{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T17:48:47Z","timestamp":1760204927322},"reference-count":0,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1995,5,1]]},"abstract":"<jats:p> Sarcoplasmic reticulum (SR) Ca2+ release channel function is modified by ligands (Mg2+, Ca2+, ATP, and H+) that are generated during a bout of exercise. We have examined the effects of changing intracellular metabolites on Ca2+ release, [3H]ryanodine binding, and single-Ca2+ release channel activity of SR isolated from white rabbit skeletal muscle. Increasing Mg2+ (from 0 to 4 mM) and decreasing pH (7.1\u20136.5) inhibited SR Ca2+ release and [3H]-ryanodine binding. In addition, increasing lactate concentrations from 2 to 20 mM inhibited [3H]ryanodine binding to SR vesicles, inhibited SR Ca2+ release, and decreased the single-channel open probability. These findings suggest that intracellular modifications that disrupt excitation-contraction coupling and decrease Ca2+ transients will promote a decline in tension development and contribute to muscle fatigue. In addition, we show that hydrogen peroxide induces Ca2+ release and increases [3H]ryanodine binding to its receptor, suggesting that reactive oxygen species produced during exercise may compromise muscle function by altering the normal gating of the SR Ca2+ release channel. <\/jats:p>","DOI":"10.1152\/jappl.1995.78.5.1665","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T06:05:54Z","timestamp":1513922754000},"page":"1665-1672","source":"Crossref","is-referenced-by-count":61,"title":["Metabolic end products inhibit sarcoplasmic reticulum Ca2+ release and [3H]ryanodine binding"],"prefix":"10.1152","volume":"78","author":[{"given":"T. G.","family":"Favero","sequence":"first","affiliation":[{"name":"Department of Biology, University of Portland 97203, Oregon, USA."}]},{"given":"A. C.","family":"Zable","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Portland 97203, Oregon, USA."}]},{"given":"M. B.","family":"Bowman","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Portland 97203, Oregon, USA."}]},{"given":"A.","family":"Thompson","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Portland 97203, Oregon, USA."}]},{"given":"J. J.","family":"Abramson","sequence":"additional","affiliation":[{"name":"Department of Biology, University of Portland 97203, Oregon, USA."}]}],"member":"24","container-title":["Journal of Applied Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/jappl.1995.78.5.1665","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T13:57:52Z","timestamp":1567951072000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jappl.1995.78.5.1665"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1995,5,1]]},"references-count":0,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1995,5,1]]}},"alternative-id":["10.1152\/jappl.1995.78.5.1665"],"URL":"https:\/\/doi.org\/10.1152\/jappl.1995.78.5.1665","relation":{},"ISSN":["8750-7587","1522-1601"],"issn-type":[{"value":"8750-7587","type":"print"},{"value":"1522-1601","type":"electronic"}],"subject":[],"published":{"date-parts":[[1995,5,1]]}}}