Effect of adrenaline on the post-tetanic potentiation in mouse skeletal muscle

We report the influence of adrenergic stimulation on the amplitude and time course of post-tetanic potentiation of twitch contraction. This was complemented by measurements of the peak of [Ca2+](i) transients in twitches and of the level of myosin light chain 2 (LC2) phosphorylation, before, 20 and 300 s after the conditioning tetanus. Soon after the tetanus, twitch potentiation and increases of LC2 phosphorylation and of [Ca2+](i) peak were similar in control conditions and in the presence of adrenaline. In control conditions, twitch potentiation, LC2 phosphorylation and [Ca2+](i) peak returned to, or close to, pre-tetanic values in 300 s. On the contrary, in the presence of adrenaline, twitch potentiation and LC2 phosphorylation were partially or fully maintained respectively, while the increase of [Ca2+](i) peak was not. This situation allowed us to analyse the relative contributions of elevated LC2 phosphorylation and [Ca2+](i) peak in the twitch post-tetanic potentiation phenomenon. Moreover, it was shown that the increase of LC2 phosphorylation (up to 0.5 mol P/mol LC2) affected neither the kinetic parameters of the twitch nor the maximal velocity of shortening. It is proposed that the maintenance of LC2 phosphorylation in the presence of adrenaline results from the inhibition of myosin light chain phosphatase. This could be achieved through the production of the active, phosphorylated form of the inhibitor-1, an endogenous inhibitor, which binds to the catalytic sub-units common to class 1 protein phosphatases.