De Ruiter C J, Wevers R A, Van Engelen B G, Verdijk P W, De Haan A
Institute for Fundamental and Clinical Human Movement Sciences, Vrije Universiteit, Amsterdam, The Netherlands.
Muscle Nerve. 1999 Jun;22(6):704-11. doi: 10.1002/(sici)1097-4598(199906)22:6<704::aid-mus6>3.0.co;2-z.
Adductor pollicis muscle function of a 21-year-old man with genetically confirmed Brody's disease (sarcoplasmic reticulum [SR] -Ca2+ATPase deficiency) was investigated to study the possible effects of reduced SR-Ca2+ATPase activity on muscle relaxation and force production. Following maximal electrical activation of the ulnar nerve, tetanic muscle half-relaxation time was greater in the patient (246 +/- 10 ms) than control subjects (97 +/- 4 ms, n = 8). During repetitive activation, there was a similar decline in maximal shortening velocity in the patient and controls, indicating a comparable reduction in cross-bridge cycling rate. The finding that the slowing of relaxation was greater in the patient (329 ms versus 138 +/- 20 ms) suggests that there was a further reduction of SR-Ca2+ATPase activity in the patient's muscle during fatigue. Following a voluntary contraction, involuntary activity of the antagonist muscles facilitated force decline and masked the impaired relaxation in the patient. This antagonist-induced relaxation indicates that it might be difficult to establish impaired muscle relaxation with voluntary contractions.
对一名经基因确诊患有布罗迪病（肌浆网[SR]-Ca2+ATP酶缺乏症）的21岁男性的拇内收肌功能进行了研究，以探讨SR-Ca2+ATP酶活性降低对肌肉舒张和力量产生的可能影响。在尺神经进行最大程度的电刺激后，患者的强直肌半舒张时间（246±10毫秒）比对照组受试者（97±4毫秒，n=8）更长。在重复刺激过程中，患者和对照组的最大缩短速度出现了类似程度的下降，表明横桥循环速率有类似程度的降低。患者的舒张减慢更为明显（329毫秒对138±20毫秒），这一发现表明患者肌肉在疲劳时SR-Ca2+ATP酶活性进一步降低。在一次随意收缩后，拮抗肌的非随意活动促进了力量下降，并掩盖了患者受损的舒张功能。这种拮抗肌诱导的舒张表明，通过随意收缩可能难以确定肌肉舒张功能受损。
