Cardiorespiratory plasticity in humans following two patterns of acute intermittent hypoxia.

Peripheral respiratory chemoreceptors monitor breath-by-breath changes in arterial CO2 and O2 , and mediate ventilatory changes to maintain homeostasis. Intermittent hypoxia (IHx) elicits hypoxic ventilatory responses, with well-described experience-dependent effects (EDEs), derived mostly from animal work involving intermittent 5-min cycles of hypoxia and normoxia. These EDEs include post-hypoxia frequency decline (PHxFD), progressive augmentation (PA) and long-term facilitation (LTF). Comparisons of these EDEs between animal models and humans using similar IHx protocols are lacking. In addition, it is unknown whether shorter bouts of hypoxia, which may be more relevant to clinical conditions, elicit EDEs of similar magnitudes in humans. Respiratory (frequency, tidal volume and minute ventilation ( V ̇ I ) and cardiovascular (heart rate and mean arterial pressure (MAP)) variables were measured during and following two patterns of acute isocapnic IHx in 14 healthy human participants (four female): (1) 5 × 5 min and (2) 5 × 90 s on/off hypoxia. Participants' end-tidal P O 2 was clamped at 45 Torr during hypoxia and 100 Torr during normoxia. We found that (1) PHxFD and PA were not present in either IHx pattern (P > 0.14), (2) LTF was present in V ̇ I following both 5-min (P < 0.001) and 90-s isocapnic IHx trials (P < 0.001), and (3) LTF was present in MAP following 5-min isocapnic IHx (P < 0.001), and trended towards significance following 90-s IHx (P = 0.058). We demonstrate that acute isocapnic IHx alone may not elicit all of the EDEs that have been described in animal models. Additionally, ventilatory LTF occurred regardless of the length of hypoxia-normoxia cycles.