Chapter 23
Cardiopulmonary Response to Exercise in Health and Disease
After reading this chapter you will be able to:
• Describe why continual regeneration of adenosine triphosphate (ATP) is necessary to sustain exercise
• Explain how aerobic and anaerobic metabolic processes differ in their ability to generate ATP
• Explain how oxygen consumption and carbon dioxide production differ in aerobic metabolism of carbohydrates and fats
• Explain why the changes in respiratory, cardiovascular, and metabolic processes are different below than above the anaerobic threshold
• Explain how caloric expenditure is related to oxygen consumption
• Use exercise test data to differentiate cardiac and pulmonary limitations to exercise
• Explain why sedentary and athletically trained individuals differ in their ability to perform exercise
• Use exercise test data to differentiate obstructive and restrictive pulmonary limitations to physical activity
• Use exercise test data to prescribe appropriate physical activity in cardiopulmonary rehabilitation programs
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maximum oxygen consumption (
Physiology of Exercise
Strenuous exercise greatly increases the body’s requirements for oxygen delivery and carbon dioxide elimination. Close coupling between increased metabolic activity and cardiopulmonary function is necessary to supply adequate oxygen to exercising muscles and maintain a normal blood acid-base balance. This coupling is schematically represented in Figure 23-1.
Normal exchange of O2 and CO2 between muscle cells and the air requires the following:1 (1) efficient alveolar ventilation, (2) pulmonary blood flow matched to ventilation, (3) adequate blood hemoglobin content, (4) adequate cardiac pump function, (5) systemic blood flow matched to tissue requirements, and (6) ventilatory control mechanisms sensitive to arterial blood gas changes. These factors normally interact in a finely coordinated fashion, responding precisely to the metabolic needs of exercising muscle.
Metabolism during Exercise
The source of energy for skeletal muscle contraction is adenosine triphosphate (ATP). The structure of the ATP molecule is symbolized as follows:2
The bonds between the
ATP stores in skeletal muscle are extremely small and can sustain strenuous muscular activity for only about 3 seconds.2 Therefore ATP molecules must be reconstituted continuously during exercise through aerobic (with oxygen) and anaerobic (without oxygen) metabolic processes.
The energy required for sustained exercise is derived from internal and external mechanisms.3 Internal mechanisms include anaerobic production of ATP, O2 release from hemoglobin, and dissolved O2 uptake from plasma and tissue fluids. External mechanisms involve the delivery of atmospheric O2 molecules to the tissues. Atmospheric O2 is relatively unimportant for power surges of a few seconds and the first few minutes of exercise. Internal mechanisms are crucial for initiating exercise because of the delay involved in transporting atmospheric O2 to the tissues. As exercise continues, energy production becomes primarily dependent on the adequate delivery of atmospheric O2 to the tissues. As exercise intensity reaches maximum limits, internal anaerobic sources of energy become increasingly important.
Aerobic Metabolism
Aerobic metabolism of carbohydrates (glucose), fats (fatty acids), and proteins (amino acids) provides the major energy source for ATP synthesis.2 During exercise, stored glycogen in the muscles breaks down into glucose. Glucose breaks down into pyruvic acid, which reacts with O2 in the cell’s mitochondria, forming ATP, CO2, and water; thus the aerobic or oxidative process of ATP synthesis consumes O2 and generates CO2.
Aerobic metabolism of fatty acids also produces ATP molecules. For a given rate of ATP production, fat metabolism requires more O2 than carbohydrate metabolism (Figure 23-2). This means carbohydrate metabolism uses O2 more efficiently and requires less cardiovascular work per mole of ATP synthesis. However, fat metabolism generates less CO2 per mole of ATP produced than carbohydrate metabolism (see Figure 23-2); in other words, fat metabolism requires less ventilatory work than carbohydrate metabolism in generating a given amount of energy.2
Anaerobic Metabolism and Lactic Acid Production
The breakdown of this bond supplies the immediate energy for ATP resynthesis from ADP, as shown:
However, this process produces only enough ATP to fuel muscle contraction for 8 to 10 seconds during heavy exercise.2
If the cardiovascular system does not supply enough O2 for aerobic metabolism, glucose from muscle glycogen is metabolized in a process called anaerobic glycolysis. In this process, pyruvic acid is metabolized anaerobically into lactic acid and ATP (see Figure 23-2). The lactic acid subsequently diffuses into the interstitial fluid and blood, creating lactic acidosis, a form of metabolic acidosis. Increased blood lactic acid concentration indicates the presence of anaerobic metabolism, implying inadequate O2 delivery to the tissues.
Anaerobic Threshold
As exercise intensity increases, energy requirements gradually increase until aerobic metabolism alone can no longer meet the demand for ATP resynthesis. Consequently, the body must rely on anaerobic metabolism to generate additional ATP. The onset of anaerobic metabolism, the anaerobic threshold, normally occurs at about 50% to 65% of the body’s maximum oxygen consumption (
Figure 23-2 shows that aerobic metabolism produces ATP far more efficiently than anaerobic metabolism. In aerobic metabolism, one molecule of glucose produces 36 molecules of ATP compared with only two molecules of ATP in anaerobic glucose metabolism. In addition, anaerobic glucose metabolism generates two lactic acid molecules. Blood bicarbonate immediately buffers newly formed lactic acid, generating more CO2, adding to the CO2 already produced by aerobic metabolism (see Figure 23-2). This increased CO2 production stimulates a proportional increase in ventilation.3
Respiratory Quotient and Respiratory Exchange Ratio
The respiratory quotient (RQ) is the ratio of CO2 molecules produced to O2 molecules consumed by the tissues (
The respiratory exchange ratio (R) is the ratio between CO2 elimination and O2 uptake, measured from inhaled and exhaled gases at the mouth (see Figure 23-1).2 In steady-state conditions, R equals RQ. The steady state is characterized by a CO2 elimination rate that matches the CO2 production rate; likewise, the lung’s O2 uptake rate equals the tissue’s O2 consumption rate in steady-state conditions. During short bursts of maximal exercise such as the 100-yard dash, RQ and R are different because tissue O2 consumption and CO2 production momentarily exceed the lung’s O2 uptake and CO2 elimination. Like RQ, R increases as exercise intensity increases; the onset of anaerobic metabolism further increases R as bicarbonate reacts with lactic acid and generates more CO2
Exercise Testing Methods
bicycle’s pedal resistance. For example, the subject may exercise at a certain treadmill speed and angle for 3 minutes, after which the speed and angle are increased for the next 3 minutes, and so on. The subject exercises through a well-defined series of stages, each more difficult than the last, until maximum capacity is reached. During this time, a machine called a metabolic cart measures the inhaled and exhaled O2 and CO2 concentrations, tidal volume (VT), respiratory rate, and minute ventilation.
To obtain these measurements, the subject breathes through a specially designed mouthpiece attached to the metabolic cart by large-bore tubes. Nose clips prevent breathing through the nose. The lips must be sealed tightly around the mouthpiece to prevent mixing of respiratory gases with atmospheric air. An electrocardiogram (ECG) machine measures the heart rate (HR) and ECG pattern during the exercise test. Depending on the data desired, various other physiological parameters may be measured. Table 23-1 lists physiological measurements grouped according to the invasiveness of the test and the monitoring equipment needed.
TABLE 23-1
Measurements during Graded Exercise Testing
Level of Rest | Measurements |
Group 1 | No mouthpiece |
Patient response and symptoms | |
Heart rate | |
Blood pressure | |
ECG | |
SaO2 by oximetry | |
Group 2 | Mouthpiece, oxygen, and carbon dioxide analyzer |
Respiratory rate | |
Tidal volume | |
Minute ventilation | |
End-tidal gas measurements | |
Respiratory exchange ratio | |
Group 3 | Arterial line |
Blood gas values: PaO2, PaCO2, and pH | |
VD/VT | |
Group 4 | Right-sided heart catheter |
Pulmonary artery pressures | |
Cardiac output | |
Mixed venous PO2 and SO2 |
Modified from Martin L: Pulmonary physiology in clinical practice: the essentials for patient care and evaluation, St Louis, 1987, Mosby.
Physiological Changes during Exercise
Oxygen Consumption, Cardiac Output, and Blood Pressure
Figure 23-3 represents the exercise performance of a normal person.
As exercise intensifies, contracting muscles consume ever greater amounts of ATP, which means aerobic ATP regeneration requires an increasingly greater O2 supply from the blood flow. Cardiac output rises to meet this demand by increasing stroke volume (SV) and heart rate. SV increases to its maximum value within the first half of the tolerable work rate range (at about 45% of the maximum
As cardiac output increases with exercise, systolic blood pressure rises significantly (often ≥200 mm Hg). Diastolic pressure changes little, if at all, in normal, healthy people because the peripheral vasculature dilates significantly in response to increased O2 demand, which greatly reduces vascular resistance.2,3 Thus, the pulse pressure (systolic – diastolic) increases significantly, forcing open all of the capillaries in working skeletal muscle. In heavy exercise, up to 80% of the cardiac output is diverted to skeletal muscle, making possible greatly increased O2 delivery and
HRmax is age related and does not change with fitness. The predicted HRmax for adults is as follows:4
HRmax, and thus, cardiac output are reduced in older persons because their hearts are less responsive to beta-adrenergic stimulation.4 An unconditioned person and a conditioned athlete of the same age have the same HRmax, but the conditioned athlete has a much greater SV and therefore a much higher cardiac output at HRmax. For a given amount of submaximal exercise, a conditioned person’s HR is much lower than the HR of a sedentary person. This explains why a sedentary person reaches the HRmax sooner and at much lower exercise intensity than an athlete. Because the unconditioned person’s cardiac output is lower at the HRmax, maximum O2 delivery and
Carbon Dioxide Production, Respiratory Exchange Ratio, and Minute Ventilation
The increased metabolic activity of exercising muscles raises not only the
Although it is generally accepted that increased
The ventilatory response to exercise was discussed in Chapter 11. The immediate hyperpnea of exercise has long been a controversial subject and remains incompletely understood.3 The abrupt increase in
Normal people increase
Figure 23-5 shows that dead space-to-tidal volume ratio (VD/VT) decreases as exercise progresses. The initial steep reduction in VD/VT reflects early increases in VT with respect to the fixed anatomical dead space. VD/VT decreases from normal values of 0.3 to 0.4 at rest to 0.15 to 0.2 in exercise, in part due to a larger VT but also because of significant blood flow diversion to previously underperfused upper lung zones.3,8 As the respiratory rate begins to account for more of the increase in
Events Occurring after Anaerobic Threshold
As shown in Figure 23-3, the anaerobic threshold is the point at which the
As bicarbonate stores diminish and arterial pH falls, ventilation is stimulated more intensely, causing a second-phase increase in