Edelman N H, Santiago T V, Conn H L
J Appl Physiol. 1975 Nov;39(5):857-9. doi: 10.1152/jappl.1975.39.5.857.
The oxygen cost of exercise and chemical control of breathing were studied in a subject with Luft's syndrome, a disorder in which skeletal muscle mitochondria have a high "resting" O2 consumption which is imcreased only slightly by stimulation with excess phosphate acceptor, but a normal P/O ratio. The O2 consumption was more than three times normal (1.05 1/min) at rest but could be doubled when stimulated by maximal exercise. The O2 cost of exercise was similar to that of normal subjects. At rest, arterial blood PCO2 and ventilatory response to CO2 were normal, while ventilatory response to hypoxia was four times the predicted value. The data 1) confirm, in vivo, the normal respiratory efficiency of skeletal muscles in this disorder; 2) suggest that in vitro estimates of the extent to which mitochondrial respiration can be stimulated may not correlate with in vivo determinations; and 3) suggests that hypermetabolism per se can cause the ventilatory adjustments which are associated with exercise in normal subjects.
在一名患有 Luft 综合征的受试者中，研究了运动的氧耗和呼吸的化学控制。Luft 综合征是一种疾病，其骨骼肌线粒体具有较高的“静息”氧消耗，仅通过过量磷酸受体刺激时略有增加，但磷氧比正常。静息时氧消耗超过正常的三倍（1.05升/分钟），但在最大运动刺激下可增加一倍。运动的氧耗与正常受试者相似。静息时，动脉血二氧化碳分压和对二氧化碳的通气反应正常，而对缺氧的通气反应是预测值的四倍。这些数据：1）在体内证实了该疾病中骨骼肌正常的呼吸效率；2）表明体外对线粒体呼吸可被刺激程度的估计可能与体内测定不相关；3）表明高代谢本身可导致与正常受试者运动相关的通气调节。
