RESUMO
Enterically coated (ENT) or delayed-release (DEL) capsules may lessen gastrointestinal symptoms (GIS) following acute sodium citrate (SC) ingestion, although the effects on blood acid-base balance are undetermined. Fourteen active males ingested 0.4 g.kg-1 body mass (BM) SC, within gelatine (GEL), DEL and ENT capsules or 0.07 g.kg-1 BM sodium chloride control (CON). Blood acid-base balance and GIS were measured for 4 h. Ingestion form had no significant effect on total GIS experienced (GEL: 2 ± 7; DEL: 1 ± 8; ENT: 1 ± 4 AU). Most (7/14) participants experienced zero symptoms throughout. Peak GIS typically emerged ≤100 min post-ingestion, with a similar time to reach peak GIS between ingestion form (GEL: 36 ± 70; DEL: 13 ± 28; ENT: 15 ± 33 AU). Blood [HCO3-] was significantly higher with ENT versus GEL (ENT: 29.0 ± 0.8; GEL: 28.5 ± 1.1 mmol.L-1, P = 0.037). Acute ingestion of a reduced SC dose elicited minimal GIS, producing significant changes in blood [HCO3-] from rest, irrespective of ingestion form (GEL: 6.0 ± 0.9; DEL: 5.1 ± 1.0; ENT: 6.2 ± 0.8 mmol.L-1). The necessity of individualized ingestion strategies is also challenged, with sustained increases in blood [HCO3-] of ≥4 mmol.L-1 for up to 153 min highlighted. If commencing exercise at peak alkalosis augments subsequent performance above starting at a standardized time point where HCO3- is still elevated remains unclear.
RESUMO
To compare the bicarbonate kinetics and gastrointestinal (GI) symptom responses between an equal dose of sodium bicarbonate and sodium citrate using delayed-release capsules. Thirteen active males (age 20.5 ± 2.1 y, height 1.8 ± 0.1 m and body mass [BM] 76.5 ± 9.6 kg) consumed either 0.3 g.kg-1 BM sodium bicarbonate, sodium citrate or a placebo, using a double-blind, randomized crossover design. Blood bicarbonate ion (HCO3-) concentration, pH and GI symptoms were measured pre-consumption and every 10 min for 180 min post-consumption. Blood HCO3- concentration (P < 0.001) and pH (P = 0.040) were significantly higher in the sodium bicarbonate condition compared with sodium citrate condition up to 3 h post-consumption. Peak blood HCO3- concentration was significantly higher with the sodium bicarbonate compared with citrate (P < 0.001). Mean GI symptom scores were lower (P = 0.037) for sodium citrate (1.5 ± 1.8 AU) than bicarbonate (2.6 ± 3.1 AU), with considerable inter-individual variability. No GI symptoms were reported following consumption of the placebo. Both substances increase HCO3- values significantly, with sodium bicarbonate causing significantly higher pH and HCO3- values than the same dose of sodium citrate, but results in slightly more severe GI symptoms.