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Background Chronic kidney disease with metabolic acidosis is common in older people, but the effectiveness of oral sodium bicarbonate therapy in this group is unclear. We tested whether oral sodium bicarbonate provides net health benefit for older people with advanced chronic kidney disease and serum bicarbonate concentrations < 22 mmol/L. Methods Pragmatic multicentre, parallel group, double-blind, placebo-controlled randomised trial. We recruited adults aged ≥ 60 years with estimated glomerular filtration rate of < 30 mL/min/1.73 m 2 , not receiving dialysis, with serum bicarbonate concentration < 22 mmol/L, from 27 nephrology and geriatric medicine departments in the UK. Participants received oral sodium bicarbonate (up to 3 g/day) or matching placebo given for up to 2 years, randomised in a 1:1 ratio. The primary outcome was between-group difference in the Short Physical Performance Battery (SPPB) at 12 months, adjusted for baseline values, analysed by intention to treat. Secondary outcomes included generic and disease-specific quality of life (EQ-5D and KDQoL tools), anthropometry, renal function, walk distance, blood pressure, bone and vascular health markers, and incremental cost per quality-adjusted life year gained. Results We randomised 300 participants between May 2013 and February 2017, mean age 74 years, 86 (29%) female. At 12 months, 116/152 (76%) participants allocated to bicarbonate and 104/148 (70%) allocated to placebo were assessed; primary outcome data were available for 187 participants. We found no significant treatment effect for the SPPB: bicarbonate arm 8.3 (SD 2.5) points, placebo arm 8.8 (SD 2.2) and adjusted treatment effect − 0.4 (95% CI − 0.9 to 0.1, p  = 0.15). We found no significant treatment effect for glomerular filtration rate (0.6 mL/min/1.73 m 2 , 95% CI − 0.8 to 2.0, p  = 0.39). The bicarbonate arm showed higher costs and lower quality of life as measured by the EQ-5D-3L tool over 1 year (£564 [95% CI £88 to £1154]); placebo dominated bicarbonate under all sensitivity analyses. Adverse events were more frequent in those randomised to bicarbonate (457 versus 400). Conclusions Oral sodium bicarbonate did not improve physical function or renal function, increased adverse events and is unlikely to be cost-effective for use by the UK NHS for this patient group. Trial registration European Clinical Trials Database (2011-005271-16) and ISRCTN09486651 ; registered 17 February 2012.

The consequences of chronic subclinical metabolic acidosis, characterized by an increase in single nephron ammonium generation, contribute to the progression of chronic kidney disease (CKD). Therefore, sodium bicarbonate (NaHCO₃) supplementation in CKD with normal serum bicarbonate patients may reduce kidney fibrosis and slow CKD progression. This study aimed to evaluate the impact of high-dose NaHCO₃ supplementation on urinary transforming growth factor-beta (TGF-β), a biomarker of kidney fibrosis, in non-diabetic CKD patients with normal serum bicarbonate levels. We conducted a single-center, randomized, open-label controlled trial in patients with non-diabetic CKD stage 3–4 and normal serum bicarbonate (22–26 mEq/L). Participants were randomized to receive high-dose NaHCO₃ (0.8 mEq/kg/day) or standard care for 12 weeks. The primary outcome was the change in urinary TGF-β-to-creatinine ratio from baseline. Secondary outcomes included changes in urinary albumin-to-creatinine ratio (UACR), urine pH, serum electrolytes, blood pressure, and adverse events. A total of 64 participants were randomized (NaHCO₃ group: n = 32; control group: n = 32). There was no significant difference in the percentage change of urinary TGF-β (NaHCO₃: −1.86% vs. control: 5.75%; p = 0.477). However, the NaHCO₃ group demonstrated a significant increase in urine pH mean difference (0.56; 95% CI: 0.3,0.82 vs. 0,95% CI −0.24,0.24; p = 0.002) compared to the control group. Similarly, no significant differences were observed in UACR, serum electrolytes, blood pressure, or body weight between groups. No serious adverse events were reported. High-dose NaHCO₃ supplementation in non-diabetic CKD patients with normal serum bicarbonate levels did not significantly reduce urinary TGF-β over 12 weeks but effectively increased urine pH without adverse effects. These findings suggest that NaHCO₃ is safe; however, its role in modulating profibrotic biomarkers in CKD requires further investigation. Longer-term studies and alternative alkali therapies should be explored to determine the optimal strategies for preserving kidney function in this population. Clinical trial registration: TCTR20240817007 (17/08/2024).

This study quantified blood bicarbonate (HCO3−) kinetics and gastrointestinal upset to determine the gender-related ergogenic potential of sodium bicarbonate (0.15-, 0.25- and 0.35 gSB·kgFat-free mass (FFM)–1) in high intensity functional training. Double-blind randomized placebo-controlled crossover. Thirty female and male athletes performed two bouts of the Wingate Anaerobic Test (WAnTPRE-HIFT and WAnTPOST-HIFT) interspaced with two 3-min bouts of Wall Balls and Burpees 120 min after ingestion of three sodium bicarbonate doses. Blood HCO3− was determined pre-ingestion, after supplementation and before/post exercise. Gastrointestinal upset was evaluated 120 min post-ingestion. Control (CTRL) measurements were performed. There were significant gender × treatment interactions for: changes in blood HCO3− at 60 min post-ingestion (p = 0.014; η2p = 0.104; at 0.15 gSB·kgFFM−1 males experienced higher increase than females); peak power (p = 0.015; η2p = 0.103) and average power (p = 0.005; η2p = 0.124) during WAnTPOST-HIFT, and changes in peak power between the Wingate Anaerobic Test bouts (p = 0.049; η2p = 0.081). Sodium bicarbonate compared to PLA had no significant impact on Wall Balls and Burpees performance. The dose of 0.35 gSB·kgFFM−1 resulted in higher less severe gastrointestinal symptoms compared to CTRL and 0.15 gSB·kgFFM−1 (p = 0.001; W = 0.178); and higher total gastrointestinal upset compared to CTRL, PLA and 0.15 gSB·kgFFM−1 (p < 0.001; W = 0.323). There were dose- and gender-related differences in extracellular buffering capacity and ergogenic potential of sodium bicarbonate. The study suggested a detrimental impact of gastrointestinal upset on performance.

Purpose: We evaluated the feasibility of individualized sodium bicarbonate (NaHCO3) supplementation and its physiological effects on simulated artistic swimming duet performance, including blood buffering responses, perceived exertion, gastrointestinal (GI) tolerance, and performance scores. Methods: Seventeen (n = 17) elite adolescent female artistic swimmers completed an initial trial to determine individual time-to-peak blood bicarbonate concentration (Part 1). Subsequently, a subset (n = 7) completed a randomized, double-blind, crossover intervention (Part 2), performing competition duet routines (4 min) after ingesting either 0.3 g/kg NaHCO3 or a placebo timed to their individual alkalosis peak. Blood gas and lactate samples were taken pre- and post-performance. Performance was scored by blinded FINA adjudicators. GI discomfort was assessed before and after each routine. Results: Peak blood bicarbonate occurred at 52 ± 9 min post-ingestion, with a mean increase of 6.7 ± 1.8 mmol/L (g = 5.03). In Part 2 (n = 7), NaHCO3 significantly elevated pre- and post-performance pH (7.46 ± 0.02 vs. 7.37 ± 0.01; 7.34 ± 0.02 vs. 7.26 ± 0.03), HCO3− (29.5 ± 0.9 vs. 22.4 ± 0.4 mmol/L; 21.5 ± 1.2 vs. 15.7 ± 1.5 mmol/L), and base excess (5.9 ± 0.6 vs. −2.9 ± 0.5 mmol/L; −4.3 ± 0.8 vs. −10.3 ± 1.1 mmol/L) compared to the placebo (all p < 0.05, g = 3.99–14.93). Post-performance lactate was higher (9.3 ± 1.0 vs. 8.4 ± 0.9 mmol/L, g = 0.89), while rating of perceived exertion (RPE) was lower (12.9 ± 0.7 vs. 14.4 ± 0.7, p < 0.05, g = −2.14). Propulsion improved (6.66 ± 0.16 vs. 6.52 ± 0.20, g = 0.85), with no change in execution. Mild gastrointestinal symptoms were transiently elevated with NaHCO3. Conclusions: Individualized NaHCO3 dosing is a feasible and effective ergogenic strategy for artistic swimmers, enhancing systemic alkalosis and perceptual tolerance while preserving technical execution. These findings support the sport-specific integration of NaHCO3 to optimize anaerobic performance elements in high-level artistic swimming.

Purpose Enteric-coated sodium bicarbonate (NaHCO 3 ) can attenuate gastrointestinal (GI) symptoms following acute bicarbonate loading, although the subsequent effects on exercise performance have not been investigated. The purpose of this study was to examine the effects of enteric-coated NaHCO 3 supplementation on high-intensity exercise performance and GI symptoms. Methods Eleven trained male cyclists completed three 4 km time trials after consuming; a placebo or 0.3 g∙kg –1 body mass NaHCO 3 in enteric-coated or gelatin capsules. Exercise trials were timed with individual peak blood bicarbonate ion concentration ([HCO 3 – ]). Blood acid–base balance was measured pre-ingestion, pre-exercise, and post-exercise, whereas GI symptoms were recorded pre-ingestion and immediately pre-exercise. Results Pre-exercise blood [HCO3 − ] and potential hydrogen (pH) were greater for both NaHCO 3 conditions ( P  < 0.0005) when compared to placebo. Performance time was faster with enteric-coated (− 8.5 ± 9.6 s, P  = 0.044) and gelatin (− 9.6 ± 7.2 s, P  = 0.004) NaHCO 3 compared to placebo, with no significant difference between conditions (mean difference = 1.1 ± 5.3 s, P  = 1.000). Physiological responses were similar between conditions, although blood lactate ion concentration was higher with gelatin NaHCO 3 (2.4 ± 1.7 mmol∙L –1 , P  = 0.003) compared with placebo. Furthermore, fewer participants experienced GI symptoms with enteric-coated ( n  = 3) compared to gelatin ( n  = 7) NaHCO 3 . Discussion Acute enteric-coated NaHCO 3 consumption mitigates GI symptoms at the onset of exercise and improves subsequent 4 km cycling TT performance. Athletes who experience GI side-effects after acute bicarbonate loading may, therefore, benefit from enteric-coated NaHCO 3 supplementation prior to exercise performance.

Patients with advanced chronic kidney disease lose the capacity to fully excrete endogenous acid, resulting in chronic metabolic acidosis that increases the risk of disease progression and causes muscle catabolism and bone resorption. Veverimer, a non-absorbed, counterion-free, polymeric drug, selectively binds and removes hydrochloric acid from the gastrointestinal lumen, unlike current oral sodium bicarbonate therapy for metabolic acidosis that only neutralises accumulated acid. We assessed the efficacy and safety of veverimer as a treatment for metabolic acidosis in patients with chronic kidney disease. We did a multicentre, parallel, randomised, double-blind, placebo-controlled study at 37 sites (hospitals and specialty clinics) in Bulgaria, Croatia, Georgia, Hungary, Serbia, Slovenia, Ukraine, and the USA. Eligible participants were patients aged 18–85 years with non-dialysis-dependent chronic kidney disease (estimated glomerular filtration rate of 20–40 mL/min per 1·73 m2) and metabolic acidosis (serum bicarbonate concentration of 12–20 mmol/L). Patients were randomly assigned (4:3) to veverimer 6 g/day or placebo for 12 weeks while they consumed their typical diet. Both drugs were taken as oral suspensions in water with lunch. Randomisation was done by study site personnel with a computer-generated randomisation code with balanced permuted blocks (block size of seven) and stratified by baseline bicarbonate (≤18 mmol/L vs >18 mmol/L). Patients and investigators were masked to treatment allocation; however, because the appearance of placebo differed from veverimer, a non-masked site staff member who had no other role in the study dispensed, prepared, and supervised dosing of the study drugs. The composite primary efficacy endpoint was the difference (veverimer–placebo) in the proportion of patients achieving at week 12 either an increase of 4 mmol/L or more from baseline in serum bicarbonate concentration or serum bicarbonate in the normal range of 22–29 mmol/L, assessed in the modified intention-to-treat population (all patients with a baseline and at least one post-baseline serum bicarbonate value). Patients fasted for at least 4 h (consuming only water) before measurements of bicarbonate. Safety was assessed in all patients who received any amount of study drug. This trial is registered with ClinicalTrials.gov, number NCT03317444. Between Sept 26, 2017, and Feb 9, 2018, we randomly assigned 124 participants to veverimer and 93 to placebo. The composite primary endpoint was met by 71 (59%) of 120 patients in the veverimer group versus 20 (22%) of 89 patients in the placebo group (a difference of 37%, 95% CI 23–49; p<0·0001). The most common body system in which adverse events in the veverimer group occurred was gastrointestinal; of these, non-treatment limiting diarrhoea was the most common event (11 [9%] vs three [3%] in the veverimer and placebo groups, respectively). The most common treatment-related adverse events were gastrointestinal (diarrhoea, flatulence, nausea, and constipation) occurring in 16 (13%) patients with veverimer and five (5%) patients with placebo. Two deaths occurred during the study, both in the placebo group (unstable angina and pneumonia). Veverimer effectively and safely corrected metabolic acidosis. Longer-term studies are warranted to assess the effects of veverimer on physical functioning and to assess other deleterious consequences of metabolic acidosis including progression of chronic kidney disease and bone health. Tricida.

Introduction β-alanine (BAl) and NaHCO 3 (SB) ingestion may provide performance benefits by enhancing concentrations of their respective physiochemical buffer counterparts, muscle carnosine and blood bicarbonate, counteracting acidosis during intense exercise. This study examined the effect of BAl and SB co-supplementation as an ergogenic strategy during high-intensity exercise. Methods Eight healthy males ingested either BAl (4.8 g day −1 for 4 weeks, increased to 6.4 g day −1 for 2 weeks) or placebo (Pl) (CaCO 3 ) for 6 weeks, in a crossover design (6-week washout between supplements). After each chronic supplementation period participants performed two trials, each consisting of two intense exercise tests performed over consecutive days. Trials were separated by 1 week and consisted of a repeated sprint ability (RSA) test and cycling capacity test at 110 % Wmax (CCT 110 % ). Placebo (Pl) or SB (300 mg kgbw −1 ) was ingested prior to exercise in a crossover design to creating four supplement conditions (BAl-Pl, BAl-SB, Pl–Pl, Pl-SB). Results Carnosine increased in the gastrocnemius ( n  = 5) ( p  = 0.03) and soleus ( n  = 5) ( p  = 0.02) following BAl supplementation, and Pl-SB and BAl-SB ingestion elevated blood HCO 3 − concentrations ( p  < 0.01). Although buffering capacity was elevated following both BAl and SB ingestion, performance improvement was only observed with BAl-Pl and BAl-SB increasing time to exhaustion of the CCT 110 % test 14 and 16 %, respectively, compared to Pl–Pl ( p  < 0.01). Conclusion Supplementation of BAl and SB elevated buffering potential by increasing muscle carnosine and blood bicarbonate levels, respectively. BAl ingestion improved performance during the CCT 110 % , with no aggregating effect of SB supplementation ( p  > 0.05). Performance was not different between treatments during the RSA test.

Background Correction of metabolic acidosis (MA) with nutritional therapy or bicarbonate administration is widely used in chronic kidney disease (CKD) patients. However, it is unknown whether these interventions reduce insulin resistance (IR) in diabetic patients with CKD. We sought to evaluate the effect of MA correction on endogenous insulin action in diabetic type 2 (DM2) CKD patients. Methods A total of 145 CKD subjects (83 men e 62 women) with DM2 treated with oral antidiabetic drugs were included in the study and followed up to 1 year. All patients were randomly assigned 1:1 to either open-label (A) oral bicarbonate to achieve serum bicarbonate levels of 24–28 mmol/L (treatment group) or (B) no treatment (control group). The Homeostatic model assessment (HOMA) index was used to evaluate IR at study inception and conclusion. Parametric and non-parametric tests as well as linear regression were used. Results At baseline no differences in demographic and clinical characteristics between the two groups was observed. Average dose of bicarbonate in the treatment group was 0.7 ± 0.2 mmol/kg. Treated patients showed a better metabolic control as confirmed by lower insulin levels (13.4 ± 5.2 vs 19.9 ± 6.3; for treated and control subjects respectively; p  < 0.001), Homa-IR (5.9[5.0-7.0] vs 6.3[5.3–8.2]; p  = 0.01) and need for oral antidiabetic drugs. The serum bicarbonate and HOMA-IR relationship was non-linear and the largest HOMA-IR reduction was noted for serum bicarbonate levels between 24 and 28 mmol/l. Adjustment for confounders, suggests that serum bicarbonate rather than treatment drives the effect on HOMA-IR. Conclusions Serum bicarbonate is related to IR and the largest HOMA-IR reduction is noted for serum bicarbonate between 24 and 28 mmol/l. Treatment with bicarbonate influences IR. However, changes in serum bicarbonate explains the effect of treatment on HOMA index. Future efforts are required to validate these results in diabetic and non-diabetic CKD patients. Trial registration The trial was registered at www.clinicaltrial.gov (Use of Bicarbonate in Chronic Renal Insufficiency (UBI) study - NCT01640119 )

Background Sodium bicarbonate intake has been shown to improve exercise tolerance, but the effects on high-intensity intermittent exercise are less clear. Thus, the aim of the present study was to determine the effect of sodium bicarbonate intake on Yo-Yo intermittent recovery test level 2 performance in trained young men. Method Thirteen men aged 23 ± 1 year (height: 180 ± 2 cm, weight: 78 ± 3 kg; VO 2 max: 61.3 ± 3.3 mlO 2  · kg −1  · min −1 ; means ± SEM) performed the Yo-Yo intermittent recovery test level 2 (Yo-Yo IR2) on two separate occasions in randomized order with (SBC) and without (CON) prior intake of sodium bicarbonate (0.4 g · kg −1 body weight). Heart rate and rating of perceived exertion (RPE) were measured during the test and venous blood samples were taken frequently. Results Yo-Yo IR2 performance was 14 % higher (P = 0.04) in SBC than in CON (735 ± 61 vs 646 ± 46 m, respectively). Blood pH and bicarbonate were similar between trials at baseline, but higher (P = 0.003) immediately prior to the Yo-Yo IR2 test in SBC than in CON (7.44 ± 0.01 vs 7.32 ± 0.01 and 33.7 ± 3.2 vs 27.3 ± 0.6 mmol · l −1 , respectively). Blood lactate was 0.9 ± 0.1 and 0.8 ± 0.1 mmol · l −1 at baseline and increased to 11.3 ± 1.4 and 9.4 ± 0.8 mmol · l −1 at exhaustion in SBC and CON, respectively, being higher (P = 0.03) in SBC. Additionally, peak blood lactate was higher (P = 0.02) in SBC than in CON (11.7 ± 1.2 vs 10.2 ± 0.7 mmol · l −1 ). Blood glucose, plasma K + and Na + were not different between trials. Peak heart rate reached at exhaustion was 197 ± 3 and 195 ± 3 bpm in SBC and CON, respectively, with no difference between conditions. RPE was 7 % lower (P = 0.003) in SBC than in CON after 440 m, but similar at exhaustion (19.3 ± 0.2 and 19.5 ± 0.2). Conclusion In conclusion, high-intensity intermittent exercise performance is improved by prior intake of sodium bicarbonate in trained young men, with concomitant elevations in blood alkalosis and peak blood lactate levels, as well as lowered rating of perceived exertion.

This study aimed to investigate the ability of highly trained athletes to consistently perform at their highest level during a simulated three-day 400 m race and to examine the impact of an alkaline diet associated with chronic consumption of bicarbonate-rich water or placebo on their blood metabolic responses before and after the three races. Twenty-two highly trained athletes, divided into two groups—one with an alkalizing diet and placebo water (PLA) and the other with an alkalizing diet and bicarbonate-rich water (BIC)—performed a 400 m race for three consecutive days. Performance metrics, urine and blood samples assessing acid-base balance, and indirect markers of neuro-muscular fatigue were measured before and after each 400 m race. The evolution of the Potential Renal Acid Load (PRAL) index and urinary pH highlights the combination of an alkalizing diet and bicarbonate-rich hydration, modifying the acid-base state (p < 0.05). Athletes in the PLA group replicated the same level of performance during three consecutive daily races without an increase in fatigue-associated markers. Athletes experienced similar levels of metabolic perturbations during the three 400 m races, with improved lactate clearance 20 min after the third race compared to the first two (p < 0.05). This optimization of the buffering capacity through ecological alkaline nutrition and hydration allowed athletes in the BIC group to improve their performance during the third 400 m race (p < 0.01). This study highlights athletes’ ability to replicate high-level performances over three consecutive days with the same extreme level of metabolic disturbances, and an alkaline diet combined with bicarbonate-rich water consumption appears to enhance performance in a 400 m race.