Mutations in the chloride channel (CLCN1) are causative for Thomsen and Becker´s myotonia. Repetitive contractions reduce the myotonic stiffness by unknown mechanisms. The objective of this study was to investigate changes of microenvironmental conditions on this so called warm-up phenomenon. Force registrations were performed on freshly dissected mouse gastrocnemius muscle. Experimental myotonia was induced by Cl-free solution, blocking CLCN1 with 9-antracene carboxylic acid, and the use of myotonic mice (ADR-mouse). Elevated osmolarity promoted the warm-up phenomenon. This effect was partially antagonized by bumetanide, an inhibitor of the Na⁺K⁺Clcotransporter (NKCC). Therefore, the antimyotonic effects of increased osmolarity may be explained by electrical stabilisation via NKCC. [K⁺]_o increase prevented the relaxation deficit in a concentration and time dependent manner. At 7 mM [K⁺]_o the relaxation time reached control levels. We conclude that the efflux of K⁺ from muscle fibres after repetitive voluntary contractions reduces myotonic activity and enhances T-tubular function. Potential mechanisms as inactivation of voltage gated Na⁺-channels and increased K⁺-conductance via BK⁺-channels are discussed.