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https://doi.org/10.1038/nm954

has been cited by the following article:

• TITLE: Effect of Dietary Nitrate on Force Production and Sarcoplasmic Reticulum Ca2+ Handling in Rat Fast-Twitch Muscles Following Eccentric Contraction

  AUTHORS: Satoshi Matsunaga, Chihiro Aibara, Daiki Watanabe, Keita Kanzaki, Yurie Morizaki, Sumiko Matsunaga-Futatsuki, Masanobu Wada

  KEYWORDS: Supplementation, Ca2+-ATPase Activity, Ca2+ Uptake, Ca2+ Release

  JOURNAL NAME: Open Journal of Applied Sciences, Vol.8 No.12, December 27, 2018

  ABSTRACT: 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.