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KIN321 Week 5 Class Notes

by: askcch

KIN321 Week 5 Class Notes 321

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About this Document

These notes cover Lecture 7 & 8
Introduction to Systemic Exercise Physiology
Dr. Kevin Jacobs
Class Notes
Systemic, Physiology, KIN321
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This 9 page Class Notes was uploaded by askcch on Tuesday October 4, 2016. The Class Notes belongs to 321 at University of Miami taught by Dr. Kevin Jacobs in Fall 2016. Since its upload, it has received 5 views. For similar materials see Introduction to Systemic Exercise Physiology in Kinesiology at University of Miami.


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Date Created: 10/04/16
KIN321   Class     otes     eek      (9/19­9/23)  ________________________________________________________________________________  From    revious  ections    ­ Amino acidmetabolism  ­ Neural­endocrincontro   metabolism  ________________________________________________________________________________  Lecture 7 The Heart and the Cardiac Cycle  ● Cardiovascular Functions  ○ Distribution   ■ O 2o tissues and CO f2om tissues to lungs  ■ Nutrients to tissues  ■ Hormones  ■ Waste products  ○ Hemostatic regulation   ■ Fluid balance and blood pressure (blood ow)  ■ Maintain pH  ■ Maintain thermal balance  ● Vasodilation to get rid of heat  ● Vasoconstriction to keep warm  ○ Protection  ■ Prevention of blood loss (vasoconstrict)  ■ Prevention of infection  ● Basics of Heart  ○ Size of st → approx. ½ pound  ○ Four chambers  ■ Left & Right Atria (thin myocardium because of low resistance & short  distance)  ■ Left ventricle  ● Thicker and usually larger ventricle, pump blood to the whole  body  ● Left ventricle hypertrophy is due to:  ○ Hypertension, increased resistance & pressure in the aorta   ○ Endurance training, volume overload overtime   ○ Resistance training, pressure overload   ■ Right ventricle pump blood to the lungs   ● Thinner due to low BP in the lungs (due to very high surface area)  ● Right ventricle hypertrophy is due to COPD, increased pressure in  lungs   ○ Base at 2nd rib  ○ Apex at 5th or 6th rib  ■ Important for placing electrodes for ECG  ○ Non-contractile layers:  ■ Pericardium → double-walled, loose-tting sac  ● Parietal → brous protection, anchor + smooth surface  ● Pericardial cavity   ● Visceral (epicardium) → smooth surface + coronary arteries   ○ Contractile layers:  ■ Myocardium → Cardiac muscle  ○ Endocardium (innermost layer)  ○ Valves of the heart assure unidirectional ow of blood  ■ Atrioventricular   ● Tricuspid on right  ● Mitral on left   ● Chordae tendonae and papillary muscles hold valves closed  during ventricular contraction  ■ Semilunar   ● Pulmonic on right  ● Aortic on left   ● The Cardiac Cycle   ○ Systole - Contraction phase (ventricular contraction)  ○ Diastole - Relaxation phase (lling of the ventricle)  ■ Where the perfusion to myocardium occurs  ○ When HR goes up, time for diastole decreases dramatically   1. Waste-carrying, oxygen-poor blood enters the right atrium from the superior  and inferior venae cavae  2. Blood ows from the right atrium into the right ventricle; from there it is  pumped through the pulmonary arteries into the lungs  3. In the lungs, blood picks up oxygen and discards carbon dioxide; it then ows  through the pulmonary veins into the left atrium  4. Oxygen-rich blood ows from the left atrium into the left ventricle; from  there it is pumped through the aorta into the rest of the body’s blood vessels  ● The Myocardium  ○ Similarities to skeletal muscle:  ■ Striated with myobrils containing actin (thin) and myosin (thick)  laments  ■ Surrounded by sarcolemma  ■ Depolarize before contracting  ○ Dierences from skeletal muscle:  ■ Tightly connected by intercalated disks and gap junctions → complete  synchronous contraction (contract at the same time; no lag/delays)  ● Minimal electrical resistance → all or none contraction of entire  heart compared to entire motor unit of skeletal muscle  ■ More developed capillary network  ■ Greater mitochondrial volume (~40%) than skeletal muscle (~2-6%)  ■ Inherent rhythm (involuntary) → no need for neural innervation   ■ 10-15min lack of Q to myocardium can cause death of tissue  ● Action Potentials in Cardiac Tissue   ○ Atrial and ventricular syncytium separated by atrioventricular brous tissue   ■ This allow time for blood to ll the ventricle before the action potential  arrives and forces the contraction to pump blood out  1. Sinus node (SA node)  2+ a. SA node is leaky to Na → less negative resting membrane potential   i. Thus it has an inherent rhythm of 100-120bpm  b. Parasympathetic nervous system (Vagal tone) slows it down to  60-80bpm  2. Atrioventricular node (AV node)  a. Impulse delayed at AV node to allow ventricular lling  3. Right & Left bundle branch  4. Purkinje bers  a. Nearly instantaneous transmission → 0.03s from top bundle of  branches to furthest ends  b. Ventricular muscle bers wrap around heart in double spiral →  ventricles are emptied in a wringing motion (擠毛巾)  ● Normal ECG  ○ Atrial repolarization is hidden behind QRS  ○ Shape of QRS curve is due to the spread of action potential is AV node → 2  branches → tons of purkinje bers           ● Blood Vessels              ● Systemic and Pulmonary Blood Pressure              ● Physical Characteristics of Blood  ○ Plasma  ■ Liquid portion of blood  ■ Contains ions, proteins, hormones  ○ Cells  ■ Red Blood Cells  ● Contain hemoglobin to carry oxygen  ■ White Blood Cells  ■ Platelets  ● Important in blood clotting                                  ________________________________________________________________________________  Lecture 8 Control of Circulation; Cardiovascular dynamics during  exercise  ● Vascular Smooth Muscle  ● Vascular smooth muscle designed to:  ○ Regulate blood ow to active tissue  ○ Maintain systemic BP  ● Dierences from skeletal muscle bers include:  ○ Smaller and not striated  ○ Contract more slowly  ○ Capable of maintaining vascular tone with little energy  ● Controlled by factors including:  ○ Local → (exclusively vasodilator)  ○ Humoral → substances owing in the blood  ○ Neural → (exclusively vasoconstrictor)    ● Determinants of Blood Flow  ○ Rate of Q is determined by blood pressure  ○ BP = CO x TPR  ○ At constant cardiac output (rest, steady state exercise), Q is regulated by  changing TPR via vasoconstriction or dilation  ○ Increased TPR is common cause of hypertension  ○ Q is aected by:  ■ Pressure dierence between inow and outow → ^P1-P2 = ^ow  ● CO primarily inuences P1  ■ Radius → ^R = ^ow (small changes in radius, big changes in ow)  ■ Viscosity → ^V = dec. ow (higher viscosity more sticky)  ○ How do you accomplish 25 fold increase in Q to active skeletal muscle during  exercise?  ■ ^CO (^P1)  ■ Vasodilate at areas of need (decrease P2)  ■ Vasoconstric at areas of unnecessity   ■ Maintain viscosity   ○ Perfusion to brain unchanged during exercise   ● Local control of Q  ○ Q increases exponentially with increased metabolism  ○ Increased rate of local metabolism signaled by:  ■ Metabolites → ^adenosine, ^lactate  ■ Gas partial pressures → dec. PO and2^PCO   2 + + ■ Ions → ^H and ^K   ■ NO, potent vasodilator at endothelium  ● Damage to the arterial wall is the rst step for coronary diseases  ■ Flow mediated dilation: decrease when people have disease, ^ with  endurance training  ● Renin-Angiotensin System  1. Reduced blood ow through kidneys  2. Kidneys secrete hormone renin  3. Renin splits angiotensinogen from liver to produce angiotensin I  4. Angiotensin converting enzyme (ACE) from the lungs converts angiotensin I  to angiotensin II  a. Vasoconstriction   b. Aldosterone release by adrenal cortex → water retention by kidneys   5. Increased BP  - Caused by:  - Dehydration (^viscosity, decreased ow, decreased BP)  - Acute blood loss from injury   ● Neural Control of Blood Flow  ○ Sympathetic nerve bers innervate all blood vessels except capillaries →  almost exclusively vasoconstrictor  ○ Kidneys, gut, spleen, and skin most heavily innervated → skeletal muscle and  brain under less inuence  ○ Neural control does not distinguish between active & inactive muscles   ■ It needs to be layered with local factors, so Q goes to desired places  ■ Therefore neural and local controls need to work together for it to  work  ● Myocardial Blood Supply   ○ Danger of high DBP: low perfusion to myocardium   ○ DBP don’t usually drift that much during exercise; so if DBP goes up, exercise  needs to stop  ● Cardiovascular Regulation and Control   ○ Ultimate goal of neural regulation of cardiovascular function is to maintain  arterial BP  ○ Heart is directly innervated by both the parasympathetic and sympathetic  division of the ANS  ■ Parasympathetic nervous system  ● Vagus nerve innervates SA and AV nodes, atrial myocardium  ● Slows HR by inhibiting SA node  ● Decreases atrial contractility   ■ Sympathetic nervous system  ● Innervates SA and AV nodes and ventricular myocardium (wide  spread eects)  ● Increases HR by stimulating SA node  ● Increases ventricular contractility (^SV)  ■ (Parasympathetic inuence predominates at rest)  ○ HR has a linear increase with exercise intensity and VO    2 ○ HR is the most important factor increasing CO during exercise. (SV can only  goes up so much)  ○ SV plateaus ~40-50% VO 2max ■ SV = EDV - ESV  ● ^EDV when:  ○ ^HR  ○ ^Venous Return  ○ ^Ventricular compliance  ● ^ESV when: ^Afterload (pressure the heart must pump against to  eject blood)  ● Decreased ESV when: ^Contractility   ■ Frank-Starling mechanism:  ● Greater preload results in stretch of ventricles and in a more  forceful contraction  ● ^venous return = ^contractility  ● Intrinsic to the heart (can beat on its own)  ● Length-tension relationship of muscle cross bridges   ■ ^Venous return → ^EDV (stretch of cardiac muscle bers + sympathetic  stimulation) → ^contractility → deceased ESV → ^SV  ● Oxygen Delivery During Exercise  ○ ^O delivery accomplished by:  2 ■ ^CO  ■ Redistribution of Q to skeletal muscle  ● (a-v)O D2erence  ○ VO 2max = CO maxx (a-v)O 2 dierence ○ Range of ~ 5 to 16 ml O /102ml  ○ VO 2max is limited by max CO             


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