Cardio Readings- hemostatic responses.docx

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University of Toronto St. George
Human Biology
Philip Goodman

Dority Cardio Readings: Hemostatic Responses PP.156-162 o Acute aerobic exercise has been shown to increase arterial compliance o Changes in compliance appear to be the result of real changes in the properties of the arterial wall rather than an artifact of changes in arterial pressure o Vasodilation and reduced vascular resistance most likely explain the increase in arterial compliance following exercise o In turn, a variety of factors, such as changes in sympathetic tone, circulating hormone levels, and/or release of tissue metabolites or endothelial factors may contribute to exercise –induced vasodilation o Acute exercise stimulus alter the functioning of various blood factors involved in coagulation and fibrinolysis, promoting both procoagulatory and profibrinolysis state o Also, plasma decreases as a result of fluid shifts and fluid loss during exercise o Plasma volume decreases during aerobic exercise, the result of fluid shifts between intra- and extravascular space o As steady state exercise progresses plasma volume may continue to decrease slightly as a result of fluid loss through sweat and evaporation in the lungs o Exercise in extreme heat exacerbates fluid loss and hence reductions in plasma volume, as the sweat rate increases to release body heat and maintain body temperature o During exercise the CV system has two goals:  Supplying sufficient blood to the working muscles to maintain oxygen consumption and energy production  And supplying sufficient blood to the skin to aid in heat loss and temperature regulation o Blood flow increases to both skeletal muscle and skin during aerobic exercise  This is accomplished by vasodilation in the skeletal muscles and cutaneous circulations o In this way, oxygen consumption can increase appropriately with exercise intensity , and sufficient heat is lost to allow thermal balance to be maintained o When the air is already hot, the temperature gradient between the skin and air is reduced; when humid, the water vapor gradient between the skin and air is also reduced  Therefore heat loss through sweat evaporation o But if less sweat evaporates (hot outside) then body temperature increases o While HR will increase in a compensatory manner, Q is reduced if HR cannot fully compensate as occurs in maximal exercise o Fluid ingestion prior to and during prolonged exercise in the heat prevents the decline in plasma volume and attenuates both a drop in SV and the increase in HR o MAP must be maintained to supply an adequate driving force to move blood through the circulation and maintain adequate oxygen delivery to the body’s tissues o If a person continues to exercise in the heat, not only with arterial pressure be compromised but core temperature will also increase  Leading to heat exhaustion and heat stroke o Platelets play an important role in hemostasis by stimulating thrombin generation and formation o Aerobic exercise has been shown to increase platelet activation and aggregation and to stimulate thrombosis Dority o Exercised-induced platelet activation is thought to be mediated through elevated catecholamine levels during exercise o Epinephrine stimulates and enhancing platelet adhesiveness and aggregation as well as the binding of fibrogen to platelets o Norepinephrine has been shown to decrease thrombosis and this response may be mediated through the release of the platelet-inhibiting factors such as prostacyclin and NO  P and NO increase shear stressed that is associated with increased blood flow o An acute bout of aerobic exercise is associated with a hypercoaguable state; this exercise- induced increase in coagulation is most likely explained by activation of beta-adrenergic receptors during exercise  This response may be mediated through NO production o The coagulation appears to be highest during the first house of heavy exercise o This related to that of the risk of an acute coronary event may be elevated during the early stages of recovery from exercise as well as during the exercise period itself o The exercise-induced hypercoaguable state is accompanied by an equal or greater potential for fibrinolysis o With enhanced plasmin formation, this precipitates fibrin degradation, as indicated by increased levels of fibrin degradation products o As with coagulation, activation of fibrinolysis appears to increase with exercise intensity, this is indicated by  Higher levels of plasminogen activator following high-intensity, compared to moderate - intensity exercise  Increased levels of fibrin degradation products during high0intensity but not moderate- intensity exercise o It is possible, however that the lack of elevated fibrin degradation products during moderate- intensity exercise reflect the lack of significant increase in coagulation rather than a true limitation in fibrinolysis o The enhancement of fibrinolysis appears to be greatest immediately after heavy exercise o Fibrinolysis appears to recover more quickly than coagulation following acute exercise, which may explain the increase in vulnerability to acute cardiac event during this time period PP. 175-178 o Platelet activation and aggregation are reduced with training, while fibrinolysis is enhanced in trained compared to untrained individuals o Acute aerobic exercise, particularly of high intensity , enhances platelet adhesion and aggregation; however chronic exercise training serves a protective function and has been shown to reduce platelet adhesion and aggregation at both rest and acute bouts of exercise o Implications for CV health- as acute bouts of exercise have been associated with myocardial infraction and sudden cardiac death o Training increases levels of prostacyclin and NO which inhibit platelet aggregation o Further, training
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