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To better appreciate how the circulatory system adjusts to the stress of exercise, it is important to understand elementary details of heart muscle structure as well as the electrical and mechanical activities of the heart.
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The wall of the heart is composed of three layers: (1) an outer layer called the epicardium, (2) a muscular middle layer, the myocardium, and (3) an inner layer known as the endocardium (see Fig. 9.3). It is the myocardium, or heart muscle, that is responsible for contracting and forcing blood out of the heart. The myocardium receives its blood supply via the right and left coronary arteries, which branch off the aorta and encircle the heart. The coronary veins run alongside the arteries and drain all coronary blood into a larger vein called the coronary sinus, which deposits blood into the right atrium.
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Maintaining a constant blood supply to the heart via the coronary arteries is critical because, even at rest, the heart has a high demand for oxygen and nutrients. When coronary blood flow is disrupted (i.e., blockage of a coronary blood vessel) for more than several minutes, permanent damage to the heart occurs. This type of injury results in the death of cardiac muscle cells and is commonly called a heart attack, or myocardial infarction (see Chap. 17). The number of heart cells (i.e., muscle fibers) that die from this insult determines the severity of a heart attack. That is, a “mild” heart attack may damage only a small portion of the heart, whereas a “major” heart attack may destroy a large number of heart cells (fibers). A major heart attack greatly diminishes the heart’s pumping capacity; therefore, minimizing the amount of injury to the heart during a heart attack is critical. Importantly, strong evidence indicates that exercise training can provide cardiac protection during a heart attack (see Clinical Applications 9.1).
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CLINICAL APPLICATIONS 9.1 Exercise Training Protects the Heart
It is now well established that regular exercise training is cardioprotective. Indeed, many epidemiological studies have provided evidence that regular exercise can reduce the incidence of heart attacks and that the survival rate of heart attack victims is greater in active people than in sedentary ones. Recent experiments provide direct evidence that regular endurance exercise training reduces the amount of cardiac damage that occurs during a heart attack (26, 28, 29). The protective effect of exercise is illustrated in Figure 9.4. Notice that exercise training can reduce the magnitude of cardiac injury during a heart attack by approximately 60%. This is significant because the number of cardiac cells that are destroyed during a heart attack determines the patient’s chances of a full, functional recovery.
Animal experiments indicate that exercise-induced protection against myocardial injury during a heart attack can be achieved quickly (29). For example, it appears that as few as three to five consecutive days of aerobic exercise (~60 minutes/day) can provide significant cardiac protection against heart attack-mediated damage to the heart muscle (29).
How does exercise training alter the heart and provide cardioprotection during a heart attack? A definitive answer to this question is not available. Nonetheless, evidence suggests that the exercise-training-induced improvement in the heart’s ability to resist permanent injury during a heart attack is linked to improvements in the heart’s antioxidant capacity (i.e., the ability to remove free radicals) (18, 26, 28, 29). For more details, see Powers et al. (2014) in the Suggested Readings.
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Heart muscle differs from skeletal muscle in several ways. First, cardiac muscle fibers are shorter than skeletal muscle fibers and are connected in a tight series. Further, cardiac fibers are typically branched, whereas skeletal muscle fibers are elongated and do not branch. Also, cardiac muscle contraction is involuntary, whereas skeletal muscle contractions are under voluntary control.
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Another difference between cardiac fibers and skeletal muscle fibers is that, unlike skeletal muscle fibers, heart muscle fibers are all interconnected via intercalated discs. These intercellular connections permit the transmission of electrical impulses from one fiber to another. Intercalated discs allow ions to cross from one cardiac muscle fiber to another. Therefore, when one heart fiber is depolarized to contract, all connecting heart fibers also become excited and contract as a unit. This arrangement is called a functional syncytium. Heart muscle cells in the atria are separated from ventricular muscle cells by a layer of connective tissue that does not permit the transmission of electrical impulses. Hence, the atria contract separately from the ventricles.
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One more difference between heart and skeletal muscle fibers is that human heart fibers are not divided into different fiber types. The ventricular myocardium is considered to be a homogenous muscle containing one primary fiber type that has similarities to the type I, slow fibers found in skeletal muscle. In this regard, heart muscle fibers are highly aerobic and contain large numbers of mitochondria. Note, however, that cardiac muscle fibers contain many more mitochondria than type I, slow skeletal muscle fibers. This fact highlights the importance of continuous aerobic metabolism in the heart.
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A final difference between cardiac and skeletal muscle fibers is the ability to recover following an injury to the muscle fibers. Recall from Chap. 8 that skeletal muscle fibers are surrounded by muscle precursor cells called satellite cells. These satellite cells are important because they provide skeletal muscle with the ability to regenerate (i.e., recover) from injury. However, cardiac muscle fibers do not contain satellite cells, and therefore, these heart muscle cells have limited regeneration capacity.
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Although heart muscle and skeletal muscle differ in many ways, they are also similar in several ways. For example, both heart and skeletal muscle fibers are striated and contain the same contractile proteins: actin and myosin. Further, both heart and skeletal muscle fibers require calcium to activate the myofilaments (17), and both fibers contract via the sliding filament model of contraction (see Chap. 8). In addition, like skeletal muscle, heart muscle can alter its force of contraction as a function of the degree of overlap of actin-myosin filaments due to changes in fiber length. Table 9.1 contains a point-by-point comparison of the structural/functional similarities and differences between cardiac and skeletal muscle fibers.
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The cardiac cycle refers to the repeating pattern of contraction and relaxation of the heart. The contraction phase is called systole and the relaxation period is called diastole. Generally, when these terms are used alone, they refer to contraction and relaxation of the ventricles. However, note that the atria also contract and relax; therefore, there is an atrial systole and diastole. Atrial contraction occurs during ventricular diastole, and atrial relaxation occurs during ventricular systole. The heart thus has a two-step pumping action. The right and left atria contract together, which empties atrial blood into the ventricles. Approximately 0.1 second after the atrial contraction, the ventricles contract and deliver blood into both the systemic and pulmonary circuits.
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At rest, contraction of the ventricles during systole ejects about two-thirds of the blood out of the ventricles, leaving about one-third in the ventricles. The ventricles then fill with blood during the next diastole. A healthy 21-year-old female might have an average resting heart rate of 75 beats per minute. This means that the total cardiac cycle lasts 0.8 second, with 0.5 second spent in diastole and the remaining 0.3 second dedicated to systole (17) (see Fig. 9.5). If the heart rate increases from 75 beats per minute to 180 beats per minute (e.g., heavy exercise), there is a reduction in the time spent in both systole and diastole (11). This point is illustrated in Figure 9.5. Note that a rising heart rate results in a greater time reduction in diastole, whereas systole is less affected.
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Pressure Changes during the Cardiac Cycle
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During the cardiac cycle, the pressure within the heart chambers rises and falls. When the atria are relaxed, blood flows into them from the venous circulation. As these chambers fill, the pressure inside gradually increases. Approximately 70% of the blood entering the atria during diastole flows directly into the ventricles through the atrioventricular valves before the atria contract. Upon atrial contraction, atrial pressure rises and forces most of the remaining 30% of the atrial blood into the ventricles.
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Pressure in the ventricles is low while they are filling, but when the atria contract, the ventricular pressure increases slightly. Then as the ventricles contract, the pressure rises sharply, which closes the atrioventricular valves and prevents backflow into the atria. As soon as ventricular pressure exceeds the pressure of the pulmonary artery and the aorta, the pulmonary and aortic valves open and blood is forced into both pulmonary and systemic circulations. Figure 9.6 illustrates the changes in ventricular pressure as a function of time during the resting cardiac cycle. Note the occurrence of two heart sounds that are produced by the closing of the atrioventricular valves (first heart sound) and the closing of the aortic and pulmonary valves (second heart sound).
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Arterial Blood Pressure
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Blood exerts pressure throughout the vascular system but is greatest within the arteries, where it is generally measured and used as an indication of health. Blood pressure is the force exerted by blood against the arterial walls and is determined by how much blood is pumped and the resistance to blood flow.
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Arterial blood pressure can be estimated by the use of a sphygmomanometer (see A Closer Look 9.1). The normal blood pressure of an adult male is 120/80, while that of adult females tends to be lower (110/70). The larger number in the expression of blood pressure is the systolic pressure expressed in millimeters of mercury (mm Hg). The lower number in the blood pressure ratio is the diastolic pressure, again expressed in mm Hg. Systolic blood pressure is the pressure generated as blood is ejected from the heart during ventricular systole. During ventricular relaxation (diastole), the arterial blood pressure decreases and represents diastolic blood pressure. The difference between systolic and diastolic blood pressure is called the pulse pressure.
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A CLOSER LOOK 9.1 Measurement of Arterial Blood Pressure
Arterial blood pressure is not usually measured directly but is estimated using an instrument called a sphygmomanometer (see Fig. 9.7). This device consists of an inflatable arm cuff connected to a column of mercury. The cuff can be inflated by a bulb pump, with the pressure in the cuff measured by the rising column of mercury. For example, a pressure of 100 mm of mercury (mm Hg) would be enough force to raise the column of mercury upward a distance of 100 mm.
Blood pressure is measured in the following way: The rubber cuff is placed around the upper arm so it surrounds the brachial artery. Air is pumped into the cuff until the pressure around the arm exceeds arterial pressure. Because the pressure applied around the arm is greater than arterial pressure, the brachial artery is squeezed shut and blood flow is stopped. If a stethoscope is placed over the brachial artery (just below the cuff), no sounds are heard, since there is no blood flow. However, if the air control valve is slowly opened to release air, the pressure in the cuff begins to decline, and the pressure around the arm will quickly reach a point that is just slightly below arterial pressure. At this point blood begins to spurt through the artery, producing turbulent flow, and a sharp sound (known as Korotkoff sounds) can be heard through the stethoscope. The pressure (i.e., height of mercury column) at which the first tapping sound is heard represents systolic blood pressure.
As the cuff pressure continues to decline, a series of increasingly louder sounds can be heard. When the pressure in the cuff is equal to or slightly below diastolic blood pressure, the sounds heard through the stethoscope cease because turbulent flow ceases. Therefore, resting diastolic blood pressure represents the height of the mercury column when the sounds disappear.
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The average pressure during a cardiac cycle is called mean arterial pressure. Mean arterial blood pressure is important because it determines the rate of blood flow through the systemic circuit.
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Determination of mean arterial pressure is not easy. It is not a simple average of systolic and diastolic pressure, because diastole generally lasts longer than systole. However, mean arterial pressure can be estimated at rest in the following way:
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Here, DBP is the diastolic blood pressure, and the pulse pressure is the difference between systolic and diastolic pressures. Let’s consider a sample calculation of mean arterial pressure at rest.
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For example, suppose an individual has a blood pressure of 120/80 mm Hg. The mean arterial pressure would be:
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Note that this equation cannot be used to compute mean arterial blood pressure during exercise because it is based on the timing of the cardiac cycle at rest. That is, arterial blood pressure rises during systole and falls during diastole across the cardiac cycle. Therefore, to accurately estimate the average arterial blood pressure at any time, systolic and diastolic blood pressure must be measured and the amount of time spent in both systole and diastole must be known. Recall that the time spent in systole and diastole differs between rest and exercise. For example, the formula estimates that the time spent in systole occupies 33% of the total cardiac cycle at rest. However, during maximal exercise, systole may account for 66% of the total cardiac cycle time. Therefore, any formula designed to estimate mean arterial blood pressure must be adjusted to reflect the time spent in systole and diastole.
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High blood pressure (called hypertension) is classified as blood pressures above 140/90 mm Hg. Unfortunately, approximately 33% of all adults (>20 years old) in the United States have hypertension (13). Hypertension is generally classified into one of two categories: (1) primary, or essential, hypertension and (2) secondary hypertension. The cause of primary hypertension is multifactorial; that is, there are several factors whose combined effects produce hypertension. This type of hypertension constitutes 95% of all reported cases in the United States. Secondary hypertension is a result of some known disease process, and thus the hypertension is “secondary” to another disease.
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Hypertension can lead to a variety of health problems. For example, hypertension increases the workload on the left ventricle, resulting in an adaptive increase in the muscle mass of the left heart (called left ventricular hypertrophy). In the early phases of hypertension-induced left ventricular hypertrophy, the increase in cardiac mass helps to maintain the heart’s pumping ability. However, with time, this left ventricular hypertrophy changes the organization and function of cardiac muscle fibers, resulting in diminished pumping capacity of the heart, which can lead to heart failure. Further, the presence of hypertension is a major risk factor for developing arteriosclerosis and heart attacks. Finally, hypertension also increases the risk of kidney damage and the rupture of a cerebral blood vessel resulting in localized brain injury (i.e., a stroke).
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Factors That Influence Arterial Blood Pressure
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Mean arterial blood pressure is determined by two factors: (1) cardiac output and (2) total vascular resistance. Cardiac output is the amount of blood pumped from the heart, and total vascular resistance is the sum of resistance to blood flow provided by all systemic blood vessels. Mathematically, mean arterial blood pressure is defined as the product of cardiac output times total vascular resistance, as given in the following equation:
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Therefore, an increase in either cardiac output or vascular resistance results in an increase in mean arterial blood pressure. In the body, mean arterial blood pressure depends on a variety of physiological factors, including cardiac output, blood volume, resistance to flow, and blood viscosity. These relationships are summarized in Figure 9.8. An increase in any of these variables results in an increase in arterial blood pressure. Conversely, a decrease in any of these variables causes a decrease in blood pressure. The relationships between these factors will be discussed in detail in a later section.
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How is blood pressure regulated? Acute (short-term) regulation of blood pressure is achieved by the sympathetic nervous system, whereas long-term regulation of blood pressure is primarily a function of the kidneys (4). The kidneys regulate blood pressure by controlling blood volume.
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Pressure receptors (called baroreceptors) in the carotid artery and the aorta are sensitive to changes in arterial blood pressure. An increase in arterial pressure triggers these receptors to send impulses to the cardiovascular control center (located within the medullar oblongata), which responds by decreasing sympathetic activity. A reduction in sympathetic activity may lower cardiac output and/or reduce vascular resistance, which in turn lowers blood pressure. Conversely, a decrease in blood pressure results in a reduction of baroreceptor activity to the brain. This causes the cardiovascular control center to respond by increasing sympathetic outflow, which raises blood pressure back to normal. For a complete discussion of blood pressure regulation, see Hall (2015) or Fox (2016) in the Suggested Readings.
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Electrical Activity of the Heart
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Many myocardial cells have the unique potential for spontaneous electrical activity (i.e., each has an intrinsic rhythm). However, in the normal heart, spontaneous electrical activity is limited to a special region located in the right atrium. This region, called the sinoatrial node (SA node), serves as the pacemaker for the heart (see Fig. 9.9). Spontaneous electrical activity in the SA node occurs due to a decay of the resting membrane potential via inward diffusion of sodium during diastole. When the SA node reaches the depolarization threshold and “fires,” the wave of depolarization spreads over the atria, resulting in atrial contraction. The wave of atrial depolarization cannot directly cross into the ventricles but must be transported by way of specialized conductive tissue. This specialized conductive tissue radiates from a small mass of muscle tissue called the atrioventricular node (AV node). This node, located in the floor of the right atrium, connects the atria with the ventricles by a pair of conductive pathways called the right and left bundle branches (Fig. 9.9). Note that atrial-mediated depolarization of the AV node is delayed by approximately 0.10 second. This time delay is important because it allows atrial contraction to empty atrial blood into the ventricles prior to ventricular depolarization and contraction. Upon reaching the ventricles, these conductive pathways branch into smaller fibers called Purkinje fibers. The Purkinje fibers then spread the wave of depolarization throughout the ventricles.
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A recording of the electrical changes that occur in the myocardium during the cardiac cycle is called an electrocardiogram (ECG or EKG). Analysis of ECG waveforms allows the physician to evaluate the heart’s ability to conduct impulses and therefore determine if electrical problems exist. Further, analysis of the ECG during exercise is often used in the diagnosis of coronary artery disease (see A Closer Look 9.2). Figure 9.11 illustrates a normal ECG pattern. Notice that the ECG pattern contains several different deflections, or waves, during each cardiac cycle. Each of these distinct waveforms is identified by different letters. The first deflection on the ECG is called the P wave and represents the depolarization of the atria. The second wave, the QRS complex, represents the depolarization of the ventricles and occurs approximately 0.10 second following the P wave. The final deflection, the T wave, is the result of ventricular repolarization. Notice that atrial repolarization is usually not visible on the ECG because it occurs at the same time as the QRS complex (Fig. 9.12). That is, atrial repolarization is “hidden” by the QRS complex.
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Finally, Figure 9.13 illustrates the relationship between changes in the intraventricular pressure and the ECG. Note that the QRS complex (i.e., depolarization of the ventricles) occurs at the beginning of systole, whereas the T wave (i.e., repolarization of the ventricles) occurs at the beginning of diastole. Also, notice that the rise in intraventricular pressure at the beginning of systole results in the first heart sound, due to closure of the atrioventricular valves (AV valves), and that the fall in intraventricular pressure at the end of systole results in the second heart sound, due to the closure of the aortic and pulmonary semi-lunar valves.
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A CLOSER LOOK 9.2 Diagnostic Use of the ECG During Exercise
Cardiologists are physicians who specialize in diseases of the heart and vascular system. One of the diagnostic procedures commonly used to evaluate cardiac function is to make ECG measurements during an incremental exercise test (commonly called a stress test). This allows the physician to observe changes in blood pressure as well as changes in the patient’s ECG during periods of exercise-induced stress.
The most common cause of heart disease is the collection of fatty plaque (called atherosclerosis) inside coronary vessels. This collection of plaque reduces blood flow to the myocardium. The adequacy of blood flow to the heart is relative—it depends on the metabolic demand placed on the heart. For example, a small obstruction in a coronary artery may permit adequate blood flow to meet the metabolic needs during rest, but a coronary blockage would likely result in inadequate blood flow to the heart during exercise because of the large increase in metabolic demands. Therefore, a graded exercise test may serve as a “stress test” to evaluate cardiac function.
An example of an abnormal exercise ECG is illustrated in Figure 9.10. Myocardial ischemia (reduced blood flow) may be detected by changes in the S-T segment of the ECG. Notice the depressed S-T segment in the picture on the right when compared to the normal ECG on the left. This S-T segment depression suggests to the physician that ischemic heart disease may be present and that additional diagnostic procedures may be warranted.
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IN SUMMARY
The myocardium is composed of three layers: (1) epicardium (outer layer); (2) myocardium (middle layer composed of cardiac muscle fibers); and (3) endocardium (inner layer).
The contraction phase of the cardiac cycle is called systole and the relaxation period is called diastole.
The average blood pressure during a cardiac cycle is called mean arterial blood pressure.
Blood pressure can be increased by one or all of the following factors:
Increase in blood volume
Increase in heart rate
Increased blood viscosity
Increase in stroke volume
Increased peripheral resistance
The pacemaker of the heart is the SA node.
A recording of the electrical activity of the heart during the cardiac cycle is called the electrocardiogram (ECG or EKG).