总觉得，这句话理解的不对

Expiration against a pressure of up to 1 kPa (10 cmH2O) does not usually result in activation of the expiratory muscles in conscious or anaesthetized subjects. The additional work to overcome this resistance is, in fact, performed by the inspiratory muscles. The subject augments his inspiratory force until he achieves a lung volume (i.e., FRC) at which the additional elastic recoil is sufficient to overcome the expiratory resistance (Fig. 3.11). The mechanism for resetting the FRC at a higher level probably requires accommodation of the intrafusal fibres of the spindles to allow for an altered length of diaphragmatic muscle fibres because of the obstructed expiration. This would reset the developed inspiratory tension in accord with the increased FRC. The conscious subject normally uses his expiratory muscles to overcome expiratory pressures in excess of about 1 kPa (10 cmH2O).

清醒或麻醉状态下，≦1 kPa（10 cmH₂O）的呼气阻力通常不激活呼气肌。事实上，是由吸气肌来克服这种额外呼气阻力。受试者增大吸气努力，直到（新的、增大的）肺容积（即FRC）增大的弹性回缩力足以克服呼气阻力（图3.11）。增大的FRC需要更大的吸气力量。为能在呼气气流受阻时改变膈肌纤维长度（即增加吸气力量），将FRC重置到较高水平可能包括调节肌梭内纤维的机制。清醒的受试者通常只在呼气阻力＞1 kPa（10 cmH₂O）时才激活呼气肌。

​Spirogram showing the response of an anaesthetized patient to the sudden imposition of an expiratory resistance. Note that there is an immediate augmentation of the force of contraction of the inspiratory muscles. This continues with successive breaths until the elastic recoil is sufficient to overcome the expiratory resistance. (From Nunn JF, Ezi-Ashi TI. The respiratory effects of resistance to breathing in anaesthetised man. Anesthesiology. 1961;22:174-185.)

麻醉患者呼气阻力突然增加时代偿反应的肺量图。注意吸气肌收缩力立即增强，在弹性回缩力足以克服呼气阻力之前，呼吸连续增强。

Patients show a remarkable capacity to compensate for acutely increased resistance, such that arterial Pco2 is usually normal. However, the efficiency of these mechanisms in maintaining alveolar ventilation carries severe physiological consequences. In common with other muscles, the respiratory muscles can become fatigued, which is a major factor in the onset of respiratory failure. A raised Pco2 in a patient with increased respiratory resistance is therefore always serious. Also, intrathoracic pressure will rise during acutely increased expiratory resistance, and so impede venous return and reduce cardiac output (page 390) to the point that syncope may occur.

患者代偿急剧增加阻力的能力显著，因此动脉PCO₂多正常。但该机制在有效维持肺泡通气同时也可带来严重生理后果。与其他肌肉一样，呼吸肌也会疲劳，这是呼吸衰竭的主要原因之一。因此，呼吸阻力增加的患者CO₂分压升高通常很显著。此外，当呼气阻力急剧增加时，胸腔内压也会升高，从而使静脉回流受阻和心排血量减少，甚至出现晕厥（见第390页）。

总觉得，这句话理解的不对

是否这么理解：无论如何，该机制在维持肺泡通气效率方面具有重要意义？