EFFECT OF CHRONIC HYPOXIA ON BREATHING AND EMGS OF RESPIRATORY MUSCLES IN AWAKE PONIES

Breathing, diaphragmatic and transversus abdominis electromyograms (EMGdi and EMGta, respectively), and arterial blood gases were studied during normoxia (arterial PO2 = 95 Torr) and 48 h of hypoxia (arterial PO2 = 40-50 Torr) in intact (n = 11) and carotid body-denervated (CBD, n = 9) awake ponies. In intact ponies, arterial PCO2 was 7, 5, 9, and 11 Torr below control (P < 0.01) at 1 and 10 min and 5 and 24-48 h of hypoxia, respectively. In CBD ponies, arterial PCO2 was 3-4 Torr below control (P < 0.01) at 4, 5, 6, and 24 h of hypoxia. In intact ponies, pulmonary ventilation, mean inspiratory flow rate, and rate of rise of EMGdi and EMGta changed in a multiphasic fashion during hypoxia; each reached a maximum during the 1st h (P < 0.05), declined between 1 and 5 h (P < 0.05), and increased between 5 and 24-48 h of hypoxia. As a result of the increased drive to the diaphragm, the mean EMGdi was above control throughout hypoxia (P < 0.05). In contrast, as a result of a sustained reduction in duration of the EMGta, the mean EMGta was below control for most of the hypoxic period. In CBD ponies, pulmonary ventilation and mean inspiratory flow rate did not change during chronic hypoxia (P > 0.10). In these ponies, the rate of rise of the EMGdi was less than control (P < 0.05) for most of the hypoxic period, which resulted in the mean EMGdi to also be less than control (P < 0.05). In contrast, rate of rise of the EMGta was above control (P < 0.05) for most of hypoxia, which resulted in the mean EMGta to increase above control (P < 0.05). We conclude that during hypoxia in ponies the carotid chemoreceptors increase respiratory drive, which is attenuated in a time-dependent manner by a central nervous system (CNS) inhibitory mechanism. The paradoxical relationship between respiratory drive and the hyperventilation during much of the hypoxia suggests that a component of the CNS inhibition might be through a depression of metabolic rate. Finally, during chronic hypoxia a CNS mechanism stimulates expiratory muscles, but in normal ponies this effect is masked by carotid chemoreceptor and/or CNS inhibition of these muscles.