4010 Pg108-172, 68-90

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Department
Kinesiology & Health Science
Course
KINE 4010
Professor
David Hood
Semester
Fall

Description
Pg. 108 • Looking at what happens at altitude • At Seas level the Pb is 760mmHg and gets thinner as you go up to altitude • Fractions of the gases do not change (20.93) • Inspired gas is always the same fraction but going down o How does this affect PAO2 is always about 40-50 mmHg less than PiO2 (inspired) o PaO2 is always 4-10 less than PAO2 o Severe hypoxemia at 82, moderate at 93 • Total oxygen coming is less, impacts PAO2 and PaO2 • Not until 50 though is when you start to see some desaturation of Hb • People have tried to improve O2 carrying capacity by Living high and Training Low o Living high makes you increase RBC (you are in aan Erythropoemic situation) o Its like blood doping o You don't train high because it makes you tired Pg. 109 • Some people respond well to Live high, Train low • Live at a high enough altitude to elicit an increase in RBC mass due to an acute increase in EPO (erythropoetin), and train at a low enough altitude to maintain interval- training velocity. For runners who experience a significant desaturation of Hb at sea level even low altitude training may be inconsistent with maintaining interval training • Suggested to live for at least 22hours a day for 4 weeks to induce an increase in RBC mass Pg. 110 • What else affects O2 delivery • CO is in cigarettes and CO has a tremendous affinity for Hb o Will affect O2 transport because CO binds onto Hb • Nicotine induces Bronchoconstriction o Takes more effort to get air in and out • Smokeless tobacco o Increase HR, sympathetic response and incidence of oral cancer Pg. 111 • Polycythemia- more Hb • Anemia- low Hb • Hematocrit is the % of Blood volume that is RBC • At Normal conditions 45% is RBC in our example • AtAnemic condition you may have the same volume but only 30% RBC- Thinner blood • Polycythemia, same volume but 70% RBC- Thicker blood • Dehydration, lower volume (less plasma), RBC may be same as normal but ratio of RBC to Plasma is higher thus 60% Hematocrit Pg. 112 • Make yourself Anemic by taking out RBC, and body creates RBC to compensate then you add the RBC back which increases your RBC content o Withdraw blood, replace fluid loss with Saline (diluting blood volume)  Reduce Hct <45 and Hb to <15 o Kidney senses reduction of O2 delivery (ex. Hypoxemia) this and makes EPO o Stimulates bone marrow RBC synthesis o Hct 55 and Hb 15 comes back o 1 week prior to competition, add back the RBC o You now have Hct 55 and Hb is 20 • Phlebotomy- removal of blood • Autologous- transfusion of your own blood back into you • Everything goes up and lasts for weeks and in this time you have your competition • You have induced Polycythemia • Another way to increase Epo secretion o Going up to altitude o Hemmorhage will also do this (ex. Take a razor blade to your wrist...) • Risks: Increases blood viscosity (better chance of blood clots, and cause strokes), increase resistance to blood flow and blood pressure • Results: Increase VO2max up to 25% and increase endurance Pg. 113 • How does EPO work? o When you have reduced O2 carrying capacity your under hypoxic condition o Kidney (endocrine organ) detects this and secretes EPO o EPO acts on Bone marrow to create RBC  Bone marrow contain Stem cells and with the presence of EPO it differentiates Stem cells into Erythroblasts • Differentiation- used for when cells become Specialized  Then become Reticulocytes- they have nuclei • They become Enucleated which is stimulated by EPO  To become an Erythrocyte to go into the blood • A nice Negative feedback loop o Low O2 delivery o Stimulates process to restore O2 delivery o Restores homeostasis • Vitamin B12 stimulates Bone marrow, assists in making RBCs o Dietary component and rarely deficient • AplasticAnemia- when Bone marrow is destroyed by radiation or chemicals (paint remover long term exposure) o would require a Bone marrow transplant to get Stem cells back o If producing cancerous RBC like Lymphocytes, you then need to kill the Stem cells using Chemotherapy to treat Blood cancers  Then you need a Bone marrow transplant to get Stem cells back Pg. 114 • Anemias are characterized by Low Hct and Hb • Anemias cause fatigue which would impair endurance performance • Several types 1. AplasticAnemia 2. Sickle CellAnemia 3. PerniciousAnemia 4. Iron-deficiencyAnemia- most common  Usually due to low iron from diet, not eating meat  Dieters maintaining low weight: dancers, gymnasts, wrestler • Iron is incorporated into Heme (red pigment) which is in Hemoglobin, Cytochromes (in the ETC of the Mitochondria, the more Mitochondria the redder the muscle), and Myoglobin o More Heme, more red o Dark meat is red muscle Pg. 115- Don't need to know- Recreational reading- Example of Iron-deficiencyAnemia • Former Triathlon Paula Findley former No.1 finished dead last • Found out she was Anemic when they took her blood at the end o She went into the raceAnemic • Apparently she had a hip injury and only 6 weeks of training before Olympics o So poor performance probably due to not training enough Pg. 116 • Experiment done in the mid 80s • Wanted to see what Iron-deficiency did to Performance, VO2max and Mitochondria • If you take away Iron you can imagine that the Mitochondria content might go down cause of Heme o Iron is found in the Heme, and Heme is found in the Cytochromes which is found in the Mitochondria • Depletion of Iron decreased VO2max, Hct, Mitochondria, and Endurance • During restoration VO2max and Hct both climb in a straight line o Shows that VO2max is closely related to O2 delivery • Mitochondria and Endurance have a relationship, also don't increase until after 3 days • PerniciousAnemia- story about something affecting Vit B12 absorption o Stomach has a lining of cells ( some are called Parietal cells that secrete Intrinsic Factor [IF] ) o IF usually binds Vit B12 o IF-B12 complex is absorbed by the gut by Endocytosis and travels to the Bone marrow o At the Bone marrow Vit B12 will dissociate from IF and stimulate RBC synthesis • Intrinsic Factor problem if you have a condition like cancer or ulcers which cause deficient IF Pg. 117- Sickle cellAnemia • Agenetic disease • Hb have 4 Polypeptide chains o 2 Alphas and 2 Beta sub units • Story- 141 Alpha amino acids, 146 Beta o Each subunit is bound to heme, which contains a central iron atom which binds O2 o Sickle cell anemia is a genetic disease due to a Point mutation in the B-globin gene, affects more of the black population in the US  Point mutation (genetic disease) is one Nucleotide substitution in the codon for Glutamate results in amino acid switch in the primary structure (Valine instead of Glutamate) • GGC change to GAC (one has changed) o Beta proteins polymerize in the cell at low PO2 leads to distorted RBC shape and stiff cells, which look like a sickle shape  They also plug up capillaries  Hemolysis- breakdown of RBC Pg. 118 • There are 3 globin genes: alpha, beta, and gamma (y) • In fetal stage we had a2y2 • Adults have a2b2 • If we could restore this fetal Hb to ourselves we would get rid of Beta, and it is the Beta that mutates, so we can do this by using a drug • Hydroxyurea- increase the production of Fetal Hb (Hb F) by inducing Gamma subunit expression which will compete with the Beta and drive it out o So you end up as an adult with Fetal Hb o Fetal Hb does not have mutated Beta subunit which causes Sickling • Many isoforms of proteins are developmentally regulated o Fetal Hb have a stronger affinity for O2, so when a fetus is developing they need more O2 Pg. 119 • Myoglobin is like one of the Hb subunits- has one heme and one segment as opposed to 4 o Hb in the blood, in the RBC o Drops off the O2 which goes into the Interstitial Fluid o Diffuses into the muscle o Where Myoglobin is freely diffuseable protein floating around in the Cytoplasm o Has a high affinity for O2 and grabs onto it o Myoglobin facilitates diffusion of O2 to the Mitochondria (Mb the taxi cab) • Mb Knockout animal o Assumed it would affect performance and impair it o Endurance is not impaired o Strengthens the fact that O2 is plentiful and can diffuse by itself without the need of this taxi cab, not a limiting factor of performance o Heart and muscles become pale because Mb has heme but function not affected Pg.120- Lung disease • Obstructive also called COPD • Classified by on their compliance o Compliance is how easy it is to open up the lung • Obstructive have high Compliance and low Elastance (floppy lung) o Easy to get air in, but hard to get air out o On expiration, largeAlveoli collapse, large pockets of air remain (high Residual volume) • Ex. Small airway disease- Emphysema, Bronchitis, Large airway disease-Asthma Pg. 121 • Emphasematous lung has: o Weak bronchiolar walls o DisruptedAlveoli o Amarkedly reduced surface area for diffusion • Loss a lot of folding, Surface area is important for diffusion o More SA, more diffusion Pg. 122 • Easy to get air in but difficult to get out • Exercise strategy that COPD patients use is they don't take very deep breaths but they take many of them, kind of like panting breathing o Higher frequency • Getting to 30 L/min o VE=30 L/min, VE= f * Vt o Healthy : 2000mls/b * 15b/min o Patient: 1000 mls/b * 30 b/min • Borg scale- Index of discomfort, whether it is hard or not Pg. 123 1. No treatment- they find it really difficult at around 4-5 minutes 2. Now give them a Bronchodilator to open up the airways, they can now perform a longer time and lower Rating of perceived exertion 3. Bronchodilator and if they can carry some O2 during exercise (not practical), o This will reduce Hypoxemia o Will help to maintain a high O2 dissolved in the plasma o Helps reduce diffusion distance 4. If the person could exercise train in a limited way to improve respiratory muscle endurance and strength accompanied by O2 therapy and bronchodilator will have the best overall resulted • Can improve quality of life Pg. 124 • Is an exercise test useful? Is exercise training important or useful for some of these patients • What can an exercise test do? It could tell you how much labour breathing is going on • Sometimes a patient at rest seems okay, put them on a Stress test and pathologies show up like Dyspnea • Will training help? Yes • Pulmonary rehabilitation exercise training can Increase: o Lactate threshold o Peripheral muscle adaptations:Work capacity and sense of well being o Respiratory muscle adaptations  FEV1 and VE capacity o Reduce VE during submaximal exercise o Trained person has a higher capacity to Ventilate, but during submaximal exercise lower Ventilation compared to untrained Pg. 125- Restrictive disease • Low Compliance, High Elastance (opposite to Obstructive) • Ex. Pulmonary fibrosis- stiff lung, hard to inflate but easy get air out • Compliance curve- restrictive has flatter curve Pg. 126 • FEV1 test using Spirometry • How much did you blow out in 1 second • Normal- can blow out 4 of the 5 L- 80% • Obstructive- blows out 2 of 5L, less than 80% • Restrictive- Cant breath in as much, so only breaths in 3.5L , but no problem breathing it out Pg. 127-Asthma • Children in particular suffer fromAsthma but they grow out of it • Is an Obstructive disease of large airways characterized by o Increased sensitivity to a variety of stimuli like dust o Inflammation • Risk factors- smoke, dust, pet exposure (chronic), genetic predispostion, chest infections, cold exposure • Asthmatic airways have smooth muscle constriction, mucous plug, Mucosal layer inflammation Pg. 128 • 3 tissues we don't usually think about • Mast cells found in airway mucosa, secrete Histamine o Bronchial smooth muscle that will respond to Histamine, will contract or relax and cause bronchoconstriction/ dilation o Leukocyte that also respond and promote inflammation o Receptors are on Mast cells, a kind ofAnti-body- Immunoglobulin E, that recognize specificAllergens  When bound causes release of Histamine • Degranulation (exocytosis) occurs to spit out the Histamine o Histamine comes out and binds to H1 which lead to Smooth muscle constriction o Histamine also binds onto H1 of the Leukocyte which triggers the process of PhosolipaseA2  Which breaks down Phospholipids intoArachidonic acid and is converted into Leukotrienes  Leukotrienes undergo Exocytosis and promote inflamation (swelling, pain, and secretions) • Epinephrine can counteract this, and it binds onto Mast cells through the Beta2 receptor, cAMP inhibits Degranulation so Histamine is not released • Binds onto B2 of Smooth muscle and promotes Dilation • Anti-inflammatory drugs have non-steroid type, and steroid types o Prednisone is a steroid, and you take it chronically  It inhibits the PhospholipaeA2- which means less breakdown of Phosopholipids, reducing swelling o B2 receptor Agonist like Salbutamol (popular name: Ventolin) is a short term treatment  TheseAgonist last longer (longer half life) thus have a prolong effect o Cromolyn sodium blocks the Degranulation effect, it preveents Ca from being taken up  In order for Exocytosis to occur you need Ca uptake • Ca causes fusion of Vesicle into the membrane  Cromolyn has no effect on Smooth muscle o Antihistamines have too many side effects, not ideal to take for long term Pg. 129 • Asthma triggers include: smoke, dust, pollen, cold air, laughter, exercise • Exercise causes Exercise induced Bronchoconstriction (EIB) o Proportional to exercise intensity, duration, and type of exercise • EIB proportional to intensity, up to 70%- up to 70% is as much constriction as you can get • Duration- at 1-10mins you see progressive EIB seen post-exercise o Greater than 10 mins sometimes you can run through theAsthma  Due to increased Catecholamines (Epi and NE)= bronchodilation  Not everyone experiences this • Type of Exercise o Worst- exercising in the dry, cold air (running) o Best- warm, most air (swimming) • You use FEV1 test to measure Bronchoconstriction • The graph shows the change of FEV1 results o Most EIB seen after exercise o Asthma us an Obstructive disease, so difficult to get air out o Working at 50% VO2max- Someone prone to EIB after exercise their performance on the FEV1 test starts to fall- this person has Bronchoconstriction- they fall to around 70% and take around One hour for them to recover to normal o Working at 70% VO2max their performance is reduced even further o Working at 30% will lose not as much as 50% o Working at 90% would have same results as 70% VO2max Pg. 130 • There are some parameters that provoke EIB and is proportional to Ventilation (up until 70%) and inversely proportional toAir temperature and Humidity o The lower the temp and lower the Humidity, the higher the EIB  Cold temp and Dry air • Suggestions for people with Asthma o Select exercise type and intensity carefully o Nasal rather than mouth breathing- more airway resistance which moistens the air o Training can reduce VE at submaximal and may reduce medication required o Use drugs: use 10-15 min pre-exercise which decrease EIB post-exercise o People with asthma can exercise regularly o Maybe a slow warm up to get the Catecholamines up to get airways open Pg. 131 • Right ventricles- thin wall • Left ventricles- thick wall- pumps against high BP, has a high load to deal with o Left is hypertrophied • After Load- is the load that the heart to working against • Intercalated disk- the morphological structure between cells- allows current to flow from one cell to another o Aunique feature of the Heart, you can conduct electricity from one cell to the next, this does not happen in muscle cells o Connexin proteins at gap junctions allow Ion flow • Two types of Hypertrophy that result in cells which leads to the different shape of heart o Eccentric hypertrophy- same thickness as normal but longer cell  Caused by Volume Overload  Like elevating Cardiac output for long time, like endurance training  Longer cells- means the chambers get bigger and hold more volume o Concentric hypertrophy- same length but thicker  This is in response to Pressure overload  An example is High BP 24/7 will lead to thicker cells, the heart is trying to get stronger to pump theAfter load • Will lead to Cardiac failure because the heart can't handle this  Chambers get thicker and the inside gets smaller, less room  Resistance exercise will have a higher pressure • Resistance trainers won't have this pathology because they dont have this high BP for 24/7 but only one hour each day, so it results in a stronger heart Pg. 132 • SAnode is where the conduction begins o FastAction potential from SAto Internodal and slows down at theAV node o AV node characterized by a bunch of cells that have a very low conduction velocity  AP slows down here because it allows theAtria to pump and allow blood to fill up the Ventricles o After AV nodeAP speeds up again and rapidly depolarizes and contracts the Ventricles • Cardiac conduction is revealed on the surface of the body using the ECG o P wave- depolarization ofAtria o QRS complex- depolarization of Ventricles and repolarization ofAtria o T wave- repolarization of Ventricles • All cells are bathed in salt water (useful to remember forAP) o Na, Cl, and Ca are high outside, K is high inside (also always negative inside) o ex. Skeletal muscle- Na comes in, making the cell positive, then K moves out and it goes back to negative ( restoring resting potential ) o These ions move through Voltage sensitive channels • AP in the SAnode graph o Starts at around -60mv and NAchannels start to slowly open, increasing positively o At around -30mv hits the threshold, Ca channels open and increases at a faster rate than Na o K starts to leave and the potential goes back to -60mv, o Then Na channels start to open up until threshold again- there is nothing stable about this, changes all the time  The slope of this Pacemaker potential can change (fast or slow, used to control heartbeat) based on Na current- Called the Funny Na current and it's slow Pg. 133 • Electrical events are faster than Mechanical events • Skeletal muscle graph o 1 AP, 1 twitch- the mechanical is so much slower, but this is an advantage o Refractory period- the period where you cannot get anAP  The cell is saying “ I'm recovering, don't bother me” • When anAP happens right before the Muscle has relaxed, it causes more Ca and force to come out before relaxing, theAP are so close together you just get a constant contraction o Tetanic (tetanus) contraction is summation and maximum force output of Skeletal muscle • Ventricle graph o LongAP and it matches the Mechanical in time o At around 30ms Ca channels are open keeping the cell +, and Na are closed o Producing a longer Refractory period o Heart contracts in twitches, there is no Tetanic contraction because theAP are so long you cannot create a summation o Ventricular muscle has Ca keeping cell + Pg. 134 • Coronary blood flow- is blood flow to the heart • Heart is responsible for blood flow sent to the rest of the body • Atherosclerotic plaque have Lipid rich plaque and there isAbnormal connective tissue, Smooth muscle, and Macrophages to block up blood flow • Ischemia means lower than normal blood flow o Blocked arteries mean that the down flow will be Ischemic o Blocked completely is no blood flow and that will be Total Ischemia • Angina pectoris- chest pain because of the Ischemia • Necrosis- is cell death because of Ischemia • Myocardial infarction- heart attack because of cell death • Exercise protects the heart from cell death • Heart is characterized by very high BP and very high Mitochondria per cell • Blood flow to the heart occurs when the heart is relaxing • When heart contracts it compresses all the blood vessels inside the heart and they all flatten out and can't deliver blood flow o When they contract they are all squashed until you relax, and all vessels open • While beating during Systole blood flow to the heart is 20%, more blood flow (80%) during relaxing which is at Diastole • The longer the Diastolic period the better the blood flow to myocardium o The lower the heart rate the better the blood flow • Blood flow to the heart is important because O2 extraction is at maximum Pg. 135 • In the Muscle 5 vol % is extracted at rest, during exercise you extract 15% o During exercise you can get a high extraction for muscle • In the Heart you have high blood flow and high Mitochondria, at rest it extracts 15%, during exercise you extract 17% ( not much room for improvement) o Extraction is maxed out so the way to improve is to increase blood flow • How do we getAerobic activity for the heart measured as VO2 o We have two ways of supplying O2 to the heart: Extraction and Blood flow o Blood flow is more important factor because extraction is already so high • In Muscle we have low extraction initially and increased extractionAND flow during exercise • Why is Blood flow important to the Heart? Because the only way to increase O2 delivery to the heart is Blood flow Pg. 136 • Exercise done at a certain degree protects your heart, and results are fairly significant • If you have exercised all your life and you get a heart attack then the damage done is 60% less than if you did not do exercise • Why a trained person suffers less injury? 1. Exercise training is linked to an improvement in the heart'sAnti oxidant capacity, the ability to remove Free radicals which arise in injury also called Reactive Oxygen Species  Trained heart can remove and metabolize these ROS before they get to damaging levels 2. Increased synthesis of “stress” response proteins , which help refold damaged proteins  Training elevates these Stress proteins to repair proteins 3. Improved blood flow distribution to cell  IncreasedAngiogensis- development of new capillaries that occur with training  In muscle you getAngiogensis also Pg. 137 • First we have a Ventricular AP- NAcomes in, Ca comes in, K going out • QRS is the ventricular depolarization, Repolarization is the T wave • When you depolarize the Ventricle starts to contract and generate pressure • Blood fills up the Ventricle and Ventricle starts to contract which makes pressure that closes theAV valve (makes a noise called S1) • Blood is now flowing out to theAortic valve, pressure continues to rise • When the pressure in the Ventricle falls below that of theAorta around 80mmHg the Aortic valves are shut due to theAorta pressure (creating the second noise S2) • Ventricle pressure continue to fall and when it is below theAtria pressure, it starts to fill up with blood again ( Ventricular filling) • Systolic phase was when blood was leaving the Ventricle, the time between S1 and S2 is Systole o In this example it is from 0-250ms, and beyond is Diastole • Cardiac Cycle Time from 0 to 0.8s corresponds to 75 beats/min • Summary o Ventricular depolarization, the plateau phase then Ventricular repolarization reflected by the QRS complex and T wave o Mechanical event and electrical event very closely matched in time which means a long Refractory period, preventing a Tentanic contraction o Heart starts to generate pressure, and pressure in Ventricle shuts theAV valve making the sound S1 o Pressure continues and pushes open theAortic valve o Ventricle starts to relaxes and the pressure falls below that of theAorta and the Aortic valve shuts making the sound S2 o Pressure continues to drop in the Ventricle and flow can occur again fromAtrium to Ventricle o Time between S1 and S2 is when the blood is leaving the heart and this is Systole • During exercise o Rate of rise is steeper o Extent of rise is greater o Rate of relaxation is greater, o Due to catecholamines affecting contractility Pg. 138 • 60 beats/min is 1 beat every 1 second o 1 Beat is 1000msec o Assume that Systole is 300 msec long, Diastole is 700 msec ( ventricular filling) • 75 beats/min, How much time does it take for 1 beat? o 75 beats occurs in 60 seconds o 75 beats= 60s o 1 beat= X o 75/60 =1/X  75X= 60  X= 0.8 sec  = 800 msec/beat o If Systole is still 300ms then Diastole is now 500 ms  Less time to fill the Ventricle • The longer the period of Diastole, the healthier it is for the heart in terms of getting proper blood flow, a little bit of atherosclerosis means getting longer period of Coronary blood flow • Alower HR like 60 beats/min means you are consuming less energy, don't need as much ATP • Two things benefit for the heart of having a lower HR is longer Perfusion with a longer Diastolic period and Less ATP demand b/c heart is beating less o That is supply and demand • Benefit for rest of the body, if you have more filling time then the ejection time will be higher Pg. 139 • Example of a 40 yr old person • At Rest o CCT=0.8s, Sys= 0.3, Dia= 0.5 • Heavy exercise o CCT= 0.33, Sys= 0.2, Dia=0.13 o Huge change in Diastole o This will affect Stroke volume o At very high Hrs, Systolic time also decreases Pg. 140 • Arrhymthmia- electrical activity disturbances of the heart o Depression of S-T segment of the QRS is an indicator of Myocardial Ischemia or lower than normal blood flow o At rest may not see a difference but may be inadequate during exercise • Hypertrophy of cells vs. Hypertrophy of the Heart o Eccentric and Concentric • Tachy and Bradycardia- High and slow heart rate • Inotropic effect- effects that have an influence on the force of contraction o Postive Inotropic agent would be Epinephrine o Negative- Ca channel blocker • Chronotropic effect- affects the time, like increasing/ decreasing HR o Negative- Acetylcholine • Vagal tone-Action potentials in the Vagus nerve which is part of the Parasympathetic Nervous System- AP in Vagus nerve reducing in frequency • Sympathetic tone- AP frequency in Sympathetic neurons innervating the heart Pg. 141 • Q= HR*SV • At Rest: Q=75 beats/min*65 mls blood/beat o =4875 mls blood/min • Exercise: Q= 150 beats/min * 120mls blood/ beat o =18000 mls blood/min • These two parameters come to a steady state • 60-70 is typical SV at rest • At prolonged exercise things change, especially in the heat o Cardiac drift occurs Pg. 142 • Graph C- Heart rate starts to go up and up gradually from Steady state this is called Cardiac Drift o 10-20mins will be flat but with prolonged and particularly in hot environment HR goes up o When you exercise you get hot and start to sweat, you are losing water (plasma volume) as you exercise  From a Heart perspective- you have less blood, so it is not receiving as much blood and not pumping out as much • Graph B- shows the SV going down • Graph A- Q stays relatively constant even with the loss of volume, HR increases to maintain Q • Take some fluid to replace the fluid loss from sweat o Cardiac drift is less, SV doesn’t change as much, and Q remains constant Pg. 143 • SAnode: Control- Na coming in through the Funny channel to reach threshold, then Ca comes in, and then repolarization with K leaving • Increase in Pacemaker potential slope by making it steeper will reach threshold faster.AP will occur sooner o To increase we have to increase current through the Funny Na channels o Sympathetic stimulation will do this through the action of NE, NE acts on cells and opens Na channels more rapidly, allowing more Na in o Positive Chronotropic agent- NE • Reduce the slope it will take longer to reachAP o There is a Hyperpolarization which also prolongs reaching threshold o Parasympathetic stimulation releases the Negative chronotropic agent Acetylcholine- reduces the current  Acetylcholine also increases K coming out and causes Hyperpolarization Pg. 144 • HR goes up in a straight line with Exercise intensity, the harder you work the more HR • SAnode becomes less sensitive to Epi and NE as we age o Can't get HR as high than when younger o Max HR is dependent on Sympathetic action • When you start to exercise something happens in your b
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