Potentiation of force by extracellular potassium is not dependent on muscle length in mouse EDL muscle.

Increases in myofiber extracellular potassium with prolonged contractile activity can potentiate twitch force. Activity-dependent potentiation, another mechanism of force increase in skeletal muscle, has a strong dependence on muscle or sarcomere length. Thus, potassium-mediated twitch potentiation could also be length-dependent. However, this has not been previously investigated. To this end, we used isolated C57BL/6 mouse extensor digitorum longus (EDL) muscles and elicited twitches at 0.9 , , and 1.1 ( refers to optimal length) in normal (5 mM) and high (10 mM) potassium solutions. Potentiation magnitude was similar to previous observations and was not significantly different between lengths (0.9 : 12.3 ± 4.4%, : 12.2 ± 3.6%, 1.1 : 11.8 ± 4.8%, values are means ± SD). Exposure to dantrolene sodium, a compound that attenuates calcium release, reduced twitch force across lengths by ∼70%. When dantrolene-affected muscles were subsequently exposed to high potassium, potentiation was similar to that observed in the absence of the former. In total, these findings provide novel information on potassium-mediated twitch potentiation. Here, we investigated the length-dependence of twitch force potentiation by extracellular potassium in mouse extensor digitorum longus (EDL) in vitro, at 25°C. Potentiation magnitude did not display a statistically significant difference between the examined muscle lengths. These results describe, for the first time, the relationship of this form of potentiation with muscle length, thus furthering the understanding of how it is integrated in in vivo muscle function.