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HLSC 3P90 (2)

CHSC 3P90 Midterm 2 notes.docx

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Health Sciences
Deborah O' Leary

CHSC 3P90 –MIDTERM 2 NOTES Exercise is an acute bout of exertion – requires energy above resting level, is planned to improve fitness Resistance exercise -- exertion of force against a load. Aerobic exercises -- use oxygen to meet the energy demands during exercise. VO m2x = maximum capacity of body to transport oxygen during exercise, reflects physical fitness of ppl Cardiac Output • 5x greater during exercise -- ~25 L/min during maximal exercise • Depends on exercise intensity & oxygen demand Vascular Responses • Increased metabolic demands increases blood flow: Increase oxygen, nutrient, removal of by-products • Cardiac Blood Flow = 4x greater • Muscle Blood Flow = 20x greater • Skin Blood Flow = 8 – 18x greater • Blood flow proportional to perfusion pressure and vascular resistance, increases to active tissues Mean arterial Pressure • increase in Cardiac output = MAP via  SBP • Vasoconstriction of non-exercising muscles MAP • Vasodilation of active muscles TPR • Net effect is unchanged diastolic pressure • Rate-pressure product – myocardial oxygen consumption • RPP = SBP x HR Vascular resistance • TPR decreases during aerobic exercise – vasodilation of active muscle • Sympatholysis • Exercise blunts sympathetically mediated vasoconstriction in active muscle beds • Vasoconstriction maintains perfusion pressure • Q has an upper limit – results in vasoconstriction to active muscle Arterial compliance • Compliance increased 30 min after exercise • Pulse wave velocity decreased up to 1h post • Due to: Vasodilation and reduced TPR, Decrease SNS & circulating hormones Acute Resistance Exercise • Static/Isometric contraction – muscle tension, not movement • Dynamic contraction – force exerted varies as the muscle shortens while moving a constant load • Concentric contraction = tension during shortening • Eccentric contraction = tension during lengthening • magnitude of the cardiovascular response depends on intensity of load and number of repetitions Valsalva Maneuver • Forcefully exhaling against a closed glottis – lungs remain inflated • Protective effect on cerebral arteries and cardiac load Endothelial function Improvements occur via: NO, Prostacyclin, EDHF • Aerobic training increases flow-mediated dilation Vascular remodeling • Aerobic training stimulates vascular remodeling • Larger arterial diameter • Repeated exposure to shear stress = stimulate growth of collateral vessels • Capillary-to-muscle fibre ratio increases = increasing gas exchange & oxygen diffusing capacity…greater oxygen extraction & VO m2x Coronary flow • Enhanced blood flow and oxygen delivery to cardiac muscle • Enhanced vasodilatory capacity – 2x greater • Remodeling in cardiac microvasculature • Growth of capillaries develop into arterioles • Enhanced sensitivity of smooth muscle to vasodilators • Myocardial oxygen consumption & Rate pressure product lower after training Resistance training  Cardiac Structure o Left ventricular mass o Left ventricular posterior wall thickness o Interventricular septal wall thickness  Cardiac Function o Stroke volume = no change or slightly higher o Ejection fraction = no change o Enhanced diastolic function = enhanced early diastolic filling  Blood Pressure o Reduced SBP & DBP – 3-4 mmHg o Central changes may be greater than peripheral changes o Lower BP response to resistance exercise = increase muscle strength and decrease intensity  Arterial Stiffness o no effect of training o Why? – large pressure increases can alter wall properties Myocardial Ischemia – heart not recieveing enough oxygen due to narrowed coronary artey Angina – temporary chest pain, pressure from ischemia Myocardial Infarction (MI) – death of heart tissue Monocytes – mature into macrophages, important germ eating cells Macrophages – phagocytic cell protects from infection Lymphocytes – white blood cells (20-30% of blood) Thrombogenic – promotes blood coagulation Normal state of endothelial cells - Permeable barrier -- Limits the passage of large molecules into subendothelial space - Anti-thrombotic o on the surface (hparan sulfate/plasminogen activators) o in circulation (nitric oxide/ prostacyclin) o **in healthy arteries a net anticoagulant state exists - Vasodialation Properties o substances moderate contraction of smooth muscles in response to shear stress o Vasodilating (NO, prostacyclin) --*normal state* o Vasoconstricting (endothelin) - Inhibit smooth muscle migration & proliferation -- (heperan sulfate, NO) - Immune function o Respond to injury by secreting chemokines (attract circulating WBC) o endothelium increases production of cell-surface adhesion molecules that attach leukocytes NORMAL STATE - Intimal endothelial layer = a protective nonthrombogenic surface w/homeostatic vasodilator (likes to stay vasodialated) and has anti-inflammatory properties - no coagulation, leukocyte adhesion, inflammation Atherosclerosis -- endothelial dysfunction (injury) = primary event Endothelial Injury 1. Physical forces a. Arterial branch points disturb laminar flow i. Laminar flow promotes NO production = vasodilation, anti-inflammatory and inhibit platelet aggregation, prevents ROS – reactive oxygen species b. Alters atheroprotective functions of the endothelium c. Lesions develop around arterial branch points 2. Toxic chemical env’t a. High levels of circulating lipids (LDL) b. Increase of ROS (damages cells) & has negative effect on NO c. Will vasoconstrict, thrombosis, smooth muscle proliferation d. Increase permeability Lipoproteins Entry - LDL correlates with atherosclerosis - HDL protects against atherosclerosis – transports lipids away from peripheral tissues back to liver - Injury  holes in lining  LDL entry into intima binding to proteoglycans  Accumulates near matrix  atherosclerotic lesions  Oxidation of LDL  inflammatory response Recruitment of Leukocytes - Modified LDL (mLDL) – recruits monocytes and leukocytes to the vessel wall and these may penetrate into subendothelial surface by slipping b/w junctions & differentiate into macrophages - mLDL increases inflammation - mLDL ingested by macrophages = no –ve feedback inhibition. - foam cells -- Macrophages engorged on mLDL Fatty streak - Foam cell accumulation forms fatty streak - First sign of atherosclerosis - Yellow colour on inner surface of artery - Doesn’t disturb flow or cause symptoms - Exist in aorta and coronary artery in most ppl by age 20! Transition from fatty streak to fibrous plaque involves: - Migration & Proliferation of SMC’s from media to injured intima & Secretion of fibrous connective tissue by SMC’s - fibrous plaque = SMC mass, leukocytes, foam cells and fibrous cap (ECM w/embedded SMC’s) Plaque Rupture - Due to shear forces & vasoconstriction - Thrombus forms at the site of rupture o Incorporated into plaque - Artery will expand to accommodate plaque formation to a certain point - Stable plaque – small lipid core or pool, thick fibrous cap, preserved lumen - Vulnerable plaque – large lipid pool/core, thin fibrous cap, inflammatory cells, breaks and forms thrombus o Healed ruptures narrow the lumen and it becomes fibrous Pathogenesis of Atherosclerosis Endothelial dysfunction  subendothelial lipid accumulation & leuckocyte recruitment  foam cell formation and fatty streak  SMC migration and proliferation  plaque rupture & thrombosis formation Pathophysiology of Ischemia - Imbalance b/w myocardial oxygen supply and demand due to limited myocardial blood supply o Fixed vessel narrowing  Proximal coronary arteries = atherosclerosis and stenoic plaques  Distal vessels free of plaque dev’p – adjust vasomotor tone to metabolic need  Resistance vessels increase in diameter to meet increasing O2 demand o Endothelial dysfunction 1. Inappropriate vasoconstriction a. Happens when you should have vasodilation b. Healthy individuals =  sympathetic activity increases coronary blood flow & vasodilation c. Atherosclerosis – endothelial dysfunction i. Impaired release of vasodilators ii. Vasoconstriction & Reduced coronary flow 2. Loss of antithrombotic properties a. Endothelial dysfunction = reduced antithrombotic properties b. Impaired release of NO and prostacyclin allows platelet aggregation & vasoconstrictor effects 3. 90% blocked at rest -- exercise it is 70% blockage before you notice Consequences of Ischemia - inadequate oxygen supply and accumulation of metabolic waste products - Reduced O2 supply  anaerobic metabolism prevails  reduced ATP production and metabolite accumulation  reduced ventricular function Fates of the ischemic myocardium 1. Stunned myocardium a. acute transient ischemia = no necrosis b. prolonged systolic dysfunction – even when blood flow is restored c. alterations are reversible and contraction gradually restores d. Delayed recovery due to Myocyte calcium overload, Accumulation of free radicals 2. Hibernating myocardium a. Chronic ventricular contractile dysfunction b. Due to persistently reduced blood supply – multivessel coronary artery disease c. NO Irreversible damage – function improves if blood supply is restored by angioplasty or bypass surgery 3. Myocardial infarction a. 30 mins after onset -- damage irreversible & Necrosis occurs Ischemic Syndromes Stable Angina - Predictable, transient discomfort during exertion or emotional stress - Caused by fixed plaque in one or more coronary arteries Unstable Angina - Increase in freq & duration if ischemic episodes with lesser degree of exertion or even at rest - Associated with rupture of an unstable plaque with platelet aggregation Silent Ischemia - Occurs in 40% of patients with stable angina - absence of pain or perceptible discomfort Theories of Aging 1. Wear and tear theories  Accumulation of normal injury, used cells just wear out  Free radicals  disruptive at mitochondria  Damage DNA & protein synthesis  Cross-linking = tangles of proteins  Collagen stiffens with age  stiffening of tissue, rigidity of blood vessels, tight ligaments, atherosclerosis 2. Genetic theories  Programmed cell death – apoptosis part of the genetic code  Genetic mutations o mutational changes accelerate aging o Synthesis of
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