A hypothesis in which intramembrane charge reflects a voltage sensing process allosterically coupled to transitions in ryanodine receptor (RyR)-Ca²⁺ release channels as opposed to one driven by release of intracellularly stored Ca²⁺ would predict that such charging phenomena should persist in skeletal muscle fibres unable to release stored Ca²⁺. Charge movement components were accordingly investigated in intact voltage-clamped amphibian fibres treated with known sarcoplasmic reticular (SR) Ca²⁺-ATPase inhibitors. Cyclopiazonic acid (CPA) pretreatment abolished Ca²⁺ transients in fluo-3-loaded fibres following even prolonged applications of caffeine (10 mM) or K⁺ (122 mM). Both CPA and thapsigargin (TG) transformed charge movements that included delayed (q) 'hump' components into simpler decays. However, steady-state charge-voltage characteristics were conserved to values (maximum charge, Q_max ~ 20-25 nC µF^-1; transition voltage, V* ~ -40 to-50 mV; steepness factor, k ~ 6-9 mV; holding voltage -90 mV) indicating persistent q charge. The features of charge inactivation similarly suggested persistent q_ß and q charge contributions in CPA-treated fibres. Perchlorate (8.0 mM) restored the delayed kinetics shown by 'on' q charge movements, prolonged their 'off' decays, conserved both Q_max and k, yet failed to restore the capacity of such CPA-treated fibres for Ca²⁺ release. Introduction of perchlorate (8.0 mM) or caffeine (0.2 mM) to tetracaine (2.0 mM)-treated fibres, also known to restore q charge, similarly failed to restore Ca²⁺ transients. Steady-state intramembrane q charge thus persists with modified kinetics that can be restored to their normally complex waveform by perchlorate, even in intact muscle fibres unable to release Ca²⁺. It is thus unlikely that q charge movement is a consequence of SR Ca²⁺ release rather than changes in tubular membrane potential.