Department of Physical Therapy, School of Health Sciences, Ariel University, Ariel, Israel.
J Appl Physiol (1985). 2019 Apr 1;126(4):1103-1109. doi: 10.1152/japplphysiol.01121.2018. Epub 2019 Feb 7.
The effects of temperature elevation after intense repeated contractions on glycogen and energy metabolism as well as contractile function of isolated mouse soleus muscle (slow twitch, oxidative) were investigated. Muscles were stimulated electrically to perform repeated tetanic contractions for 10 min at 25°C, which reduced tetanic force by 85% and glycogen by 50%. After 120-min recovery at 25°C glycogen was fully restored (125% of basal), whereas after recovery at 35°C glycogen decreased further (25% of basal). Glycogen synthase fractional activity averaged 31.8 ± 3.1% (baseline = 33.8 ± 3.4%) after 120-min recovery at 25°C but was increased after recovery at 35°C (63.8 ± 4.8%; < 0.001 vs. 25°C). Phosphorylase fractional and total activities were not affected by the higher temperature. However, recovery at 35°C resulted in a significantly higher content of the phosphorylase substrate inorganic phosphate (20%; < 0.01 vs. 25°C). Finally, fatigue development during a subsequent bout of repeated contractions at 25°C was similar after 120-min recovery at 25°C and 35°C. These data demonstrate that after intense contractions elevated temperature inhibits glycogen accumulation, likely by increasing the availability of the phosphorylase substrate inorganic phosphate, but has no effect on fatigue development. Thus after heat exposure phosphorylase plays a significant role in glycogen accumulation, and glycogen does not limit muscle performance in isolated mouse soleus muscle after recovery from elevated temperature. Whether elevated temperature affects glycogen biogenesis and contractile performance of isolated slow-twitch muscle is not known. Here we show that after a bout of repeated contractions in isolated mouse soleus muscle at 25°C, increasing muscle temperature during recovery to 35°C blocked glycogen accumulation compared with recovery at 25°C. Surprisingly, during a subsequent bout of repeated contractions at 25°C, the rate of fatigue was not different between groups after recovery at the two temperatures.
研究了剧烈重复收缩后温度升高对分离的小鼠比目鱼肌（慢收缩、氧化）糖原和能量代谢以及收缩功能的影响。肌肉在 25°C 下通过电刺激进行 10 分钟的重复强直收缩，使强直力降低约 85%，糖原减少 50%。在 25°C 下恢复 120 分钟后，糖原完全恢复（约为基础值的 125%），而在 35°C 下恢复后糖原进一步减少（约为基础值的 25%）。在 25°C 下恢复 120 分钟后，糖原合酶分数活性平均为 31.8±3.1%（基线为 33.8±3.4%），但在 35°C 下恢复后增加（63.8±4.8%；<0.001 与 25°C 相比）。较高的温度对磷酸化酶分数和总活性没有影响。然而，在 35°C 下恢复导致磷酸化酶底物无机磷的含量显著增加（约 20%；<0.01 与 25°C 相比）。最后，在 25°C 下进行随后的重复收缩收缩时，在 25°C 和 35°C 下恢复 120 分钟后疲劳发展相似。这些数据表明，在剧烈收缩后，升高的温度会抑制糖原的积累，可能是通过增加磷酸化酶底物无机磷的可用性来实现的，但对疲劳发展没有影响。因此，在热暴露后，磷酸化酶在糖原积累中发挥重要作用，并且在从高温恢复后，糖原不会限制分离的小鼠比目鱼肌的肌肉性能。升高的温度是否会影响分离的慢收缩肌肉的糖原生物发生和收缩性能尚不清楚。在这里，我们表明，在 25°C 下进行一次分离的小鼠比目鱼肌重复收缩收缩后，在恢复期间将肌肉温度升高至 35°C 会阻止糖原的积累，与在 25°C 下恢复相比。令人惊讶的是，在两个温度下恢复后，在随后的 25°C 重复收缩收缩中，两组之间的疲劳速度没有差异。
