Abstract

Exposure to chronic sustained hypoxia in healthy subjects, for example during acclimatization to high altitude, increases ventilation in normoxia and increases the ventilatory response to acute hypoxia or hypercapnia. Laboratory rodents have proved to be a useful model for studying the mechanisms of such ventilatory acclimatization to hypoxia. However, it is not known if all respiratory muscles contribute similarly to increases in ventilatory drive and chemoreflexes with acclimatization. Here we tested the hypothesis that the diaphragm contributes to increases in ventilatory responses to hypoxia and hypercapnia equally before and after acclimatization. Therefore, we measured diaphragm electromyogram activity and related the amplitude of the rectified and integrated signal (EMGdia) to tidal volume (Vt) in rats exposed to one week of sustained hypoxia. We made an abdominal incision in male Sprague‐Dawley rats and implanted a two‐electrode transmitter to telemeter EMG activity from the diaphragm muscle. After recovery, we simultaneously measured ventilation with barometric pressure plethysmography and EMGdia with telemetry in awake, unrestrained rats before and after 7 days of exposure to hypobaric hypoxia (PO2 = 80 Torr). EMGdia positively correlated with Vt when breathing was stimulated by hypoxia, hypercapnia or both, and this relationship was not changed after chronic hypoxia. This shows that ventilatory acclimatization to hypoxia does not change the contribution of the diaphragm to ventilatory drive and chemoreflexes.
 Supported by NIH RO1 HL‐081823.

Full Text
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