Bicarbonate (Sodium Bicarbonate): A Comprehensive Reference
1. Identity, Chemical Nature, and Common Forms
Sodium bicarbonate (IUPAC name: sodium hydrogen carbonate), commonly known as baking soda or bicarbonate of soda (or simply "bicarb," especially in the UK), is a chemical compound with the formula NaHCO₃. It is a salt composed of a sodium cation (Na⁺) and a bicarbonate anion (HCO₃⁻). Sodium bicarbonate is a white solid that is crystalline but often appears as a fine powder, with a slightly salty, alkaline taste resembling that of sodium carbonate ("washing soda").
Its IUPAC name is sodium hydrogen carbonate; other common names include baking soda, bicarb, and bicarbonate of soda. In clinical and pharmaceutical contexts it is referred to simply as "sodium bicarbonate" or abbreviated as "SB" or "NaHCO₃." In European food regulation, it carries an E-number designation as a permitted food additive.
Natural Sources and Mineral Forms
Sodium bicarbonate is a crystalline salt found in a natural mineral form in nahcolite deposits. The natural mineral form is nahcolite, although it is more commonly found as a component of the mineral trona. It is a component of the mineral natron and is found dissolved in many mineral springs.
Nahcolite commonly forms by reaction of carbon dioxide with the mineral trona in evaporated lake basins. It is found in large quantities in the central salt body of Searles Lake, California, and as concentrations up to 5 feet (1.5 metres) thick in oil shale deposits in the Piceance Basin of the Green River Formation in Colorado, where it is commercially mined. It has also been mined in Botswana and Kenya, and there are sizable deposits in Uganda, Turkey, and Mexico. Nahcolite can be used in traditional applications of sodium bicarbonate—e.g., in baking soda and toothpaste.
Naturally, sodium bicarbonate occurs in deposits of minerals such as trona (formed in alkaline lake environments primarily located in the Americas) and nahcolite (found in several locations including parts of Africa and Asia). More recently, synthetic manufacturing has been used to create the substance on a larger scale through the Solvay process. The Solvay process involves chemically transforming sodium chloride through various reactions into sodium bicarbonate.
Dosage Forms and Preparations
Sodium bicarbonate is available in numerous forms across dietary, pharmaceutical, and clinical settings:
- Powder/bulk: Fine white powder for oral dissolution in water, the most traditional preparation.
- Tablets and capsules: Standard uncoated oral tablets and gelatin capsules, typically used in clinical trials and supplement products.
- Enteric-coated capsules/tablets: Enteric-coated tablet formulation protects sodium bicarbonate under acidic conditions and releases bicarbonate in the intestine. Enteric-coated tablet formulation also reduced the oral dose required to achieve a blood bicarbonate concentration over 5 mmol·L⁻¹ from 300 mg·kg⁻¹ of uncoated tablet formulation to 225 mg·kg⁻¹.
- Intravenous solution: Used in acute clinical settings for rapid correction of severe metabolic acidosis.
- Dentifrice/toothpaste: Incorporated into oral care products for its mild abrasive and buffering properties.
2. Traditional and Historical Use
Ancient Egypt and the Greco-Roman World
The ancient Egyptians discovered sodium bicarbonate in the form of natron, a naturally occurring mineral. Natron was indispensable in the mummification process, prized for its ability to preserve bodies and ward off decay. Its mildly abrasive texture also made it a favored cleaning agent, used to purify homes and temples alike.
Natron is a naturally occurring mixture of sodium carbonate decahydrate and around 17% sodium bicarbonate (also called baking soda, NaHCO₃) along with small quantities of sodium chloride and sodium sulfate. It is widely believed that natron was the main desiccation agent in the preparation of Egyptian mummified bodies in the 18th Dynasty. Natron is a natural mixture of sodium chloride, sodium sulphate, sodium carbonate and sodium bicarbonate found in the Nile Delta, which has significant desiccation properties.
Natron was known as "netjeri," the Ancient Egyptian word for "pure" or "divine," and through several thousand years would become the word natron, which is also the reason why the chemical symbol for sodium is Na.
Natron or native soda, a natural compound of sodium salts, was a very important product in ancient history. It was produced in Egypt, the Middle East, and Greece. Natron was used for medicine, cookery, agriculture, in glass-making, and to dehydrate Egyptian mummies. The medicinal uses are known thanks to Egyptian pharaonic, Greek, and Latin texts, which are rich in hundreds of recipes. Those treatments concerning almost every part of the body were essentially applied externally, often intended to treat dermatological pathology, hydro-electrolytic disorders, and lesions caused by fungi and parasites.
Sodium bicarbonate's reputation spread across the Mediterranean, where the Greeks and Romans found new ways to exploit its versatility. The Romans referred to it as "nitrum" and used it both for medicinal purposes and in the creation of amphorae, the iconic vessels that stored wine and oil.
Babylonian and Early Medicinal Traditions
Babylonian clay tablets describe a substance remarkably similar to sodium bicarbonate, highlighting its use in soap making and medicinal preparations.
Traditional Internal Use as an Antacid
Sodium bicarbonate-rich natron variants served as antacids in traditional medicine by neutralizing stomach acid and relieving heartburn or indigestion. In some cultures, natron was dissolved in water and consumed in small amounts to alleviate gastrointestinal discomfort. The mildly abrasive texture of powdered natron also allowed it to be used as a natural toothpaste or tooth cleanser, and its alkaline nature helped neutralize acids in the mouth that cause tooth decay.
Industrial Era and Modern Availability
First isolated by Nicolas Leblanc in the 1790s, it wasn't until the Solvay process was introduced in the 1860s that industrial-scale production became possible. Today, this chemical powerhouse is produced globally, with an estimated volume of 2 million tons per year.
Infusion of sodium carbonate (Na₂CO₃) into cholera patients to compensate for loss of serum alkali in diarrhea was recorded in the 1830s, and the commercial production of sodium bicarbonate (NaHCO₃) for use as an antacid (Brioschi®) apparently dates back to the 1880s.
3. Key Constituents and Mechanisms of Action
Chemical Composition
Sodium bicarbonate (NaHCO₃) reveals its chemical identity as a salt composed of sodium (Na⁺) and bicarbonate (HCO₃⁻) ions. The bicarbonate ion (HCO₃⁻) is the primary pharmacologically active species. It is the same ion that constitutes the body's principal endogenous extracellular buffer. Because sodium bicarbonate is 27% sodium, ergogenic doses (i.e., 300 mg·kg⁻¹) result in sodium intakes well above the Dietary Reference Intake's upper limit of 2300 mg/day.
Buffering Mechanism
The onset of muscular fatigue is associated with a rapid increase in the production of metabolic acids. The tolerance of high-intensity exercise may be limited by the ability of the body to counteract decreases in intracellular (muscle) and extracellular (blood) pH through its intrinsic buffering systems.
Sodium bicarbonate ingestion increases the extracellular buffering and dynamic buffering capacity, increasing the rate at which accumulating H⁺ is removed from the working muscles during high-intensity exercise, which ultimately contributes to intramuscular pH maintenance.
Sodium bicarbonate ingestion increases the concentration of HCO₃⁻ in the stomach lumen, some of which neutralizes HCl to form CO₂ and increases luminal pH. The rise in pH stimulates the Cl⁻/HCO₃⁻ antiporter in the parietal cells, which transports HCO₃⁻ into the extracellular fluid. This transport is coupled with the H-K-ATPase pump that secretes H⁺ into the stomach lumen to restore the pH.
The ergogenic effect of sodium bicarbonate on exercise performance stems from the reinforced extracellular bicarbonate buffer capacity to regulate acid-base balance during high-intensity exercise. The elevated bicarbonate enlarges the gradient between extracellular and intracellular H⁺, which stimulates the lactate/H⁺ cotransporter. The rationale for the ergogenic effects of bicarbonate is that the increase in extracellular pH and bicarbonate can enhance the efflux of lactate and H⁺ from the muscle cell.
Sodium bicarbonate also appears to influence phosphocreatine degradation (PCr) and inorganic phosphate (Pi) accumulation, glycolytic intermediates (muscle protons and lactate), and intra- and extracellular distribution of metabolites and other strong ions (Na⁺, K⁺, and Cl⁻), which appear to contribute to a performance-enhancing effect.
The ergogenic mechanisms of sodium bicarbonate are not yet fully understood. Nevertheless, an increase in extracellular buffering capacity is a widely accepted mechanism.
Extracellular Bicarbonate Concentration
Extracellular bicarbonate concentration can be increased by about 20% following ingestion of sodium bicarbonate (~0.3 g per kg body mass 1–2 hours before exercise).
Acid-Base Neutralization in the Gastrointestinal Tract
When sodium bicarbonate contacts hydrochloric acid (HCl) in the stomach, it undergoes a neutralization reaction, producing water, carbon dioxide, and sodium chloride. This is the basis for its long-standing use as an antacid. The most commonly reported side effect is gastrointestinal discomfort, including stomach bloating, belching, bowel urgency, stomachache, stomach cramps, flatulence, diarrhea, nausea, and vomiting. Some of these side effects are caused by carbon dioxide gas, which is produced through carbonic acid after neutralization of sodium bicarbonate by gastric acid in the stomach.
4. Scientific Evidence by Area of Use
4.1 Athletic and Exercise Performance
According to recent literature, sodium bicarbonate (NaHCO₃) has been proposed as a performance-enhancing aid by reducing acidosis during exercise. This is one of the most extensively studied areas of sodium bicarbonate supplementation, with decades of research and multiple meta-analyses now available.
ISSN Position Stand (2021)
The International Society of Sports Nutrition (ISSN) published a comprehensive position stand on sodium bicarbonate and exercise performance in 2021. The ergogenic effects of sodium bicarbonate are mostly established for exercise tasks of high-intensity that last between 30 seconds and 12 minutes. Sodium bicarbonate improves performance in single- and multiple-bout exercise. Sodium bicarbonate improves exercise performance in both men and women. For single-dose supplementation protocols, 0.2 g/kg of sodium bicarbonate seems to be the minimum dose required to experience improvements in exercise performance. The optimal dose of sodium bicarbonate for ergogenic effects seems to be 0.3 g/kg.
Higher doses (e.g., 0.4 or 0.5 g/kg) may not be required in single-dose supplementation protocols, because they do not provide additional benefits (compared with 0.3 g/kg) and are associated with a higher incidence and severity of adverse side-effects. For single-dose supplementation protocols, the recommended timing of sodium bicarbonate ingestion is between 60 and 180 minutes before exercise or competition.
Multiple-day protocols of sodium bicarbonate supplementation can also be effective in improving exercise performance. The duration of these protocols is generally between 3 and 7 days before the exercise test, and a total sodium bicarbonate dose of 0.4 or 0.5 g/kg per day produces ergogenic effects. The total daily dose is commonly divided into smaller doses, ingested at multiple points throughout the day (e.g., 0.1 to 0.2 g/kg of sodium bicarbonate consumed at breakfast, lunch, and dinner).
Umbrella Review of Meta-Analyses
An umbrella review found eight reviews of moderate and high methodological quality met inclusion criteria. Using the GRADE framework, evidence for the ergogenic effects of sodium bicarbonate supplementation on peak and mean power in the Wingate test and Yo-Yo test performance was classified as being of moderate quality.
High-Intensity Exercise and Time-to-Exhaustion
Sodium bicarbonate shows ergogenic potential in physical exercise and sports activities, although there is no strong evidence which performance markers show the greatest benefit from this supplement. A systematic review was conducted using three databases, including 17 clinical trials. Time to exhaustion was assessed in six studies, while time trial performance was evaluated in five studies. A significant beneficial effect of supplementation on time to exhaustion was found in a random effects model (effect size 1.48; 95% CI, 0.49 to 2.48).
In recent years, NaHCO₃ has attracted considerable attention as it was shown to significantly improve performance by up to 3% in swimming and cycling athletes.
Continuous Running Performance — Null Findings
Sodium bicarbonate supplementation may enhance short-term, high-intensity exercise performance through improved extracellular buffering capacity, but its effect on continuous running performance has not been systematically evaluated until recently. A systematic review with meta-analysis of randomized, double-blind, placebo-controlled trials was conducted examining the effects of oral single-dose SB supplementation on continuous running performance. The results of this 2025 review suggest negligible benefit for continuous (as opposed to intermittent or short-burst) running, highlighting that while several reviews have reported improved athletic performance with SB supplementation, the magnitude and consistency of these ergogenic benefits are highly variable.
Combat Sports
According to the ISSN position stand, supplementation with sodium bicarbonate (doses from 0.2 to 0.5 g/kg) improves performance in muscular endurance activities and various combat sports, including boxing, judo, karate, taekwondo, and wrestling, and in high-intensity cycling, running, swimming, and rowing.
A separate systematic review and meta-analysis examined the effects of NaHCO₃ supplementation on biochemical and physical measurements of combat sports athletes. However, performance measures (rating of perceived exertion, power, and specific performance) did not show a significant difference (p < 0.05). In conclusion, NaHCO₃ supplementation causes a significant increase in blood lactate, consistent with the proposed mechanism of enhanced lactate/H⁺ efflux from working muscle cells.
Ergolytic Potential
Studies have shown that NaHCO₃ may not only be an ergogenic, but also an ergolytic substance. The reasoning behind this may lie within the mechanism of action, as the bicarbonate buffer system is not solely responsible for blood pH but is also vital in other systems, such as the stomach and duodenum by neutralizing gastric acid. Gastrointestinal distress induced by supplementation can impair rather than enhance performance in some individuals.
Evidence strength summary (exercise performance): Moderate-quality evidence (GRADE classification) supports ergogenic effects for high-intensity, short-to-medium duration exercise (30 seconds to 12 minutes). Effects on continuous endurance running are not well-supported. Individual variability is substantial, partly driven by GI tolerance.
4.2 Chronic Kidney Disease (CKD) and Metabolic Acidosis
Chronic kidney disease (CKD) is a global health burden, with metabolic acidosis being a common complication that accelerates disease progression and contributes to muscle wasting, bone demineralization, and systemic inflammation. Oral sodium bicarbonate has been used for decades to counteract metabolic acidosis.
Systematic Reviews and Meta-Analyses
Sodium bicarbonate supplementation is widely used to correct acidosis, but its effects on kidney function and clinical outcomes remain inconsistent. A 2025 PRISMA-compliant systematic review searched PubMed, Scopus, MEDLINE, and the Cochrane Library through May 2025. Nine randomized controlled trials (RCTs) involving 1,354 patients were included. Studies assessed the effects of SB on estimated glomerular filtration rate (eGFR), serum bicarbonate, muscle mass, blood pressure, and adverse events.
SB supplementation consistently improved serum bicarbonate levels across all included studies, with statistically significant increases reported. The impact on kidney function was variable, with some trials demonstrating improved eGFR while others showed no significant benefit. Positive effects on muscle mass preservation were observed in several studies, though physical function and blood pressure outcomes remained inconsistent.
A separate 2021 meta-analysis of 1,853 patients with chronic metabolic acidosis found that there was a significant increase in serum bicarbonate level (MD 2.37 mEq/L; 95% CI, 1.03 to 3.72) and slowed decline in estimated glomerular filtration rate (eGFR) (MD −4.44 mL/min per 1.73 m², 95% CI, −4.92 to −3.96) compared with control groups.
The BiCARB Trial
The primary objective of the BiCARB trial was to determine whether oral bicarbonate therapy improves physical function compared to placebo in older people with CKD and mild acidosis. The secondary objectives were to assess the effect of bicarbonate supplementation on health-related quality of life, biochemical markers of CKD, bone and vascular health, adverse events, and healthcare costs. The trial was conducted as a parallel group, double-blind, placebo-controlled randomised trial, designed in response to a commissioning brief issued by the National Institute for Health Research (NIHR) Health Technology Assessment board. Participants were recruited from nephrology and geriatric medicine outpatients at 27 UK hospitals.
This pragmatic, multicentre RCT found that administration of oral sodium bicarbonate using a dose regimen similar to that currently used in UK practice did not improve physical function or quality of life or slow down deterioration of renal function compared with placebo in older people with category 4 or 5 CKD and a serum bicarbonate concentration of <22 mmol/L. Data from the BiCARB study, a multicenter, double-blind, placebo-controlled trial which enrolled patients aged ≥60 years with CKD stage IV or V, failed to observe any significant treatment effect of sodium bicarbonate on renal outcome including eGFR or risk of dialysis initiation. Moreover, oral sodium bicarbonate did not improve physical function but increased adverse events.
The evidence regarding the impact of SB on kidney function and acid-base balance in CKD remains heterogeneous. While several randomized controlled trials and cohort studies report improvements in estimated glomerular filtration rate and stabilization of kidney function, others raise concerns about sodium load, fluid retention, hypertension, and cardiovascular risk, particularly in patients with advanced CKD or comorbid heart failure.
Alkali therapy in CKD may have beneficial effects, but the effects may differ depending on the stage of CKD.
Evidence strength summary (CKD): SB reliably corrects serum bicarbonate levels (consistent across trials). Effects on eGFR preservation are mixed across trials; the largest UK pragmatic trial (BiCARB) found no significant benefit on physical function or kidney function decline in advanced CKD. Evidence is moderate in quality but heterogeneous; optimal patient selection, dosing strategy, and long-term safety require further investigation.
4.3 Bone Health and Acid Load
Both in vitro and in vivo studies in animals and humans suggest that bone base helps neutralize part of the dietary net acid load. This raises the question of whether decades of eating a high acid diet might contribute to the loss of bone mass in osteoporosis. If this idea is true, then additional alkali ingestion in the form of net base-producing foods or alkalinizing salts could potentially prevent this acid-related loss of bone.
The nutritional acid load hypothesis of osteoporosis has been reviewed extensively. This hypothesis posits that foods associated with an increased urinary acid excretion are deleterious for the skeleton, leading to osteoporosis and enhanced fragility fracture risk. Conversely, foods generating neutral or alkaline urine would favour bone growth and Ca balance, prevent bone loss, and reduce osteoporotic fracture risk. This theory currently influences nutrition research, dietary recommendations, and the marketing of alkaline salt products or medications meant to optimize bone health and prevent osteoporosis.
Recent reports have not sustained the existence of a pathophysiological mechanism linking the consumption of some nutrients, particularly animal protein, to the induction of a biologically significant metabolic acidosis that would result in a negative Ca balance, bone loss, and eventually osteoporotic fracture. Presently, data exist that support both the proponents as well as the opponents of this hypothesis. Recent literature reviews have tended to support either one side or the other.
Metabolic acidosis has been associated in observational studies with a range of adverse health outcomes in patients with CKD, including worse cardiovascular health, lower bone mineral density and increased fracture risk, impaired muscle function, and more rapid progression of kidney disease.
Evidence strength summary (bone health): Preliminary and conflicting. The acid-load hypothesis linking dietary acid burden to bone loss, and the corollary that bicarbonate supplementation protects bone, remains debated. Existing clinical trial evidence is insufficient to support a definitive recommendation for sodium bicarbonate as a bone-protective intervention in the general population; stronger evidence exists only in the CKD context where frank metabolic acidosis is present.
4.4 Muscle Preservation in CKD
Metabolic acidosis may play a key role in the pathogenesis of protein-energy wasting (PEW) in patients with chronic kidney disease. Potential benefits of SB may extend to muscle preservation, bone health, and reduced risk of adverse cardiovascular outcomes.
Results of one clinical study support an improvement in serum albumin level and muscle mass in patients who were supplemented with oral sodium bicarbonate, suggesting that bicarbonate supplementation helps in delaying the progression of CKD by relieving the effects of metabolic acidosis. However, adding the results of the BiCARB trial to meta-analysis findings showed no overall effect of bicarbonate on weight or mid-arm muscle circumference.
Evidence strength summary (muscle wasting in CKD): Mixed. Some individual RCTs show preservation of lean body mass; meta-analytic pooling (including the BiCARB data) does not confirm a significant effect. Larger, longer-duration studies targeting specific CKD stages are needed.
4.5 Acute Medical Conditions
Sodium bicarbonate has been used in the treatment of different pathologies, such as hyperkalemia, cardiac arrest, tricyclic antidepressant toxicity, aspirin toxicity, acute acidosis, lactic acidosis, diabetic ketoacidosis, rhabdomyolysis, and adrenergic receptor resistance to catecholamine in patients with shock. An ongoing debate about bicarbonate's efficacy and potential harm has been raised for decades because of the lack of evidence supporting its potential efficacy. Despite the guidelines' restrictions, sodium bicarbonate has been overused in clinical practice.
It is believed that sodium bicarbonate may reverse acidosis-induced myocardial depression, hemodynamic instability, ventricular arrhythmias, impaired cellular energy production, resistance to catecholamines, altered metabolism, enzyme suppression, immune dysfunction, and ineffective oxygen delivery.
Evidence strength summary (acute medicine): The clinical evidence base for several acute indications is limited and contested; many uses persist from historical practice rather than high-quality RCT evidence. This remains an area of ongoing research and institutional guideline review.
4.6 Cancer Microenvironment — Preliminary / Preclinical Evidence
The potential of tumor alkalization therapy using sodium bicarbonate in the treatment of malignant ascites has been studied. The concept of intraperitoneal perfusion with an alkalizing solution to increase the extracellular pH and its antitumor effect was explored. Not only oral but also intraperitoneal treatment with sodium bicarbonate reduced the pH gradient in mouse models of breast cancer, enhancing the response to weak-base chemotherapy drugs. It was shown that sodium bicarbonate inhibits the growth of breast cancer tumors in animal studies when injected subcutaneously surrounding the tumors every other day.
Despite numerous specious claims that baking soda is a miracle cure for cancer, the therapeutic value of controlling acid-base balance is indisputable and is the basis of FDA-approved treatments for constipation, epilepsy, metabolic acidosis, and peptic ulcers.
Evidence strength summary (cancer): Preclinical (animal model) only. No robust human RCT data exist supporting sodium bicarbonate supplementation as an anti-cancer intervention. Current evidence does not support its use for this purpose outside of controlled research settings.
4.7 Gastrointestinal (Antacid) Use
In medical contexts, sodium bicarbonate is used to treat indigestion and may improve renal function in individuals with chronic kidney disease. Its role as an antacid is historically its oldest medicinal application, and it remains a component of over-the-counter antacid preparations. The mechanism is straightforward chemical neutralization of gastric hydrochloric acid.
Evidence strength summary (antacid): Well-established pharmacological mechanism and long-standing clinical and traditional use. Comparable to other antacid salts. Short-term relief of dyspepsia and heartburn is clinically accepted; not recommended as a long-term substitute for investigation of underlying conditions.
5. Body Systems and Health Areas
- Renal/Kidney System: Correction of metabolic acidosis in CKD; potential modulation of eGFR decline; urinary alkalinization (including for uric acid stone prevention and some drug toxicities).
- Musculoskeletal System: Extracellular buffering during high-intensity exercise; potential preservation of lean body mass in CKD-associated acidosis; role in the acid-load/bone-loss hypothesis.
- Gastrointestinal System: Neutralization of gastric acid; short-term relief of heartburn and indigestion; source of GI side effects at higher doses.
- Cardiovascular System: Sodium bicarbonate raises concerns about sodium load, fluid retention, hypertension, and cardiovascular risk, particularly in patients with advanced CKD or comorbid heart failure.
- Skeletal/Bone System: Associated with reduced urinary calcium excretion in some alkali supplementation studies; the acid-load/osteoporosis hypothesis involves bicarbonate as a theoretical bone-protective agent.
- Acid-Base Homeostasis: The bicarbonate/carbonic acid system is the body's primary extracellular buffer; exogenous sodium bicarbonate directly augments this system.
6. Dosage Forms and Dosages Reported in Studies
Exercise Performance
- For single-dose supplementation protocols, 0.2 g/kg of sodium bicarbonate seems to be the minimum dose required to experience improvements in exercise performance. The optimal dose for ergogenic effects seems to be 0.3 g/kg.
- Higher doses (e.g., 0.4 or 0.5 g/kg) are associated with a higher incidence and severity of adverse side-effects without providing additional benefits compared with 0.3 g/kg. The recommended timing is between 60 and 180 minutes before exercise or competition.
- Multiple-day protocols generally span 3 to 7 days before the exercise test, and a total sodium bicarbonate dose of 0.4 or 0.5 g/kg per day produces ergogenic effects. The total daily dose is commonly divided into smaller doses ingested at multiple points throughout the day (e.g., 0.1 to 0.2 g/kg consumed at breakfast, lunch, and dinner).
- Enteric-coated tablet formulation reduces the oral dose required to achieve a blood bicarbonate concentration over 5 mmol·L⁻¹ from 300 mg·kg⁻¹ to 225 mg·kg⁻¹.
CKD / Metabolic Acidosis
- In the BiCARB trial, participants received up to 3,000 mg per day of sodium bicarbonate to achieve serum bicarbonate ≥22 mEq/L.
- In one 9-month RCT, bicarbonate supplementation decreased metabolic acidosis in CKD patients; serum bicarbonate level increased time-dependently from 16.62 to 18.02 and 19.77 mEq/L after 6 and 9 months, respectively.
Strategies to Reduce GI Side Effects
Ingesting sodium bicarbonate (i) in smaller doses (e.g., 0.2 g/kg or 0.3 g/kg), (ii) around 180 minutes before exercise or adjusting the timing according to individual responses to side-effects, (iii) alongside a high-carbohydrate meal, and (iv) in enteric-coated capsules are possible strategies to minimize side effects.
7. Safety Considerations and Interactions
Gastrointestinal Adverse Effects
Sodium bicarbonate supplementation has the possibility of causing gastrointestinal discomfort, resulting in symptoms such as nausea, stomach pain, diarrhea, and vomiting. In one study, 10 of 11 subjects (91%) experienced diarrhea, 64% experienced bloating and thirst, and 45% experienced nausea after bicarbonate loading. Abdominal distress was found to be significantly more prominent in the sodium bicarbonate trial than the placebo, resulting in an increase in stomach cramping, stomachache, and diarrhea immediately after consumption.
Electrolyte Disturbances
Sodium bicarbonate may cause paradoxical respiratory acidosis, intracellular acidosis, hypokalemia, hypocalcemia, alkalosis, impaired oxygen delivery, cerebrospinal fluid acidosis, and neurologic dysfunction. These risks are most relevant in acute, high-dose intravenous administration, but electrolyte monitoring is prudent in any chronic oral supplementation context.
Sodium Load and Hypertension Risk
Because sodium bicarbonate is 27% sodium, ergogenic doses (300 mg·kg⁻¹) result in sodium intakes well above the Dietary Reference Intake's upper limit of 2,300 mg/day. It is therefore conceivable that bicarbonate loading could have hypertensive effects. Although oral sodium bicarbonate is widely used to correct metabolic acidosis, there exist potential risks of therapy including worsening hypertension and fluid overload.
Metabolic Alkalosis
Excessive or prolonged intake can induce metabolic alkalosis. It is crucial to pay attention to the potential harm that could be caused by excessive sodium bicarbonate administration.
Fluid Retention and Cardiovascular Risk in CKD
Concerns about sodium load, fluid retention, hypertension, and cardiovascular risk are particularly relevant in patients with advanced CKD or comorbid heart failure. A prior systematic review suggested that bicarbonate therapy may improve eGFR but increase diastolic blood pressure by 2.8 mmHg.
Impaired Ergogenic Effect Due to GI Distress
The discrepancy in previous performance findings may be due to side effects of typical dosing strategies. Most studies of the effects of SB on performance have administered a standard acute dose of sodium bicarbonate (300 mg·kg⁻¹ body weight), which may cause gastrointestinal distress and potentially minimize any ergogenic effect of the bicarbonate ingestion.
Overuse in Critical Care
The overuse of sodium bicarbonate in critical care may occur because of the desire to correct arterial blood gas parameters rapidly instead of achieving homeostasis by treating the cause of the metabolic acidosis.
Interactions with Other Supplements and Drugs
Studies have investigated the interaction of sodium bicarbonate with other ergogenic aids, such as beta-alanine, caffeine, and creatine. In the pharmacological context, sodium bicarbonate's alkalinization of urine can alter the renal clearance of drugs that are weak acids or weak bases, potentially increasing or decreasing their plasma concentrations. The influence of acid-base status on the pharmacokinetic properties of drugs is a recognized clinical consideration.
References
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