Effects of reduced muscle glycogen concentration on force, Ca2+ release and contractile protein function in intact mouse skeletal muscle
Effects of reduced muscle glycogen concentration on force, Ca2+ release and contractile protein function in intact mouse skeletal muscle
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DOI：
10.1113/jphysiol.1997.sp021838
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发表时间：
1997-01-01
影响因子：
5.5
通讯作者：
Allen, DG
中科院分区：
文献类型：
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作者：
Chin, ER;Allen, DG
1.本研究旨在探讨骨骼肌疲劳过程中糖原浓度降低对肌力、钙离子释放和肌原纤维蛋白功能的影响。方法：1.在相同条件下，测定单个哺乳动物骨骼肌纤维在疲劳过程中的受力和细胞内游离钙离子浓度([Ca~(2+)](I))，以及同一肌肉中20~40束纤维的恢复糖原。反复最大强度破伤风诱导疲劳，直至力降至初始的30%。这与肌肉糖原降低到控制值的27+/-6%有关。在5.5 mM葡萄糖存在下恢复60min的纤维(n=6)，强直力(100 Hz)完全恢复，但强直性[Ca~(2+)](I)保持在初始值的82+/-8%。由于肌糖原已恢复到疲劳前的水平(157+/-42%)，这种钙离子释放的长期抑制与肌糖原下降无关。为了检测肌肉糖原浓度降低时的反应，在无葡萄糖的情况下疲劳60min的纤维恢复(n=6)。无糖恢复后，强直力和[Ca~(2+)](I)的下降仅部分逆转(分别降至初始值的+/-8%和57+/-7%)。这些改变与肌肉糖原浓度的持续降低(初始值的27+/-4%)有关。在另一组纤维中，疲劳后给予50赫兹间歇刺激22.6+/-4min。在此方案下，强直力和[Ca~(2+)](I)分别部分恢复到初始水平的76+/-9%和55+/-6%。这些变化与肌糖原的恢复有关(恢复到85+/-10%)。疲劳时，钙敏感性和最大钙激活力(F-max)受到抑制，但当肌糖原恢复后，这些变化被完全逆转。当糖原未恢复时，钙敏感性仍受抑制，但F-max部分恢复。肌原纤维蛋白功能的改变可能是由于无机磷水平的改变或与肌肉糖原水平降低相关的其他代谢物的改变。这些数据表明，在疲劳过程中观察到的力量减少、钙离子释放和收缩蛋白抑制与肌肉糖原浓度的降低密切相关。这些发现还表明，与疲劳和恢复相关的钙释放的变化有两个组成部分-一个是糖原依赖的，另一个是不依赖糖原的，但依赖于宝贵的活动。
1. The purpose of this study was to examine the effects of reduced glycogen concentration on force, Ca2+ release and myofibrillar protein function during fatigue in skeletal muscle. Force and intracellular free Ca2+ concentration ([Ca2+](i)) were measured in single mammalian skeletal muscle fibres during fatigue and recovery Glycogen was measured in bundles of 20-40 fibres from the same muscle under the same conditions.2. Fatigue was induced by repeated maximum tetani until force was reduced to 30% of initial. This was associated with a reduction in muscle glycogen to 27 +/- 6% of control values. In fibres allowed to recover for 60 min in the presence of 5.5 mM glucose (n = 6), tetanic (100 Hz) force recovered fully but tetanic [Ca2+](i) remained at 82 +/- 8% of initial values. This prolonged depression in Ca2+ release was not associated with decreased muscle glycogen since glycogen had recovered to pre-fatigue levels (157 +/- 42%).3. To examine the responses under conditions of reduced muscle glycogen concentration, fibres recovered from fatigue for 60 min in the absence of glucose (n= 6). After glucose-free recovery, the decreases in tetanic force and [Ca2+](i) were only partially reversed (to 64 +/- 8% and 57 +/- 7% of initial values, respectively). These alterations were associated with a sustained reduction in muscle glycogen concentration (27 +/- 4% of initial values).4. In another set of fibres, fatigue was followed by 50 Hz intermittent stimulation for 22.6 +/- 4 min. With this protocol, tetanic force and [Ca2+](i) partially recovered to 76 +/- 9% and 55 +/- 6% of initial levels, respectively. These changes were associated with a recovery of muscle glycogen (to 85 +/- 10%).5. During fatigue, Ca2+ sensitivity and maximum Ca2+-activated force (F-max) were depressed but these alterations were fully reversed when muscle glycogen recovered. When glycogen did not recover, Ca2+ sensitivity remained depressed but F-max partially recovered. The altered myofibrillar protein function is probably due to alterations in inorganic phosphate levels or other metabolites associated with reduced levels of muscle glycogen.6. These data indicate that the reductions in force, Ca2+ release and contractile protein inhibition observed during fatigue are closely associated with reduced muscle glycogen concentration. These findings also suggest that the changes in Ca2+ release associated with fatigue and recovery have two components - one which is glycogen dependent and another which is independent of glycogen but depends on precious activity.