It has been proposed¹ that an influx of calcium ions into twitch muscle fibres during an action potential might initiate contraction. However, when external Ca²⁺ is lowered to 10⁻⁸ M with EGTA, the fibres can produce normal twitches for many minutes^2,3. Nevertheless, a clear Ca²⁺ influx during contraction has been demonstrated^4,5, and it has been found that phasic skeletal muscle has an inward calcium current (I_Ca)^6,7 which can give rise to calcium spikes⁸. In certain conditions, a reduction in external Ca²⁺ with 80–90 mM EGTA results in reversible blockade of excitation–contraction (e–c) coupling⁹, leading some authors to suggest^7,9–11 that extracellular Ca²⁺ moved into the myoplasm due to I_Ca may be involved in the e–c coupling mechanism that triggers contraction. This proposition was further supported by the localization of I_Ca in the T-system, which circumvented the problem of the delay due to calcium diffusion from the surface membrane. We have now investigated whether I_Ca has a clear role in initiating or sustaining contractions in twitch muscle fibres. Our approach was to decrease or eliminate I_Ca with the calcium-blocking agent diltiazem (Herbesser) and to see how the twitch, tetanic and potassium-contracture tensions were affected. We found that I_Ca could be decreased or cancelled with the calcium-blocking agent, but that the same concentration of the drug potentiated the twitch, tetanus and contractures. We conclude, therefore, that I_Ca has no role in e–c coupling. A preliminary report of these results has been presented elsewhere¹².