Chapter 9: Circulatory Responses to Exercise

By studying this chapter, you should be able to do the following:

1. Provide an overview of the design and function of the circulatory system.

2. Describe the cardiac cycle and the associated electrical activity recorded via the electrocardiogram.

3. Discuss the pattern of redistribution of blood flow during exercise.

4. Outline the circulatory responses to various types of exercise.

5. Identify the factors that regulate local blood flow during exercise.

6. List and discuss those factors responsible for regulation of stroke volume during exercise.

7. Discuss the regulation of cardiac output during exercise.

• Organization of the Circulatory System 194

  • Structure of the Heart 194

  • Pulmonary and Systemic Circuits 195

• Heart: Myocardium and Cardiac Cycle 195

  • Myocardium 196

  • Cardiac Cycle 197

  • Arterial Blood Pressure 199

  • Factors That Influence Arterial Blood Pressure 201

  • Electrical Activity of the Heart 202

• Cardiac Output 204

  • Regulation of Heart Rate 204

  • Heart Rate Variability 207

  • Regulation of Stroke Volume 208

• Hemodynamics 210

  • Physical Characteristics of Blood 210

  • Relationships among Pressure, Resistance, and Flow 210

  • Sources of Vascular Resistance 211

• Changes in Oxygen Delivery to Muscle during Exercise 212

  • Changes in Cardiac Output during Exercise 212

  • Changes in Arterial-Mixed Venous O₂ Content during Exercise 214

  • Redistribution of Blood Flow during Exercise 214

  • Regulation of Local Blood Flow during Exercise 215

• Circulatory Responses to Exercise 216

  • Emotional Influence 217

  • Transition from Rest to Exercise 217

  • Recovery from Exercise 217

  • Incremental Exercise 217

  • Arm Versus Leg Exercise 218

  • Intermittent Exercise 219

  • Prolonged Exercise 219

• Regulation of Cardiovascular Adjustments to Exercise 220

arteries

arterioles

atrioventricular node (AV node)

autoregulation

capillaries

cardiac accelerator nerves

cardiac output

cardiovascular control center

central command

diastole

diastolic blood pressure

double product

electrocardiogram (ECG or EKG)

heart rate variability

intercalated discs

mixed venous blood

myocardium

pulmonary circuit

sinoatrial node (SA node)

stroke volume

systole

systolic blood pressure

vagus nerve

veins

venules

One of the major challenges to homeostasis posed by exercise is the increased muscular demand for oxygen; during heavy exercise, the demand may be 15 to 25 times greater than at rest. The primary purpose of the cardiorespiratory system is to deliver adequate amounts of oxygen and remove wastes from body tissues. Further, the circulatory system also transports nutrients and aids in temperature regulation. It is important to remember that the respiratory system and the circulatory system function together as a “coupled unit”; the respiratory system adds oxygen and removes carbon dioxide from the blood, while the circulatory system is responsible for the delivery of oxygenated blood and nutrients to tissues in accordance with their needs. In simple terms, the “cardiorespiratory system” works as a unit to maintain oxygen and carbon dioxide homeostasis in body tissues. A British physician, William Harvey, proposed the first complete theory about how the cardiovascular system works in humans (see A Look Back—Important People in Science).

To meet the increased oxygen demands of muscle during exercise, two major adjustments of blood flow must be made: (1) an increased cardiac output (i.e., increased amount of blood pumped per minute by the heart) and (2) a redistribution of blood flow from inactive organs to the active skeletal muscles. However, while the needs of the muscles are being met, other tissues, such as the brain, cannot be denied blood flow. This is accomplished by maintaining blood pressure, the driving force behind blood flow. A thorough understanding of the cardiovascular responses to exercise is important for the student of exercise physiology. Therefore, this chapter describes the design and function of the circulatory system and how it responds during exercise. We begin with a brief review of the anatomy and function of the heart and blood vessels.

The human circulatory system is a closed loop that circulates blood to all body tissues. Circulation of blood requires the action of a muscular pump, the heart, that creates the “pressure head” needed to move blood through the system. Blood travels away from the heart in arteries and returns to the heart by way of veins. The system is considered “closed” because arteries and veins are continuous with each other through smaller vessels. Arteries branch extensively to form a “tree” of smaller vessels. As the vessels become microscopic, they form arterioles, which eventually develop into “beds” of much smaller vessels called capillaries. Capillaries are the smallest and most numerous of blood vessels; all exchanges of oxygen, carbon dioxide, and nutrients between tissues and the circulatory system occur across capillary beds. Blood passes from capillary beds to small venous vessels called venules. As venules move back toward the heart, they increase in size and become veins. Major veins empty directly into the heart. The mixture of venous blood from both the upper and lower body that accumulates in the right side of the heart is termed mixed venous blood. Mixed venous blood, therefore, represents an average of venous blood from the entire body.

Structure of the Heart

The heart is divided into four chambers and is often considered to be two pumps in one. The right atrium and right ventricle form the right pump, and the left atrium and left ventricle combine to make the left pump (see Fig. 9.1). The right side of the heart is separated from the left side by a muscular wall called the interventricular septum. This septum prevents the mixing of blood from the two sides of the heart.

Blood movement within the heart is from the atria to the ventricles, and from the ventricles, blood is pumped into the arteries. To prevent backward movement of blood, the heart contains four one-way valves. The right and left atrioventricular valves connect the atria with the right and left ventricles, respectively (Fig. 9.1). These valves are also known as the tricuspid valve (right atrioventricular valve) and the bicuspid valve (left atrioventricular valve). Backflow from the arteries into the ventricles is prevented by the pulmonary semilunar valve (right ventricle) and the aortic semilunar valve (left ventricle).

Pulmonary and Systemic Circuits

As mentioned previously, the heart can be considered two pumps in one. The right side of the heart pumps blood that is partially depleted of its oxygen content and contains an elevated carbon dioxide content as a result of gas exchange in the various tissues of the body. This blood is delivered from the right heart into the lungs through the pulmonary circuit. At the lungs, oxygen is loaded into the blood and carbon dioxide is released. This “oxygenated” blood then travels to the left side of the heart and is pumped to the various tissues of the body via the systemic circuit (Fig. 9.2).

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.

Myocardium

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.

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).

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.

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.

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.

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.

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.

Cardiac Cycle

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.

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.

Pressure Changes during the Cardiac Cycle

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.

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).

Arterial Blood Pressure

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.

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.

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.

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:

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.

For example, suppose an individual has a blood pressure of 120/80 mm Hg. The mean arterial pressure would be:

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.

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.

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).

Factors That Influence Arterial Blood Pressure

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:

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.

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.

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.

Electrical Activity of the Heart

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.

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.

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.

Cardiac output $(Q˙)$ is the product of the heart rate (HR) and the stroke volume (SV) (amount of blood pumped per heartbeat):

Thus, cardiac output can be increased due to a rise in either heart rate or stroke volume. During exercise in the upright position (e.g., running, cycling, etc.), the increase in cardiac output is due to an increase in both heart rate and stroke volume. Table 9.2 presents typical values at rest and during maximal exercise for heart rate, stroke volume, and cardiac output in both untrained and highly trained endurance athletes. The gender differences in stroke volume and cardiac output are due mainly to differences in body sizes between men and women (2) (see Table 9.2).

Regulation of Heart Rate

During exercise, the quantity of blood pumped by the heart must change in accordance with the elevated skeletal muscle oxygen demand. Because the SA node controls heart rate, changes in heart rate often involve factors that influence the SA node. The two most prominent factors that influence heart rate are the parasympathetic and sympathetic nervous systems (11).

The parasympathetic fibers that supply the heart arise from neurons in the cardiovascular control center in the medulla oblongata and make up a portion of the vagus nerve (4). Upon reaching the heart, these fibers make contact with both the SA node and the AV node (see Fig. 9.14). When stimulated, these nerve endings release acetylcholine, which causes a decrease in the activity of both the SA and AV nodes due to hyperpolarization (i.e., moving the resting membrane potential further from threshold). The end result is a reduction of heart rate. Therefore, the parasympathetic nervous system acts as a braking system to slow down heart rate.

Even at rest, the vagus nerves carry impulses to the SA and AV nodes (11). This is often referred to as parasympathetic tone. As a consequence, changes in parasympathetic activity can cause heart rate to increase or decrease. For instance, a decrease in parasympathetic tone to the heart can elevate heart rate, whereas an increase in parasympathetic activity causes a slowing of heart rate.

The initial increase in heart rate during low- intensity exercise, up to approximately 100 beats per minute, is due to a withdrawal of parasympathetic tone (34). This occurs because, without neural input to the SA node, the intrinsic firing rate of the SA node is typically 100 beats per minute. At higher work rates, stimulation of the SA and AV nodes by the sympathetic nervous system is responsible for increases in heart rate (34). Sympathetic fibers reach the heart by means of the cardiac accelerator nerves, which innervate both the SA node and the ventricles (Fig. 9.14). Endings of these fibers release norepinephrine upon stimulation, which act on beta receptors in the heart and cause an increase in both heart rate and the force of myocardial contraction. (See Clinical Applications 9.2.)

At rest, a normal balance between parasympathetic tone and sympathetic activity to the heart is maintained by the cardiovascular control center in the medulla oblongata. The cardiovascular control center receives impulses from various parts of the circulatory system relative to changes in important parameters (e.g., blood pressure, blood oxygen tension), and it relays motor impulses to the heart in response to a changing cardiovascular need. For example, an increase in resting blood pressure above normal stimulates pressure receptors in the carotid arteries and the arch of the aorta, which in turn send impulses to the cardiovascular control center (Fig. 9.14). In response, the cardiovascular control center increases parasympathetic activity to the heart to slow the heart rate and reduce cardiac output. This reduction in cardiac output causes blood pressure to decline back toward normal.

Another regulatory reflex involves pressure receptors located in the right atrium. In this case, an increase in right atrial pressure signals the cardiovascular control center that an increase in venous return has occurred; hence, to prevent a backup of blood in the systemic venous system, an increase in cardiac output must result. The cardiovascular control center responds by sending sympathetic accelerator nerve impulses to the heart, which increase heart rate and cardiac output. The end result is that the increase in cardiac output lowers right atrial pressure back to normal, and venous blood pressure is reduced.

Finally, a change in body temperature can influence heart rate. An increase in body temperature above normal results in an increase in heart rate, whereas lowering of body temperature below normal causes a reduction in heart rate (34). For example, exercise in a hot environment results in increased body temperatures and higher heart rates than if the same exercise was performed in a cool environment. This topic is discussed in more detail in Chap. 12.

Heart Rate Variability

As discussed previously, heart rate is regulated by the autonomic nervous system (i.e., balance between the parasympathetic and sympathetic nervous systems). The term heart rate variability (HRV) refers to the variation in the time between heartbeats (19). In practice, the time interval (expressed in milliseconds) between two heartbeats can be measured as the R-R time interval using an ECG tracing, as illustrated in Figure 9.11. The HRV is then calculated as the standard deviation of the R-R time interval during a selected time period. A wide variation in HRV is considered to be a good index of a “healthy” balance between the sympathetic and parasympathetic nervous systems, whereas low HRV indicates an imbalance exists in autonomic regulation.

The physiological significance of HRV is that the time variation between heartbeats reflects autonomic balance and is an excellent noninvasive screening tool for many diseases. For example, low HRV has been shown to predict future cardiovascular events, such as sudden cardiac death. Further, low HRV is an independent risk factor for the development of cardiovascular disease, including heart failure, myocardial infarction, and hypertension (20). Epidemiological studies have also established that low HRV is an excellent predictor of increased cardiovascular morbidity and mortality in patients with existing cardiovascular disease.

What is the physiological cause of low HRV variability? Again, the autonomic nervous system regulates many cardiovascular parameters, including both heart rate and HRV. Recall that heart rate can be elevated by increasing sympathetic activity or decreased by increasing parasympathetic (vagal) activity. The balance between the effects of the sympathetic and parasympathetic systems, the two opposite-acting branches of the autonomic nervous system, is referred to as the sympathovagal balance and is reflected in the beat-to-beat changes of the cardiac cycle (19).

Numerous factors can influence the sympathovagal balance and thus affect HRV. For example, with advancing age or some disease states, there is a decrease in parasympathetic tone at rest (19) or an increase in sympathetic nervous system outflow (8). This results in a disturbance in sympathovagal balance and a decrease in HRV. Some specific examples of diseases that promote a decrease in HRV are as follows: HRV is decreased in patients suffering from depression, hypertension, and heart disease, and in individuals following a myocardial infarction (19). Importantly, research indicates that physical inactivity promotes a decrease in HRV, whereas regular bouts of aerobic exercise result in increased HRV (19). Therefore, investigation of the types of exercise and specific training programs that have positive influences on HRV has become an important area of research.

Regulation of Stroke Volume

Stroke volume, at rest or during exercise, is regulated by three factors: (1) the end-diastolic volume (EDV), which is the volume of blood in the ventricles at the end of diastole; (2) the average aortic blood pressure; and (3) the strength of ventricular contraction.

EDV is often referred to as “preload,” and it influences stroke volume in the following way. Two physiologists, Frank and Starling, demonstrated that the strength of ventricular contraction increased with an enlargement of EDV (i.e., stretch of the ventricles). This relationship has become known as the Frank-Starling law of the heart. The increase in EDV results in a lengthening of cardiac fibers, which improves the force of contraction in a manner similar to that seen in skeletal muscle (discussed in Chap. 8). The mechanism to explain the influence of fiber length on cardiac contractility is that an increase in the length of cardiac fibers increases the number of myosin cross-bridge interactions with actin, resulting in increased force production. A rise in cardiac contractility results in an increase in the amount of blood pumped per beat; the relationship between EDV volume and stroke volume is illustrated in Figure 9.15.

The principal variable that influences EDV is the rate of venous return to the heart. An increase in venous return results in a rise in EDV and, therefore, an increase in stroke volume. Increased venous return and the resulting increase in EDV play a key role in the increase in stroke volume observed during upright exercise.

What factors regulate venous return during exercise? There are three principal mechanisms: (1) constriction of the veins (venoconstriction), (2) pumping action of contracting skeletal muscle (called the muscle pump), and (3) pumping action of the respiratory system (termed the respiratory pump).

1. Venoconstriction. Venoconstriction increases venous return by decreasing the diameter of the vessels and increasing the pressure within the vein. The end result of increased venous pressure is to drive blood back toward the heart. Venoconstriction occurs via a reflex sympathetic constriction of smooth muscle in veins draining skeletal muscle, which is controlled by the cardiovascular control center (4).

2. Muscle pump. The muscle pump is a result of the mechanical action of rhythmic skeletal muscle contractions. Therefore, when muscles contract during exercise, they compress veins and push blood back toward the heart. Between contractions, blood refills the veins and the process is repeated. Blood is prevented from flowing away from the heart between contractions by one-way valves located in large veins (Fig. 9.16). During sustained muscular contractions (isometric exercise), the muscle pump cannot operate, and venous return to the heart is reduced.

   Figure 9.16

   The action of the one-way venous valves. Contraction of skeletal muscles helps to pump blood toward the heart, but is prevented from pushing blood away from the heart by closure of the venous valves.

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3. Respiratory pump. The rhythmic pattern of breathing also provides a mechanical pump by which venous return is promoted. The respiratory pump works in the following way. During inspiration, the pressure within the thorax (chest) decreases and abdominal pressure increases. This creates a flow of venous blood from the abdominal region into the thorax and therefore promotes venous return. Although quiet breathing (rest) aids in venous return, the role of the respiratory pump is enhanced during exercise due to the greater respiratory rate and depth. Indeed, recent evidence indicates that the respiratory pump is a dominant factor that promotes venous return to the heart during upright exercise (22).

A second variable that affects stroke volume is the aortic pressure (mean arterial pressure). In order to eject blood, the pressure generated by the left ventricle must exceed the pressure in the aorta. Therefore, aortic pressure or mean arterial pressure (called afterload) represents a barrier to the ejection of blood from the ventricles. Stroke volume is thus inversely proportional to the afterload; that is, an increase in aortic pressure produces a decrease in stroke volume. However, afterload is minimized during exercise due to arteriole dilation. This arteriole dilation in the working muscles reduces afterload and makes it easier for the heart to pump a large volume of blood.

The final factor that influences stroke volume is the effect of circulating catecholamines (i.e., epinephrine and norepinephrine) and direct sympathetic stimulation of the heart by cardiac accelerator nerves. Both of these mechanisms increase cardiac contractility by increasing the amount of calcium available to the myocardial cell (34). In particular, epinephrine and norepinephrine both increase the entry of extracellular calcium into the cardiac muscle fiber, which increases cross-bridge activation and force production. The relationship between sympathetic stimulation of the heart and stroke volume is illustrated in Figure 9.17. Notice that compared to control conditions (i.e., limited sympathetic stimulation), increased sympathetic stimulation of the heart increases stroke volume at any level of EDV.

To summarize, stroke volume is regulated by three factors: EDV, cardiac contractility, and cardiac afterload. During upright exercise, the exercise-induced increases in stroke volume occur due to both increases in EDV and increased cardiac contractility due to circulating catecholamines and/or sympathetic stimulation. In contrast, an increase in cardiac afterload results in a decrease in stroke volume.

One of the most important features of the circulatory system is that the system is a continuous “closed loop.” Blood flow through the circulatory system results from pressure differences between the two ends of the system. To understand the physical regulation of blood flow to tissues, it is necessary to appreciate the interrelationships between pressure, flow, and resistance. The study of these factors and the physical principles of blood flow is called hemodynamics.

Physical Characteristics of Blood

Blood is composed of two principal components: plasma and cells. Plasma is the “watery” portion of blood that contains numerous ions, proteins, and hormones. The cells that make up blood are red blood cells (RBCs), platelets, and white blood cells. Red blood cells contain hemoglobin used for the transport of oxygen (see Chap. 10). Platelets play an important role in blood clotting, and white blood cells are important in preventing infection (Chap. 6).

The percentage of the blood that is composed of cells is called the hematocrit. That is, if 42% of the blood is cells and the remainder is plasma, the hematocrit is 42% (see Fig. 9.19). On a percentage basis, RBCs constitute the largest fraction of cells found in blood. Therefore, the hematocrit is principally influenced by increases or decreases in RBC numbers. The average hematocrit of a normal college-age male is 42%, and the hematocrit of a normal college-age female averages approximately 38%. These values vary among individuals and are dependent on a number of variables.

Blood is several times more viscous than water, and this viscosity increases the difficulty with which blood flows through the circulatory system. One of the major contributors to viscosity is the concentration of RBCs found in the blood. Therefore, during periods of anemia (decreased RBCs), the viscosity of blood is lowered. Conversely, an increase in hematocrit results in an elevation in blood viscosity. The potential influence of changing blood viscosity on performance is discussed in Chap. 25.

Relationships among Pressure, Resistance, and Flow

As mentioned earlier, blood flow through the vascular system is dependent upon the difference in pressure at the two ends of the system. For example, if the pressures at the two ends of the vessel are equal, no flow will occur. In contrast, if the pressure is higher at one end of the vessel than the other, blood will flow from the region of higher pressure to the region of lower pressure. The rate of flow is proportional to the pressure difference (P₁ – P₂) between the two ends of the tube. In other words, the blood flow is directly related to the pressure differences across the tube, whereby an increase in driving pressure will increase flow. Figure 9.20 illustrates the “pressure head” driving blood flow in the systemic circulatory system under resting conditions. Here, the mean arterial pressure is 100 mm Hg (i.e., this is the pressure of blood in the aorta), while the pressure at the opposite end of the circuit (i.e., pressure in the right atrium) is 0 mm Hg. Therefore, the driving pressure across the circulatory system is 100 mm Hg (100 – 0 = 100).

It should be pointed out that the flow rate of blood through the vascular system is proportional to the pressure difference across the system, but it is inversely proportional to the resistance. In simple terms, this means that when vascular resistance increases, blood flow decreases. Inverse proportionality is expressed mathematically by the placement of this variable in the denominator of a fraction, because a fraction decreases when the denominator increases. Therefore, the relationship between blood flow, pressure, and resistance is given by the equation

where Δ pressure means the difference in pressure between the two ends of the circulatory system. Therefore, blood flow can be increased by either an increase in blood pressure or a decrease in resistance. A fivefold increase in blood flow could be generated by increasing pressure by a factor of five; however, this large increase in blood pressure would be hazardous to health. Fortunately, increases in blood flow during exercise are achieved primarily by a decrease in resistance with a small rise in blood pressure.

What factors contribute to the resistance of blood flow? Resistance to flow is directly proportional to the length of the vessel and the viscosity of blood. However, the most important variable determining vascular resistance is the diameter of the blood vessel, because vascular resistance is inversely proportional to the fourth power of the radius of the vessel:

In other words, an increase in either vessel length or blood viscosity results in a proportional increase in resistance. However, reducing the radius of a blood vessel by one-half would increase resistance 16 fold (i.e., 2⁴ = 16)!

Sources of Vascular Resistance

The viscosity of blood and the length of the blood vessels are not manipulated in normal physiology. Therefore, the primary factor regulating blood flow through organs is the diameter of the blood vessel. Indeed, a small decrease in the radius of the blood vessel (vasoconstriction) results in a large increase in vascular resistance and a decrease in blood flow. Specifically, the effect of changes in radius on changes in flow rate are magnified by a power of four and therefore, blood can be diverted from one organ system to another by varying degrees of vasoconstriction and vasodilation. This principle is used during heavy exercise to divert blood toward contracting skeletal muscle and away from less-active tissue. This concept is discussed in detail in the next section, “Changes in Oxygen Delivery to Muscle During Exercise.”

The greatest vascular resistance in blood flow occurs in arterioles. This point is illustrated in Figure 9.21. Note the large drop in arterial pressure that occurs across the arterioles; approximately 70% to 80% of the decline in mean arterial pressure occurs across the arterioles.

During intense exercise, the metabolic need for oxygen in skeletal muscle increases many times over the resting value. To meet this rise in oxygen demand, blood flow to the contracting muscle must increase. As mentioned earlier, increased oxygen delivery to exercising skeletal muscle is accomplished via two mechanisms: (1) an increased cardiac output and (2) a redistribution of blood flow from inactive organs to the working skeletal muscle.

Changes in Cardiac Output During Exercise

Cardiac output increases during exercise in direct proportion to the metabolic rate required to perform the exercise task. This is shown in Figure 9.22. Note that the relationship between cardiac output and percent maximal oxygen uptake is essentially linear. The increase in cardiac output during exercise in the upright position (i.e., running or cycling) is achieved by an increase in both stroke volume and heart rate. However, in untrained or moderately trained subjects, stroke volume does not increase beyond a workload of 40% to 60% of $V˙O2 max$ (Figure 9.22).

Therefore, at work rates greater than 40% to 60% $V˙O2$ max, the rise in cardiac output in these individuals is achieved by increases in heart rate alone. The examples presented in Figure 9.22 for maximal heart rate, stroke volume, and cardiac output are typical values for a 70-kg, active (but not highly trained) college-age male. See Table 9.2 for examples of maximal stroke volume and cardiac output for trained men and women.

Note that although most experts agree that stroke volume reaches a plateau between 40% and 60% of $V˙O2 max$ during upright exercise in untrained and moderately trained individuals, evidence exists that stroke volume does not plateau in highly trained athletes during running exercise. This point is discussed in more detail in Research Focus 9.1. Further, differences exist in exercise-induced changes in stroke volume between upright exercise (e.g., running) and supine exercise (e.g., swimming). See A Closer Look 9.3 for more details.

Maximal cardiac output tends to decrease in a linear fashion in both men and women after 30 years of age (12). This is primarily due to a decrease in maximal heart rate with age (12). For example, because cardiac output equals heart rate times stroke volume, any decrease in heart rate would result in a decrease in cardiac output. The decrease in maximal heart rate with age in young adults can be estimated by the following formula:

According to this formula, a 20-year-old subject might have a maximal heart rate of 200 beats per minute (220 − 20 = 200), whereas a 35 year-old would have a maximal heart rate of 185 beats per minute (220 − 35 = 185). However, this is only an estimate, and values can be 20 beats × min⁻¹ higher or lower.

The previous formula for adults is not a good predictor of maximal heart rate in older adults or children. In adults (>40 years old) and children (ages 7–17), the following formula can be used to predict maximal heart rate (21, 39):

According to this formula for children, a 12-year-old child would have a maximal heart rate of 200 beats (208 − 8 = 200). Similar to the formula used to predict maximal heart rates in young adults, the formula for children and older adults provides only an estimate of maximal heart rates, and wide variability in maximal heart rates can exist between different individuals (21, 29).

Changes in Arterial-Mixed Venous O₂ Content during Exercise

Figure 9.22 illustrates the exercise-induced changes in the arterial-mixed venous oxygen difference ($a−v¯O2$ diff). The $a−v¯O2$ difference represents the amount of O₂ that is taken up from 100 ml of blood by the tissues during one trip around the systemic circuit. An increase in the $a−v¯O2$ difference during exercise is due to an increase in the amount of O₂ taken up and used for the oxidative production of ATP by skeletal muscle. The relationship between cardiac output $(Q˙)$, $a−v¯O2$ diff, and oxygen uptake is given by the Fick equation:

Simply stated, the Fick equation says that $v˙O2$ equal to the product of cardiac output and the $a−v¯O2$ diff. This means that an increase in either cardiac output or $a−v¯O2$ diff would elevate $v˙O2$. Figure 9.2 illustrates that, during exercise, oxygen consumption increases due to both an increase in cardiac output and an increase in the $a−v¯O2$ difference.

Redistribution of Blood Flow during Exercise

To meet the increased oxygen demand of the skeletal muscles during exercise, it is necessary to increase muscle blood flow while reducing blood flow to less active organs such as the liver, kidneys, and GI tract. Figure 9.23 points out that the change in blood flow to muscle and the splanchnic (pertaining to the viscera) circulation is dictated by the exercise intensity (metabolic rate). That is, the increase in muscle blood flow during exercise and the decrease in splanchnic blood flow change as a linear function of % $V˙O2 max$ (34).

Figure 9.24 illustrates the change in blood flow to various organ systems between resting conditions and during maximal exercise. Several important points need to be stressed. First, at rest, approximately 15% to 20% of total cardiac output is directed toward skeletal muscle (2, 34). However, during maximal exercise, 80% to 85% of total cardiac output goes to contracting skeletal muscle (34). This is necessary to meet the huge increase in muscle oxygen requirements during intense exercise. Second, notice that during heavy exercise, the percentage of total cardiac output that goes to the brain is reduced compared to that during rest. However, the absolute blood flow that reaches the brain is slightly increased above resting values; this is due to the elevated cardiac output during exercise (6, 45). Further, although the percentage of total cardiac output that reaches the myocardium is the same during maximal exercise as it is at rest, the total coronary blood flow is increased due to the increase in cardiac output during heavy exercise. Also, note that skin blood flow increases during both light and moderate exercise but decreases during maximal exercise (6). Finally, compared to rest, blood flow to abdominal organs is also decreased during maximal exercise (Fig. 9.24). This reduction in abdominal blood flow during heavy exercise is an important means of shifting blood flow away from “less active” tissues and toward the working skeletal muscles.

Regulation of Local Blood Flow during Exercise

What regulates blood flow to various organs during exercise? Muscle as well as other body tissues have the unique ability to regulate their own blood flow in direct proportion to their metabolic needs. Blood flow to skeletal muscle during exercise is regulated in the following way. First, the arterioles in skeletal muscle have a high vascular resistance at rest. This is due to adrenergic sympathetic stimulation, which causes arteriole smooth muscle to contract (vasoconstriction) (41). This produces a relatively low blood flow to muscle at rest (4 to 5 ml per minute per 100 grams of muscle), but because to muscles have a large mass, this accounts for 20% to 25% of total blood flow from the heart.

During exercise, skeletal muscle blood flow increases in direct proportion to the metabolic demand (25). In fact, compared to blood flow at rest, blood delivery to contracting skeletal muscle during intense exercise may rise 100 times (25). This increased muscle blood flow occurs because of a decrease in vascular resistance and is combined with “recruitment” of the capillaries in skeletal muscle. At rest, only 50% to 80% of the capillaries in skeletal muscle are open at any one time. However, during intense exercise, almost all of the capillaries in contracting muscle are open, resulting in increased oxygen delivery to the contracting muscle fibers (34).

The increase in muscle blood flow that occurs during exercise is regulated by several factors that promote vasodilation (25). This type of blood flow regulation is termed autoregulation and is the most important factor in regulating blood flow to muscle during exercise. The level of vasodilation that occurs in arterioles and small arteries leading to skeletal muscle is regulated by the metabolic (i.e., oxygen and nutrients) need of the muscle. Specifically, the intensity of exercise and the number of motor units recruited determine the overall need for blood flow to the muscle. For example, during low-intensity exercise, a relatively small number of motor units are recruited into action, resulting in a relatively small demand for blood flow to the contracting muscle. In contrast, high-intensity exercise results in the recruitment of a large number of motor units and, therefore, results in a large increase in muscle blood flow.

What factors are responsible for the autoregulation of muscle blood flow to match the metabolic demand? Skeletal muscle blood flow is controlled by an interaction between several locally formed vasodilators including nitric oxide, prostaglandins, ATP, adenosine, and endothelium derived hyperpolarization factors (25). Further, separate from these substances that promote vasodilation, some locally produced substances inhibit the vasoconstrictor effect of increased sympathetic nerve activity during exercise. The local inhibition of sympathetic-induced vasoconstriction that occurs during exercise is called sympatholysis (25). Although it is clear that sympatholysis occurs and increases muscle blood flow during exercise, the relative importance of this phenomenon on the control of muscle blood flow continues to be a debated topic (25).

Let’s discuss the local factors involved in the control of muscle blood flow during exercise in more detail. The increased metabolic rate of skeletal muscle during exercise causes local changes such as increased production of nitric oxide, prostaglandins, ATP, adenosine, and endothelium derived hyperpolarization factors. Each of these factors has been independently shown to promote vasodilation by increasing smooth muscle relaxation in arterioles (25). For example, both nitric oxide and prostaglandins (e.g., prostacyclin) are potent vasodilators. Further, both ATP and adenosine are important vasodilators that increase muscle blood flow during exercise. Finally, endothelium derived hyperpolarization factors act to promote hyperpolarization of smooth muscle cells in arterioles with the end result being smooth muscle relaxation and dilation of the arterioles (25). Current evidence indicates that an interplay between these vasodilatory factors exists so that these elements work together to cause vasodilation of arterioles feeding the contracting skeletal muscle; this vasodilation reduces the vascular resistance and, therefore, increases blood flow (25). To summarize, the exercise-induced increase in local factors result in increased vasodilation of arterioles/small arteries and promote increased blood flow to the contracting muscle in order to match the metabolic demand.

While the vascular resistance in skeletal muscle decreases during exercise, vascular resistance to flow in the visceral organs and other inactivity tissue increases. This occurs due to an increased sympathetic output to these organs, which is regulated by the cardiovascular control center. As a result of the increase in visceral vasoconstriction during exercise (i.e., resistance increases), blood flow to the viscera can decrease to only 20% to 30% of resting values (34).

The changes in heart rate and blood pressure that occur during exercise reflect the type and intensity of exercise performed, the duration of exercise, and the environmental conditions under which the work was performed. For example, heart rate and blood pressure are higher during arm work when compared to leg work at a given oxygen uptake. Further, exercise in a hot/humid condition results in higher heart rates when compared to the same exercise in a cool environment. The next several sections discuss the cardiovascular responses to exercise during a variety of exercise conditions.

Emotional Influence

Submaximal exercise in an emotionally charged atmosphere results in higher heart rates and blood pressures when compared to the same work in a psychologically “neutral” environment. This emotional elevation in heart rate and blood pressure response to exercise is mediated by an increase in sympathetic nervous system activity. If the exercise is maximal (e.g., 400-meter dash), high emotion elevates the pre-exercise heart rate and blood pressure but does not generally alter the peak heart rate or blood pressure observed during the exercise itself.

Transition from Rest to Exercise

At the beginning of exercise, there is a rapid increase in heart rate, stroke volume, and cardiac output. It has been demonstrated that heart rate and cardiac output begin to increase within the first second after muscular contraction begins (see Fig. 9.25). If the work rate is constant and below the lactate threshold, a steady-state plateau in heart rate, stroke volume, and cardiac output is reached within two to three minutes. This response is similar to that observed in oxygen uptake at the beginning of exercise (see Chap. 4).

Recovery from Exercise

Recovery from short-term, low-intensity exercise is generally rapid. This is illustrated in Figure 9.25. Notice that heart rate, stroke volume, and cardiac output all decrease rapidly back toward resting levels following this type of exercise. Recovery speed varies from individual to individual, with well-conditioned subjects demonstrating better recuperative powers than untrained subjects. In regard to recovery heart rates, the slopes of heart-rate decay following exercise are generally the same for trained and untrained subjects. However, trained subjects recover faster following exercise because they don’t achieve as high a heart rate as untrained subjects during a particular exercise.

Recovery from long-term exercise is much slower than the response depicted in Figure 9.25. This is particularly true when the exercise is performed in hot/ humid conditions, because an elevated body temperature delays the fall in heart rate during recovery from exercise (36).

Incremental Exercise

The cardiovascular responses to dynamic incremental exercise were illustrated in Figure 9.22. Heart rate and cardiac output increase in direct proportion to oxygen uptake. Further, blood flow to muscle increases as a function of oxygen uptake (see Fig. 9.23). This ensures that as the need to synthesize ATP to supply the energy for muscular contraction increases, the supply of $O2$ reaching the muscle also increases. However, both cardiac output and heart rate reach a plateau at approximately 100% $V˙O2 max$ (see Fig. 9.22). This point represents a maximal ceiling for oxygen transport to exercising skeletal muscles, and it is thought to occur simultaneously with the attainment of maximal oxygen uptake.

The increase in cardiac output during incremental exercise is achieved via a decrease in vascular resistance to flow and an increase in mean arterial blood pressure. The elevation in mean arterial blood pressure during exercise is due to an increase in systolic pressure, because diastolic pressure remains fairly constant during incremental work (see Fig. 9.22).

As mentioned earlier, the increase in heart rate and systolic blood pressure that occurs during exercise results in an increased workload on the heart. The increased metabolic demand placed on the heart during exercise can be estimated by examining the double product. The double product (also known as rate-pressure product) is computed by multiplying heart rate times systolic blood pressure:

Table 9.3 contains an illustration of changes in the double product during an incremental exercise test. The take-home message in Table 9.3 is simply that increases in exercise intensity result in an elevation in both heart rate and systolic blood pressure; each of these factors increases the workload placed on the heart.

Careful examination of Table 9.3 reveals that the double product during exercise at $V˙O2 max$ is five times greater than the double product at rest. This implies that maximal exercise increases the workload on the heart by 500% over rest.

The practical application of the double product is that this measure can be used as a guideline to prescribe exercise for patients with coronary artery blockage. For example, suppose a patient develops chest pain (called angina pectoris) at a certain intensity of exercise due to myocardial ischemia at a double product of 30,000. Because chest pain appears at a double product of 30,000, the cardiologist or exercise physiologist would recommend that this patient perform types of exercise that result in a double product of 30,000. This would reduce the risk of the patient developing chest pain due to a high metabolic demand on the heart.

Arm Versus Leg Exercise

As mentioned earlier, at any given level of oxygen consumption, both heart rate and blood pressure are higher during arm work when compared to leg work (1, 24, 33) (see Fig. 9.26). The explanation for the higher heart rate seems to be linked to a greater sympathetic outflow to the heart during arm work when compared to leg exercise (2). In addition, isometric exercise also increases the heart rate above the expected value based on relative oxygen consumption (1).

The relatively large increase in blood pressure during arm work is due to a vasoconstriction in the inactive muscle groups (2). In contrast, the larger the muscle group (e.g., legs) involved in performing the exercise, the more resistance vessels (arterioles) that are dilated. Therefore, this lower peripheral resistance is reflected in lower blood pressure (because cardiac output × resistance = pressure).

Intermittent Exercise

If exercise is intermittent (e.g., interval training), the extent of the recovery of heart rate and blood pressure between exercise bouts depends on the level of subject fitness, environmental conditions (temperature, humidity), and the duration and intensity of the exercise. With a relatively light effort in a cool environment, there is generally complete recovery between exercise bouts within several minutes. However, if the exercise is intense or the work is performed in a hot/humid environment, there is a cumulative increase in heart rate between efforts, and thus recovery is not complete (38). The practical consequence of performing repeated bouts of light exercise is that many repetitions can be performed. In contrast, the nature of high-intensity exercise dictates that a limited number of efforts can be tolerated.

Prolonged Exercise

Figure 9.27 illustrates the change in heart rate, stroke volume, and cardiac output that occurs during prolonged exercise at a constant work rate. Note that cardiac output is maintained at a constant level throughout the duration of the exercise. However, as the duration of exercise increases, stroke volume declines while heart rate increases (6). Figure 9.27 demonstrates that the ability to maintain a constant cardiac output in the face of declining stroke volume is due to the increase in heart rate being equal in magnitude to the decline in stroke volume.

The increase in heart rate and decrease in stroke volume observed during prolonged exercise is often referred to as cardiovascular drift and is due to the influence of rising body temperature on dehydration and a reduction in plasma volume (5, 30, 34). A reduction in plasma volume acts to reduce venous return to the heart and therefore reduce stroke volume. If prolonged exercise is performed in a hot/humid environment, the increase in heart rate and decrease in stroke volume is exaggerated even more than depicted in Figure 9.27 (27, 32). In fact, it is not surprising to find near-maximal heart rates during submaximal exercise in the heat. For example, it has been demonstrated that during a 2.5-hour marathon race at a work rate of 70% to 75% $V˙O2 max$, maximal heart rates may be maintained during the last hour of the race (10).

Does prolonged exercise at high heart rates pose a risk for cardiac injury? The answer to this question is almost always “no” for healthy individuals. However, sudden cardiac deaths have occurred in individuals of all ages during exercise. See Clinical Applications 9.3 for more details on sudden cardiac death during exercise.

The cardiovascular adjustments at the beginning of exercise are rapid. Within one second after the commencement of muscular contraction, there is a withdrawal of vagal outflow to the heart, which is followed by an increase in sympathetic stimulation of the heart (34). At the same time, there is a vasodilation of arterioles in active skeletal muscles and a reflex increase in the resistance of vessels in less active areas. The end result is an increase in cardiac output to ensure that blood flow to muscle matches the metabolic needs (see Fig. 9.28). What is the signal to “turn on” the cardiovascular system at the onset of exercise? This question has puzzled physiologists for many years (15). At present, a complete answer is not available. However, recent advances in understanding cardiovascular control have led to the development of the central command theory (42).

The term central command refers to a motor signal developed within the brain (42). The central command theory of cardiovascular control argues that the initial cardiovascular changes at the beginning of dynamic exercise (e.g., cycle ergometer exercise) are due to centrally generated cardiovascular motor signals, which set the general pattern of the cardiovascular response. However, it is clear that cardiovascular activity is also regulated by afferent feedback to higher brain centers from heart mechanoreceptors, muscle chemoreceptors, muscle mechanoreceptors, and pressure-sensitive receptors (baroreceptors) located within the carotid arteries and the aortic arch (31, 42). Muscle chemoreceptors are sensitive to increases in muscle metabolites (e.g., potassium, lactic acid) and send messages to higher brain centers to fine-tune the cardiovascular responses to exercise (42). This type of peripheral feedback to the cardiovascular control center (medulla oblongata) is called the exercise pressor reflex (7, 23).

Muscle mechanoreceptors (e.g., muscle spindles, Golgi tendon organs) are sensitive to the force and speed of muscular movement. These receptors, like muscle chemoreceptors, send information to higher brain centers to aid in modification of the cardiovascular responses to a given exercise task (34, 35, 43).

Finally, baroreceptors, which are sensitive to changes in arterial blood pressure, may also send afferent information back to the cardiovascular control center to add precision to the cardiovascular activity during exercise. These pressure receptors are important because they regulate arterial blood pressure around an elevated systemic pressure during exercise (34).

In summary, the central command theory proposes that the initial signal to the cardiovascular system at the beginning of exercise comes from higher brain centers. However, fine-tuning of the cardiovascular response to a given exercise test is accomplished via a series of feedback loops from muscle chemoreceptors, muscle mechanoreceptors, and arterial baroreceptors (see Fig. 9.29). The fact that there appears to be some overlap among these three feedback systems during submaximal exercise suggests that redundancy in cardiovascular control exists (34). This is not surprising considering the importance of matching blood flow to the metabolic needs of exercising skeletal muscle. Whether one or many of these feedback loops becomes more important during heavy exercise is not currently known and poses an interesting question for future research.

1. What are the major purposes of the cardiovascular system?

2. Briefly outline the design of the heart. Why is the heart often called “two pumps in one”?

3. Outline the cardiac cycle and the associated electrical activity recorded via the electrocardiogram.

4. Graph the heart rate, stroke volume, and cardiac output response to incremental exercise.

5. What factors regulate heart rate during exercise? Stroke volume?

6. How does exercise influence venous return?

7. What factors determine local blood flow during exercise?

8. Graph the changes that occur in heart rate, stroke volume, and cardiac output during prolonged exercise. What happens to these variables if the exercise is performed in a hot/humid environment?

9. Compare heart rate and blood pressure responses to arm and leg work at the same oxygen uptake. What factors might explain the observed differences?

10. Explain the central command theory of cardiovascular regulation during exercise.