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A NOVEL REGULATORY ROLE FOR THE LACTATE ION ON EXCITABILITY AND FORCE
Author(s) -
Paoli Frank Vincenzo,
Jørgensen Rasmus,
Pedersen Thomas Holm,
Ørtenblad Niels,
Nielsen Ole Bækgaard
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.962.9
Subject(s) - chemistry , osmotic concentration , stimulation , analytical chemistry (journal) , chromatography , biochemistry , endocrinology , biology
We examined the effect of lactate (lac) per se on excitability and tetanic force development. Rat soleus muscles were incubated in KR‐buffer (95% O 2 ) containing 20 mM Na‐methanosulfonate (MS). Lac was added as Na‐lac and an equimolar of MS was omitted to maintain osmolarity and constant Na + and Cl − concentrations. Elevation of [K + ] o to 11 mM reduced M‐wave area and force in muscles stimulated via the nerve to 16 and 17% of control values at 4 mM [K + ] o , respectively. Subsequent addition of 20 mM lac recovered M‐wave area and force to 53 and 70% of control values at 4 mM [K + ] o , respectively. In similar experiments with field stimulation, the force recovered from 29 to 88% of control values at 4 mM [K + ] o . 20 mM lac reduced pH i from 7.19 to 7.06 within 40 sec, followed by a recovery of pH i to 7.21 over the next 45 min. We have previously shown that a reduction in pH i can lead to force recovery in K + depressed muscles, it was of interest to estimate to what extend the reduction in pH i after addition of lac was responsible for the recovery of force. The reduction in pH i induced by lac was mimicked by increasing CO 2 to 7%, which reduced pH i from 7.19 to 7.04. This pH i reduction, however, only produced a negligible and insignificant recovery of force in muscles depressed by elevated [K + ] o . Conclusion: In K + depressed muscles, a physiological increase in intracellular lac restores excitability and force. Danish Medical Research Council: j.nr. 271‐05‐0304