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J Appl Physiol 89: 517-528, 2000;
8750-7587/00 $5.00
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Vol. 89, Issue 2, 517-528, August 2000

Effects of high myoplasmic L-lactate concentration on E-C coupling in mammalian skeletal muscle

Giuseppe S. Posterino and Martin W. Fryer

School of Physiology and Pharmacology, Faculty of Medicine, The University of New South Wales, Sydney, New South Wales 2052, Australia

The effects of high myoplasmic L-lactate concentrations (20-40 mM) at constant pH (7.1) were investigated on contractile protein function, voltage-dependent Ca2+ release, and passive Ca2+ leak from the sarcoplasmic reticulum (SR) in mechanically skinned fast-twitch (extensor digitorum longus; EDL) and slow-twitch (soleus) fibers of the rat. L-Lactate (20 mM) significantly reduced maximum Ca2+-activated force by 4 ± 0.5% (n = 5, P < 0.05) and 5 ± 0.4% (n = 6, P < 0.05) for EDL and soleus, respectively. The Ca2+ sensitivity was also significantly decreased by 0.06 ± 0.002 (n = 5, P < 0.05) and 0.13 ± 0.01 (n = 6, P < 0.001) pCa units, respectively. Exposure to L-lactate (20 mM) for 30 s reduced depolarization-induced force responses by ChCl substitution by 7 ± 3% (n = 17, P < 0.05). This inhibition was not obviously affected by the presence of the lactate transport blocker quercetin (10 µM), or the chloride channel blocker anthracene-9-carboxylic acid (100 µM). L-Lactate (20 mM) increased passive Ca2+ leak from the SR in EDL fibers (the integral of the response to caffeine was reduced by 16 ± 5%, n = 9, P < 0.05) with no apparent effect in soleus fibers (100 ± 2%, n = 3). These results indicate that the L-lactate ion per se has negligible effects on either voltage-dependent Ca2+ release or SR Ca2+ handling and exerts only a modest inhibitory effect on muscle contractility at the level of the contractile proteins.

muscle fatigue; excitation-contraction coupling; contractile apparatus; calcium release


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