Exercise Physiology A Tale of Two Pumps
The Respiratory System During Exercise
The Controller ↑
In Chapter 6, we began our discussion of the control of ventilation during exercise. Although we can characterize the response fairly accurately at this point, the exact physiological mechanisms responsible for each of the components of the ventilatory response remain the subject of some controversy and speculation.
Phase 1: The Neurological Phase
During the neurological phase of exercise ventilation, breathing increases out of proportion to the metabolic needs of the body. The increase in ventilation, in essence, starts before or accelerates more quickly than the increase in oxygen consumption and carbon dioxide production. Furthermore, the increase in ventilation does not appear to be the consequence of changes in arterial blood gases.
Studies in animals suggest either a central or peripheral neurological mechanism for this first stage of exercise hyperventilation. Electrical stimulation of areas in the hypothalamus in animals, for example, has been shown to produce respiratory responses that mimic those observed during exercise. Alternatively, experiments in which the limbs of sedated animals were passively moved to simulate exercise demonstrated an increase in ventilation similar to that seen with physical activity. The stimulation of joint or muscle receptors by this movement may trigger neural impulses to the brain that lead to an increase in ventilation.
Some have termed this early stage of exercise ventilation an “anticipatory” response to the metabolic needs that are to follow. It remains unclear whether there is a learned or behavioral component to this response.
Phase 2: The Metabolic Stage
During the second stage of exercise breathing, ventilation increases in concert with the increase in oxygen consumption and carbon dioxide production. The relationship between ventilation and either metabolic parameter is linear. Thus, whether you plot ventilation as a function of carbon dioxide production or oxygen consumption, a straight-line relationship is seen (Fig. 9-1).
The close link between these metabolic parameters and ventilation suggests that the body has a mechanism for monitoring carbon dioxide production or oxygen consumption (or both) and translating that information into a signal to the ventilatory controller. There is no known receptor, however, that serves this purpose. Because PaCO2 changes little during this phase of exercise, the chemoreceptors are not likely candidates for the very dramatic increases in ventilation that we observe (easily up to a 10-fold increase over resting ventilation). Some evidence suggests that there may be receptors sensitive to changes in the local metabolic environment at the tissue level located in the skeletal muscles. These so-called metaboreceptors could play a role in the increased ventilation during the metabolic phase of exercise. Metaboreceptors are hypothesized to respond to the local accumulation of metabolic byproducts and may send signals to the brain that lead to an increase in ventilation as well as the sensation of shortness of breath with which we associate exercise.
Phase 3: The Compensatory Phase ↑
In our discussion of exercise metabolism earlier in this chapter, we outlined the sequence of events that leads to the production of energy in the muscles. Both aerobic and anaerobic processes lead to the creation of carbon dioxide molecules that must be eliminated via the respiratory system. The exhaled carbon dioxide is what we measure as carbon dioxide production. However, anaerobic metabolism also leads to the production of protons, or acid, that, when buffered by bicarbonate, lead to a further increase in carbon dioxide. Thus, the compensation for the acid that results from anaerobic metabolism involves a further increase in ventilation. At this point, the carbon dioxide exiting the lungs reflects, in part, the consequence of processes that result in the production of energy as well as the compensation necessary to maintain acid–base balance within the body. As protons accumulate and the pH begins to decrease, the peripheral chemoreceptors respond by sending messages to the controller that result in an increase in ventilation.
As one follows the increase in ventilation as a function of oxygen consumption during the metabolic phase of exercise hyperpnea, the slope of the relationship changes as the intensity of exercise increases. Ventilation increases at an even faster rate during the compensatory phase (Fig. 9-2).
The change in slope of the relationship between ventilation and oxygen consumption reflects the compensation of the respiratory system for the accumulation of metabolic acid. The level of oxygen consumption at which the slope changes is the AT. The use of the plot of ventilation as a function of oxygen consumption to measure the AT is termed the “V-dot” method, a phrase that signifies that you are using ventilation
Use Animated Figure 9-2 to vary the level of exercise and observe the effects on parameters, including pH and PaCO2. Pay special attention to the changes as you exceed AT and enter the compensatory phase.
Animated Figure 9-2 (Work in progress)
The Ventilatory Pump ↑
The controller is stimulated by a variety of factors during exercise, and the demand for increased ventilation is great. The neural messages descend from the controller to the ventilatory muscles, and the pump must respond.
The respiratory system may generate the necessary ventilation during exercise by increasing the respiratory rate, increasing the tidal volume, or a combination of the two. The initial increase in ventilation is achieved primarily by enlarging the tidal volume. After doubling the tidal volume, the system relies to a greater degree on changes in respiratory rate to achieve even higher levels of ventilation (Fig. 9-3).
The “choice” between enlarging the tidal volume versus increasing the respiratory rate or frequency to achieve the desired ventilation probably represents an effort by the body to minimize the work of breathing and, hence, the discomfort associated with exercise. Until the tidal volume is doubled, the ventilatory pump operates on a relatively compliant portion of the pressure-volume curve for the respiratory system. (For a review of compliance, see Chapter 3 and Animated Figure 3-5.) Relatively small changes in transmural pressure lead to substantial tidal volumes. As soon as tidal volume has doubled, however, further increases in tidal volume begin to take you to flatter portions of the curve, and compliance decreases. Now it may be more energy efficient to increase ventilation by keeping the tidal volume constant and increasing the frequency of breaths (assuming airway resistance is normal).
The Gas Exchanger ↑
The absolute amount of dead space in the lungs and the proportion of each breath that is attributed to dead space are both reduced during exercise. You recall from Chapter 5 that a normal individual in the upright position has a small amount of alveolar dead space because of the poor perfusion pressure in the pulmonary capillaries in the apex of the lung (zone 1 of the lung). These regions are ventilated but not perfused because most of the blood flow goes to the bases of the lungs primarily as a consequence of the effect of gravity. With exercise, however, the amount of blood pumped by the heart each minute, the cardiac output, increases, and perfusion is more evenly distributed throughout the lung. Previously nonperfused alveoli, therefore, now receive blood, and dead space is reduced.
The proportion of each breath that is composed of dead space ventilation—the ratio of dead space to tidal volume, or VD/VT—is also reduced. First, the absolute amount of dead space, as we have just discussed, is smaller during exercise. Second, the tidal volume increases through the early stages of exercise and typically doubles during moderate to very intense activity. For any given amount of dead space, therefore, the VD/VT ratio is reduced.
The ability to get oxygen into the blood is also affected by exercise. Capillary blood volume increases during exercise because of the increase in cardiac output. This is favorable for gas exchange because more red blood cells (RBCs) are in contact with the alveolus at any moment in time. However, the increase in cardiac output also results in a shorter period of time that any given RBC is in the alveolar capillary. Recall that at rest, the hemoglobin in an RBC is fully saturated after approximately one third of the transit time through the alveolar capillary. Although this provides substantial reserve capacity at rest, cardiac output may increase fivefold during exercise, thereby leading to a diffusion limitation for gas exchange, i.e., the ability of oxygen to cross from the alveolus to the RBC is limited by the rate of diffusion of the gas (see Animated Figure 5-10). Patients with lung diseases that cause a mild abnormality in the alveolar-capillary interface and prolong diffusion may have normal oxygen saturation at rest, but they desaturate with exercise because of this effect.
The alveolar-to-arterial oxygen gradient, or A-aDO2, tends to widen during heavy exercise. The alveolar PO2 tends to increase with the hyperventilation seen in the compensatory phase of the increased ventilation of exercise, and the arterial PO2 tends to remain constant, thereby resulting in a widened A-aDO2. The lack of increase in the PaO2 is attributable to the reduced level of PO2 in the venous blood returning to the heart during exercise as the metabolically active tissue extracts larger amounts of oxygen from the blood (more on this shortly).