Effect of sodium citrate on performance and metabolism of human skeletal muscle during supramaximal cycling exercise.

The aim of this study was to examine whether the alkalosis-induced improvement in supramaximal performance could be explained by a less-altered muscle metabolic status. Eight subjects first performed exhausting exercise at 120% peak oxygen uptake after ingesting either a placebo (PLC) or sodium citrate (CIT) at a dose of 0.5 g.kg-1 body mass to determine exhaustion time (texh). They then, performed exercise (Lim-EX) at the same relative intensity lasting PLCtexh minus 20 s in both treatments. Samples were taken from vastus lateralis muscle at rest (90-min after the ingestion) and at the end of Lim-EX. Arterial blood samples were obtained at rest (immediately prior to and 90 min after ingesting the drug) and during the 20-min post-exercise recovery. The texh was significantly increased by CIT [PLC 258 (SD 29) s, CIT 297 (SD 45) s]. The CIT raised the rest [citrate] in blood [PLC 0.11 (SD 0.01) mmol.l-1, CIT 0.34 (SD 0.07) mmol.l-1] and in muscle [PLC 0.78 (SD 0.23) mmol.kg-1 dry mass, CIT 1.00 (SD 0.21) mmol.kg-1 dry mass]. Resting muscle pH and buffering capacity were unchanged by CIT. The same fall in muscle pH was observed during Lim-EX in the two conditions. This was associated with similar variations in both the cardio-respiratory response and muscle energy and metabolism status in spite of a better blood acid-base status after CIT. Thus, CIT would not seem to allow the alkalinization of the muscle cytosolic compartment. Though sodium citrate works in a similar way to NaHCO3 on plasma alkalinization and exercise performance, the exact nature of the mechanisms involved in the delay of exhaustion could be different and remains to be elucidated.