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Feb 8th, 2012 Human PhysioII.docx

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Kinesiology & Health Science
KINE 2011
Gillian Wu

th Feb 8 ,2012 Human Physiology II How does the SA node drive heart, what is important in SA node that allows it to control heart node? Ans: Pace maker potential Different shape than the muscle action pot; Pacemaker membrane potential goes -60 to +5 ; 30 to -90 for musle membrane potential The slowly rising line with the dotted blue is the pacemaker potential Green: The threshold potential As you get a slow rise in mem poten you hit threshold, you get a spike in the action potential when it comes down and it starts all over again. The slope of the line is going to determine the heart rate. If that pacemaker potential rises(heart rate high) The rate/ slope of the line is dependent upon these things: (i) At resting potential, Decrease in potassium (K) permeablility (channels close potassium is not moving out retaining the +ve charge inside) (ii) F-type Na channel has fluctuating permeability ; sodium is starting to increase inside the cell, moves from outside to inside, it also contributes to the INCREASEING charge (iii) T-type calcium channels ( t is for transient=short period of time) Calcium is high outside the cell, and it moves inside the cell. Calcium moves in and slow rise occurs in mem pot until we hit threshold (-40mV), we get opening of L-type Calcium Channels and allows Caclium to move in and mem pot hits its PEAK . then the L-type Calcium channels close and potassium channels open and that’s because they are voltage gated and depend on mem potential. -When you stop calcium from going in , potassium is allowed to go out, membrane potential comes back to NORMAL, and it restarts and goes over and over again. -The closeness of this action potential that determine heart rate. The depolarization of the SA node leads to depolarization of the arterial muscle that leads to wave of depolarization travelling across the heart rate. Why does the heart beat on its own? Since these cardiac action potential don’t need any out put. They are self-excitationary. The slop of this pacemaker potential how fast these action potential can be generated. Without any external input? SA node can generate 100Aps/ Minute ( means 100 beats per minute) Intrinsic fire rate of AV node is 100 Aps/min Resting heart rate is 65-72 beats per/min; heart rate is lower than intrinsinc firing rate of SA node? 2 inputs into the SA node: Parasympathetic activity (acetylcholine)decreases heart rate; Sympathetic activity(epinephrine/norepinephrine) increases heart rate. Parasympathetic activity is keeping our heart lower which dominates over our sympathetic activity..Its better because if we want to increase our heart rate (for e.g exercising); we wouldn’t be able to do it,.. Many exercising heart are 150 beats per minute. The parasympathetic activity keeps our heart down, and we can increase it almost 3-folds. Sleeping heart rate: 60 beats/min Heart rate at any given time is going to dependant on parasympathetic and sympathetic activity AV node -AV node also has a pacemaker potential -The excitation is much slower than SA node, -Intrinsic fire rate of AV node is 25-40 Aps/min (much lower) -AV node is able to control the firing rate by the SA node, so the SA node depolarizes the arterial muscle and AV node senses that and causes depolarization. -Under normal conditions, AV node the firing is regulated by SA node, and depolarization of the aterial muscle. Could have problems between communications. If we completely remove the communication, the firing rate will be 40 beats/min in the ventricle. 80 will be the resting heart rate, in the SA node, you will get 80 contractions of atria per min and only 40 in the ventricle (NOT GOOD) Pacemaker can be put in (pacemaker surgery) to sync again. How do these electrical activities turn in depolarization turn in to muscle contraction? -Excitation – contraction coupling -Action potential red: goes up (in cardiac muscle); Na channels make mem pot go up; L-type Ca channels cause the plateau, K brings mem poten back to 0. The contraction starts after the spike of action potential and its going to hit a peak where the action potential starts to come, contraction is coming down with the action potential. What is linking Action Potential to muscle contraction? Similarities 1. Mem depolarization carried into center of cardiac muscles which leads to opening of T- tubules (this is how depolarization goes to the muscles via T-tubules) 2. Depolarization of that leads to the Ca2+ into the cell through L-type Ca2+ channels Entry of Ca into the cell through L-type Ca 2+ (facilitates muscle contraction but its very small to cause contraction ) 3.Calcium comes from out side to inside the cell and binds to receptor (RYANIDINE Rece) Ryanodine Receptor is a calcium channel and its located on the sarcoplasmic reticulum and it’s the same in cardiac and muscle cell. It’s a storage for calcium, (sarcoplasmic reticulum). Ryanodine Receptor is a LIGAND-RECEPTOR channel. (Ligand is calcium , calcium release into the cells through L type channels, Ca binds to these receptor and causes them to open up which allows huge amount of Ca stored in Sarcoplasmic reticulum to be released).. (THIS ALLOWS MUSCLE CONTRACTION) How does Ca allow Contraction? Resting condition, actin mysosin (where they interact) is blocked by troponin and tropomyosin, Ca binds to troponin & causes it to change its shape, by exposing the actin-myosin interaction sites, once that’s done there is cross-bridge formation and this allows for muscle contraction. We also have Ryanodine receptor in skeletal muscles but THEY ARE NOT OPENED by calcium they are opened in a diff way. Cardiac vs Skeletal muscle -The strength of Contraction depends on how much calcium is released.(dependant on intracellular calcium) ** VERY IMPORTANT (Cardiac) -If you want to contract stronger , you will recruit more muscle fibre ( Skeletal muscle) VERY IMPORTANT Ca pumped back to where it came from, RELAXTATION (Decreased intracellular calcium) CONTRACTION (Increased intracellular calcium) Summary [PROCESS OF GOING FROM ACTION POTENTIAL TO MUSCLE CONTRACTION] Action potent on the cardiac muscle cell, Travels down the depolarization and T-tubules Opens the L-type calcium channels that allows little bit of calcium to migrate from outside into the cell This leads to plaetu of action potential but the Ca also migrates to Ryanodine receptors located in the sarcoplasmic reticulum. Calcium release from the Sarcoplasmic reticulum which causes the intracellular increase in calcium Calcium binds to troponin and tropomyosin, That allows the actin filments and myosin to be exposed to each other and make cross bridges, This causes contraction ( muscle shortens) If you remove that calcium the muscle releaxes Electrical activity of the heart can be done by Electrocardiogram, -Summation of all those action potential that
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