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The increases in muscular oxygen consumption (V̇O2) and carbon dioxide production (V̇CO2) accompanying whole-body exercise present a greater challenge to the maintenance of pulmonary gas exchange than any other physiologic stressor. This chapter discusses the responses of the healthy respiratory system to exercise with an emphasis on the following problems: what neurochemical mechanisms regulate the ventilatory response to exercise and what are the consequences of this hyperpnea to the work and to the fatigue of the respiratory muscles? What mechanisms underlie the widening of the alveolar to arterial partial pressure of oxygen (Po2) difference during exercise? How do the unique characteristics of the pulmonary circulation determine its response to exercise? How does respiration impact the cardiovascular response to exercise? Under what circumstances might the respiratory system provide a limitation to O2 transport and/or exercise performance? We consider these problems primarily in the healthy, young, normally fit adult, with reference to special cases of the highly trained athlete and to the effects of healthy aging, high altitude hypoxia, and physical training.

Exercise Hyperpnea

In healthy humans, breathing in all physiological states is remarkably well controlled. Accordingly, the partial pressures of oxygen and carbon dioxide, in systemic arterial blood along with its acidity, are regulated precisely throughout mild to moderate exercise.14

These relationships are shown in the following alveolar gas equations, where alveolar gas partial pressures are approximately equal to the ratio of the metabolic requirement to alveolar ventilation.



PaCO2 and PaO2 = alveolar carbon dioxide and oxygen partial pressures (it is assumed PaCO2 ≈ arterial PCO2)

CO2 and V̇O2 = volumes of carbon dioxide produced and oxygen consumed

a = alveolar ventilation

PiO2 = inspired partial pressure of oxygen

K = constant (0.863). This constant allows alveolar gases to be calculated from these equations if V̇O2 and V̇CO2 are expressed in mL/min and V̇a in L/min.

Table 18-1 illustrates the interrelation of these variables, as one goes from rest to exercise. With exercise, there is an increased metabolic rate, with alveolar ventilation increasing to regulate arterial blood gases near resting levels. In health, dead space (VD) increases slightly as intrathoracic airways stretch and dilate with increased tidal volume (VT) – but VT rises out of proportion; thus, VD/VT falls to about one-half its resting value during exercise. In order that PaCO2 be precisely controlled, overall minute ventilation (V̇e) during exercise must be regulated in such a fashion so as to compensate both for the increasing CO2 production as well ...

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