Adaptability of the pulmonary system to changing metabolic requirements

The conventional view of the healthy pulmonary system during exercise is of a very precise and mechanically efficient homeostatic regulator of ventilation and gas exchange occurring within the reserves of a near ideal architecture of the lung and chest wall. These regulatory and architectural limits may be exceeded in the healthy pulmonary system when extremely high levels of metabolic demand are needed. For example, arterial hypoxemia will often occur at exercise intensities demanding greater than 25 liters/min cardiac output. This may be due to inadequate red cell transit time in the pulmonary capillary bed whose blood volume has been maximally recruited, thereby resulting in alveolar-end-capillary oxygen disequilibrium. At these extreme levels of exercise the hyperventilatory response may be minimal (and clearly inadequate in terms of alveolar oxygenation) despite substantial and progressive metabolic acidosis or hypoxemia or both. This evidence of compromised ventilatory response and inadequate gas exchange in the highly fit human suggests that the pulmonary system may not be reasonably designed or adaptable (with long-term physical training) to the extreme demands imposed on gas transport by a truly adapted cardiovascular system.