test 2 kin 321 study guide
test 2 kin 321 study guide kin 321
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This 12 page Study Guide was uploaded by Annmarie Jaghab on Sunday February 28, 2016. The Study Guide belongs to kin 321 at University of Miami taught by Dr.Jacobs in Winter 2016. Since its upload, it has received 43 views. For similar materials see in Physiology at University of Miami.
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Date Created: 02/28/16
KIN 321 Test 2 Notes Lecture 7 -distribution consists of distributing oxygen to tissues, nutrients to tissues, hormones around and wastes -cardiovascular system reaches out to many different systems in the body -heart runs from the base of the second rib to the 6 rib -the outer portion of the heart is non-contractile. The heart sits within the pericardium. -the thickest portion of your heart is the myocardium -the endocardium is the thinnest portion of your heart -atria have a thin myocardium (only moving to the ventricles so they need to move a short distance. There is little to no resistance if the heart has healthy valves and gravity assists in pushing the blood) -ventricles have thick myocardium due to resistance (pressure that the chamber has to push against) as well as the distance (how far does it have to move blood) -the left ventricle is thicker than the right because the left ventricle pushes blood through systemic circulation while the right ventricle only needs to pump to the lungs which is a short distance away. The left ventricle pushes against more resistance (about 120/80) while the right ventricle only needs to go against the pressure of the lungs which is low (due to the huge capillary beds, lots of surface area so blood spreads over a large area and pressure drops) -thickening of either ventricle can occur. In athletes we see thickening of the left ventricle why? You can push more blood out to the rest of the body. For endurance athlete it is a volume over load. On the other hand for a resistance trained athlete left ventricular hypertrophy is due to a pressure overload. -val salva maneuver increases the blood pressure from exertion and due to pressure over load the left ventricle gets stronger. -clinically, someone with hypertension would have left ventricular hypertophy since they always have high blood pressure -right ventricular hypertophy would be seen with COPD (lung disease) since there is an increased pressure in the lungs -valves make sure blood only flows in one direction as it moves through the heart -chordae tendonae prevent the AV valves from opening up backwards into the atria due to the pressure build up in the ventricles -when the ventricles contract, so do the papillary muscles which pull on the chordae tendonae -aortic semi lunar valve makes sure it goes out through the aorta and doesn’t come back though the left ventricle -most common valve disease is mitral valve prolapse. Disease of the mitral valve, it doesn’t seal well so some of the blood regurgitates back into the atria -systole is contraction of ventricles -diastole is relaxation and filling of the ventricles -time for diastole decreases the most as you move to a high heart rate -heart gets most of it’s oxygen supply during diastole. -during systole, the heart is contracting against its own capillary beds and restricts flow slightly -cut down time for diastole, at high heart rates. This is why you can’t sustain high heart rates for very long or you go into ischemia (lack of adequate oxygen supply) -cardiac output=HR x SV and at rest CO is usually 5L/min -three sources for deoxygenated blood: superior vena cava, inferior vena cava, and coronary sinus (deoxygenated blood from the myocardium enters there, since your heart uses blood too) -intercalated disks allow for the heart to contract with little or no electrical resistance. The heart is just one motor unit so once one part contracts, the whole heart contracts. This is unlike skeletal muscle, which is divided into multiple motor units -the heart has a more developed capillary network because it has to have more blood flow go to it than skeletal muscle since it is constantly contracting -huge mitochondrial volume since it is always contracting -because the heart is highly aerobic, it relies on a constant flow of blood. This is dangerous because if there is any drop in myocardial blood flow, the heart tissue can die easily -no need for neural innervations meaning that if you took away the parasympathetic or sympathetic stimulation, the heart would still contract -atria and ventricles are electrically separated from each other by this fibrous tissue that is not conductive at all. There is one narrow gap, which the electrical stimulation can pass through. Action potential spreads through the atria via the SA node and then once it passes the middle non-conductive portion it can enter through the gap called the AV node so that the electrical stimulation can go to the ventricles. A delay is built into the AV node and this allows for filling. -SA node is the pacemaker. It has the highest inherent electrical rhythm and dictates the pace of the heart -electrical signal pathway: SAAVBundle of HisPurkinje Fibers (pneumonic: Start A Blood Pump) -the heart is leaky to sodium so it is less negative than you would see in skeletal muscle. If you are leaky to sodium, the resting membrane potential is never constant and is depolarizing randomly until an action potential is reached. -don’t need to know speeds of conduction exactly. The AV node has slow conduction velocity. There is a pause at the AV node to allow for the filling of the ventricles -ventricles are slightly twisted -P wave: atrial depolarization. Where the SA node fires an action potential and it spreads through the atria -Flat portion after the P wave is when the heart pauses at the AV node while the ventricles are filling -QRS: ventricular depolarization. Ventricles are pushing blood out to systemic circulation -T wave: re-polarization of the ventricles -P wave is very small in magnitude vs the QRS. Why? The P wave is small because of the thin myocardium of the atria not having much electrical activity. There is thicker myocardium in the ventricles so they get a large magnitude of electrical activity. Also the P wave is uniform while the QRS has 3 separate parts to it and has to go through both the bundle of his and then comes back up through the purkinje fibers -resistance vessels: aorta and arteries since they are under high pressure -capillary beds have a large surface area so the pressure drops -once you get to the veins the pressure is nearly zero -pressure goes back up in the lungs -everything but capillaries have a smooth muscle layer. Smooth muscle layer is a lot thicker in arteries than in veins. This is because arteries have a higher average pressure. -capillaries have no smooth muscle layer because there is exchange of fluid, nutrients, and gas. If there were a thicker muscle layer, this exchange would be prevented. -veins have valves which are not present in arteries. This helps prevent pooling of blood in the extremities -blood is made of plasma and cell portions -oxygen carrying capacity is more in the cell portion -things more dense go to the bottom of the centrifuge tube so this is why the cell layer is at the bottom -hematocrit: the percentage of blood volume that is made up of red blood cells. -hematocrit is increased at altitude. Increased red blood cells and decreased plasma -training slightly increases hematocrit. Training in Miami may actually slightly drop hematocrit since plasma volume goes up -blood doping increases hematocrit -dehydration increases hematocrit Lecture 8 -when you go from rest to exercise, you need blood flow to go to working muscle and vascular smooth muscle is designed for this regulation. -smooth muscle all contracts slowly, no fast twitch activity -local: anything floating in the blood -blood flow is determined by blood pressure -blood pressure is equal to the cardiac output x total peripheral resistance -TPR is a function of vasoconstriction and vasodilatation -BP increases when you do exercise, why? Cardiac output goes up and TPR either remains the same or fluctuates a little -hypertension is caused by a high TPR usually due to arterial disease meaning they can dilate the blood vessels well -poiseuille’s equation is used for tubes and blood vessels act as tubes -P1 is the pressure in the aorta -P2 is at the arterioles going to the leg -blood flow is dependent directly on pressure difference, radius and inversely related to length of tube and viscosity -dehydration leads to blood becoming thicker which would lead to decreased blood flow -blood doping would also lead to decreased blood flow -How do you accomplish 25 fold increase in blood flow to active skeletal muscle during exercise? increase P1, vasodilate to active skeletal muscle, try to maintain normal viscosity by staying hydrated -gut is a large amount of tissue. Absolute amount of blood to the gut isn’t changed much -what provides the signal to link local metabolism to blood flow? Lactate, decreased oxygen and increased carbon dioxide, increase in adenosine from breakdown of ATP, and H+ ions being released which drops pH -local induced vasodilatation is only to active muscle -endothelium is a vasodilator in response to catecholamines -sheer stress is sensed by artery which releases NO and it vasodilates -first step to arterial disease is damage to the endothelium -if arteries can vasodialate well it reduces risk of arterial disease -reactive hyperemia is an increase in blood flow from baseline. Happens when you take blood pressure since you cut off the stress of blood flow to 0 and then when you release the blood rushes -kidneys sense a reduction in normal blood flow to start the Renin Angiotensin System -ACE is located in the lungs. The conversion to angiotensin II is the most important step because angiotensin II is a potent vasoconstrictor -vasoconstriction and water retention serve to increase blood pressure -when you become dehydrated, blood volume drops which would cause blood pressure to drop significantly and in turn cause blood flow to decrease, but this drop in blood pressure doesn’t occur because there are regulatory mechanisms of the renin angiotensin system in place -ACE inhibitor is given to people with hypertension, which reduces the amount of angiotensin II that is produced so it would lower your blood pressure -local control is exclusively vasodilatory -humoral can be vasodilation or constriction -neural is strictly vasoconstriction -kidneys, gut, spleen, and skin are most heavily innervated by the sympathetic nervous system ** -local control pulls the blood flow to active muscle -this system is messed up in people with spinal chord injuries since they lack the ability to vasoconstrict to areas below their injury -area of the brain that controls blood flow is the motor cortex -you constantly maintain slight vasoconstriction to maintain resting blood pressure -dangerous to have high diastolic pressure because that is directly linked to reductions in blood flow to the heart -systolic blood pressure could fluctuate due to stress (like white coat syndrome) but this does not occur with diastolic blood pressure -vasomotor region controls circulation -ultimate goal of neural regulation of CV function is to maintain arterial BP because the blood to the brain needs to be sufficient -any influence on the SA node would influence heart rate because it is the pacemaker -any influence on the rest of the myocardium would influence cardiac output -contractility is the force of contraction -main influence of the Parasympathetic nervous system is to lower heart rate. -sympathetic affects both HR and SV while parasympathetic only influences HR -Cardiac output is mainly changed by changes in heart rate -at 50% and below Vo2 max the rise is in cardiac output is driven by increases in HR and SV, but once you get above 50% SV plateaus and HR becomes a major factor -EDV: volume of blood after filling -ESV: leftover blood after emptying -Afterload: pressure outside of the heart that the heart has to work against. Avg for left ventricle is around 100mmHg -ventricular compliance is how much your ventricles can stretch -increase contractility, increase end systolic volume -hypertension can lead to ischemia over time -Frank-Starling Method: as you fill the ventricles and they stretch more, it increases their contractility -when you stretch the ventricles enough there is optimal overlap between the actin and myosin -increased venus return from heart rate increase increase EDV stretching of cardiac muscle and sympathetic stimulation is from the frank starling methodsincreased contractilitydecreased ESVincreased SV -AV O2 difference can be looked at and shows peripheral O2 use Lecture 9 -alveoli shows respiratory zone -conducting zone has no alveoli and no exchange of gases -diaphragm is the primary muscle for inspiration and is assisted by the external intercostals -expiration uses mainly internal intercostals and rectus abdominus -move air in and out of lungs by changing thoracic volume which thus changes pressure inside of lungs -diaphragm in resting position is an upside down U -higher rates of ventilation during exercise -during exercise you need to breathe more rapidly to bring air into the lungs -tidal volume is depth of normal breath -vital capacity: difference between max inspiration and max expiration. Working volume of lungs -residual volume: what is left in lungs after you maximally expire. It is there to prevent lungs from collapsing -minute ventilation is how much air you exhale in a minute. Depth of breath x how frequently you breathe -at maximal exercise you increase both the depth and the frequency of breaths -why do you max out tidal volume? Breathing more quickly is more efficient than taking deeper breaths -in the lungs there are two types of dead space: anatomical and physiological -anatomical: V EV …A is Alveolar. Anatomical dead space is the conducting zone -physiological dead space is down in the respiratory zone -more physiological dead space at the top of your lungs -change body position, change physiological dead space -oxygen has a low solubility in fluid, so most oxygen is found bound to hemoglobin -V is alveolar V is arterial A a -concentration of hemoglobin in the blood is the only part of the equation that changes. It can change which changes oxygen amount. When does the hemoglobin concentration change? Being at altitude increases oxygen carrying capacity and blood doping (take own blood cells out and the body makes more RBC and then you re-inject it. OR you can take EPO which is intended for people with anemia but people use it anyway to blood dope) -As you increase PO ,2you increase hemoglobin’s affinity for oxygen (curvilinear relationship) -PO2 in lungs is 100-105 and in the tissues it is only around 40. So there is a higher affinity for oxygen in the lungs and in the tissues, it lowers its affinity so it can deliver oxygen -myoglobin (located inside skeletal muscle) has a greater affinity for oxygen than hemoglobin -myoglobin gives muscle it’s red color so that is why slow twitch fibers tend to be red -chicken meat: dark meat has more myoglobin and is more fatty since it is more oxidative and stores more fat and has a higher oxidative capacity -ducks have a lot of dark meat under breasts because they migrate while chickens don’t really fly so there is less dark meat near breast bone -drop in pH causes oxyhemoglobin dissociation curve to shift to the right with exercise. rightward shift is beneficial because it lowers hemoglobin’s affinity for oxygen mostly in the steep portions of the curve where the tissues are. At the lungs there is not much of a change in affinity because during exercise you don’t want to change the lung affinity just the tissue affinity and this is why it makes sense that the graph is curvilinear -increase in temperature causes a rightward shift also -we also have to move CO fro2 the tissues to the lungs -CO 2s slightly more soluble than O (52 is freely floating while for O it2 was 1%) -bicarbonate is produced within the RBC and then is kicked out into the plasma -in the tissues, hemoglobin is binding CO and hydrogen ions 2 -size of a tennis court is the amount of surface area in our alveoli -small vessels form a weblike network around alveoli to allow for gas exchange to occur -gasses move down concentration gradient (from high to low partial pressures) -if you maintain P AO2and P ACO2you maintain the gradient which keeps gasses moving -lung disease/COPD you would have accumulation of fluid in the lungs and increased tissue thickness which makes gas diffusion harder. So you give them oxygen to help and change the pressure difference to increase gas diffusion -neural mechanisms increase ventilation as body anticipates exercise -respiratory center of the brain is in the lower portion of the brain. It has an inspiratory and expiratory center -motor cortex has a heavy impact on ventillatory center -peripheral chemoreceptors are in the aortic arch and carotid bodies because these are the points that show how well the heart and lungs are working together to re-oxygenate blood. Carotid bodies control blood flow to the brain. -muscle afferents are from the muscle to the brain -mechanoreceptors inhibit inspiration to prevent over inflation of lungs -motor cortex signal switches between expiratory and inspiratory -conditions in which peripheral chemoreceptors increase ventilation : drop in PO2 increase in PCO2and drop in PH -greater regulation over the inspiratory than expiratory because expiratory is passive at rest whereas inspiration is always active requiring contraction of the diaphragm Lecture 10 -pH equations involve levels of H+ and CO 2 -any increase in CO w2uld decrease pH -increase in bicarbonate (a base) would make blood more basic (raise pH) -tolerate narrow ranges of pH, usually lower in the muscle -hydrolyzing ATP produces a hydrogen ion -oxidation reduction reactions produce a hydrogen ion -CO 2omes from citric acid cycle -CO 2s buffered by being converted to bicarbonate which liberates a hydrogen ion -ATP hydrolysis and red-ox reactions are the parts that produce hydrogen ions (2 hydrolysis and 1 redox in glycolysis) -with high rates of glycolysis there is a reduction in pH since 3 steps are producing hydrogen ions -lactate production is not what lowers pH, it is the high rates of hydrogen ion production -3 steps of the citric acid cycle (decarboxylation) form CO . It all occurs 2 in the mitochondria so it is metabolic CO p2oduction -a reduction in pH is bad because within the muscle there are 3 enzymes that are inhibited with reductions in pH (phosphorylase, PFK, and PDH) -phosphorylase triggers breakdown of glycogen in muscle to glucose 6 phosphate -pyruvate dehydrogenase allows carbohydrates to enter into the TCA cycle because it converts them to acetyl coA -why does a drop in pH turn off these enzymes? pH is low and we don’t want it to drop even lower so by stopping glycolysis you stop the production of hydrogen ions –drops in pH reduces high intensity exercise performance. As you become more trained, your buffering capacity is improved so you can sustain more high intensity training -hydrogen ions compete with calcium for binding sites with troponin. Hydrogen ions therefore block calcium and there is a drop in peak power output because cross bridge cycling is disrupted -muscle pH drops more quickly than blood pH -muscle is the site of the majority of hydrogen ion production and it has a lower buffering capacity -hemoglobin is key buffer that binds CO and H+ ions and offloads O 2 2 -primary buffer in the blood is bicarbonate plus ventilatory compensation -first line of defense is weak in the muscle as a buffering system, but the second line in the blood is better -still producing hydrogen ions as glycolysis is occurring -pH is maintained at rest and low intensity of exercise -greater amount of hydrogen ions drive the reaction down to CO (seen 2 in high intensity exercise) -why is body making conversion to CO ? so 2ou can breathe it out to the atmosphere -only can buffer hydrogen ions to CO if y2u can blow it out so it has to be paired to ventillatory compensation -increase in CO i2 blood results in an increase in ventilation which is sensed by peripheral chemoreceptors -non-metabolic CO is 2he result of buffering (not structurally different from metabolic CO ). 2eripheral chemoreceptors still sense the non- metabolic CO 2 -increase ventilation rate increases during exercise to maintain pH in blowing of the CO an2 to regulate the P CO2and the P O2 -as you move up in intensity, there is a linear increase in ventilation. Ventilation is increasing because the amount of CO in th2 blood is increasing -once you get to higher rates of glycolysis you have more non- metabolic CO pr2duction so there is thus an exponential rise in ventilation -lactate thresholds are more predictive for performance than VO max 2 Lecture 11 -Infants are mostly made of water -most fluid loss comes from urine production and a lot is lost from breathing -fluid balance can be thrown off with prolonged exercise in the heat (fluid loss exceeds fluid gain) -For every liter of oxygen consumed we make 5 Kcals of energy and 4 of those Kcals are in the form of heat -when you do high intensity exercise, you produce enough heat to raise core temperature by 1 degree celcius every 5 minutes -core temperature is a balance of factors that promote heat gain as well as heat loss -once ambient temperature exceeds skin temperature, radiation, conduction and convection become means of heat gain and you can only rely on evaporation for heat loss -in hot humid conditions, there is very limited ability to get rid of heat compared to hot and dry conditions -radiation is exchange of heat with objects you are not in contact with (IR) -in dry environments, it is not that you aren’t sweating because you aren’t soaking wet, you are still sweating but the sweat is just evaporating -more surface area exposed results in more sweating -if sweat is not evaporating, you have water loss without cooling -the rate at which body produces heat at a cold and warm environment is the same. Heat production is driven by exercise intensity. -core temperature increases fairly steadily -rectal temperature is the best measure with exercise -as you increase intensity heat production increases linearly -total heat loss is mostly in the form of evaporation -ability to produce heat exceeds ability to get rid of heat starting at a low intensity (occurs above 60 watts, anything above a warm up) -intense exercise in a hot, humid environment would give the greatest increase in core temperature -hypothalamus acts as a thermostat -vasodilatation and increased heart rate allows blood to be moved more from the core to the skin and then combined with sweating allows it to be evaporated -pilloerrection occurs because hair standing up would allow warm air to be trapped within the skin (evolutionarily vestigial, we used to have a lot more hair on skin) -exercise in the heat is tough on the cardiovascular system -cardiovascular system moves oxygen and nutrients -sweat production is driven primarily from plasma volume which decreases due to high sweat rates -when plasma volume drops, stroke volume drops so the heart beats faster to compensate -why does SV drop? EDV goes down so then contractility of ventricles goes down -in a dehydrated condition at a constant intensity (CO will stay the same), HR drifts upward -sweat rates are highly variable between people -as you repeatedly expose your body to heat, your body adapts -at lower core temperatures, you start sweating earlier -if you exercise in the heat, acclimatization is rapid and you will mostly hold on to these adaptations for a longer period of time than it took to gain them -HR is easiest to measure to see if someone is acclimatizing -in dehydrated states, VO 2ax decreases since you drop SV -in the heat you deplete carbohydrate sources more rapidly so you rely on muscle glycogen use more. Lecture 12 -as you increase exercise intensity, you increase the amount of blood low. Reduction in blood flow to muscle training in heat. Increase in blood flow to skin training in the heat. -people exhaust sooner in the heat -heat exhaustion results in hypotension from acute plasma volume loss so blood volume drops and vasodilatation occurs so blood pressure drops ***-What distinguishes heat exhaustion from heat stroke? Core temperatures! 39.5 degrees Celsius for heat exhaustion and 41 degrees Celsius for heat stroke -ignoring signs and symptoms of heat exhaustion, you can push yourself to the point of heat stroke -hypothalamus controls sweating and vasodilatation amount. -plasma volume is low so sweat rate decreases -blood pressure can swing one way or the other in heat injuries -football linemen are athletes that are susceptible to heat stroke especially in pre-season (gear inhibits evaporation of sweat) -ice packs should be in armpit, groin, and neck -hyponatremia: low sodium concentration -takes a dilute substance like straight water to get to the point of hyponatremia -anything below 135 serum sodium levels is hyponatremic -run lower, more time to drink so they are less likely to become hyponatremic -the occurrence of dehydration is much more common than hyponatremia -drinking ahead of thirst but not over-consuming is best -lack of sleep, glycogen depletion, and hypoglycemia all are associated with a stressed state which predisposes to hyperthermia -alcohol consumption leads to dehydration so that is why you are more susceptible to heat injuries then -sweat rate is related to genetics and previous heat exposure -body weight from day to day should not change by more than % or you are not properly hydrated -glycerol lowers heart rate and core temperature. Increasing plasma volume by trying to hyperhydrate -combining water and carbohydrate results in an additive effect -first drop in plasma volume is due to increased blood pressure -plasma volume during exercise is better maintained with a less concentrated hypotonic drink. Why? Things that are highly concentrated stay in the stomach longer. Reduced gastric emptying with something hypertonic -active water absorption activates SGLT 1 -having sodium and carbohydrates is better for rehydration -consuming a lot of plain water during recovery results in an increase excretion of water in urine so you lose a lot of the rehydration -coke has no sodium so it is bad for rehydration
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