In the present work, we investigate whether changes in EC coupling mode occur in skeletal muscles from ageing mammals by examining the dependence of EC coupling on extracellular Ca²⁺. Single intact muscle fibres from flexor digitorum brevis muscles from young (2-6 mo) and old (23-30 mo) mice were subjected to tetanic contractile protocols in the presence and absence of external Ca²⁺. Contractile experiments in the absence of external Ca²⁺ show that about half of muscle fibres from old mice are dependent upon external Ca²⁺ for maintaining maximal tetanic force output, while young fibres are not. Decreased force in the absence of external Ca²⁺ was not due to changes in charge movement as revealed by whole-cell patch-clamp experiments. Ca²⁺ transients, measured by fluo-4 fluorescence, declined in voltage-clamped fibres from old mice in the absence of external Ca²⁺. Similarly, Ca²⁺ transients declined in parallel with tetanic contractile force in single intact fibres. Examination of inward Ca²⁺ current and of mRNA and protein assays suggests that these changes in EC coupling mode are not due to shifts in DHPR and/or ryanodine receptor isoforms. These results indicate that a change in EC coupling mode occurs in a population of fibres in ageing skeletal muscle, and is responsible for the age-related dependence on extracellular Ca²⁺.