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.
Highlights
Fatigue-induced changes in force production can be analyzed in terms of a generally decreased ability of cross-bridges formation to generate force, decreased myofibrillar Ca2+ sensitivity, decreased sarcoplasmic reticulum (SR) Ca2+ release, or combination of these [1]
eccentric contraction (ECC) decreased the Ca2+-ATPase activity and Ca2+ uptake rate, irrespective of the period of dietary nitrate supplementation. 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
There were no significant differences among the measurement results of the three resting groups
Summary
Fatigue-induced changes in force production can be analyzed in terms of a generally decreased ability of cross-bridges formation to generate force, decreased myofibrillar Ca2+ sensitivity, decreased sarcoplasmic reticulum (SR) Ca2+ release, or combination of these [1]. Unaccustomed eccentric contraction (ECC) induces skeletal muscle damage characterized by a long-lasting decrease in muscle strength and delayed onset muscle soreness [7]. Muscles damaged by unaccustomed ECC are characterized by sarcolemmal disruption and myofibrillar disorganization during ECC [8] and crystallized structures within the Z disk and SR swelling immediately following ECC [9]; overstretched sarcomeres act as the origin of such muscle damage [10]. Impaired excitation-contraction coupling occurs in eccentrically damaged mammalian muscles [8]. It has been suggested that sarcomeres within myofibrils, transverse tubules (t-tubules), and SR are susceptible to damage in the overstretched regions, possibly marking the basis of excitation-contraction coupling damage [11]
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