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Mechanical factors in the initiation of eccentric contraction-induced injury in rat soleus muscle.

机译:引发大鼠比目鱼肌离心收缩损伤的机械因素。

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摘要

1. Mechanical factor(s) associated with the initiation of eccentric contraction-induced muscle injury were investigated in isolated rat soleus muscles (n = 180; 42 protocols with 4-6 muscles per protocol). Five eccentric contractions were performed with 4 min between contractions. Three levels of peak eccentric contraction force (100, 125 and 150% of pre-injury maximal isometric tetanic tension, P0), length change (0.1, 0.2 and 0.3 muscle length, L0) and lengthening velocity (0.5, 1.0 and 1.5 L0/s) were utilized. Force was varied with stimulation frequency (10-150 Hz). The eccentric contractions were initiated at muscle lengths of 0.85 or 0.90 L0. Following the fifth eccentric contraction, the muscle was incubated in Krebs-Ringer buffer for 60 min. Peak isometric twitch tension (PT), P0, maximal rate of tension development (+ dP/dt), maximal rate of relaxation (-dP/dt), and creatine kinase (CK) release were measured prior to the five eccentric contractions and at 15 min intervals during the incubation period. Total muscle [Ca2+] was measured after 60 min incubation. 2. The mean (+/- S.E.M.) initial decline in P0 for the muscles performing the most injurious protocol was 13.6 +/- 4.8% (n = 6); P0 in control muscles immediately following performance of five isometric contractions was elevated 1.2 +/- 1.0% (n = 8). These means were different at probability, p = 0.005. Mean [ATP] in muscles immediately following the isometric control and most injurious protocols, respectively, were 16.30 +/- 1.49 and 19.84 +/- 1.38 mumol/g dry wt (p = 0.229). 3. Decrements in P0, PT, +dP/dt, and -dP/dt immediately after the injury protocol were related most closely to the peak forces produced during the eccentric contractions; greater initial declines in P0, +dP/dt and -dP/dt were also observed at higher lengthening velocities independent of peak force. Slow declines in P0 and -dP/dt during the 60 min incubation following the injury protocol were greatest for muscles performing contractions at the longer initial length. CK release was independent of all mechanical factors with the exception of lengthening velocity. CK activity at 45 and 60 min into the incubation period was greater for muscles lengthened at the highest velocity used (1.5 L0/s). Mean total muscle [Ca2+] for muscles performing the eccentric contractions was elevated by 38% over isometric control muscles but the elevation was unrelated to any of the four mechanical factors. 4. These data support the hypothesis that eccentric contraction-induced injury is initiated by mechanical factors, with muscle tension playing the dominant role.(ABSTRACT TRUNCATED AT 400 WORDS)
机译:1.在离体的大鼠比目鱼肌中研究了与偏心收缩引起的肌肉损伤的开始相关的机械因素(n = 180; 42个实验方案,每个实验方案4-6块肌肉)。进行五次离心收缩,每次收缩间隔4分钟。三种水平的峰值偏心收缩力(损伤前最大等距张紧度P0的100%,125%和150%),长度变化(肌肉长度L0分别为0.1、0.2和0.3)和延伸速度(0.5、1.0和1.5 L0 / s)被利用。力随刺激频率(10-150 Hz)变化。离心收缩始于0.85或0.90 L0的肌肉长度。第五次离心收缩后,将肌肉在克雷布斯-林格氏缓冲液中孵育60分钟。在五次离心收缩之前和在5分钟时测量峰值等距抽搐张力(PT),P0,最大张力产生率(+ dP / dt),最大松弛率(-dP / dt)和肌酸激酶(CK)释放。孵育期间间隔15分钟。孵育60分钟后,测量总肌肉[Ca2 +]。 2.进行最有害实验的肌肉的P0平均初始(+/- S.E.M.)下降为13.6 +/- 4.8%(n = 6);紧接执行五次等距收缩后,对照肌肉中的P0升高了1.2 +/- 1.0%(n = 8)。这些均值的概率不同,p = 0.005。紧接等距对照和大多数伤害性治疗方案后,肌肉中的平均[ATP]分别为16.30 +/- 1.49和19.84 +/- 1.38 mumol / g干重(p = 0.229)。 3.受伤后立即降低P0,PT,+ dP / dt和-dP / dt与离心收缩过程中产生的峰值力密切相关;在较高的加长速度下(与峰值力无关),还观察到了P0,+ dP / dt和-dP / dt更大的初始下降。在损伤方案之后的60分钟孵育过程中,P0和-dP / dt的缓慢下降对于在较长的初始长度执行收缩的肌肉最大。 CK的释放与所有机械因素无关,除了延长速度。在以所使用的最高速度(1.5 L0 / s)加长的肌肉中,潜伏期为45和60分钟的CK活性较高。与等轴测对照肌肉相比,进行偏心收缩的肌肉的平均总肌肉[Ca2 +]升高了38%,但升高与四个机械因素中的任何一个都不相关。 4.这些数据支持以下假设,即偏心收缩引起的损伤是由机械因素引起的,其中肌肉张力起主要作用。(摘要截断为400个字)

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