The lactate ion protects excitability and force in depolarized muscle fibres by inhibiting chloride conductance.

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The lactate ion protects excitability and force in depolarized muscle fibres by inhibiting chloride conductance. 1Institute of Sport Science and Clinical Biomechanics, University of South Denmark, 2Institut of Physiology and Biophysic, University of Aarhus1.


Impaired muscle function during high intensity exercise is a complex phenomenon which is associated with loss of excitability and increase in lactate ion and decrease in pH. Here, we demonstrate that in contrast to the general view of lactate as a culprit and a cause of fatigue the lactate ion (Lac-) per se preserve the transverse (t-) tubular membrane excitability, thereby maintaining muscle function.

In this series of experiments we used rat muscle fibres, where the peripheral surface membrane was removed by micro-dissection whereby the extensive t-system reseals and becomes normally polarized. With this preparation it is possible to measure fibre excitability and force production while at the same time having direct access to the intracellular environment enabling the estimation of the effects of Lac- per se while the intracellular environment, e.g. pH and Na+, was be kept constant.

When normally polarised (Con, incubated in control buffer with 127 mM cellular K+) exposure to Lac- had no effect on the twitch and tetanic force responses of the fibres. Further, there is no effect of Lac- on maximum Ca2+ activated force or the force-pCa relationship. Depolari-zing the fibres, by incubation in 75 mM K+, reduced twitch and tetanic force to 58±7 and 66±7% of Con, respectively. However, when the fibers were placed in 75 mM K+ with 10 mM Lac-, twitch and tetanic force were only reduced to 81±3 and 83±6%, respectively (Figure). Moreover, when the fibers were further depolarized, by incubation in 60 mM K+, the tetanic force was depressed to 43±10% of Con, while only reduced to 68±9% incubated in 60 mM K+ in the presence of 10 mM Lac- (Figure). The data clearly demonstrates that Lac- significantly recovers twitch and tetanic force responses in depolarized fibers. When the t-system chloride conductance was eliminated, either by removal of all Cl- from the solution or by block of the chloride channels with 9-anthracene carboxylic acid (a specific inhibitor of ClC-1 channels), Lac- was without effect on the excitation-induced force response in depolarised skinned fibres. These data strongly suggests that Lac- increases excitability in depolarised muscle fibres, by mediating a reduction in the ClC-1 Cl- conductance, which enables action potentials to still be generated in the t-system of the muscle fibres despite the inhibitory effects of depolarization.
Period26. Aug 2009
Event titleMyoNak Conference
Event typeConference
LocationPalm Cove, Australia