In vivo, Ba2+ produces flaccid paralysis of mammalian skeletal muscle and lowers serum K+ concentration. An episode of hypokalaemic periodic paralysis (h.p.p.) produces similar changes. Reduced K+ permeability may be involved in the onset of h.p.p., and Ba2+ is known to block K+ channels in some types of excitable cells. I have investigated the mechanism of Ba2+ action in mammalian skeletal muscle (mouse and pig) in vitro. Ba2+ (1‐10 mM) initially potentiated twitch force but subsequently depressed both twitches and tetani. These effects were enhanced by low external K+ concentration (0 mM) and diminished by doubling the external K+ (8 mM). Muscle paralysed by Ba2+ responded to caffeine (25 mM) or K+ (100‐200 mM) with a contracture. The Ca2+ channel blocker verapamil did not prevent paralysis and, in fact, enhanced Ba2+ depression of tetani. Mouse long digital extensor (e.d.l.) muscles were depolarized by approximately 35 mV after 5 min in the presence of 1 mM‐Ba2+. Action potentials from porcine muscles exposed to Ba2+ for 30 min rose and fell more slowly than controls and thus had a longer duration. Continuous recordings of membrane potential from individual cells revealed that 5 mM‐Ba2+ depolarized mouse e.d.l. muscle at about 0.05 times the rate with high K+ (200 mM). I conclude that Ba2+ acts relatively slowly to block K+ channels, to decrease K+ fluxes and to induce depolarization. The rate of spontaneous inactivation of the contraction was apparently faster than the rate of activation. This would account for the Ba2+‐induced flaccid paralysis without an initial contracture. These results with Ba2+‐treated muscle illustrate similarities to h.p.p. and indicate that Ba2+ may create a useful model for studies relevant to h.p.p. Furthermore, Ba2+ may provide an appropriate means for evaluating K+ channel function in other muscle disorders.