Abstract
1. 1. The ventilatory and pulmonary gas exchange responses during moderate exercise can be appropriately modelled with first-order dynamics. 2. 2. A delay term, reflecting tissue-to-lung transit time, is needed for accurate characterization, however. 3. 3. The O 2 uptake time constant ( τ V ̇ O 2 reflects the enzymatically controlled tissue O 2 utilization. 4. 4. τ V ̇ CO 2 is appreciably longer than τ V ̇ O 2 , consequent to the tissue CO 2 capacitance. 5. 5. As τ V ̇ E typically longer than τ V ̇ CO 2 , transient errors in alveolar and arterial blood gas tensions are predicted: small for P CO 2 but much larger for P O 2. 6. 6. At work rates above the lactate threshold, a slow and delayed component of V̇ O 2 induces an additional V̇ component (“excess” V̇ O 2), leading to more rapid fatigue. 7. 7. The ventilatory compensation for the metabolic acidemia at these work rates is slow, with compensation being poor for rapid-incremental exercise. 8. 8. A justifiable control model of the coupling of ventilation to metabolism must cohere with these demonstrable physiological characteristics.
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