To gain a more complete understanding of mechanisms relevant to HyperKPP and to answer the above questions, we assessed how Na+ influx, electromyographic (EMG) activity, hindlimb immobility, force generation at different [K+]e, muscle fiber type composition, and myofiber damage change as a function of NaV1.4 protein content during the first 12 months of age in the M1592V HyperKPP mouse model. The gene discussed is SCN4A; the disease is hyperkalemic periodic paralysis.