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High metabolic activity and existence of a large transmembrane inward electrochemical gradient for H +  at rest promote intracellular acidification of skeletal muscle. Exchangers and cotransports efficiently contend against accumulation of intracellular H +  and associated deleterious effects on muscle functions. Voltage-gated H +  channels have also been found to represent another H +  extrusion pathway in cultured muscle cells. Up to now, the skeletal muscle cell was therefore the unique vertebrate excitable cell in which voltage-gated H +  currents have been described. In this study, we show that, unlike cultured cells, single mouse muscle fibers do not generate H +  currents in response to depolarization. In contrast, expression of human voltage-gated H +  channels in mouse muscle gives rise to robust outward voltage-gated H +  currents. This result excludes that inappropriate experimental conditions may have failed to reveal voltage-gated H +  currents in control muscle. This work therefore demonstrates that fully differentiated mammalian muscle fibers do not express functional voltage-gated H +  channels and consequently can no longer be considered as the only vertebrate excitable cells exhibiting voltage-gated H +  currents.

Mammalian skeletal muscle does not express functional voltage-gated H+ channels

Mammalian skeletal muscle does not express functional voltage-gated H⁺ channels