Abstract

Using 6 chronically instrumented awake dogs, we constrasted the ventilatory and respiratory muscle EMG responses to steady-state normoxic hypercapnia with those occurring at similar levels of ventilation during steady-state treadmill exercise. During hypercapnia, increases in ventilatory output were primarily due to increments in Vt whereas during exercise, increases in minute ventilation were due primarily to increases in frequency. With either hypernea, augmentation of both inspiratory and expiratory muscle EMG activity occured but only diaphragmatic EMG activity was strongly correlated with tidal volume changes in both conditions. Using both EMGs and thoraco-abdominal pressures, we found that with increasing chemical or locomotory stimuli, during inspiration (1) diaphragmatic EMG activation occurred sooner relative to the onset of mechanical flow and (2) that respiratory muscles other than the diaphragm contributed significantly to the generation of inspiratory flow and Vt either actively or passively through recoil. Post-inspiratory activity of the crural diaphragm shortened relative to control in hypercapnia but did not change in exercise. Finally, during mild hyperpneas, end-expiratory lung volume did not change significantly in either hypercapnia or exercise but decreased at the higher levels of hyperpnea only during exercise. This may reflect differences not in the magnitude of phasic expiratory muscle activity, but rather in the degree of tonic abdominal muscle activation between the two conditions.

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