首页> 外文期刊>The Journal of Physiology >Increased fatigue resistance linked to Ca2+-stimulated mitochondrial biogenesis in muscle fibres of cold-acclimated mice.
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Increased fatigue resistance linked to Ca2+-stimulated mitochondrial biogenesis in muscle fibres of cold-acclimated mice.

机译:与冷适应小鼠的肌肉纤维中Ca2 +刺激的线粒体生物发生有关的增强的抗疲劳性。

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Mammals exposed to a cold environment initially generate heat by repetitive muscle activity (shivering). Shivering is successively replaced by the recruitment of uncoupling protein-1 (UCP1)-dependent heat production in brown adipose tissue. Interestingly, adaptations observed in skeletal muscles of cold-exposed animals are similar to those observed with endurance training. We hypothesized that increased myoplasmic free [Ca2+] ([Ca2+]i) is important for these adaptations. To test this hypothesis, experiments were performed on flexor digitorum brevis (FDB) muscles, which do not participate in the shivering response, of adult wild-type (WT) and UCP1-ablated (UCP1-KO) mice kept either at room temperature (24 degrees C) or cold-acclimated (4 degrees C) for 4-5 weeks. [Ca2+]i (measured with indo-1) and force were measured under control conditions and during fatigue induced by repeated tetanic stimulation in intact single fibres. The results show no differences between fibres from WT and UCP1-KO mice. However, muscle fibres from cold-acclimated mice showed significant increases in basal [Ca2+]i ( approximately 50%), tetanic [Ca2+]i ( approximately 40%), and sarcoplasmic reticulum (SR) Ca2+ leak ( approximately fourfold) as compared to fibres from room-temperature mice. Muscles of cold-acclimated mice showed increased expression of peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) and increased citrate synthase activity (reflecting increased mitochondrial content). Fibres of cold-acclimated mice were more fatigue resistant with higher tetanic [Ca2+]i and less force loss during fatiguing stimulation. In conclusion, cold exposure induces changes in FDB muscles similar to those observed with endurance training and we propose that increased [Ca2+]i is a key factor underlying these adaptations.
机译:暴露在寒冷环境中的哺乳动物最初会通过重复的肌肉活动(发抖)产生热量。颤抖逐渐被棕色脂肪组织中依赖于解偶联蛋白1(UCP1)的热量产生所取代。有趣的是,在冷暴露的动物的骨骼肌中观察到的适应性与耐力训练中观察到的相似。我们假设增加的肌质游离[Ca2 +]([Ca2 +] i)对于这些适应很重要。为了验证这一假设,我们对成年野生型(WT)和UCP1消融(UCP1-KO)小鼠均保持在室温下,不参与发抖反应的屈指短屈(FDB)肌肉进行了实验( 24摄氏度)或冷适应(4摄氏度)持续4-5周。 [Ca2 +] i(用indo-1测得)和力在对照条件下以及在完整的单根纤维中反复进行破伤风刺激引起的疲劳过程中进行了测量。结果显示WT和UCP1-KO小鼠的纤维之间没有差异。但是,与经过冷驯化的小鼠相比,肌纤维的基础[Ca2 +] i(约50%),破伤风[Ca2 +] i(约40%)和肌浆网(SR)Ca2 +泄漏显着增加(约四倍)室温小鼠的纤维。冷适应小鼠的肌肉显示过氧化物酶体增殖物激活的受体-γ共激活因子-1alpha(PGC-1alpha)的表达增加,柠檬酸合酶活性增加(反映线粒体含量增加)。冷适应小鼠的纤维在疲劳刺激期间具有更高的破伤风[Ca2 +] i和更低的力损失,从而更耐疲劳。总之,冷暴露会引起FDB肌肉的变化,类似于耐力训练中观察到的变化,因此我们认为增加的[Ca2 +] i是导致这些适应的关键因素。

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