The Controller: Directing the Orchestra

Exercise and Ventilatory Control

We started this chapter by asking you, “Why do you breathe?” You have been learning that the answer to that question is more complicated than you may have thought originally. Now we ask you, “Why do you breathe more when you exercise?” A person with a normal cardiovascular system does not become hypoxemic during exercise, nor does she become acutely hypercapnic. As you might have guessed, the answer to this question is also a bit complicated.

Ventilation increases during exercise in three phases. The first phase is sometimes called the neurological phase. Next, one sees a metabolic phase. The third phase may be considered the compensatory phase.

The initial increase in ventilation occurs almost instantaneously with the onset of exercise. This increase is too quick to be explained by changes in metabolism. It is possible that this first phase is partly a learned response, what some call an anticipatory increase in ventilation. Data from animal studies suggest a possible role for stimulation of the controller by information arising in joint and muscle receptors in the limbs. Passive movement of animals’ limbs that simulates exercise has been shown to lead to an increase in ventilation. Because of these hypothesized mechanisms, this first phase of the increase in ventilation has been termed the neurological phase.

As exercise continues, ventilation increases linearly with the increase in oxygen consumption and carbon dioxide production that results from the increased physical activity. Thus, we call this phase of exercise ventilation the metabolic phase. As noted, P_aO₂ and P_aCO₂ remain normal during this phase of exercise, and we refer to the increase in ventilation as exercise hyperpnea. Although the increase in ventilation is tightly associated with the changes in oxygen consumption and carbon dioxide production, we do not know how the controller monitors these metabolic changes. For a time, scientists hypothesized the presence of receptors within the pulmonary vasculature that might have the capability of responding to changes in the flux of carbon dioxide returning from the extremities. Definitive proof of these receptors, however, has remained elusive.

As the intensity of exercise continues, the energy needs of the muscles outstrip the ability of the cardiovascular system to supply oxygen for aerobic metabolism. Cells increasingly shift to anaerobic metabolism to supplement their needs. A byproduct of anaerobic metabolism is the production of lactic acid. The acid lowers the pH of arterial blood, which then stimulates the peripheral and central chemoreceptors (with the caveat that the response of the central chemoreceptor may be delayed, given the time it takes for the hydrogen ions to diffuse into the CSF, as discussed previously). Ventilation now increases at a rate faster than the increase in oxygen consumption. The incremental increase in ventilation is a compensation for the development of metabolic acidosis (see Chapter 7) and, consequently, we term this phase of exercise ventilation the compensatory phase. The level of oxygen consumption above which anaerobic metabolism leads to an accumulation of lactic acid in the blood is called the anaerobic threshold and, in normal individuals, it occurs between 40% and 60% of the maximal oxygen consumption (see Chapter 9).