In vivo Ca2+ dynamics during cooling after eccentric contractions in rat skeletal muscle.
In vivo Ca2+ dynamics during cooling after eccentric contractions in rat skeletal muscle.
复制标题
大鼠骨骼肌离心收缩后冷却过程中的体内 Ca2 动力学。
DOI：
10.1152/ajpregu.00253.2020
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Kano Y.
中科院分区：
文献类型：
--
作者：
Takagi R;Tabuchi A;Asamura T;Hirayama S;Ikegami R;Tanaka Y;Hoshino D;Poole DC;Kano Y.
冷却对偏心收缩（ECs）后体内细胞内钙离子浓度[Ca2+]的影响仍有待确定。我们验证了这样一个假设，即ECs后的冷冻治疗促进了[Ca2+]的增加，并在具有大量IIb和IIx纤维群的两块肌肉中诱导了更大的肌肉损伤。Wistar大鼠的薄斜方棘肌（SPINO）用于体内[Ca2+]成像，胫骨前肌（TA）提供了更高的保真度和可重复性的收缩功能测量。SPINO [Ca2+]是用fura 2-AM估计的，[Ca2+]的大小、位置和时间分布是在ecs后肌肉表面附近的温度从30°C（对照）降低到20°C或10°C时确定的。随后，在TA中，在ECs后1天和2天测定ECs后冷却至10°C对肌肉收缩性能的影响。采用苏木精和伊红染色检测TA肌肉样本的损伤程度。在SPINO中，ECs后将肌肉温度从30°C降低到10°C，导致ECs产生的高[Ca2+]离子的扩散增加3.7倍（P< 0.05）。当重新加热到30°C时，这些高[Ca2+]含量表现出部分可逆性。丹trolene，一种ryanodine受体Ca2+释放抑制剂，在10°C时减少了高[Ca2+]位点的存在。在TA组，冷却通过增强肌纤维损伤加重了ecs诱导的肌力缺陷（P< 0.05）。通过证明冷却后的ecs增强了[Ca2+]的变化，这种体内方法支持了运动后冷冻疗法如何增加肌肉纤维损伤和降低随后的运动表现的假设机制基础。
The effect of cooling on in vivo intracellular calcium ion concentration [Ca2+]iafter eccentric contractions (ECs) remains to be determined. We tested the hypothesis that cryotherapy following ECs promotes an increased [Ca2+]iand induces greater muscle damage in two muscles with substantial IIb and IIx fiber populations. The thin spinotrapezius (SPINO) muscles of Wistar rats were used for in vivo [Ca2+]iimaging, and tibialis anterior (TA) muscles provided greater fidelity and repeatability of contractile function measurements. SPINO [Ca2+]iwas estimated using fura 2-AM and the magnitude, location, and temporal profile of [Ca2+]idetermined as the temperature near the muscle surface post-ECs was decreased from 30°C (control) to 20°C or 10°C. Subsequently, in the TA, the effect of post-ECs cooling to 10°C on muscle contractile performance was determined at 1 and 2 days after ECs. TA muscle samples were examined by hematoxylin and eosin staining to assess damage. In SPINO, reducing the muscle temperature from 30°C to 10°C post-ECs resulted in a 3.7-fold increase in the spread of high [Ca2+]isites generated by ECs (P< 0.05). These high [Ca2+]isites demonstrated partial reversibility when rewarmed to 30°C. Dantrolene, a ryanodine receptor Ca2+release inhibitor, reduced the presence of high [Ca2+] sites at 10°C. In the TA, cooling exacerbated ECs-induced muscle strength deficits via enhanced muscle fiber damage (P< 0.05). By demonstrating that cooling post-ECs potentiates [Ca2+]iderangements, this in vivo approach supports a putative mechanistic basis for how postexercise cryotherapy might augment muscle fiber damage and decrease subsequent exercise performance.
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