Abstract

Breathing is dependent on the coordination of respiratory muscles. The timing and contribution of the respiratory muscles determine the balance between breathing frequency and tidal volume. At rest, the mammalian breathing cycle has three phases: active inspiration (I), expiratory braking (E1) and an expiratory pause (E2). With elevated respiratory drive, expiratory muscles may contract to produce active expiration. This study investigated how respiratory muscles are recruited under hypercapnic and hypoxic conditions. These stimuli modify the breathing response by primarily increasing tidal volume or breathing frequency, respectively. EMG electrodes were placed in the diaphragm, intercostal and abdominal muscles. Anesthetized and unanesthetized rats were then exposed to progressive hypercapnia and hypoxia. Progressive hypercapnia (0% to 10% CO2) induced active expiration at the end of the breathing cycle (E3 phase) at 8% and 10% inspired CO2 in unanesthetized rats. The placement in E3 correlated with an increase in tidal volume. Active expiration was not observed in anesthetized rats, even at the highest level of CO2. Progressive hypoxia (21% to 9% O2) never induced active expiration, in either unanesthetized or anesthetized rats indicating that passive expiration was sufficient even at the highest breathing frequencies. This further suggests that the control mechanisms that coordinate the respiratory muscles during hypercapnia and hypoxia are different and dependent on higher brain centers. Supported by the NSERC of Canada.

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