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大鼠比目鱼肌离心收缩诱导损伤起始中的力学因素

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

作者信息

Warren G L, Hayes D A, Lowe D A, Armstrong R B

机构信息

Muscle Biology Laboratory, University of Georgia, Athens 30602.

出版信息

J Physiol. 1993 May;464:457-75. doi: 10.1113/jphysiol.1993.sp019645.

DOI:10.1113/jphysiol.1993.sp019645
PMID:8229813
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1175396/
Abstract
  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)
摘要
  1. 在离体大鼠比目鱼肌中(n = 180;42个实验方案,每个方案4 - 6块肌肉)研究了与离心收缩诱导的肌肉损伤起始相关的机械因素。进行5次离心收缩,每次收缩间隔4分钟。采用了三种峰值离心收缩力水平(损伤前最大等长强直张力P0的100%、125%和150%)、长度变化(0.1、0.2和0.3肌肉长度L0)以及拉长速度(0.5、1.0和1.5 L0/s)。通过刺激频率(10 - 150 Hz)改变力量。离心收缩在肌肉长度为0.85或0.90 L0时开始。在第5次离心收缩后,将肌肉在 Krebs - Ringer 缓冲液中孵育60分钟。在5次离心收缩前以及孵育期间每隔15分钟测量峰值等长单收缩张力(PT)、P0、最大张力发展速率(+ dP/dt)、最大松弛速率(-dP/dt)以及肌酸激酶(CK)释放。孵育60分钟后测量肌肉总[Ca2+]。2. 执行最具损伤性方案的肌肉,P0的平均(±标准误)初始下降为13.6 ± 4.8%(n = 6);执行5次等长收缩后立即测量,对照肌肉的P0升高了1.2 ± 1.0%(n = 8)。这些平均值在概率p = 0.005时存在差异。等长对照和最具损伤性方案后立即测量,肌肉中的平均[ATP]分别为16.30 ± 1.49和19.84 ± 1.38 μmol/g干重(p = 0.229)。3. 损伤方案后立即出现的P0、PT、+dP/dt和 -dP/dt的下降与离心收缩期间产生的峰值力最密切相关;在较高拉长速度下,无论峰值力如何,P0、+dP/dt和 -dP/dt也出现更大的初始下降。损伤方案后的60分钟孵育期间,P0和 -dP/dt的缓慢下降在初始长度较长时进行收缩的肌肉中最为明显。CK释放与所有机械因素无关,但拉长速度除外。在孵育期45和60分钟时,以最高使用速度(1.5 L0/s)拉长的肌肉的CK活性更高。进行离心收缩的肌肉的平均总肌肉[Ca2+]比等长对照肌肉升高了38%,但这种升高与四个机械因素中的任何一个都无关。4. 这些数据支持这样的假设,即离心收缩诱导的损伤由机械因素引发,肌肉张力起主导作用。(摘要截断于400字)
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/0d3b69a592d8/jphysiol00418-0470-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/e845733816ff/jphysiol00418-0464-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/0e934bb570f0/jphysiol00418-0465-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/aae13f051050/jphysiol00418-0468-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/0d3b69a592d8/jphysiol00418-0470-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/e845733816ff/jphysiol00418-0464-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/0e934bb570f0/jphysiol00418-0465-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/aae13f051050/jphysiol00418-0468-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fb42/1175396/0d3b69a592d8/jphysiol00418-0470-a.jpg

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