{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T10:29:39Z","timestamp":1762079379630},"reference-count":27,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,2,4]],"date-time":"2013-02-04T00:00:00Z","timestamp":1359936000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:p>Myotonia is a heritable disorder in which patients are unable to willfully relax their muscles. The physiological basis for myotonia lies in well\u2010established deficiencies of skeletal muscle chloride and sodium conductances. What is unclear is how normal muscle function can temporarily return with repeated movement, the so\u2010called \u201cwarm\u2010up\u201d phenomenon. Electrophysiological analyses of the skeletal muscle voltage\u2010gated sodium channel Na<jats:sub>v<\/jats:sub>1.4 (gene name <jats:italic>SCN4A<\/jats:italic>), a key player in myotonia, have revealed several parallels between the Na<jats:sub>v<\/jats:sub>1.4 biophysical signature, specifically slow\u2010inactivation, and myotonic warm\u2010up, which suggest that Na<jats:sub>v<\/jats:sub>1.4 is critical not only in producing the myotonic reaction, but also in mediating the warm\u2010up. 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