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在不同细胞外氧分压下疲劳的非洲爪蟾单根肌纤维中钙(Ca²⁺)释放的损伤

Impairment of Ca(2+) release in single Xenopus muscle fibers fatigued at varied extracellular PO(2).

作者信息

Stary C M, Hogan M C

机构信息

Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623, USA.

出版信息

J Appl Physiol (1985). 2000 May;88(5):1743-8. doi: 10.1152/jappl.2000.88.5.1743.

DOI:10.1152/jappl.2000.88.5.1743
PMID:10797138
Abstract

We tested the hypothesis that the mechanisms involved in the more rapid onset of fatigue when O(2) availability is reduced in contracting skeletal muscle are similar to those when O(2) availability is more sufficient. Two series of experiments were performed in isolated, single skeletal muscle fibers from Xenopus laevis. First, relative force and free cytosolic Ca(2+) concentrations (Ca(2+)) were measured simultaneously in single fibers (n = 6) stimulated at increasing frequencies (0.25, 0.33, 0.5, and 1 Hz) at an extracellular PO(2) of either 22 or 159 Torr. Muscle fatigue (force = 50% of initial peak tension) occurred significantly sooner (P < 0.05) during the low- (237 +/- 40 s) vs. high-PO(2) treatments (280 +/- 38 s). Relative Ca(2+) was significantly decreased from maximal values at the fatigue time point during both the high- (72 +/- 4%) and low-PO(2) conditions (78 +/- 4%), but no significant difference was observed between the treatments. In the second series of experiments, using the same stimulation regime as the first, fibers (n = 6) exposed to 5 mM caffeine immediately after fatigue demonstrated an immediate but incomplete relative force recovery during both the low- (89 +/- 4%) and high-PO(2) treatments (82 +/- 3%), with no significant difference between treatments. Additionally, there was no significant difference in relative Ca(2+) between the high- (100 +/- 12% of prefatigue values) and low-PO(2) treatments (108 +/- 12%) on application of caffeine. These results suggest that in isolated, single skeletal muscle fibers, the earlier onset of fatigue that occurred during the low-extracellular PO(2) condition was modulated through similar pathways as the fatigue process during the high and involved a decrease in relative peak Ca(2+).

摘要

我们验证了这样一个假设

当收缩的骨骼肌中氧气供应减少时,疲劳更快发作所涉及的机制与氧气供应更充足时的机制相似。在来自非洲爪蟾的分离单根骨骼肌纤维上进行了两组实验。首先,在细胞外氧分压为22或159托的条件下,以递增频率(0.25、0.33、0.5和1赫兹)刺激单根纤维(n = 6),同时测量相对力和游离胞质钙浓度([Ca²⁺]c)。在低氧分压(237 ± 40秒)处理期间,肌肉疲劳(力 = 初始峰值张力的50%)明显比高氧分压处理(280 ± 38秒)更早出现(P < 0.05)。在高氧分压(72 ± 4%)和低氧分压条件(78 ± 4%)下,相对[Ca²⁺]c在疲劳时间点均从最大值显著降低,但处理之间未观察到显著差异。在第二组实验中,使用与第一组相同的刺激方案,疲劳后立即暴露于5 mM咖啡因的纤维(n = 6)在低氧分压(89 ± 4%)和高氧分压处理(82 ± 3%)期间均表现出立即但不完全的相对力恢复,处理之间无显著差异。此外,施加咖啡因后,高氧分压(疲劳前值的100 ± 12%)和低氧分压处理(108 ± 12%)之间的相对[Ca²⁺]c无显著差异。这些结果表明,在分离的单根骨骼肌纤维中,低细胞外氧分压条件下更早出现的疲劳是通过与高氧分压期间疲劳过程相似的途径调节的,并且涉及相对峰值[Ca²⁺]c的降低。

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