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Which mechanism contributes to the increased arterial pressure observed during exercise?
What primary effect does norepinephrine have on blood vessels during strenuous exercise?
How does epinephrine primarily influence vasodilation during exercise?
What effect does sympathetic nervous system activation have during exercise?
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What is a likely consequence of reduced oxygen levels in muscles during exercise?
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What general impact does exercise have on vascular responses?
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What is the effect of large increases in systemic filling pressure during exercise?
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What effect does the vasodilation of active muscle vessels have during exercise?
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What is a primary consequence of muscle contraction during exercise on blood flow?
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Which vasodilator substance is noted for its significance during exercise?
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What effect does oxygen deficiency have on blood vessels during exercise?
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Which of the following factors continues to maintain increased capillary blood flow during prolonged exercise?
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How does sympathetic activation affect heart rate during exercise?
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Which of the following substances is NOT a vasodilator factor that aids in increased blood flow during exercise?
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During intense exercise, what happens to the parasympathetic signals to the heart?
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Which of the following observations is true regarding adenosine's role in blood flow during exercise?
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How does lactic acid contribute to the exercise response?
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What is the general impact of strong rhythmic exercise on vascular response?
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What is the primary purpose of performing coronary artery angioplasty?
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What effect does the inflation of the balloon in angioplasty have on the artery?
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How much can blood flow through the vessel increase after angioplasty?
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Which physiological response is triggered by skeletal muscle mechanoreflex activation during exercise?
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What is a key factor affecting blood flow to muscles during exercise?
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What happens to blood flow rates in coronary vessels during physical exercise?
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What mechanism primarily regulates coronary blood flow during heavy exercise?
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What physiological condition is often relieved in more than 75% of patients after undergoing angioplasty?
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What happens to the resistance in blood vessels during heavy exercise?
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What is a potential predictor of stent thrombosis that impacts clinical practice?
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How does exercise impact cardiac output in competitive runners?
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Which of the following does NOT contribute to increased blood flow during exercise?
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What role do tensed skeletal muscles play during exercise?
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What is the effect of maximal exercise on mean systemic filling pressure?
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How does oxygen delivery to muscles change during exercise?
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What primarily contributes to muscle blood flow increasing during maximal activity?
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What is the maximum heart rate observed in marathon runners during intense exercise?
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How much can muscle blood flow increase during maximal activity in comparison to rest?
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What is the main consequence of increased arterial pressure during exercise?
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What effect does sympathetic stimulation have on veins during heavy exercise?
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What is a key factor preventing cardiac output from rising significantly without changes in venous return curves?
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Which physiological changes occur during exercise that help increase cardiac output?
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Which response is seen in muscle blood flow during laboratory experiments versus real exercise conditions?
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What changes occur in venous return during heavy exercise?
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What primarily limits the increase of cardiac output to only 2.5-fold in an untrained runner?
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Blood flow during muscle contractions is greater than blood flow between contractions in the calf of a leg.
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Low oxygen levels in muscles cause blood vessels to constrict.
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Adenosine cannot sustain vasodilation in skeletal muscle for more than about two hours during intense exercise.
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Potassium ions, ATP, lactic acid, and carbon dioxide are factors that maintain increased capillary blood flow during exercise.
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The sympathetic nervous system activation decreases heart rate and pumping strength during exercise.
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Experiments have shown that large amounts of infused adenosine greatly increase blood flow during intense exercise.
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During strong tetanic contraction, there is minimal compression of blood vessels.
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Sympathetic discharge during exercise initiates signals not only to the muscles but also to the vasomotor center.
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During strenuous exercise, epinephrine predominantly causes vasoconstriction in blood vessels.
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The mean systemic filling pressure decreases during exercise.
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Increased sympathetic nervous system activation during exercise leads to decreased arterial pressure.
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When the area of ischemia is small, it generally results in dead muscle cells and abnormal conduction pathways.
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The heart’s pumping activity increases during exercise, contributing to higher cardiac output.
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The cardiac reserve can be reduced to as low as 100% while still allowing a person to perform most daily activities.
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The role of norepinephrine during exercise is mainly as a vasodilator.
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Immediately after a myocardial infarction, there is a high risk of rupture in the ischemic portion of the heart.
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A 20 mm Hg increase in arterial pressure can occur during exercise.
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Increased blood flow to the muscles during exercise is primarily due to reduced mean systemic filling pressure.
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After a large myocardial infarction, muscle fibers begin to die rapidly within 5 to 6 hours of blood supply cessation.
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Sympathetic stimulation can lead to an overall increase in both heart rate and arterial pressure during exercise.
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The area surrounding ischemic muscle fibers can continue to contract but in a weakened state due to mild ischemia.
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Exercise generally results in vasodilation of arterioles and small arteries in most tissues except the brain and active muscles.
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The beta-adrenergic receptors are more excited by norepinephrine than epinephrine during exercise.
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Immediately after an acute coronary occlusion, blood flow stops entirely in the coronary vessels beyond the occlusion.
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The area of cardiac muscle that sustains a minimal blood flow is referred to as infarcted.
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Collaterals can supply enough blood flow to maintain cardiac muscle viability immediately after an occlusion.
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Cardiac muscle requires approximately 1.3 ml of oxygen per 100 g of tissue per minute to survive.
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Collateral blood flow can increase and potentially reach normal levels within a few hours of a myocardial infarction.
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After the onset of myocardial infarction, the affected area takes on a pinkish hue due to blood pooling.
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Diminished cellular metabolism leads to the swelling of cardiac muscle cells shortly after the blood supply is cut off.
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Anastomoses among larger coronary arteries are very common.
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During the first 8 to 24 hours after an occlusion, collateral vessels undergo significant enlargement.
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The cardiac muscle can sustain its function with only small amounts of collateral flow from surrounding vessels.
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Fibrillation is most likely to occur during the first 10 minutes after a coronary infarction.
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The second period of cardiac irritability begins approximately 5 hours after a coronary infarction.
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An elevated extracellular potassium concentration decreases the likelihood of cardiac muscle fibrillation.
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Fibrillation can occur many days after a myocardial infarction but is less likely.
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A common factor contributing to cardiac fibrillation is the acute loss of blood supply to the cardiac muscle.
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Cardiac muscle injury current is a phenomenon solely pertaining to blood vessel dilation.
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After a coronary infarction, the heart can become less prone to fibrillation as time passes.
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The extracellular fluids surrounding cardiac muscle fibers have no influence on cardiac irritability.
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Functional dead fibers rarely contribute to a heart's propensity to fibrillate.
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Injury currents arise from ischemic conditions affecting cardiac muscle.
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Match the following phases of the cardiac cycle with their corresponding effects on coronary blood flow:
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Match the following substances with their role in coronary blood flow regulation:
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Match the following characteristics with the ventricular muscles:
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Match the following events with their outcomes in the heart's oxygen supply:
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Match the following terms with their definitions related to cardiac physiology:
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Match the following coronary circulation terms with their definitions:
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Match the following exercise effects with their outcomes:
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Match the following factors with their roles during exercise:
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Match the following heart physiology aspects with their descriptions:
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Match the following physiological changes during exercise with their characteristics:
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Match the following neurotransmitters with their primary effects on coronary blood flow:
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Match the following terms with their descriptions related to cardiac muscle metabolism:
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Match the following physiological processes with their effects on the heart:
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Match the following components of the autonomic nervous system with their roles in heart function:
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Match the following types of blood flow regulation with their characteristics:
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Match the following factors influencing coronary blood flow with their influences:
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Match the following concepts with their associated outcomes in cardiac physiology:
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Match the following substances with their effects on the cardiovascular system:
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Match the following actions with their related cardiovascular responses:
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Match the following effects with their underlying mechanisms in cardiac function:
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Study Notes
Circulatory Readjustments During Exercise
- Three major effects occur in the circulatory system during exercise:
- Sympathetic nervous system activation for increased circulatory stimulation
- Increase in arterial pressure
- Increase in cardiac output
Sympathetic Stimulation May Increase Arterial Pressure During Exercise
- Increased arterial pressure occurs due to:
- Vasoconstriction of arterioles and small arteries in most tissues except the brain and active muscles
- Increased pumping activity of the heart
- Increased mean systemic filling pressure due to venous contraction
Effects of Sympathetic Activation
- Sympathetic activation leads to:
- Increased heart rate and strength due to sympathetic stimulation and reduced parasympathetic inhibition
- Arterioles constriction in the peripheral circulation, except in the brain and active muscles
- Vasoconstriction of the veins leading to increased blood return to the heart
Importance of Increased Cardiac Output During Exercise
- Marathon runners with higher cardiac output tend to have better running times, indicating the importance of cardiac output for efficient oxygen delivery
- The increase in cardiac output during exercise is achieved through changes in both cardiac output and venous return curves
- The venous return curve shifts upward due to increased mean systemic filling pressure and decreased resistance to venous return
Graphic Analysis of Changes in Cardiac Output During Heavy Exercise
- The cardiac output and venous return curves shift to higher levels during heavy exercise
- The mean systemic filling pressure increases from 7 mm Hg during rest to 30 mm Hg during maximal exercise
- This increase in pressure is a result of sympathetic contraction of veins and compression of internal vessels
- The slope of the venous return curve rotates upwards due to decreased resistance in active muscle tissue
Muscle Blood Flow During Exercise
- Blood flow in the calf during strong rhythmic contractions is much less during contractions than between contractions.
- Contracted muscles compress blood vessels, reducing blood flow.
- During intense exercise, blood flow increases despite the compression of vascular muscles.
- Vasodilator factors released during exercise, such as potassium ions, ATP, lactic acid, and carbon dioxide, maintain increased capillary blood flow.
- Even large amounts of adenosine infused directly into a muscle artery cannot increase blood flow to the same extent as during intense exercise.
- Increased sympathetic activation during exercise causes a significant increase in heart rate and force of contraction.
- Sympathetic activation also constricts arterioles in many parts of the body, except the brain and active muscles, which increases mean systemic filling pressure and venous return.
- Epinephrine, released during exercise, often has a slight vasodilator effect because of its action on beta-adrenergic receptors of blood vessels.
Circulatory Readjustments During Exercise
- Three major effects occur during exercise to increase blood flow to muscles: sympathetic nervous system activation, increased arterial pressure, and increased cardiac output.
- Sympathetic stimulation causes increased heart rate and force of contraction, as well as a vasoconstricting effect on various arterioles, enhancing venous return.
- Increased arterial pressure during exercise results from vasoconstriction in most tissues except the brain and active muscles, increased cardiac pumping activity, and elevated mean systemic filling pressure.
Coronary Blood Flow and Myocardial Infarction
- During myocardial infarction, blood flow ceases in coronary vessels beyond the occlusion, resulting in an infarcted area.
- Collateral blood flow develops gradually after coronary occlusion, increasing over time to potentially reach normal or near-normal levels within a month.
- Infarcted areas become dark blue-brown, engorged with blood, and edema develops due to increased vascular permeability.
- Cardiac muscle cells die when deprived of blood supply for a prolonged period (about 1.3 ml of oxygen/100 g of muscle tissue/min is required for survival).
Cardiac Fibrillation and Myocardial Infarction
- Cardiac fibrillation is more likely to occur during the initial 10 minutes and later during the first few hours after myocardial infarction.
- Elevated extracellular potassium concentration due to ischemic musculature contributes to cardiac irritability and fibrillation risk.
- Ischemia causes injury currents and abnormal conduction pathways, which can lead to circus movements and sustain fibrillation.
Recovery from Myocardial Infarction
- Dead muscle tissue in the center of an ischemic area enlarges over time as the surrounding marginal fibers succumb to ischemia.
- Small ischemic regions may not cause cell death but can still lead to temporary muscle dysfunction due to compromised nutrition.
- Non-functional area surrounding the dead muscle exhibits failure of contraction and impulse conduction.
- Areas with mild ischemia still contract, but weakly.
- Infarcted areas are usually replaced with scar tissue over time.
- The heart's ability to increase cardiac output beyond resting levels (cardiac reserve) is affected by the size of the infarct.
- Even with a reduced cardiac reserve, a person can still perform most daily activities but may struggle with strenuous exercise.
Coronary Circulation
- Coronary artery disease is a significant cause of death in industrialized nations.
- Most older adults have some degree of coronary artery impairment.
- Coronary blood flow averages about 5% of cardiac output.
- Coronary blood flow in a resting person averages 70 ml/min/100 g of heart weight, or about 225 ml/min.
Physiological Anatomy of the Coronary Blood Supply
- The main coronary arteries are located on the surface of the heart and branch into smaller arteries that penetrate the heart muscle.
- The coronary arteries supply the heart with blood during diastole (relaxation).
- During systole (contraction), compression of the intramuscular blood vessels by the left ventricle reduces blood flow.
- Right ventricular blood flow is less affected by systole due to the lower force of contraction.
- Local muscle metabolism heavily influences coronary flow, with increased metabolic demand triggering vasodilation.
Coronary Blood Flow Regulation
- Increased oxygen consumption by the heart results in increased coronary blood flow, almost proportionally.
- The specific mechanism for coronary dilation is not fully understood.
- A decrease in oxygen concentration in the heart is thought to trigger the release of vasodilator substances like adenosine.
- Adenosine, a potent vasodilator, is released from the heart muscle when ATP degrades to AMP in low-oxygen conditions.
- Sympathetic stimulation, releasing norepinephrine and epinephrine, increases heart rate and cardiac metabolism, indirectly increasing coronary blood flow.
- Vagal stimulation, releasing acetylcholine, slows heart rate and slightly depresses contractility, indirectly decreasing coronary blood flow.
Cardiac Ischemia
- During prolonged heavy exercise, coronary venous blood flow may decrease.
- Moderate exercise can cause a marked increase in right atrial pressure in patients with weakened hearts.
- Lactic acid buildup in cardiac tissue during ischemia may contribute to cardiac pain.
Coronary Artery Disease Treatment
- Vasodilator drugs, such as nitroglycerin and nitrates, can relieve anginal pain during an acute attack.
- Long-term treatment for angina pectoris includes drugs like beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers, and ranolazine.
- Angioplasty is a procedure used to expand and unblock coronary arteries.
- Stents can be inserted into coronary arteries to keep them open, but restenosis (reblocking) can occur.
- Drug-eluting stents release medication to help prevent restenosis.
- Laser therapy can dissolve atherosclerotic lesions in coronary arteries without damaging arterial walls.
Coronary Artery Bypass Surgery
- Aortic-coronary bypass grafting (CABG) involves grafting a section of vein from an arm or leg to a coronary artery beyond a blockage, improving blood flow.
- CABG can relieve anginal pain and improve life expectancy in patients with coronary ischemia.
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Description
Explore how the circulatory system adapts during exercise through increased arterial pressure, cardiac output, and sympathetic nervous system activation. Understand the mechanisms involved, including heart rate changes and vasoconstriction. This quiz delves into the intricate responses of the circulatory system under physical stress.