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  • 标题:Effect of Dietary Nitrate on Force Production and Sarcoplasmic Reticulum Ca2+ Handling in Rat Fast-Twitch Muscles Following Eccentric Contraction
  • 本地全文:下载
  • 作者:Satoshi Matsunaga ; Chihiro Aibara ; Daiki Watanabe
  • 期刊名称:Open Journal of Applied Sciences
  • 印刷版ISSN:2165-3917
  • 电子版ISSN:2165-3925
  • 出版年度:2018
  • 卷号:8
  • 期号:12
  • 页码:607-618
  • DOI:10.4236/ojapps.2018.812049
  • 语种:English
  • 出版社:Scientific Research Publishing
  • 摘要:Impaired excitation-contraction coupling occurs in eccentric contraction (ECC)-induced damaged muscles. It has been suggested that sarcoplasmic reticulum (SR) is susceptible to damage in the overstretched regions possibly marking the basis of excitation-contraction coupling damage. Recent studies have shown that dietary nitrate supplementation enhances SR function in fast-twitch muscles. In this study, we aimed to investigate whether dietary nitrate supplementation can alleviate a decline in muscle contractile properties and SR function following ECC. To this end, force production, Ca2+ uptake, Ca2+ release, and Ca2+-ATPase activity of the SR were examined in rat fast-twitch muscles immediately following ECC for 200 repetitions. In comparison with contralateral resting muscles, nitrate supplementation for up to 3 days resulted in an obvious decline in force production. However, there were no differences in terms of force production between 6-day nitrate-treated and contralateral muscles. Similar to the observations regarding force production, the SR Ca2+ release rate changed from an obvious decrease following the 0- and 3-day dietary nitrate supplementation to no difference following the 6-day nitrate supplementation. In contrast, ECC decreased the Ca2+-ATPase activity and Ca2+ uptake rate, irrespective of the period of dietary nitrate supplementation. Overall, these results indicate that dietary nitrate supplementation can alleviate ECC-related decreases in force production mediated through inhibited reductions in the SR Ca2+ release function.
  • 关键词:Supplementation;Ca2+-ATPase Activity;Ca2+Uptake;Ca2+Release
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