Exercise and blood flow through special regions

Feedforward Control

Anticipatory changes Made with the expectation of physical activity. Both cardiac output and TPR are adjusted in preparation for activity. Decrease parasympathetic tone and increase sympathetic activity. Also stimulate ADH as part of feedforward control to promote retention of water and decrease urine production. Also allow the resetting of baroreceptors upwards, to mute the effect of increased arterial pressure on the normal reflex mechanisms they would otherwise induce. System primed and then modified to suit demand.

Adrenaline

Beta 2 adrenergic receptors tend to be inhibitory and cause relaxation of the smooth muscle. Vascular smooth muscle in skeletal muscle contains both α1 and β2 receptors. Norepinephrine, which stimulates only the excitatory α1 receptors, causes strong vasoconstriction. However, epinephrine, which stimulates both types of receptors, causes only weak vasoconstriction. The vasodilation resulting from β2 receptor stimulation opposes and, therefore, weakens the vasoconstriction resulting from α1 receptor stimulation. Therefore if we were to shift the balance in favour of adrenaline then B2 would dominate and vasodilation would override SNS stimulation to contract in skeletal muscle.

Main points

Blood flow in lungs prevents flow going to poorly oxygenated areas. Coronary blood supply is perfused during diastole Dynamic and static exercises have many common, but some differing, effects on CVS activity.

Fick Principle

CO = (rate O2 consumption)/(arterial O2 content-venous O2 content) ie arteriovenous o2 difference (ml/L of blood) The amount of oxygen the lungs deliver to the blood is directly related to amount of oxygen the body consumes. The overall movement and utilization of oxygen in the body is dependent on five conditions: adequate concentration of inspired oxygen; appropriate movement of oxygen across the alveolar/capillary membrane into the arterial bloodstream; adequate number of red blood cells to carry the oxygen; proper tissue perfusion; and efficient off-loading of oxygen at the tissue level.

Factors promoting venous return during exercise

Cardiac output can only be increased to high levels if venous return increases to the same degree. -Increase skeletal muscle pump activity -Increase frequency and depth of inspiration -Increase venous tone via sympathetic innervation (constriction) Ease of flow from arteries to veins through dilated skeletal muscle arterioles (resistance decreased)

Brain exercise centers

Causes arterial baroreceptors to increase their set point. This and stimulated medullary cardiovascular centre cause: -decrease in parasympathetic output to heart -increase in sympathetic output to heart, veins and arterioles in abdominal organs and kidneys. This leads to: -Increased cardiac output -Increased vasoconstriction in abdominal organs and kidneys

Exercising Skeletal muscles

Contractions: -stimulate mechanoreceptors in the muscles -Afferent input sent to medullary cardiovascular centre -Local chemical changes Chemical changes cause: -stimulation of chemoreceptors in the muscle -Dilation of arterioles in the muscle Dilation causes increased blood flow to muscle

Distribution of blood flow through the lungs

Decreased alveolar O2 reduces local alveolar blood flow -Opposite to effect observed in systemic vessels -Mediator unknown In systemic if has less O2 will be screaming for more. In lungs constriction of an area of lung to stop the tissue being perfused when O2 is low.

Coronary blood flow through left ventricle

During contraction of the heart the coronary blood vessels are occluded. Perfusion window for coronary flow is during diastole. Dependent upon arterial pressure, diastolic time, and small vessel resistance Window can be closed causing lower perfusion of the heart: -increase heart rate (systole closer together and diastole shortened) -Decrease pressure in aorta due to aortic stenosis. Cant force all the blood out so EDV increases. -Increase in ventricular pressure due to increased EDV. Increased venous return or valve incompetance preventing all the blood from being ejected from the ventricles. Window for coronary flow occurs when aortic pressure>ventricular pressure

Dynamic exercise

During dynamic exercise, blood flow to exercising muscle becomes subject to similar problems seen in the myocardium: Contraction of skeletal muscle means blood perfusion is restricted to the time the muscle spends relaxed. If insufficient time is spent in the relaxed state, blood supply may not match demand. Lactic acid can also build up in skeletal muscle during anaerobic exercise.

MABP

During moderate dynamic exercise, mean arterial blood pressure may increase slightly but is generally not elevated greatly due to the changes in cardiac output and total peripheral resistance balancing out. Pulse-pressure may increase, due to increased systolic pressure (as a result of increased cardiac output into the aorta) and a mild decrease in diastolic pressure (as a result of decreased afterload due to decreased total peripheral resistance).

Static exercise

During static exercise such as weightlifting, the same changes in ANS input to the heart occur as in dynamic - therefore cardiac output increases. However the contraction of muscles for a prolonged period: -increases venous return to the heart as compress veins -occludes arteries and prevents tissue perfusion Therefore total peripheral resistance increases considerably. Even though local factors may try to cause dilation of arterioles, the physical compression caused by muscle contraction prevents this from occurring. As local factors accumulate in greater and greater concentration, metabotropic receptors cause an increase in the exercise reflex controlling cardiac output and push this higher. The result is a big increase in heart rate, which increases cardiac output alongside the increased total peripheral resistance: Mean arterial pressure increases substantially as a result of both increased systolic and diastolic pressures. So pulse pressure is greater. When add a 1/3 to diastolic pressure get a greater MABP.

Cardiac Output

Increase sympathetic and decrease parasympathetic control of the heart. Increases cardiac output by increasing heart rate and stroke volume (the latter via increased contractility) Venous return to the heart increases due to compression of veins within exercising muscles moving blood back to heart. May cause minor increase in EDV which would cause a further increase in stroke volume due to frank-starling (though contributes little) Big increase in cardiac output can be seen without necessarily big change in EDV.

Effect of exercise on cardiac output

Increases from 5L/min during exercise: -15L/min in mod intensity -30L/min in highly trained athlete at max intensity Changes distribution of cardiac output: -heart and muscle (active hypereamia Skin -initial sympathetic stimulation causes short term vasoconstriction to increase TPR and shunt blood from skin to skeletal muscle -as core temp increases -detected by hypothalamus -decreases sympathetic innervation to skin -vasodilation of blood vessels. -Skin turns pink and looses heat -Will cause a decrease in TPR

Effect of moderate exercise on arterial pressure

MABP may only increase a small amount (if at all). Pulse pressure increases: -systolic pressure increases -due to increase in stroke volume (increased venous return) - and increase in speed of ejection Massive increase in cardiac output: Increase in heart rate -decrease parasympathetic SA node -Increase sympathetic SA node Increase stroke volume -increase contractility -Increase frank-starling Total peripheral resistance decreases which can cause a slight decrease in diastolic pressure

Issues with coronary blood flow

Myocardium cannot function anaerobically -anaerobic glycolysis massively increases lactic acid production. Arterioles close mechanically during systole This causes a decrease in diastolic filling period during exercise There is an increase in O2 demand and increase metabolic demand during exercise. Work output of heart increases 6-9x during strenuous exercise -but uses 70-80% of blood flow O2 at rest -therefore increase in demand must be met by increased flow

Control of coronary blood flow

Primary controller is local metabolism -in proportion to need of cardiac musculature for O2 -Stimulates release of vasodilators (eg adenosine) -Produce dilation in relation to amount of work heart is doing -Reduces resistance of coronary arteries, thus increasing blood flow to heart tissue Sympathetic stimulation: Indirectly -Via an increase in heart and increases contractility which increases metabolism -Vasodilation caused by enhanced production of vasodilator metabolites (active hyperemia) due to increased mechanical and metabolic activity of the heart. Directly -High degree of sympathetic innervation of coronary arteries -Activation of sympathetic nerves innervating the coronary vasculature causes only transient vasoconstriction. Therefore, sympathetic activation to the heart results in coronary vasodilation and increased coronary flow due to increased metabolic activity (increased heart rate, contractility) despite direct vasoconstrictor effects of sympathetic activation on the coronaries.

Kidneys

Redistribution of the cardiac output decreases blood flow to the kidneys during exercise. This decreases urine production due to decreased pressure diuresis mechanisms. Feedforward controlled release of adh further enhances fluid retention, as does increased activity of the renin-angiotensin-aldosterone system. Result in net retention of water and substantial decrease in urine production. Increase loss of fluid does occur through sweating though

Coronary Blood Supply

Right Coronary Artery -Walls of RA and RV -SA and AV node -Posterior part of interventricular septum (proximal portion of bundle of his) -Small areas of LA and LV in some people Left Coronary Artery -Walls of LA and LV -Most of the interventricular septum including AV bundle Great and Small Cardiac veins -Via coronary sinus into right atrium

Sympathetic stimulation of skeletal muscle arteries

Sympathetic nerves: -Noradrenaline causes vasoconstriction of skeletal muscle arterioles via a1 receptors. Adrenal Medulla: -Adrenaline causes vasodilation of skeletal muscle arterioles via B2 receptors. SNS stimulates the release of adrenalin Skeletal muscle has both a1 and b2 receptors B2 receptors dominate when more adrenaline in system.

Vasodilation of muscle arterioles

Use of muscle increases metabolic activity, resulting in accumulation of local factors that stimulate vasodilation (active hyperaemia). Blood flow can thus increase to 20x normal flow. Increased arteriolar dilation in large number of muscles will greatly decrease TPR. Reduce blood-flow to non-essential organs to reduce drop in TPR by redircting blood flow to muscles. However in intensive exercise the increased blood flow to skeletal muscle may outweigh whats conserved by redirection. Overall effect of exercise can therefore be a drop in TPR from normal levels. Cardiac output has to increase to maintain arterial blood pressure.

Active Hyperemia

When more blood is needed, resistance is decreased by dilating the arteriole. Active hyperemia is the increase in organ blood flow (hyperemia) that is associated with increased metabolic activity of an organ or tissue. An example of active hyperemia is the increase in blood flow that accompanies muscle contraction, in skeletal muscle. Blood flow increases because the increased oxygen consumption during muscle contraction stimulates the production of vasoactive substances that dilate the resistance vessels in the skeletal muscle.

Coronary Blood Flow

Whenever cardiac activity and oxygen consumption increases, there is an increase in coronary blood flow (active hyperemia) that is nearly proportionate to the increase in oxygen consumption.