13.8 Lecture Circulatory System During Exercise

• Strenuous exercise significantly stresses the circulatory system
• Many capillaries have little to no blood flow during rest
• During exercise those same capillaries open due to nutritional requirements of the muscles, causing arterials to dilate
• Sympathetic stimulation affects the heart, arterials, and the walls of veins and arteries
• This leads to increased cardiac output and blood pressure through increased venous return, contractility, and heart rate
• Lower systemic vascular resistance (SVR) helps to offset the increase in blood pressure due to dilation in active muscles
• Blood pressure can rise significantly (e.g., to 170 mm Hg) when exercising or under tension using only a few muscles
• Whole-body exercises typically cause a more moderate increase in blood pressure of 20-40 mm Hg
• Sympathetic stimulation: Increases heart rate and contractility, raises systemic pressure and venous return
• In heavy exercise, cardiac output and venous return increase due to venous stimulation
• This increases mean systemic filling pressure and decreases resistance to venous return, raising right atrial pressure

Normal Coronary Blood Supply

• Main coronary arteries are located on the surface of the heart
• Smaller arteries penetrate into the muscle mass
• Only the inner 0.1 mm of the inner cardiac surface can get nutrition from blood inside the cardiac chambers
• At rest, normal coronary blood flow is about 5% of total cardiac output
• During exercise, coronary blood flow can increase 3-4 fold
• Left ventricular blood flow decreases during systole due to compression of intramuscular blood vessels
• Extra vessels of the subendocardial plexus compensate for reduced blood flow during systole
• Local arterial vessel dilation regulates blood flow according to cardiac muscle nutrition needs
• Coronary oxygen extraction is normally around 70%, limiting additional oxygen extraction when needed
• Oxygen supply is dependent on blood flow

Coronary Blood Flow Regulation

• Decreases in oxygen concentration cause the release of vasodilator substances, dilating the arterials
• Adenosine: A byproduct of ATP degradation, is a notable vasodilator
• Adenosine alone doesn't fully explain cardiac vasodilation
• Potassium, hydrogen, carbon dioxide, and nitric oxide contribute to coronary vasodilation
• Studies blocking adenosine receptors still observed coronary vessel vasodilation

Ischemic Heart Disease

• Most common cause of death in Western countries for those >65 years
• Diminished coronary blood flow due to atherosclerosis causes this disease state
• Risk factors for atherosclerosis: genetic predisposition, obesity, sedentary lifestyle, high blood pressure, endothelial cell damage

Atherosclerotic Plaques, Thrombosis & Occlusion

• Atherosclerotic plaques create an unsmooth surface
• Platelets adhere, eventually leading to thrombus formation
• Local muscle spasm in the coronary artery, alone or in combination with the above, can cause an occlusion

Myocardial Infarction

• Occurs when a coronary vessel is occluded, ceasing blood flow to an area of cardiac muscle
• Muscle can survive with 15-30% of normal resting coronary artery blood flow, but cannot contract
• Subendocardial portion of the heart muscle is more prone to infarction, even without outer surface evidence
• The subendocardial muscle has higher oxygen consumption demand
• The subendocardial muscle has increased difficulty obtaining blood flow during systole

Static Stretch

• Ischemic portions of the ventricle bulge during contraction
• Decreased cardiac output potentially leading to death

Complications

• Decreased cardiac output leads to blood accumulation in vessels of the lungs or systemic circulation
• Pulmonary edema and death from pulmonary symptoms are potential outcomes
• Causes of fibrillation during myocardial infarction include:
• Acute loss of nutrition from lack of blood flow increases extracellular potassium
• Increased likelihood of fibrillation
• Muscle injury current due to inability to repolarize
• Sympathetic reflex is a positive feedback loop:
• Decreased cardiac output leads to sympathetic stimulation
• Increased metabolic requirements for oxygen
• Further injury and sympathetic stimulation
• Ventricular dilation increases pathway length for impulse conduction
• May cause development of electrical circuit movements

Muscle Fibers During Ischemia

• Muscle fibers in the center of the ischemic region die rapidly
• Surrounding area is nonfunctional but still alive
• Over weeks, area either regains functionality or dies, depending on blood flow
• Fibrous tissue develops among the dead fibers
• Heart hypertrophies to compensate for muscle loss

Angina

• Pain felt during exercise or increased metabolism
• Cardiac muscle releases acidic substances (e.g., lactic acid, histamine, cellular proteolytic enzymes) because of diminished coronary blood flow
• These released enzymes cause pain

Treatments

• Vasodilator drugs (nitroglycerin, angiotensin-converting enzyme II inhibitors) provide immediate pain relief
• Surgical procedures: Coronary artery bypass, balloon angioplasty with stent placement