Ingestion of sodium citrate suppresses aldosterone level in blood at rest and during exercise.

The purpose of this study was to determine if the ingestion of sodium citrate (CIT) alters blood levels of fluid and electrolyte regulatory hormones at rest and during exercise. Using a randomized, double-blinded, crossover design, 13 young, male well-trained runners performed continuous incremental running tests to volitional exhaustion on a treadmill 2 h after ingestion of 0.5 g.kg-1 body mass of CIT or placebo (PLC) in 1000 mL of solution. These trials were separated by 2 weeks. Baseline (before ingestion) aldosterone concentration did not differ between the 2 trials; however, it was 36.5% (p = 0.003) lower in the CIT trial compared with the PLC trial before the running test (i.e., after ingestion). The extent of the running-induced increase in aldosterone was 33% (p = 0.009) smaller in the CIT trial. There were no between-trial differences in the levels of adrenocorticotropic hormone, N-terminal pro-B-type natriuretic peptide, or renin activity at any stage of the study. However, a greater relative increase in plasma volume (mean +/- SD, 6.41% +/- 3.78% vs. 4.08% +/- 3.33%; p = 0.042) was observed after administering the CIT compared with the PLC drink. Serum Na+ concentration increased (by 3.1 +/- 1.2 mmol.L-1; p < 0.0001) after ingestion of the CIT but not the PLC drink. A higher Na+ level was observed in the CIT trial than in the PLC trial (142.4 +/- 1.6 vs. 139.3 +/- 1.4 mmol.L-1, p = 0.00001) after completion of the run. In conclusion, pre-exercise ingestion of CIT induces a decrease in serum aldosterone concentration in the resting condition and a blunting of the aldosterone response during incremental running exercise to volitional exhaustion. The observed effect of CIT on the serum aldosterone level may be mediated by an acute increase in plasma volume and serum Na+ concentration alterations.