The pressure generated at 0.1 s after the onset of expiration measures the rate of rise of expiratory pressure potentially available for expiration. P0.1e increased with increasing the frequency of breathing and was higher in chronic obstructive pulmonary disease (COPD) patients than in controls. In normal subjects breathing under resistive load P0.1e became similar to that of patients for a given respiratory frequency. P0.1e consistently increased as the load and/or the frequency of breathing were raised. Expiratory pressure depends on elastic recoil of the respiratory system, nevertheless the action of neurally controlled respiratory muscles influence the rate of rise of expiratory pressure. The decrease of expiratory braking action by inspiratory muscles (-Pmusi) influence the rate of pressure rise in the first part of expiration, whereas the contraction of abdominal muscles (-Pmuse) increases P0.1e later from onset of expiratory occlusion. These compensatory reflexes are vagally mediated and are presumed to originate in stretch receptors. In COPD patients the braking action of inspiratory muscles was smaller and the facilitating action of abdominal muscles was higher than in controls. Both expiratory braking decay and expiratory activity increase with the rise of breathing frequency or with the increase of respiratory airflow resistance
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