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横纹肌中疲劳与缩短诱导的失活

Fatigue vs. shortening-induced deactivation in striated muscle.

作者信息

Edman K A

机构信息

Department of Pharmacology, University of Lund, Sweden.

出版信息

Acta Physiol Scand. 1996 Mar;156(3):183-92. doi: 10.1046/j.1365-201X.1996.t01-1-198000.x.

DOI:10.1046/j.1365-201X.1996.t01-1-198000.x
PMID:8729678
Abstract

Fatigue and shortening-induced deactivation, two conditions that both lead to reversible depression of the mechanical performance of striated muscle are briefly reviewed. Fatigue. Isolated fibres from frog skeletal muscle (1-3 degrees C) that are stimulated to produce a 1 s fused tetanus at 15 s intervals are brought into a state of myofibrillar fatigue, (tetanic force reduced to 70-75% of the control) that is attributable to reduced performance of the myofibrils with no significant change in activation of the contractile system. A more intense stimulation programme (a single stimulus applied at 1-2 s intervals) reduces the tetanic force below 70% of the rested-state level. Under these conditions, failure of activation becomes increasingly important as a cause of the force decline. Deficient inward spread of activation is likely to account for at least part of the force decline after a period of intense fatiguing stimulation. Shortening-induced deactivation. Striated muscle that is allowed to shorten during activity loses some of its capacity to produce force, full restoration of the contractile strength being attained 1-2 s after the shortening phase. The depressant effect of shortening is demonstrable in skinned preparations as well as in intact muscle fibres and the magnitude of the effect is dependent on the state of activation of the muscle fibre when the movement occurs. The experimental evidence supports the view that sliding of the thick and thin filaments during activity reduces the affinity for calcium at the regulatory sites on the thin filament, leading to a transitory deactivation of the contractile system.

摘要

简要回顾了疲劳和缩短诱导的失活,这两种情况都会导致横纹肌机械性能的可逆性降低。疲劳。将来自青蛙骨骼肌(1-3摄氏度)的分离纤维以15秒的间隔刺激产生1秒的强直收缩,会使其进入肌原纤维疲劳状态(强直力降至对照的70-75%),这归因于肌原纤维性能的降低,而收缩系统的激活没有显著变化。更强烈的刺激方案(以1-2秒的间隔施加单个刺激)会使强直力降至静息状态水平的70%以下。在这些情况下,激活失败作为力下降的原因变得越来越重要。激活的内向传播不足可能至少部分解释了一段时间的强烈疲劳刺激后的力下降。缩短诱导的失活。在活动期间允许缩短的横纹肌会失去一些产生力的能力,在缩短阶段后1-2秒收缩强度可完全恢复。缩短的抑制作用在去膜制剂以及完整的肌纤维中都可得到证明,其作用程度取决于运动发生时肌纤维的激活状态。实验证据支持这样一种观点,即在活动期间粗肌丝和细肌丝的滑动会降低细肌丝上调节位点对钙的亲和力,导致收缩系统的暂时失活。

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