question: What stops your heart from getting enlarged from exercise?
comment: The heart muscle responds to the type of load to which it's exposed. If you have high blood pressure, that means it has to pump out against that high pressure. **Afterload** is the force against which the heart has to pump. Increased afterload is bad for the heart, it will cause the muscles to thicken and take over much of the space inside the heart that's used to pump. The thickness will also make it much more difficult to get blood flow through the heart muscle itself which can result in heart attack. If you have a defect in the heart valves or in the muscle itself, such as regurgitation of a valve (blood flowing backwards through the valve), it can result in excessive amounts of blood in the heart that gets pumped with every beat. This causes the walls to stretch. **Preload** is the amount of blood that fills the ventricles before contraction. Increased preload in isolation like this is bad for the heart, it will cause the walls to stretch, become weak and stiff, and not pump adequately which can result in heart failure. The trick with exercise is that **contractility** of the muscle is increased in addition to the increased preload caused by vasoconstriction of large veins that hold most of the blood during rest (squeezing more blood into the heart, increasing preload) and the afterload is decreased by vasodilation of the arteries that feed the muscles. The result is your heart squeezes harder than normal, with more blood than normal. Raising your blood pressure with volume instead of resistance. This is the perfect mix, the physiological exercise that the heart desires and the muscles will respond by making this action more efficient and powerful. Increasing the strength and capacity of the heart so it doesn't have to beat as much to fill your muscles with blood. The heart will get a bit larger, but in a healthy way. If you have isolated changes in preload or afterload in absence of the sympathetic signaling that causes all those changes mentioned above in the exercise section, your heart muscle will be remodeled but not physiologically, it will lead to problems like heart attack or failure. I guess not really ELI5, but the heart is an extremely complex organ. Cardiologists spend decades learning about it and still we don't fully understand all of the interactions with the body's various systems. If you have further questions please feel free to ask :P
passages: Cardiac output, the amount of blood that leaves the heart in a given time period (i.e. liters per minute), is proportional to both the chamber sizes of the heart and the rate at which the heart beats. With a larger left ventricle, the heart rate can decrease and still maintain a level of cardiac output necessary for the body. Therefore, athletes with AHS commonly have lower resting heart rates than nonathletes.
   Factors that increase heart rate also trigger an increase in stroke volume. As with skeletal muscles the heart can increase in size and efficiency with exercise. Thus endurance athletes such as marathon runners may have a heart that has hypertrophied by up to 40%. The difference between maximum and minimum cardiac outputs is known as the cardiac reserve and this measures the residual capacity to pump blood. Heart rates may reach up to 185–195 in exercise, depending on how fit a person is.
  
  Section::::Cardiac output.
   Section::::Diagnosis.
  
  There are two main types of cardiomegaly:
  
  Dilated cardiomyopathy is the most common type of cardiomegaly. In this condition, the walls of the left and/or right ventricles of the heart become thin and stretched. The result is an enlarged heart.
  
  In the other types of cardiomegaly, the heart's large muscular left ventricle becomes abnormally thick. Hypertrophy is usually what causes left ventricular enlargement. Hypertrophic cardiomyopathy is typically an inherited condition.
  
  There are many techniques and tests used to diagnose an enlarged heart. Below is a list of tests and how they test for cardiomegaly:
   BULLET::::- Echocardiography – differentiation between physiological and pathological increases of the heart's size is possible, especially by estimating the mass of the wall (not over 130 g/m) and its end diastolic diameter (not much less 60 mm) of the left ventricle.
  
  BULLET::::- X-ray examination of the chest may show increased heart size (mimicking other possible causes of enlargement).
  
  Section::::Clinical relevance.
   The heart becomes enlarged, or hypertrophic, due to intense cardiovascular workouts, creating an increase in stroke volume, an enlarged left ventricle (and right ventricle), and a decrease in resting pulse along with irregular rhythms. The wall of the left ventricle increases in size by about 15–20% of its normal capacity. No decrease of the diastolic function of the left ventricle occurs. The athlete may also experience an irregular heartbeat and a resting pulse rate between 40 and 60 beats per minute (bradycardia).
   Regular exercise makes these systems more efficient by enlarging the heart muscle, enabling more blood to be pumped with each stroke, and increasing the number of small arteries in trained skeletal muscles, which supply more blood to working muscles. Exercise improves not just the respiratory system but the heart by increasing the amount of oxygen that is inhaled and distributed to body tissue. A 2005 Cochrane review demonstrated that physical activity interventions are effective for increasing cardiovascular fitness.
   Section::::Structure.:Coronary circulation.
  
  Heart tissue, like all cells in the body, needs to be supplied with oxygen, nutrients and a way of removing metabolic wastes. This is achieved by the coronary circulation, which includes arteries, veins, and lymphatic vessels. Blood flow through the coronary vessels occurs in peaks and troughs relating to the heart muscle's relaxation or contraction.
   Alternatively, in order to find the efficiency of the lungs in replenishing blood oxygen levels, the a-vO diff may instead be taken by comparing blood from the pulmonary artery and the pulmonary vein; in this case a negative value for a-vO diff would be obtained as the oxygen content of the blood would have increased.
  
  Section::::Impacts of exercise.
  
  Physical exercise leads to an increase in the arteriovenous oxygen difference in all individuals. As exercise intensities increase, the muscles increase the amount of oxygen they extract from the blood, and this therefore results in further increases in a-vO diff.
   The heart is cone-shaped, with its base positioned upwards and tapering down to the apex. An adult heart has a mass of 250–350 grams (9–12 oz). The heart is often described as the size of a fist: 12 cm (5 in) in length, 8 cm (3.5 in) wide, and 6 cm (2.5 in) in thickness, although this description is disputed, as the heart is likely to be slightly larger. Well-trained athletes can have much larger hearts due to the effects of exercise on the heart muscle, similar to the response of skeletal muscle.
  
  Section::::Structure.:Chambers.
   An increase in arterial stiffness also increases the load on the heart, since it has to perform more work to maintain the stroke volume. Over time, this increased workload causes left ventricular hypertrophy and left ventricular remodelling, which can lead to heart failure. The increased workload may also be associated with a higher heart rate, a proportionately longer duration of systole and a comparative reduction of duration of diastole. This decreases the amount of time available for perfusion of cardiac tissue, which largely occurs in diastole. Thus the hypertrophic heart, which has a greater oxygen demand, may have a compromised supply of oxygen and nutrients.
   Cardiogenesis products focus on the treatment of refractory angina in patients with diffuse coronary artery disease(CAD). Patients suffering from chronic angina (chest pain) are generally managed aggressively with medications to help alleviate their symptoms and frequently receive multiple coronary interventions and even bypass surgery over the course of the advancement of their disease. When chest pain continues in spite of treatments, the condition is considered, “refractory angina.”
   No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, no evidence has been found of any increased risk of long-term events. Athletes should see a physician and receive a clearance to be sure their symptoms are due to athlete's heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athlete's heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months allows the heart to return to its regular size. However, one long-term study of elite-trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning. This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athlete's heart is if athletes or nonathletes simply assume they have the condition, instead of making sure they do not have a life-threatening heart illness.
   Because cardiac output is related to the quantity of blood delivered to various parts of the body, it is an important indicator of how efficiently the heart can meet the body's demands for perfusion. For instance, physical exercise requires a higher than resting-level of oxygen to support increased muscle activity, where, in the case of heart failure, actual CO may be insufficient to support even simple activities of daily living; nor can it increase sufficiently to meet the higher metabolic demands stemming from even moderate exercise.
   Section::::Diagnosis.
  
  Athlete's heart is usually an incidental finding during a routine screening or during tests for other medical issues. An enlarged heart can be seen at echocardiography or sometimes on a chest X-ray. Similarities at presentation between athlete's heart and clinically relevant cardiac problems may prompt electrocardiography (ECG) and exercise cardiac stress tests. The ECG can detect sinus bradycardia, a resting heart rate of fewer than 60 beats per minute. This is often accompanied by sinus arrhythmia. The pulse of a person with athlete's heart can sometimes be irregular while at rest, but usually returns to normal after exercise begins.
   BULLET::::- Heart failure: One of the most serious types of enlarged heart, an enlarged left ventricle, increases the risk of heart failure. In heart failure, the heart muscle weakens, and the ventricles stretch (dilate) to the point that the heart can't pump blood efficiently throughout the body.
   People with athlete's heart do not exhibit an abnormally enlarged septum, and the growth of heart muscle at the septum and free ventricular wall is symmetrical. The asymmetrical growth seen in HCM results in a less-dilated left ventricle. This in turn leads to a smaller volume of blood leaving the heart with each beat.
  
  Section::::Screening and diagnosis.
   Respiratory pump - Intrapleural pressure decreases during inspiration and abdominal pressure increases, squeezing local abdominal veins, allowing thoracic veins to expand and increase blood flow towards the right atrium.
  
  Skeletal muscle pump - In the deep veins of the legs, surrounding muscles squeeze veins and pump blood back towards the heart. This occurs most notably in the legs. Once blood flows past valves it cannot flow backwards and therefore blood is “milked” towards the heart.
  
  Section::::See also.
  
  BULLET::::- Afterload
  
  BULLET::::- Cardiac output
  
  BULLET::::- Frank–Starling law of the heart
  
  BULLET::::- Passive leg raising test
  
  BULLET::::- Volume overload
  
  Section::::External links.
   Bradycardia is not necessarily problematic. People who regularly practice sports may have sinus bradycardia, because their trained hearts can pump enough blood in each contraction to allow a low resting heart rate. Sinus bradycardia can also be an adaptive advantage; for example, diving seals may have a heart rate as low as 12 beats per minute, helping them to conserve oxygen during long dives.
  
  Sinus bradycardia is a common condition found in both healthy individuals and those who are considered well conditioned athletes.
   The level of physical activity in a person determines what physiological changes the heart makes. The two types of exercise are static (strength-training) and dynamic (endurance-training). Static exercise consists of weight lifting and is mostly anaerobic, meaning the body does not rely on oxygen for performance. It also moderately increases heart rate and stroke volume (oxygen debt). Dynamic exercises include running, swimming, skiing, rowing, and cycling, which rely on oxygen from the body. This type of exercise also increases both heart rate and stroke volume of the heart. Both static and dynamic exercises involve the thickening of the left ventricular wall due to increased cardiac output, which leads to physiologic hypertrophy of the heart. Once athletes stop training, the heart returns to its normal size.
   Once the procedure on the heart vessels (coronary artery bypass grafting) or inside the heart such as valve replacement or correction of congenital heart defect, etc. is over, the cross-clamp is removed and the isolation of the heart is terminated, so normal blood supply to the heart is restored and the heart starts beating again.
   Angiogenesis is generally associated with aerobic exercise and endurance exercise. While arteriogenesis produces network changes that allow for a large increase in the amount of total flow in a network, angiogenesis causes changes that allow for greater nutrient delivery over a long period of time. Capillaries are designed to provide maximum nutrient delivery efficiency, so an increase in the number of capillaries allows the network to deliver more nutrients in the same amount of time. A greater number of capillaries also allows for greater oxygen exchange in the network. This is vitally important to endurance training, because it allows a person to continue training for an extended period of time. However, no experimental evidence suggests that increased capillarity is required in endurance exercise to increase the maximum oxygen delivery.
   Recent work at Johns Hopkins involving a group of athletes aged 55 to 75 with mild hypertension has found a correlation of those with exercise hypertension to a reduced ability of the major blood vessels to change in size in response to increased blood flow (probably due to impaired function of the endothelial cells in the vessel walls). This is to be differentiated from stiffness of the blood-vessel walls, which was not found to be correlated with the effect.
   The resting heart rate of a newborn can be 120 beats per minute (bpm) and this gradually decreases until maturity and then gradually increases again with age. The adult resting heart rate ranges from 60–100 bpm. Exercise and fitness levels, age and basal metabolic rate can all affect the heart rate. An athlete's heart rate can be lower than 60 bpm. During exercise the rate can be 150 bpm with maximum rates reaching from 200 and 220 bpm.
  
  Section::::Heart rate.:Cardiovascular centres.
   Quite often, HCM can be mistaken for a condition known as "athlete's heart". Both involve thickening of the myocardium. However, athlete's heart generally is not correlated with SCD. While HCM can be linked to family history, athlete's heart arises purely as a function of intense exercise (usually at least an hour every day). Since the body is operating at high training levels, the heart adapts and grows in order to pump blood more efficiently. Stoppage of exercise for three months generally leads to a decrease in wall/septum thickness in those with athlete’s heart, whereas those with HCM exhibit no decline.
   The cardiovascular system responds to changing demands on the body by adjusting cardiac output, blood flow, and blood pressure. Cardiac output is defined as the product of heart rate and stroke volume which represents the volume of blood being pumped by the heart each minute. Cardiac output increases during physical activity due to an increase in both the heart rate and stroke volume. At the beginning of exercise, the cardiovascular adaptations are very rapid: “Within a second after muscular contraction, there is a withdrawal of vagal outflow to the heart, which is followed by an increase in sympathetic stimulation of the heart. This results in an increase in cardiac output to ensure that blood flow to the muscle is matched to the metabolic needs”. Both heart rate and stroke volume vary directly with the intensity of the exercise performed and many improvements can be made through continuous training.
  
raw_presuppositions: The heart does not get enlarged from exercise.
raw_corrections: The heart gets slightly enlarged from exercise.