Division of Endocrinology, Diabetology, and Metabolism, Department of Internal Medicine, University of Turin, 10126 Turin, Italy.
J Clin Endocrinol Metab. 2010 Apr;95(4):1663-71. doi: 10.1210/jc.2009-2161. Epub 2010 Feb 5.
Glucocorticoids are known to decrease protein synthesis and impair membrane excitability of muscle fibers. However, their short-term effects on muscle structure and function of healthy subjects remain poorly understood.
Our objective was to investigate whether steroid administration could decrease the circulating levels of muscle proteins and modify myoelectric indexes of sarcolemmal excitability and fatigability.
We conducted a single-blind, placebo-controlled study in 20 men randomized to receive dexamethasone (8 mg/d) or placebo for 1 wk. Blood sampling, force measurements for knee extensors and elbow flexors, and electrophysiological tests for biceps brachii, vastus lateralis and medialis, and tibialis anterior muscles were performed before and after the intervention.
Dexamethasone administration improved force by 6.0 +/- 6.0% (P = 0.01) for elbow flexors and by 8.5 +/- 5.5% (P < 0.01) for knee extensors, decreased levels of creatine kinase by 50.5 +/- 30.0% (P < 0.01) and myoglobin by 41.8 +/- 17.5% (P < 0.01), and impaired sarcolemmal excitability, as shown by the decline of muscle fiber conduction velocity for the four muscles (range from -6 to -10.5%, P < 0.05). Moreover, significant reductions of the myoelectric manifestations of fatigue were observed for the four muscles; the decrease in the rate of change of the mean frequency of the electromyographic power spectrum ranged from -22.6 to -43.9% (P < 0.05). In contrast, no significant changes were observed in muscle excitability and fatigability in subjects who received the placebo.
The demonstration that glucocorticoid-induced muscle impairments can be unraveled by means of blood sampling and noninvasive electrophysiological tests has clinical implications for the early identification of subclinical or preclinical forms of myopathy in treated patients.
已知糖皮质激素可降低蛋白质合成并损害肌纤维的膜兴奋性。然而,它们对健康受试者的肌肉结构和功能的短期影响仍知之甚少。
我们的目的是研究类固醇给药是否会降低循环肌肉蛋白水平,并改变肌细胞膜兴奋性和疲劳性的肌电图指标。
我们在 20 名男性中进行了一项单盲、安慰剂对照研究,这些男性随机接受地塞米松(8mg/d)或安慰剂治疗 1 周。在干预前后,对股四头肌和肱二头肌、股外侧肌和股内侧肌、胫骨前肌进行了血液采样、力测量和肌电图测试。
地塞米松给药使肱二头肌的力提高了 6.0±6.0%(P=0.01),股四头肌的力提高了 8.5±5.5%(P<0.01),肌酸激酶水平降低了 50.5±30.0%(P<0.01),肌红蛋白水平降低了 41.8±17.5%(P<0.01),并损害了肌细胞膜兴奋性,表现为四头肌的肌纤维传导速度下降(-6 至-10.5%,P<0.05)。此外,还观察到四头肌的疲劳肌电表现明显减少;肌电图功率谱的平均频率变化率下降了 22.6-43.9%(P<0.05)。相比之下,接受安慰剂的受试者的肌肉兴奋性和疲劳性没有明显变化。
证明糖皮质激素引起的肌肉损伤可以通过血液采样和非侵入性电生理测试来揭示,这对早期识别治疗患者的亚临床或临床前形式的肌病具有临床意义。