Dietary nitrate, a source of nitric oxide (NO), improves the contractile properties of human muscle. We present the hypothesis that this is due to nitrosylation of the ryanodine receptor and increased NO signaling via the soluble guanyl cyclase-cyclic guanosine monophosphate-protein kinase G pathway, which together increase the free intracellular Ca2+ concentration along with the Ca2+ sensitivity of the myofilaments themselves.
Departments of 1Kinesiology and
2Cellular and Integrative Physiology, Indiana University Purdue University Indianapolis, and
Departments of 3Medicine and
4Radiology, Washington University School of Medicine, St. Louis
Address for correspondence: Andrew R. Coggan, Ph.D., FACSM, Department of Kinesiology, Indiana University Purdue University Indianapolis, IF 101C, 250 University Boulevard, Indianapolis, IN 46202, Tel.: (317) 274-0656; Fax: (317) 278-2041; Email: email@example.com
Funding: This publication was made possible by award number R34HL138253 from the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NHLBI or NIH. Conflicts of interest: None