Ventilation, EELV and diaphragmatic activity in rats during the early phase of normobaric hypoxia

We tested whether the enhancement of end-expiratory activity of the diaphragm (De) induced by acute hypoxia persists during long-lasting hypoxia and participates in the enlargement of end-expiratory lung volume (EELV). We thus measured these two parameters together with ventilation ($\text{V}\text{̇}\text{E}$) in 30 rats, either awake or anesthetized, exposed to (1) poikilocapnic hypoxia sustained for 2 or 3 h; or (2) chronic normobaric hypoxia for 7 days interrupted by short episodes of normoxia. Twelve control animals were also studied. (1) Sustained hypoxia induced a stable increase in De, Ve and EELV. (2) In awake rats, chronic hypoxia induced a transient increase in Ve after 1 day of hypoxia, and an increase persisting during acute normoxia throughout the exposure. De followed the same, although less pronounced, course as Ve. In anesthetized animals, only EELV was increased in both chronic hypoxia and acute normoxia, but its enlargement in normoxia was not associated with a concomitant increase in De. The transition from hypoxia to normoxia always induced a decrease in De and EELV. Therefore, (1) during hypoxia sustained for 2 or 3 h, the ventilatory and diaphragmatic responses were stable; (2) during chronic hypoxia lasting 1 week, a ventilatory acclimatization was expressed by a transient increase in hypoxic Ve and a hyperventilation continuing during acute normoxia; (3) EELV enlargement in chronic hypoxia was partly related to changes in De and partly due to another mechanism possibly involving morphological adaptations.