Bicarbonate attenuates intracellular acidosis

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This study was prompted by concern that administration of bicarbonate for correction of lactate acidosis aggravates a low intracellular pH (pHi). In healthy subjects we evaluated skeletal muscle pHi using 31P-magnetic resonance spectroscopy during 5-minute rhythmic handgrip to provoke intracellular acidosis. Methods:

Subjects were randomized to treatment with bicarbonate or saline infused intravenously in a cross-over study design with 1 h between trials. Results:

In response to rhythmic handgrip, muscle venous O2 hemoglobin saturation decreased from 51 ± 4% to 36 ± 2% and lactate increased from 1.0 ± 0.1 to 4.9 ± 0.5 mmol/l with a reduction in pH from 7.43 ± 0.01–7.23 ± 0.01 (P<0.05). pHi decreased from 7.06 ± 0.02–6.36 ± 0.08 (P<0.05). Infusion of bicarbonate increased the arterial blood concentration from 26 ± 1 to 39 ± 1 mmol/l (P<0.05). The arterial CO2 partial pressure decreased from 5.6 ± 0.2 to 5.2 ± 0.3 kPa during rhythmic handgrip, whereas it increased to 5.9 ± 0.2 kPa (P<0.05) during infusion of bicarbonate. Bicarbonate treatment also increased pH of arterial and venous blood (7.55 ± 0.01 vs. 7.44 ± 0.02 and 7.31 ± 0.01 vs. 7.23 ± 0.02, respectively; P<0.05). In the last min of rhythmic handgrip the decrease in pHi was attenuated by the administration of bicarbonate (6.60 ± 0.11 vs. 6.40 ± 0.12; P<0.05). Conclusion:

During exercise-induced metabolic acidosis, intravenous administration of bicarbonate increased the buffering capacity of blood and attenuated the decrease in intracellular muscle pH, although there was a small increase in the arterial carbon dioxide pressure.

Keywords: bicarbonate; buffer; intracellular acidosis

Document Type: Research Article


Affiliations: 1: the Copenhagen Muscle Research Center, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Denmark 2: NMR Center, the Panum Institute and

Publication date: May 1, 2002

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