventricle, inferior wall of L. ventricle, 1/3 of intraventricular septum When our heart is beating so fast, there is a reduced filling time in ventricles and we slow down, reducing cardiac output at increased exercise L. (main) coronary artery: supplies left side of heart, divided into circumflex, anterior descending Myocardial Tissue  Allows for delayed onset and prolonged contraction of the cardiac muscle  AP is sent to heart; every single muscle fiber is contracting every time in heart  Pacemaker tissue: does not have resting membrane, coordinate firing of myocardial  Myocardial cells have L-type Ca+ channels o Calcium induced calcium release Heart Activity Control Intrinsic Regulation: inside regulation, all alone without input from any sources Ability  maintain HR (100 BPM), increase contractibility if heart volume increases Cardiac Conduction System Does not have a resting membrane potential Spontaneous rhythmicity: special heart cels generate and spread and generate electrical signals Electrical signal spreads via gap junctions SA always fires, does not need an impulse SA node tells the myocardial tissue to contract! Force of contraction: fill the heart and it will contract with great force  Frank Starling Law: stroke volume increases in response to increased ventricular filling Extrinsic Regulations: external, operating from outside Rate and force of contraction can be modulated by external factors Main controllers: Vermaat 3 SNS: Sympathetic system Increases HR above intrinsic HR and increase contractility Release NE PNS: Parasympathetic system [reaches heart via vagus nerve] Main effect  decrease HR below intrinsic HR and decrease contractility Releases Ach, hyperpolarizes cells Enhancing Contractile Force The heart must contract only once with each heart beat and must FULLY relax between each contraction Strength of cardiac muscle contraction must be regulated by modulating the force generated during each contraction ANS: regulation of contractility As HR increases, contractility increases! Why? Due to greater calcium availability More AP = more calcium influx If we don’t fill the heart, we cannot increase cardiac output! Cardiac Cycle All mechanical and electrical events that occur during one heartbeat Vermaat 4 Peak ejection at 120 mmHg  systole Ejection occurs between 80 mmHg and 120 mmHg Aortic valve (AV) opens at 80 mmHg  diastole Ventricular pressure exceeds aortic pressure only for a short time. Diastole Relaxation phase  chambers fill with blood, twice as long as systole Systole Contraction phase Stroke Volume (SV) : volume of blood pumped in one heartbeat Most blood ejected during SYSTOLE EDV – ESV = SV Resting range = 60 mL - 70 mL Maximal exercise = 100 mL - 130 mL Ejection Fraction (EF) : percent of EDV pumped How much blood is pump proportional to how much you fill the heart Clinical index of heart contractile function Resting range 60-70% Maximal exercise 75-85% Vermaat 5 Cardiac Output (Q) : total volume of blood pumped per minute HR x SV = Q Resting cardiac output ~ 4.2 L – 6 L Maximal exercise 20 L – 32 L To increase Q = increase SV  increase HR  increase both the containers  vessels The Vascular System Arteries Arterioles Capillaries Venules Veins Arteries and Veins Arteries  distribution system Veins  collection system Capillaries  diffusion/ filtration system Blood Pressure Systolic pressure (SBP) Highest pressure in artery (during systole) ~110 to 120 mmHg Diastolic pressure (DBP) Lowest pressure in artery (during diastole) ~70 to 80 mmHg Mean arterial pressure (MAP) Average pressure over entire cardiac cycle We must maintain this! How? Two main regulators of BP  SNS and HORMONES SNS Regulation: receptors on cardiac tissue and peripheral vasculature Increase SNS activation = vasoconstriction Decrease SNS activation = vasodilation Hold most of our blood is venous circulation. Blood Measurements: total blood volume ~5 L Hematocrit values: percentage of red blood cells Hemoglobin values Plasma volume Blood Viscosity Thinkness of blood Twice as viscous as water Viscosity increase at hematocrit increase Regulation Hemodynamics – Exercise Hemodynamics BP and HR Regulation of hemodynamics: CV Control Center Vermaat 6 Pressure: force that drives flow – HR and BP Control of SNS and PNS Controls  HR, BP, vasomotor Controls ventilation and vomiting How does the Medulla regulate the CVS? Monitoring the stretch of aorta and carotid arteries Systemic mean arterial blood pressure is the principle variable that the CVS controls! How does the Medulla regulate BP? [at rest] Baroreceptors are the primary sensors for CV regulation (they sense the stretch in arterial wall), medulla turns down SNS, turns up PNS Arterial Baroreceptors Baroreceptors exert a negative drive of CV function and BP : negative feedback system What happens when you stand up too fast? Drop in BP, SNS not kicking in fast enough…medulla is not responding fast enough to baroreceptors Hemodynamics during Acute Aerobic Exercise What causes heart rate to increase during exercise? Autonomic Regulation HR increase during exercise  decrease in parasympathetic control, increase sympathetic activation The initial increase in HR (<120 bpm) is driven by a decrease in PARASYMPATHETIC (vagal) TONE! Initial drive is the backing of of parasympathetic (vagal) tone!!! Sympathetic activation and E/NE spillover from adrenal medulla can also drive HR up. Recovery? Vagal (parasympathetic) tone takes back over, profound drop in HR (18-22 beat drop within 1 minute) What drives up HR? 1. Parasympathetic control backs off, up too HR of roughly 120 bpm 2. Sympathetic activation 3. Epinephrine spillover – peak HR ACTIVATED THROUGH THE MEDULLA Stroke Volume: increases during exercise What causes an increase in stoke volume? 1. Increase venous return (preload) 2. Increase contractility (Ca++ sensitivity) 3. Sympathetic activation 4. Decrease afterload (DBP) Why does venous return increase so much? Muscle Pump SV and Exercise: resting and exercise SV is higher in trained humans The body must increase pressure and maintain pressure during exercise. Why? How? Vermaat 7 Decrease in contractility, decrease in oxygen deliver to heart Pressure increases due to: 1. Reset of baroreceptors 2. Activation of SNS (sympathetic nervous system) Why does stroke volume decrease at maximal exercise? Decreased EDV because the heart is pumping so fast it does NOT have time to fill Response to exercise: Increase SBP directly with exercise intensity Mainly due to SNS activation on larger arteries, vasoconstriction Why does DBP decrease? Decrease in peripheral resistance because of blood vessel dilatation at muscle Due to SNS activation at periphery and local factors During exercise there is a decrease in total peripheral resistance to allow more blood flow to working muscle! Why is a decrease in TPR beneficial during exercise? Increase delivery of oxygen to tissue Slower transit time through capillaries Peripheral = muscle Skeletal Muscle Oxygen Extraction a-vO 2iff local ability of muscle to extract oxygen in circulation arterial content entering tissue minus venous content leaving the muscle Peripheral extraction – skeletal muscle 1. SNS causing vasodilation at periphery 2. Local factors During exercise there is a greater extraction of oxygen. Summary: Must maintain MAP during exercise We are hemodynamically challenged Pulse pressure proportional to stroke volume (SV) At rest pulse pressure = 40 mmHg Would an increase in SV mean an increase in pulse pressure? YES Greater range for ejection to occur by maintaining low DPB and increase SBP Does MAP or Pm increase with exercise? Increase from 94 to 113 Huge drive/ increase of SBP and Q to delivery blood to periphery If we don’t drive up Q, we cannot maintain arterial pressure 1. HR and SV increase 2. Q increase 3. TPR decrease VO2 = HR x SV x a-vO2diff  ability to transport and ability to uptake/ utilize What happens to VO2 during exercise? Vermaat 8 SV is main difference between trained athlete and normal person. HR is strongest contributor to the ability to perform sustained aerobic exercise. Sustain aerobic exercise = HR Peak exercise = SV Detraining Effect on VO2max = decrease SV = decrease HR = increase What drives decrease in VO2max? Stroke volume (SV) What regulates intrinsic regulation of heart? Cardiac Conduction System Myocardial blood supply is greatest during diastole! Why? Coronary arteries are compressed during systole. What effects the size and thickness of the heart? Disease  hypertension Vermaat 9 Contraction through exercise Intrinsic factors that influence heart? Frank Starling Law  increase contractility Spontaneous rhythmicity  pacemaker cells control HR Extrinsic factors that influence heart? Sympathetic system & parasympathetic system How do we maintain flow when hear is at rest? Recoil of vessels If you want to increase EDV during exercise, where does the blood come from? Veins, increase in venous return Respiratory System Pulmonary physiology Purposes  Delivery O2 to and remove CO2 from all body tissues Regulation of CO2 levels and pH Carried out by four process 1. Pulmonary ventilation 2. Pulmonary diffusion 3. Transport of gasses 4. Exchange on O2 and CO2 between the blood and tissues Resting ventilation = 6 L/min Maximum VE = 150 L/min Rest cardiac output = 5-6 L/min Max Q = 25 L/min Inspiration = active process Causes intrapulmonary pressure to fall below atmospheric pressure Expiration = recoil of lung Decrease in lung volume = increase intrapulmonary pressure Air always moves from high pressure to low pressure! Pressure increase = venous compression/ squeezing Pressure decrease = venous filling As volume is decreasing (expiration), pressure is increasing! Takes a lot of effort at low volumes Surfactant- keeps alveoli open Pulmonary Volumes  measured using spirometry Tidal volume: amount of air each breathe Vital capacity: greatest amount of air the can be expired ater full inspiration Influences: smoking, lung disease, increase in residual volume Vermaat 10 Residual volume: the air that remains to reduce the work for inhalation Total lung capacity: sum of vital capacity and RV Inspiration and Expiration during Exercise:  Must increase TV and frequency/ rate at which we are breathing The rate and depth of inspiration increases during exercise Activation of respiratory muscles which allow for greater pressure changes Onset exercise  increase in ventilation Early light exercise  increase TV Late, high intensity  increase rate/frequency Ventilation increase proportional to metabolic needs to muscles Low-exercise intensity  increase TV only High-exercise intensity, increase rate/frequency Pulmonary diffusion: Two main functions: 1. Replenishes blood oxygen supply 2. Removes CO2 from blood Gas Exchange in Alveoli 1. Increase surface area (blood and oxygen interaction) 2. Pressure gradient (O2 moves in, CO2 moves out) 3. Diffusion rate a. Partial pressure (PO2, PN2, PCO2) b. PO2 = 20.93%, PN2 = 79.04%, PCO2 = 0.03% c. Gas percentage never changes Lung blood flow = systemic blood flow Bottom 1/3 perfused with blood at REST What is the most important factor for determining gas exchange? Partial pressure gradient  drives gas diffusion  w/o gradient = no diffusion Why is PO2 lower in alveolar in relation to atmospheric? b/c body temperature, 100% humidity which influences water vapor pressure % O2 in alveoli is lower b/c of dead space 60-65 mmHg = partial pressure gradient Gas Diffusion during Exercise: 1. O2 diffusion capacity increases due to more even lung perfusion a. Gas exchanges over full lung surface INCREASE SURFACE AREA by… 2. Vasodilation of bronchioles and pulmonary vessels 3. SNS activation Vermaat 11 During exercise, how do we increase gas diffusion/exchange? Increased lung perfusion Increased ventilation Main transporter of O2 = hemoglobin O2 must move from atmosphere  alveoli  blood  skeletal muscle Hemoglobin saturation: High PO2, high saturation As PO2 drops, increase offloading Saturation at the muscle  PO2 = 40 – 20 mmHg Hemoglobin offloading occurs during a PO2 of 40 and 100 mmHg More O2 offloading at tissue Curve shift to right indicates more O2 offloads at tissue Decreased O2 affinity When we get hot Factors that increase offloading, many increase with exercise: 1. Increase temperature 2. Increase PO2 3. 2,3 DPG 4. more acidic (Bohr effect) [Bohr Effect: increase temp, increase PO2, increase 2,3 DPG, acidosis = decrease in pH] Decreased affinity = Decrease temperature, decrease PO2, decrease 2,3 DPG, increase pH Myoglobin take O2 from hemoglobin Myoglobin offloads O2 when PO2 falls below 20 mmHg Skeletal muscle PO2 ranges from 2-40 mmHg Decreases during exercise Vasodilation CO2 Transportation: Carried in blood three ways… 1. as bicarbonate ions 2. dissolved in plasma 3. bound to Hb at tissue = CO2  bicarbonate at lung = bicarbonate  CO2  blown off O2 transport and delivery during exercise  1. vasodilation at muscle, decrease PO2, increase blood flow 2. increase O2 extraction 3. local conditions that influence hemoglobin disassociation Why do we vasodilation at the periphery? Vermaat 12 SNS activation = increase PO2 at the muscle Influence hemoglobin to offload? 1. Temperature increae 2. pH decrease 3. increase 2,3 DPG (PCO2) 4. O2 offloading How do we handle change in pH? Handle acidosis. We maintain intracellular and extracellular pH using… 1. Metabolic buffer, lactate 2. Chemical buffers in the blood, bicarbonate 3. Pulmonary ventilation increased, blow off CO2 4. Kidney function, excrete protons Lactate serves as buffer. Takes on proton. Bicarbonate take proton from blood and offload, blown off as CO2. Increase in protons and CO2 causes ventilation to increase. Kidneys can excrete bicarbonate through urine, most deals with phosphate Increase pH = kidneys will excrete bicarbonate Hyperventilate = blowing off more CO2 Medulla Regulation: PCO2 is main regulator though central/peripheral chemoreceptors Body must maintain homeostatic balance b/w blood PO2, PCO2, PN2 Coordination between respiratory and cardiovascular systems Coordination via involuntary regulation of pulmonary ventilation What happens… Step 1  onset exercise Muscle contraction begins, PO2 levels increase slightly Step 2  Increase TV, activate respiratory muscles to increase ventilation Step 3  increased intensity Increase breathing frequency/ rate Step 4 high intensity exercise Hyperventilation, further increase with PCO2, blown off as CO2, drives ventilation to maximal level Step 5  recovery Ventilation remains high to blow off protons, maintain heat production Active recovery = facilitates pH recovery 30-60 min Passive recovery = 60-120 min 1. Muscle contraction increases PCO2 levels 2. Increase TV due to activation of respiratory muscles 3. Increase intensity, increase in frequency Vermaat 13 4. Intensity approaches maximal, ventilation increases due to blow off of non-metabolic CO2 (buffer) 5. Recovery ventilation to manage protons and temperature Ventilation starts faster than cardiac output How do we buffer acidosis? What limits VO2max? [higher brain limitations] Central brain regulation: brain shuts down to prevent damage Central cardiovascular and pulmonary Limitation in O2 delivery to the tissue CV Theory: idea that skeletal muscle has capacity to consume oxygen that exceeds the cardiopulmonary system Why? Blood doping, breathing pure O2 Ventilation is NOT a limiting factor Major difference between trained and untrained person? STROKE VOLUME Other possible limitation? Metabolic limitation = not enough ATP Type of muscle being recruited – large, a lot of mitochondria Central brain regulation – brain protecting heart?


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