Spengler C M, Banzett R B, Systrom D M, Shannon D C, Shea S A
Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA.
Respir Physiol. 1998 Oct;114(1):65-74. doi: 10.1016/s0034-5687(98)00073-5.
Breathlessness arises from increased medullary respiratory center activity projecting to the forebrain (respiratory corollary discharge hypothesis). Subjects with congenital central hypoventilation syndrome (CCHS) lack the normal hyperpnea and breathlessness during hypercapnia. The corollary discharge hypothesis predicts that if CCHS subjects have normal hyperpnea during exercise, they will experience normal breathlessness during exercise. To test this, we studied four CCHS subjects and six matched controls during an exhausting constant-load cycling test requiring substantial anaerobiosis. CCHS subjects rated significantly less breathlessness at the end of the test than controls, but ventilation (index of respiratory corollary discharge) was also somewhat lower in CCHS (not significant). In both groups, breathlessness increased disproportionately more than ventilation towards the end of exercise. These data failed to disprove the corollary discharge hypothesis of breathlessness, but do suggest that the relationship between ventilation and breathlessness is non-linear and/or that projections of chemoreceptor afferents to the forebrain (presumed lacking in CCHS) is one source of breathlessness in normals.
呼吸急促源于延髓呼吸中枢活动增强并投射至前脑（呼吸伴随放电假说）。先天性中枢性低通气综合征（CCHS）患者在高碳酸血症时缺乏正常的呼吸增强和呼吸急促。伴随放电假说预测，如果CCHS患者在运动时呼吸增强正常，那么他们在运动时会经历正常的呼吸急促。为了验证这一点，我们在一项需要大量无氧代谢的力竭性恒负荷自行车测试中研究了4名CCHS患者和6名匹配的对照组。测试结束时，CCHS患者的呼吸急促评分显著低于对照组，但CCHS患者的通气量（呼吸伴随放电指标）也略低（无统计学意义）。在两组中，运动接近尾声时，呼吸急促的增加幅度比通气量的增加幅度更大。这些数据未能反驳呼吸急促的伴随放电假说，但确实表明通气与呼吸急促之间的关系是非线性的，和/或化学感受器传入纤维向前脑的投射（推测CCHS患者缺乏这种投射）是正常人呼吸急促的一个来源。
