Exercise Physiology A Tale of Two Pumps
The Cardiovascular System During Exercise
We will now explore some of the basic elements of the cardiovascular system and illustrate how, along with the respiratory system, the cardiovascular system adjusts to the metabolic demands of the body during exercise. Clearly, for those who have not yet embarked on the study of the cardiovascular system, this material will be new and challenging. Nevertheless, for those for whom this is a review, we hope to show you that the structure we have used to understand respiratory physiology (controller, pump, and gas exchanger) can be used as well for the cardiovascular system and that this approach may enhance your understanding of the heart and circulatory system. Of course, we cannot fully discuss all of the physiology of the cardiovascular system within this chapter, but we do provide some basic information that will enable you to see the similarities between the two systems and to understand the physiology of exercise.
Basic Physiology of the Cardiovascular System ↑
The “controller” is the electrical system within the heart and the various neurological and hormonal inputs that modify the rate and force with which the heart contracts. Although all of the cells within the heart have the potential to depolarize and generate an electrical signal, specialized clusters of cells, called the sinoatrial node (SA node) and the atrioventricular node (AV node), act as pacemakers for the heart. Under normal conditions, the SA node initiates an electrical impulse that is disseminated throughout the atria, leading to contraction, and then propagates to the ventricles via the AV node and the specialized conducting tissue known as the bundle of His. This electrical connection allows the contraction of the atria and ventricles to be coordinated to maximize the volume of blood pumped from the heart each minute (i.e., the cardiac output).
Unlike the respiratory system, the cardiovascular system is not subject to voluntary control. One cannot suddenly stop one’s heart, even for a few seconds, nor can one command the heart to double its rate of contraction. The pacemaker cells, similar to the inspiratory neurons in the medulla, have an intrinsic firing frequency. This frequency is modified by input from the autonomic nervous system. The two components of the system—the sympathetic and parasympathetic nervous systems—balance each other. Activation of the sympathetic system increases the heart rate (HR), and stimulation of the parasympathetic nervous system tends to slow the frequency of contraction. Output of epinephrine and norepinephrine from the adrenal gland also stimulates β-receptors within the heart to increase the HR. Recall that the sympathetic nervous system also has a role in the modulation of the tone of the smooth muscle surrounding the airways in the lungs. In contrast to the lungs, in which β-2 receptors are stimulated to cause bronchodilation, β-1 receptors are present in cardiac tissue and, when stimulated, are responsible for an increase in HR.
The autonomic nervous system may be stimulated by emotional factors such as fear or excitement. It may also respond to neurological reflexes designed to maintain blood pressure (BP).
The “pump” component of the cardiovascular system is composed of the heart muscle, the valves within the heart that ensure unidirectional flow, and the blood vessels that form a conduit for flow of blood to the tissues and then back to the right atrium (remember: the cardiovascular system is more than just the heart). The heart muscle, similar to the ventilatory muscles, contracts more strongly if it is stretched before receiving a neurological stimulus. The degree of stretch of the ventricular muscle before contraction is termed the preload. Thus, the greater the filling of the ventricle before contraction (the greater the preload), the greater the force of the contraction, which leads to a larger volume of blood ejected from the heart (stroke volume [SV]) and a larger cardiac output. The force of contraction, or contractility, of the heart can also be modified by the autonomic nervous system. Activation of the sympathetic nervous system results in an increase in contractility.
The flow of blood though arteries, capillaries, and veins obeys many of the same physiological rules as does the flow of air through the tracheobronchial tree. For example, the flow, or cardiac output, is determined by the difference in pressure across the circuit (from the aorta to the right atrium) and the resistance of the systemic vasculature (systemic vascular resistance [SVR]). Chapter 4 describes the modification of Ohm’s law for the flow of fluids through tubes and introduced the following equation:
When applied to the cardiovascular system, the systemic vascular resistance and cardiac output are substituted into the equation as follows:
This relationship is analogous to flow in the lungs, in which the driving pressure is the difference in pressure between the alveolus and the airway opening, and resistance is the airway resistance. The greatest point of resistance in the systemic vasculature is in the small muscular arteries, a location comparable to the point of highest resistance in the airways. The diameter of the muscular arteries and their corresponding resistance is determined by the activity of the autonomic nervous system as well as local factors. In contrast to the lungs, however, where hypoxia leads to vasoconstriction, low oxygen tension in the tissues causes the local systemic vasculature to dilate. This response has the advantage of bringing more blood and, therefore, more oxygen to the hypoxic tissue, thereby preserving aerobic metabolism.
The velocity of the blood (remember from the discussion in Chapter 4 that velocity and flow are not the same; see Animated Figure 4-3) is greatest in the large arteries and lowest in the millions of tiny capillaries arranged in parallel. Similarly, turbulent flow is found in the large arteries, and laminar flow is found in the capillaries. Again, the principles you learned about flow (and Reynolds number) and velocity for the respiratory pump are relevant for the cardiovascular pump.
Finally, the “gas exchanger” for the cardiovascular system is the interface between the capillaries in the tissues and the cells surrounding the vessels. Diffusion of oxygen and carbon dioxide occur in the opposite direction to that seen in the lungs. The principles you learned in Chapter 5 about the binding of oxygen and carbon dioxide to hemoglobin and the factors that affect the binding and release to tissues are all relevant and important here. For example, the accumulation of acid in the tissues from anaerobic metabolism leads to a shift to the right of the oxygen–hemoglobin dissociation curve (see Animated Figure 5-8A). This process reduces the binding of oxygen to hemoglobin and, for any given PaO2, permits more oxygen to be available to the tissues.
With this basic information in hand, we will now explore the response of the cardiovascular system to exercise and outline how it works in tandem with the respiratory system to maximize oxygen delivery to the metabolically active muscles.
Oxygen Delivery to the Tissues ↑
Having transported oxygen to the blood, the respiratory system now turns over to the cardiovascular system the responsibility for the next step in the delivery of oxygen to the exercising muscles. Systemic oxygen delivery is the total volume of oxygen transported to the tissues each minute. Simply stated, oxygen delivery is the product of the cardiac output (the volume of blood pumped each minute) and the arterial oxygen content (the amount of oxygen per unit volume of blood). This principle is summarized in the following equations.
If we represent cardiac output with the symbol Qt (total perfusion or flow) and arterial oxygen content as CaO2, the equation can be rewritten.
As the blood circulates through capillaries in the tissue, some of the oxygen leaves the blood and enters the surrounding cells. The remainder of the oxygen stays in the blood and returns to the heart and, ultimately, the lungs. The oxygen not used by the tissue returns in venous blood and can be quantified in a manner similar to oxygen delivery. Flow, or cardiac output, in the arterial system must be the same as in the venous system (because in a closed system, if this were not true, there would be a backup). We refer to the venous blood that returns from all of the venous beds, those draining tissue that is very active metabolically as well as tissue that is less active, as mixed venous blood. The amount of oxygen returned to the heart can be represented in the following equation:
The oxygen content of mixed venous blood is represented as CvO2. The equation can be rewritten as follows:
The difference between the oxygen delivered to the tissue and the oxygen returned to the heart equals the amount of oxygen actually used or consumed by the tissues. Therefore, oxygen consumption may be expressed as:
This relationship is called the Fick equation (Fig. 9-4) and is used routinely in clinical practice to calculate the cardiac output in patients in the intensive or cardiac care units as well as in the cardiac catheterization laboratory. Rearranging the equation:
We have already discussed the method for measuring oxygen consumption (
Increasing Cardiac Output: The Cardiovascular Controller and Pump During Exercise ↑
In a normal person who is resting comfortably, the cardiac output, or volume of blood pumped by the heart, is approximately 5 L/min. During exercise, as the metabolic needs of the body increase, cardiac output may increase fivefold. As we saw with the ventilatory pump, the cardiac pump can increase its output by increasing the volume moved with each contraction or by increasing the rate of contractions (in response to instructions from the controller). Typically, stroke volume doubles during exercise, and the heart rate may nearly triple from resting values (for intense exercise). Again, as discussed in our analysis of the respiratory system during exercise, there are tradeoffs between volume moved per contraction and increases in the rate of contraction.
Stroke volume increases primarily as the result of two physiological mechanisms. First, the more the ventricle fills during diastole, the interval between contractions, the greater the strength of the ensuing systole, the contraction phase of the ventricle (recall that the term preload describes the initial stretch of the muscle cells of the ventricle prior to contraction). The greater the preload, or ventricular volume at end-diastole, the longer the individual myocardial muscle fibers are. As with the ventilatory muscles, the length–tension relationship of the heart muscle dictates that there is a more forceful contraction with longer muscle fibers. This relationship can be depicted by the Starling curve, which displays SV as a function of ventricular end-diastolic volume (Fig. 9-5).
During exercise, the contraction of the muscles of the arms and legs squeezes the veins in the extremities and increases the flow of blood returning to the heart (remember: the flow of blood on the venous side of the cardiovascular circuit must increase in tandem with the increased flow on the arterial side). In addition, stimulation of the sympathetic nervous system leads to the constriction of veins, which further increases the flow of blood back to the heart. The increase in venous flow, termed venous return, causes an increase in preload of the right ventricle and, thus, an increase in cardiac output.
As you examine the Starling curve, note that the SV increases as the end-diastolic volume increases only up to a point. Further increases in end-diastolic volume do not yield any greater increases in cardiac output, but they do raise the risk of causing fluid to build up in the lung as the pressure in the pulmonary capillaries increases. Remember that pressure and volume are linked by compliance (in this case, the compliance of the ventricle during diastole).
Increases in end-diastolic volume also cause increases in end-diastolic pressure in the left ventricle. This pressure is transmitted back through the left atrium to the pulmonary veins and, ultimately, the pulmonary capillaries. At a left ventricular end-diastolic pressure (LVEDP) of 18 to 20 mm Hg, one usually begins to see fluid leak into the lungs (the exact pressure at which this occurs is affected by the balance between hydrostatic pressure, the pressure of the fluid in the vessel, and the oncotic pressure, a pressure exerted by the protein elements in the blood; you will learn more about this balance when you study renal physiology). The leakage of fluid into the lungs worsens ventilation/perfusion mismatch and leads to hypoxemia. In healthy individuals, the LVEDP does not exceed 18 mm Hg during exercise, and there is no leakage of fluid into the lungs. In individuals with a stiff or noncompliant ventricle or a ventricle whose ability to pump is severely limited, increases in ventricular pressure are common during exercise, and leakage of fluid into the lungs may occur.
As just described, SV increases during exercise because venous return increases, leading to a greater preload. SV also increases during exercise as a consequence of the effects of the sympathetic nervous system and the chemicals (i.e., epinephrine and norepinephrine) released by the adrenal gland on the contractile function of the heart muscle. For any given preload of the ventricle, the SV will be greater in the presence of increased activity of the sympathetic nervous system. This is visualized graphically by an “upward” shift of the Starling curve (Fig. 9-6).
During exercise, the sympathetic nervous system is “activated,” and the SV increases accordingly. This increase in contractility comes with a price, however: sympathetic stimulation of the myocardium increases the oxygen demands of the heart muscle. Under normal circumstances, the heart muscle extracts a very high percentage of the oxygen from the blood traveling through the coronary arteries. If flow in the coronary arteries is reduced, the heart muscle is unable to compensate by extracting more oxygen from the blood that it sees because the percent extraction is already near maximal to start. In individuals with coronary artery disease and limits on the amount of blood and oxygen that can be delivered to the myocardium, exercise can lead to chest pain, heart attack (termed myocardial infarction), and irregular heart rhythms.
Although increasing SV is a very efficient way to increase cardiac output, there are limits, as just discussed, on the ability of the heart to use this strategy to meet the increased metabolic demands of the exercising muscles. Therefore, as we saw with the respiratory system, the body relies on a combination of increased volume per contraction and increased frequency of contractions. As HR increases, oxygen demand of the myocardium also increases, and the same risks to the function and viability of the heart as we saw with increased contractility must be considered. The body ultimately balances these issues by primarily relying on increased SV during mild to moderate exercise and then exhibits greater reliance on HR as the intensity of the activity increases. A well-trained athlete, however, may continue to meet her metabolic needs by increases in SV long after the “couch potato” has shifted to an elevated HR. Physical training strengthens the heart in a way that increases its maximal contractile capability.
The Cardiovascular Gas Exchanger: Redistribution of Blood Flow ↑
The systemic circulation is regulated by the autonomic nervous system and local tissue factors in order to maximize blood flow to the areas that need oxygen and nutrients the most at any particular point. At rest, the muscles are metabolically quiet and receive only 15% of 20% of cardiac output; most blood is sent to the internal organs. During exercise, however, flow is redistributed to the muscles. Stimulation of the sympathetic nervous system causes vasoconstriction, which reduces blood flow to the internal organs. The development of hypoxia locally in the exercising muscle, along with the buildup of the products of metabolism, including lactic acid, cause the arterioles in the muscles to dilate. Arterial resistance is high in blood vessels that serve the internal organs and low in the vessels that supply the muscles. Given the relationship that governs flow:
These differential changes in resistance lead to redistribution of flow (Fig. 9-7). We saw in our study of the respiratory gas exchanger that there are regions of the apex of the lung in an upright person at rest that are poorly perfused or not perfused at all (alveolar dead space) because cardiac output is relatively low at rest. With exercise, cardiac output increases, blood flow to the apex of the lung increases, many pulmonary capillaries are “recruited” to participate in gas exchange, and dead space is reduced. Similarly, as blood flow increases to the muscles, many capillaries that are not perfused at rest are recruited into the gas exchange process. Consequently, the distance between the RBCs in a vessel and the active muscle cells in the limb is reduced, and diffusion is enhanced.