Sodium bicarbonate (commonly referred to as either 'Bicarb' or simply as Baking Soda) is a molecule with the formula of NaHCO3 that is sold in grocery stores but may also have health and performance enhancing properties. Sodium bicarbonate (as well as potassium bicarbonate) are approved for human consumption by the FDA with a GRAS rating.
Sodium bicarbonate (baking soda) is a generally recognized as safe food additive
Beyond the kidneys having a role in excreting excess hydrogen (H+) ions and reabsorbing bicarbonate into the blood (and controlling acidity via controlling what molecules get urinated), the kidneys themselves are a locus for bicarbonate production and the decline in bicarbonate production by the kidneys precedes metabolic acidosis of renal diseases or aging (associated with reduced renal function). Bicarbonate production can be reduced a certain level (during acidosis) before it stabilizes with further buffering potential coming from bone tissue.
Bicarbonate is produced by the kidneys as a buffer against excess acidity in the blood, and is capable of performing this task until the kidneys decline in function (and then a mild case of metabolic acidosis, or excess acidity that is nonlethal, ensues). Due to a preservation of bicarbonate after a certain point and buffering help from the bones, acidosis is associated with mineral loss from bones
Bicarbonate secretion can also occur in pretty much all sections of the gastrointestinal tract, and forms a barrier between the stomach and intestines (in the duodenum) to protect the intestines from the acidity of the stomach. Secretion can be induced by the hormones cholecystokinin, orexin-A, and apelin peptides and can occur via stimulation of cAMP or via Cl- dependent or independent (short chain fatty acid dependent) means.
Bicarbonate is secreted in the intestinal tract for protection against stomach acids
Dissolving sodium bicarbonate into a beverage and leaving it overnight (in the fridge) does not appear to hinder the ability of this supplement to increase blood bicarbonate levels.
It has been confirmed that the consumption of food alongside sodium bicarbonate reduces gastrointestinal side effects relative to the same dose taken on an empty stomach, and serum increases of bicarbonate appear to be highest when coingested with food.
When 300mg/kg sodium bicarbonate is given to recreationally active males at rest (400mL liquid), there is an increase in blood bicarbonate and pH within 30 minutes which plateus at 60-90 minutes and declines yet remains above baseline for up to 3 hours post ingestion which is due to a reduction in serum hydrogen ions (H+) which follow the same time course.
The plateau in serum levels (from 300mg/kg) reached 30.7-31.7mmol/L from a concentration of 23.8mmol/L, and on an individual basis people in this study seemed to peak at either 60 minutes or 90 minutes (although all subjects recorded a peak).
Bicarbonate excretion in the kidneys is mediated by a variety of transports including the Cl- dependent class (AE1-3, short for Anion Exchange), the NA+ dependent class (NBC1,3, and 4 with NBC2 being a splice variant of NBC3; NDCBE1 and AE4) and the SLC26A class (DRA/SLC26A3, Pendrin/SLC26A4, PAT-1/SLC26A6, and SLC26A7). AE receptors exchange bicarbonate for chloride in a 1:1 ratio while the sodium (Na+) dependent transporters co-transport bicarbonate across membranes in either an electrogenic (NBC1, NBC4) or electroneutral (NBC3) manner with a 2 or 3:1 ratio of bicarbonate:sodium. The SLC26A class mediates Cl-/base conversions in general, and can act upon bicarbonate.
Bicarbonate excretion from the kidneys is mediated by a variety of receptors, most of which use ions as either exchange for bicarbonate or as a cotransporter
During instances of acute metabolic/respiratory alkalosis, potassium excretion is known to be enhanced (suppressed by acidosis) and urinary excretion of sodium, potassium, and chloride all tend to correlate with one another in a positve manner (sodium can cause potassium losses, potassium can cause sodium losses). Clinical investigations into the state of alkalosis in general tend to note an increase in potassium urinary excretion which is both marked and elevated for a few days, and this increase in urinary potassium losses are highly correlated with sodium losses. In clinical settings, it is possible to induce potassium losses in the urine with sodium bicarbonate supplementation and alkalosis tends to result in a 300-500mEq loss of potassium in man.
Oral ingestion of the standard dose of sodium bicarbonate (300mg/kg) has been found to cause a rapid spike in sodium excretion measured at 24+/-2% of the oral dose of sodium (82mg/kg) within 210 minutes, which is also noted with potassium bicarbonate, but to a lesser degree (although 26+/-5% of ingested potassium is similarly excreted).
This renal excretion induced by sodium bicarbonate does not appear to significantly affect calcium homeostatis significantly in otherwise healthy controls despite potssium bicarbonate causing a slight retention of calcium.
Possible due to sodium transport being coupled with bicarbonate transport, the increase in bicarbonate excretion following supplementation (as bicarbonate is regulated and excess disposed of) is met with an increase in sodium excretion to account for about a quarter of the sodium dose.
The increase of sodium excretion is met with an increase in potassium excretion, but since potassium is not being orally supplemented (with sodium bicarbonate) it is plausible that excessive usage of sodium bicarbonate paired with low dietary potassium intake can be a risk factor for low potassium levels
Acid sensing channels on neurons are known to be involved in synaptic plasticity, learning, memory, pain, and neurodegeneration and neuronal activity itself is known to reduce brain pH (increase acidity).
Acid concentrations in the brain may be able to act on acid-sensitive receptors and modulate neuronal activity
Physical exercise is known to induce brain-derived neurotrophic growth factors (such as BDNF) which are thought to mediate the cognitive promoting effects of exercise and has been confirmed to be induced by exercise in both healthy persons and those with cognitive ailments or spinal injuries.
High intensity exercise is known to have its neuroendocrine role somewhat linked to acidity (including prolactin and growth hormone release) but it appears that buffering the increases in pH with sodium bicarbonate does not modify exercise-induced BDNF increases.
The exercise induced increase in brain neurotrophic factors does not appear to be associated with serum acidity, and there is no evidence to suggest that supplemental buffering agents (such as sodium bicarbonate) can suppress the increase
The exercise-induced changes in energy production (normally almost exclusively provided by glucose at nonfasted rest but a reduction in glucose oxidation occurs simultaneously with lactate uptake by the brain which is used as fuel) do not appear to be related to metabolic acidosis, and as such supplemental bicarbonate has been found to not affect these parameters. It was initially hypothesized that an increase in bicarbonate would reduce transport of lactate across the blood brain barrier (as the transport enzymes increase in activity with increasing H+ ion concentration).
Despite theoretically preserving the percentage of glucose used relative to lactate during exercise (there is normally a shift to lactate from glucose with exhaustive exercise), supplementation bicarbonate does not appear to have this trait
Metabolic acidosis is known to reduce cerebral blood volume, as the blood vessels are sensitive to hydrogen ions and an increase in acidity independent of carbon dioxide concentrations (hypercapnia and normocapnia) will vasodilate (widen) the blood vessels via nitric oxide dependent means and activating potassium channels.
The above mechanisms may be related to the ability of chronic low grade acidosis to reduce cerebral blood volume, and in patients (youth) with mild metabolic acidosis given intravenous sodium bicarbonate, an increase in cerebral blood volume occurs without significant changes in blood oxygenation rates.
It is plausible that sodium bicarbonate can aid an adverse influence of metabolic acidosis, but currently it is not established if the low grade acidosis seen in society is a concern in this regard and no practical studies looking at sodium bicarbonate have been undertaken
It has been observed that, in response to a flashing checkerboard test, the increase in brain lactate was exacerbated in persons with panic disorders relative to controls and some evidence currently exists to support a link between panic disorder and altered acid:base balance in the brain (specifically, the balance between CO2 and bicarbonate) including that when panic attacks are resolved there is a normalization in biomarkers of acid:base metabolism (Bicarbonate, hydrogen ions, and pH).
Furthermore, the amygdala (a brain organ involved in fear, panic, and emotional learning) has been noted to respond to acid stimulation via the ASIC1a receptor which is highly expressed in the amygdala and fear circuits. Carbon dioxide (CO2) inhalation is also an experimental test to induce panic attacks which is also thought to be the reason hyperventilation contributes to panic attacks (via increasing CO2 intake relative to O2 intake) and persons with panic disorders are more sensitive to contrlled CO2 tests than healthy controls.
Conversely, acute alkalosis (significant increase in pH and reduction of acidity) is also capable of inducing panic symptoms in research animals and both sodium bicarbonate and sodium lactate are able to induce panic symptoms when infused into persons with panic disorders.
Persons with panic disorders appear to be more sensitive to disturbances of acid:base balance, which appears to be due to signalling through acid-sensitive receptors (and likely a higher sensitivity of acid:base disturbances on these receptors). However, both an increase and decrease of acidity are able to induce panic attacks in those with panic disorders and it is unlikely that sodium bicarbonate has a therapeutic role in this regard (instead, it is possible sodium bicarbonate can actually exacerbate symptoms)
It appears that β-endorphin release from exercise (from exercise above 60% VO2 max with no significant release at lower intensities) is due to acidosis, as increased β-endorphin release is highly correlated with decreasing pH and supplemental bicarbonate (300mg/kg) to maintain a pH above 7.4 significantly suppresses the release of β-endorphin.
Due to the suppression of acidification during exercise, which appears to be causative of endorphin release, buffering agents such as sodium bicarbonate can fairly potently suppress the exercise-induced release of β-endorphin
Although administration of acids (either acetazolamide or breathing 4% CO2) to reduce serum pH has been noted to increase the adrenaline release associated with exhaustive exercise it was also shown that induced alkalosis (via hyperventilation) failed to modify serum adrenaline responses. For studies that actually use sodium bicarbonate as an intervention to increase pH, 300mg/kg taken prior to a 90s cycling test (where there was no significant influence on performance) against resistance has failed to modify adrenaline whereas a similar test that noted a slight improvement in performance also noted a reduction in plasma adrenaline (34%) and noradrenaline (30%); the difference noted does not appear to be associated with the difference in performance, as one study using intravenous bicarbonte to control pH noted an increase in performance without changes in catecholamines.
Sodium bicarbonate has mixed evidence for its interactions on adrenaline, with either no effect or attenuating the exercise-induced increase somewhat
In menopausal women given mineral water with or without added bicarbonate (1,000mmol or so via 500mL water) alongside a standardized test meal was noted to reduce postprandial lipidemia over 7 hours (peak value reduced 13.2% and AUC reduced by 15.5%) without significantly affecting cholesterol.
One study has noted an inhibition of lipid absorption, but has not been replicated nor did it propose a theory as to why this occurred
The state of metabolic acidosis is known to promote LDL oxidation due to shortening the lag phase of oxidation, which is theoretically a pro-atherosclerotic event. There are currently no studies assessing the effects of sodium bicarbonate supplementation on atherosclerosis in persons with metabolic acidosis.
Is theoretically beneficial for LDL oxidation in persons with metabolic acidosis (ie. elderly individuals or those with impaired renal function) but this has not been investigated in human trials
Polymorphisms of the sodium bicarbonate transporter SLC4A5 (NBC4) are associated with hypertension and specifically the single nucleotide polymorphisms (SNPs) of rs7571842 and rs10177833 and to a lesser degree one SNP in the transport GRK4. The SLC4A5 transporter controls cellular pH and is a cotransporter in the passing of sodium bicarbonate across the cellular membrane, and its genetic dysregulation underlies the phenomena known as 'salt-sensitive hypertension'.
There are some genetic differences on a sodium bicarbonate transporter that are highly associated with high blood pressure, but these are likely to be unrelated to nutritional supplementation of sodium bicarbonate
In normotensive older adults given a salt restricted diet and then randomized to a sodium chloride or sodium bicarbonate mineral water for 4 weeks noted reduced blood pressure (5.7+/-6.4mmHg reduction in mean arterial pressure) associated with bicarbonate, but this was mostly due to a reduction in blood pressure from the salt restricted diet (7.0+/-7.2mmHg reduction) that was not abolished by sodium bicarbonate (it was with sodium citrate).
Sodium bicarbonate, based on limited evidence, does not appear to negate the benefits of a low sodium diet on blood pressure reduction
Chronic obstructive pulmonary disease (COPD) is a cardiac condition associated with severe limitations on physical exertion, and supplementation of the standard dose of sodium bicarbonate (300mg/kg) has once failed to enhance performance in persons with severe COPD.
Limited evidnece in persons with COPD do not support the usage of sodium bicarbonate to enhance physical performance
Among adults without diabetes, lower serum bicarbonate concentrations appear to be correlated with a higher risk for insulin resistance and inducing chronic metabolic acidosis is able to temporarily induce insulin resistance hypothesized to be related to increased ACTH release and cortisol levels.
Acutely, a water drink with added bicarbonate given to menopausal women has been noted to improve insulin sensitivity with slightly more efficacy in women with worse insulin sensitivity at baseline. This is likely not due to increased insulin secretion as that has been noted to not occur with acute sodium bicarbonate.
When older adults without diabetes but impaired glucose metabolism were given 67.5mmol sodium bicarbonate daily for 84 days, there was a slight decrease in urinary biomarkers of acidity but no significant influence on cortisol, insulin, glucose, nor insulin sensitivity.
Theoretically, metabolic acidosis can contribute towards insulin resistance. Supplementation of bicarbonate does not appear to indiscriminately benefit insulin resistance, however
It is fairly established that a reduction in pH (increasing acidity) is associated with a reduction of lipolysis and some evidence to suggest the inverse effect, a mild alkalosis (increase in pH) in general is associated with increased rates of lipolysis. THis has been observed at rest, but administration of bicarbonate during exercise does not appear to alter rates of lipolysis by exercise.
A slight increase in pH in the body (which can be achieved with supplemental bicarbonate) is associated with an increase in lipolysis and free fatty acid availability while a decrease in pH is associated with decreased rates of lipolysis
Sodium bicarbonate at 2mmol/kg (16.8mg/kg) has been noted to increase energy expenditure by approximately 9.9% over 180 minutes and increased fat oxidation by 18% relative to baseline alongside an increase in plasma glycerol and NEFAs; it appeared all extra calories used were derived from fatty acids. Due to the limited time frame of measurement (180 minutes) the authors made noted that this only resulted in approximately a 0.5% increase in whole-day metabolic rate.
Other studies either in renal dialysis or in canines have also noted increaed oxygen consumption at rest (indicative of an increase in metabolic rate) or increased fat oxidation rates as assessed by the respiratory exchange ratio (these studies in persons on dialysis) following sodium bicarbonate ingestion.
Although there is a fair bit of evidence from dialysis and animal models, only one study in otherwise healthy persons has noted that oral sodium bicarbonate is able to increase the metabolic rate by 9.9% over 180 minutes (the whole day and more practical metabolic rate measurement increased by around 0.5%) associated with increased fat oxidation
Bicarbonate is of interest for ketosis diets (commonly employed by overweight persons to lose body fat) as ketosis diets are met with a benign but predictable decrease in blood pH which is effectively negated with supplemental bicarbonate.
In fasting subjects subject to either alkalosis (sodium bicarbonate) or additional acidosis (ammonium chloride), the administration of sodium bicarbonate was able to enhance ketone production and lipolysis, with an increase in 0.08+/-0.02 pH (feasible with oral supplements) increasing ketone body levels by 198+/-65mM over 210 minutes whereas in a trial in obese persons on a protein sparing modified fast (412kcal of protein only) given sodium bicarbonate (5g daily) there is a nonsignificant increase in ketone bodies by 20% with was not associated with enhanced weight loss over 4 weeks.
Ingestion of sodium bicarbonate appears to positively enhance ketone body production in a fasted state or when subject to a ketogenic diet, but the magnitude of increase appears to be fairly small and doesn't appear to greatly enhance weight loss over time
Similar to how a dietary restriction of dietary carbohydrates (ketogenic diet) is associated with both a decrease in blood pH and generally a reduction in sports performance, dietary ingestion of carbohydratse is associated with both an increase in performance and pH (including an increase in serum bicarbonate without supplementation). Due to this, it was investigated in persons who had their normal diet replaced (isocaloric) with 2.2+/-0.4% carbohydrates and 64.4% fatty acids to induce ketosis and then given 300mg/kg sodium bicarbonate whether or not performance could be preserved by supplementation. Despite an increase in serum pH, sodium bicarbonate failed to reverse the diet-induced decline in performance on a 95% VO2 cycling test.
Sodium bicarbonate has limited evidence for this claim, but does not appear to preserve physical performance which is usually hindered by a ketogenic diet
It should be noted that the usage of sodium bicarbonate in a rehabilitative manner to treat diabetic ketoacidosis (a too severe drop in blood pH) mostly fails, suggsting no therapeutic effect.
Does not appear promising to treat diabetic ketoacidosis, no information on the possibility of bicarbonate supplementation reducing the occurrence of diabetic ketoacidosis
Lactate and lactic acid form a balance within the body, where lactate may dissociated into lactic acid plus a free hydrogen ion in order to acidify (decrease pH) tissues. The conversion of lactate to lactic acid is seen as a positive modulator of acidity, whereas preservation of lactate concentrations (relative to lactic acid) is either a cause of or consequence of extra endogenous buffering (extra alkalinity to sequester hydrogen ions).
This is likely due to the increase in blood bicarbonate, usually to the degree of 5.4mmol/L (meta-analysis of studies using a 300mg/kg dosage)
An increase in lactate relative to lactic acid is sometimes used as an indicator of alkalinity of the blood
In general and in accordance with extracellular buffering, lactate is increased relative to control when sodium bicarbonate (200-500mg/kg) is ingested prior to short power exercises and can occur with or without apparent performance enhancement.
A lone study using a 60 minute cycle for time (encouraging persons to cycle as far as possible) has noted the opposite, a decrease in lactate; it is unsure if this is an inherent effect of prolonged exercise (which is not commonly studied with sodium bicarbonate) or a fluke.
Sodium bicarbonate supplementation reliably increases lactate concentrations in serum following short exhaustive exercise (such as sprints, rowing, and weight lifting). It is possible that this may be reversed with prolonged aerobic exercise
Although most studies measure serum lactate, intramuscular lactate (via biopsy) has been noted to be increased and to a degree of 72% when serum was measured at 28%; this is similar to previous research in exhaustive exercise (cycling at 90-125% VO2 max) noting approximately a 90% increase in intramuscular lactate concentrations. These results may only occur when exercising above the lactate threshold, as the range of 75-80% VO2 max has been shown to not increase intramuscular lactate in trained persons but to increase it in untrained persons who may have been above their own lactate thresholds. Converse to the influence of sodium bicarbonate, ingestion of acidifying compounds (ammonium chloride) can decrease intramuscular pH.
As extracellular alkalosis (reduction in acidity) tends to increase lactate efflux from the muscle rather than decrease, the increase in lactate concentrations within muscle are thought to not reflect impaired transit but instead reflect increased glycogen utilization. Studies that measure glycogen utilization note a significant increase in the rate of utilization (16.3%) coupled with an increase respiratory exchange ratio, indicative of more glucose oxidation relative to fatty acid oxidation and acidic conditions are known to impair the breaking of glycogen into energy.
Intramuscular lactate is also increased following supplementation of sodium bicarbonate, and usually to a larger degree than is seen in the blood. This is seen during high intensity exercises only (above the lactate threshold) and is likely due to increased glycogen utilization
It has been noted that both acute and chronic metabolic acidosis promote branched chain amino acid catabolism associated with an increase in the rate limiting catabolic enzyme and in kidney disease patients (a study population for chronic acidosis) the elevation of acidity is associated with muscle protein breakdown via stimulating for proteolysis via the ubiquitin-proteosome system.
Both acute and chronic metabolic acidosis is known to promote the breakdown of skeletal muscle. There are no interventions currently assessing proteolysis rates in persons with acidosis given bicarbonate to normalize pH
Bicarbonates main mechanism of action is an attenuation of cellular acidosis (acidosis refers to an increase in acidity that is the result of metabolic processes) and is effective in the exercising muscle in this regard. This attenuation of acidosis (and relative increase in pH) is thought to underlie a prolongation of muscle oxygenation (as the increase in acidity is paraslleled with an increase in CO2 relative to O2) seen in both rats and elite athletes, to preserve glycogen and glucose breakdown for energy (impaired during acidosis), preserve potassium release from muscle (increased during acidosis) and preserve the release of Ca2+ from the sarcoplasmic reticulum (inhibited during acidosis). Studies conducted in humans have confirmed that the exercise-induced decrease in pH is attenuated with acute loading of 0.3g/kg sodium bicarbonate (0.8-1% or around 0.05-0.1pH) in trained athletes and in untrained persons which supports this hypothesis of acid buffering being possible the mechanism of action.
A reduction in pH also occurs at rest following supplementation of sodium bicarbonate, and tends to be an increase of 0.02-0.06pH when measured at 60 minutes (peak).
A decrease in blood acidity (increase in pH) is noted with sodium bicarbonate supplementation secondary to an increase in serum sodium bicarbonate. This is thought to either attenuate the decline in muscle contractions (directly sequestering acidity) or by preserving muscle oxygenation
Sodium bicarbonate ingestion is able to alter the slow phase of pulmonary VO2 (pVO2) kinetics (for anaerobic exercise, highly associated with muscle energy turnover) without affecting the fast phase. The magnitude of reduction (in reference to the amplitude of the slow phase) has been recorded at 19, 29, and 40% following sodium bicarbonate supplementation paired with exercise with some studies failing to find a significant effect (which also appeared to be associated with less lactate production). These results suggest that sodium bicarbonate (albeit somewhat unreliably) may promote more efficient utilization of fuel substrate (such as glucose) under anaerobic conditions, thought to be from attenuating decreases in intracellular pH.
Studies that have looked at the phase II of pVO2 kinetics (usually associated with exercise below the lactate threshold) have noted opposite results (34% elongation and 32% reduction) with similar methodology (300mg/kg sodium bicarbonate on a cycling test at 80% VO2 max in active males), thus a subsequent study assessing both trials and replicating the methodology was undertaken and no significant effect was noted overall.
Sodium bicarbonate may be able to prolong energy metabolism in muscle cells during exercises associated with lactic acid production thought to be related to the intracellular buffering component, with uncertain and possibly no benefit to exercise not associated with lactic acid
A study using submaximal cycling (to induce fatigue) and then later testing force conduction velocity in the muscle of participants noted that the decline in force production seen in placebo (from the submaximal cycling) was abolished with supplemental sodium bicarbonate at 300mg/kg as assessed by isometric leg extension.
Studies assessing muscular output note higher neuromuscular function in fatigued states associated with bicarbonate supplementation, suggesting that bicarbonate may be somewhat beneficial for prolonged resistance training workouts
In practical tests, 300mg/kg sodium bicarbonate was able to enhance the amount of punches landed during boxing training (all four rounds of testing, rather than just during fatigue) and the decline in performance seen in tennis during the later stretches of a match appears to be attenuated with 300mg/kg sodium bicarbonate (an extra 100mg/kg taken before the third game) where service and stroke efficiency was preserved (declined in placebo throughout the match).
An increase in percieved readiness has been noted in elite athletes somewhat unreliably (null effects also have been reported) although this increase in readiness is independent of any alteration in the rate of percieved exertion (how fatiguing an exercise is) which does not appear to be affected.
Sodium bicarbonate supplementation appears to promote neuromuscular performance during later stages of exercise, which would be important for sports requiring a large degree of neural/muscular coordination and accuracy such as tennis and boxing
In a simulated judo test (judo tends to have 10-15s bouts and last up to 4 minutes), 300mg/kg sodium bicarbonate is able to enhance performance on a Special Judo Fitness Test (SJFT; which involves throwing one of two participants in an alternating manner for time) by increasing the amount of throws conducted in 30s (5.1%).
May be of benefit to sports with a physical power component such as judo
When subjects are doing leg presses (fours sets at 12 rep max with a set to fatigue afterwards) and preloaded with 300mg/kg sodium bicarbonate 105 minutes before activity, the typical increases in lactate and pH occur but without an increase in work conducted. A similarly structured study has also failed to find a significant benefit associated with supplementation.
The two studies conducted in weightlifting (12 rep max on the leg press) have failed to find a benefit associated with supplemental sodium bicarbonate ingestion as a pre-workout
In well trained cyclists subject to a 4 minute cycle test, both acute loading of 0.3g/kg (taken in 5 doses spread over 60 minutes) and chronic loading (0.4g/kg divided into three daily doses for three days) are able to benefit power output (2.2-3.1%) and VO2 max (1.2-2%). This trial is met by another doing a short term cycling test against resistance (where 300mg/kg sodium bicarbonate increased time to exhaustion from 61.5+/-2 to 75.3+/-8; 22.4%) and one noting that 5 days of 500mg/kg enhanced work conducted in 60s cycling by 14.2%, but in contrast to these three studies there have been numerous failures of sodium bicarbonate to enhance a 2-3 minute sprint at 110% VO2 max, 3 minute sprint in untrained persons, a 90s sprint against resistance, and in repeated short (60s) sprints in both female cyclists and BMX athletes.
In tests that are based upon prolonged and/or intermittent sprints there are benefits noted with 300mg/kg in healthy males (14s sprint followed by 16s rest, 60 sprints over 30 minutes) with a 11.5+/-5% increase in average power output, 4s sprints with 100s light pedalling (and 20s break) repeated for 36 minutes where a trend to increased work capacity was noted (not statistically significant at 400mg/kg in trained females), 5 sprints of 6s with 30s rest in between (5% work increase) and double this protocol (2% work increase), five separate 60s sprints where only the final one was compared against placebo (42% increased distance covered in 1 minute), and 10 separate 10s sprints with 50s rest in between experiencing sporadic increases in peak power output but significant increases in average power output (0.9-2%). These positive results are contrasted by one study in untrained males using 5 minute cycles (70, 80, and 90% VO2 max) followed by a 100% VO2 max sprint to fatigue where no significant effect of 300mg/kg sodium bicarbonate was detected.
A graded cycling test (more resistance added every 4 minutes, and pedalling until volitional fatigue or cadence drops below 60rpm) in females given 200mg/kg sodium bicarbonate daily for 8 weeks alongside training has noted that the improvement seen in placebo (123% more than baseline) was significantly enhanced (164%).
In short sprints, more often than not there is no significant benefit of sodium bicarbonate supplementation. However, during repeated sprints (doing the short sprint multiple times) there does appear to be more trials which note benefit than null effects
For a 3km time trial in trained cyclists, time to complete the trial is reduced by 1.2% with 300mg/kg sodium bicarbonate (similar potency to 3mg/kg caffeine) and average power output increased by 2.6% while a 60m cycling trial noted a 13.7% increase in average power output with no significant influence on peak power output.
Prolonged aerobic exercise (60 minutes or so) appears to be benefitted with supplemental sodium bicarbonate, by promoting average power production in the later stages of the test which promotes more work to be conducted
Studies that are conducted in rowers note that 300mg/kg (or in one case, 500mg/kg as well) taken either acutely 60-90 minutes prior to activity or with three days of loading before activity have sometimes noted minor improvement in time (6m16s reduced to 6m11s in a 2000m sprint; 1.3% improvement) with a similar 1.8% improvement being noted elsewhere. More often than not, however, studies fail to find any significant benefit of supplementation. All studies aside from one used a 2000m time trial, with this last one doing a 2m all out sprint.
The addition of sodium bicarbonate to a rehydation protocol (following a 4% weight loss to simulate pre-contest periods) has similarly failed to have any benefit and taking sodium bicarbonate at 300mg/kg daily for a prolonged period of time (4 weeks) has similarly failed to outperform placebo.
In studies where elite rowers are given sodium bicarbonate prior to a 2000m sprint test, supplementation more often than not fails to influence performance. It may be beneficial in some individuals (some reports are positive while other studies that note overall no benefit note a few responders) but it is not an overly reliable intervention
Supplementation of sodium bicarbonate at 300mg/kg (in 500mL powerade) 65 minutes before sprint testing in elite rugby players failed to improve performance despite increasing serum bicarbonate while other trials have noted that 300mg/kg sodium bicarbonate has failed to benefit 5 repeated sprints of 24s but benefitted 30s sprints in otherwise healthya men.
One trial has used a prefatigue method of a 30 minute run, followed by a run to exhaustion at 110% VO2 max (ended up being around 250-300s), and failed to find a significant benefit associated with sodium bicarbonate at the standard dose, similar to null results seen in prefatigue techniques on cycling sprints.
For longer sprints, a 600m run in females (trained and untrained) noted that the improvement in time seen with bicarbonate (1.4%) failed to be statistically significant and a 1500m run reduced time to complete by 1.2% and was statistically significant. In trained endurance runners performing a run to exhaustion 90 minutes after bicarbonate ingestion (300mg/kg), it was noted that sodium bicarbonate outperformed supplemental lactate and citrate (lactate can be used for muscular energy production and supplementation enhances endurance performance) where bicarbonate-chloride, bicarbonate-citrate, and bicarbonate-lactate increased performance by 2.7%, 2.2%, and 1%.
Short term sprints and multiple repeated sprints on foot have failed to find benefit with supplemental sodium bicarbonate, while there are mixed but probably benefits in longer sprints (600m or greater). It seems the longer the run is conducted, the more likely that sodium bicarbonate is beneficial
In swimmers (competitive but not elite) given 300mg/kg sodium bicarbonate prior to swim testing noted a 2% increase in performance (assessed by swim times on 8 25m front crawls with 5 second rest in between each crawl) associated with bicarbonate over placebo. Another study using 10m sprints (56 of them, in a simulated water polo game in elite athletes) failed to find a benefit associated with supplementation 90 minutes prior.
A longer swimming test (2 tests of 200m) has failed to notice an improvement of sodium bicarbonate inherently, but the decline in performance on the second 200m sprint (relative to the first) was attenuated by 1.5% in elite swimmers while another study using the 200m sprint test noted a 3.4% reduction in time associated with sodium bicarbonate in elites. Supplementation of creatine (20g) and sodium bicarbonate (300mg/kg) daily for 6 days prior to two maximal 100m fresstyle swims noted that the increase in time taken to complete the second trial in placebo (1s) was nearly abolished (0.1s) but overall the swim time was not significantly different, and a similarly structured trial (5 sprints of 91.4m after 240mg/kg sodium bicarbonate) noted significant improvements in the last two sprints (preserving velocity by about 2.5%) but no effect on the first three; control had a significant acute decline in performance on these last two sprints.
Mixed effects on how supplemental sodium bicarbonate can benefit swim performance when it is kept to short sprints, but it appears that supplementation may prevent a decline in performance seen with prolonged swimming
Most trials investigating the acute usage of sodium bicarbonate at 300mg/kg prior to exercise either have a mandatory 60 minute 'absorption' period prior to testing where the sodium bicarbonate is delivered in one acute bolus or several mini-pulses spread over the course of one hour (spanning from 90 minutes to 30 minutes before exercise). These dosing strategies are done in order to avoid gastrointestinal discomfort and the risk of diarrhea (somewhat), and blood bicarbonate appears to peak one hour post ingestion anyways with 300mg/kg and might peak a tad earlier (45-50 minutes) with a lower dose of 200mg/kg.
Some trials use a more delayed timing, and supplementation with sodium bicarbonate at 300mg/kg 150 minutes (2.5 hours) before exercise has still been noted to be effective.
In regards to dose, some studies have noted that 500mg/kg is more effective than 300mg/kg but this dose tends to be associated with significantly more stomach-related side-effects; relative to 300mg/kg (commonly seen as the standard dose), 200mg/kg is similarly effective while 100mg/kg is less effective.
Sodium bicarbonate can be used as a preworkout supplement, but it should be taken up to an hour before exercise (rather than closer to the time, as closer ingestion runs the risk of intestinal discomfort). The dosage range of 200-300mg/kg is probably best for usage before a workout, with lower doses less likely to cause stomach problems
Studies that compare acute dosing (300mg/kg taken 60-90m before exercise) or chronic loading (5 days of 400-500mg/kg in three divided doses, with no supplementation the day of testing) have mixed effects either favoring chronic loading or no significant difference (in magnitude, a more robust P-value was achieved with chronic loading).
One study having a daily bicarbonate ingestion paired with daily cycle tests noted increased performance each day, but no culumative benefit over the course of 5 days and serum concentrations of bicarbonate were similar on day one relative to day five.
Both chronic loading and acute dosing are able to confer similar benefits to performance, although chronic loading may be desired due to less risk of gastrointestinal side-effects during exercise. Benefits still appear to exist if sodium bicarbonate is loaded but then not taken for up to 2 days
Chronic low-grade metabolic acidosis has a known degratory effect on bone tissue as evidenced by the alteration in phosphate and calcium urinary excretion rates towards a more catabolic ratio. Protein losses from bone appear to be enhanced in experimentally induced acidosis in research animals associated with increased osteoclastic activity which underlies increased bone resorption (releasing of minerals) and less bone formation which are associated with increased RANKL activity via COX-dependent mechanisms.
The western diet is known to be more acidic than alkaline (due to a low vegetable intake paired with a high meat intake) with sodium being an independent risk factor. Possibly due to this, some evidence suggests more efficacy with potassium bicarbonate than sodium bicarbonate for improving mineral balance.
A high acid diet is normally a risk factor for osteoporosis and bone loss, but is mostly inconsequential assuming the kidneys can produce enough bicarbonate. There may be too much acid production relative to bicarbonate in a diet excessive in sodium, and possibly in older individuals with declining kidney function
Potassium bicarbonate at 300mmol (30g) given to young adults subject to a sodium-stress test has been able to reduce the increase in calcium excretion seen in sodium-loaded control and appears to be effective in doses as low as 60mmol (6g) when taken as potassium bicarbonate; sodium bicarbonate at this dose was ineffective but similarly failed to increase serum bicarbonate concentrations, with other studies in postmenopausal women or elderly persons (given both Vitamin D and calcium, but placebo recieved those as well) have noted that higher doses of sodium bicarbonate are effective in reducing urinary calcium losses associated with higher serum bicarbonate.
Despite sodium bicarbonate (or sodium citrate, another alkalizing agent) being demonstrated effective in several trials, the reduction in urinary calcium excretion appears to be significantly less than what is observed in trials with potassium bicarbonate or potassium citrate.
In instances of low grade metabolic acidosis, any form of supplemental bicarbonate that can increase serum bicarbonate is able to confer protection against bone loss induced by the acidosis.
Potassium bicarbonate appears to be significantly more protective than sodium bicarbonate, which may be due to potassium also inherently being osteoprotective while sodium is an independent risk factor for bone mineral losses. A high vegetable diet (high in potassium) with a concomitant reduction in sodium intake may maximize the benefits of sodium bicarbonate on bone health
Chewing gum with bicarbonate added to it is able to increase salivary pH (reduced acidity) without significantly influencing salivary flow rates.
There are mixed effects in regards to dental plaque and gingivitis, with some null results seen with chewing gum containing bicarbonate and other studies noting 5% bicarbonate in chewing gum was effective when used in conjunction with regular brushing and has been quantified at reducing plaque by approximately 17%.
Anti-staining effects have been noted with chewing gum containing sodium bicarbonate, with some efficacy seen at 2 weeks but a larger degree of benefit seen after 12 weeks of continual usage (65.3-71.9% stain reduction) relative to 4 weeks (29-51% reduction). Although some trials have noted efficacy with twice daily gum chewing (for 20 minutes following meals) there appears to be similar efficacy with one piece of gum daily after a meal.
Sodium bicarbonate added to chewing gums (around 5% of the gum) is able to beneficially influence acid:base balance in the mouth and, when consumed after acid-producing meals, can confer protective effects against both plaque and gingivitis while potentially whitening teeth
Oral malodor (halitosis or just 'bad breath') tends to be associated with production of volatile compounds which are deemed to be unpleasant in smell which affects up to 24-50% of the populace (Japan and the US, respectively) usually in reference to volatile sulfur compounds produced from oral bacteria although they are not the only causative volatile class. Sodium bicarbonate has been demonstrated to reduce volatile sulfur production (seen with dentrifices at 20-65% sodium bicarbonate and implicated in mouthwash. It is hypothesized to extend to chewing gum) although in comparative studies it has underperformed other agents (zinc acetate solution when used as mouthwash).
Although not fully demonstrated, a possible reduction in bad breath may result following usage of oral products with a sodium bicarbonate content
Metabolic acidosis is a condition that is characterized by a drop in serum bicarbonate (usually seen as the consequence of metabolic acidosis) that has both an acute and lethal component (usually induced by drugs, not in the realm of dietary supplements to address and is a clinical issue) and a chronic and mild component that is somewhat common in society in older persons; dietary stressors that are acidic in nature (such as dietary protein and sodium) may predispose the body to increasing serum acidity or reducing buffering agents.
The kidneys normally produce bicarbonate in the human body, and when optimally functioning they appear to produce enough bicarbonate to prevent acidosis in otherwise healthy adults; the age-related decline in kidney function, however, is associated with a mild state of metabolic acidosis that is exacerbated by the diet.
The diet normally confers acids, which are handled readily by the kidneys via production of sodium bicarbonate. During aging, the rate of bicarbonate production by the kidneys may be reduced (due to general kidney dysfunction) and a subsequent increase (non-lethal) increase in acidity occurs that may exacerbate disease states
In mild acidosis, sodium bicarbonate is able to at reduce blood acidity in ICU patients, those on renal dialysis, and in simulated salt-induced bone losses (which are mediated by an excess in acidity).
Oral bicarbonate as well as intravenous have both shown efficacy in attenuating some symptoms of chronic low-grade metabolic acidosis
One study using a glucose group and a sodium bicarbonate group to test the efficacy of the combination in a cycling sprint test (glucose at 8% of a 4.5mL/kg solution, sodium bicarbonate at 300mg/kg, sodium chloride as electrolytes at 22mg/kg which was also used in the glucose only group) noted that the combination was trending towards being synergistic for increasing power output and work completed.
It is possible that carbohydrate and electrolyte ingestion is either additive or synergistic with sodium bicarbonate at improving power output in anaerobic cardiovascular exercise
beta-alanine (β-alanine) is an amino acid supplement that is said to act in a similar manner as sodium bicarbonate and buffer intracellular hydrogen ion production.
One study that used beta-alanine (6.4g daily for 4 weeks) or placebo and then followed it up with either acute usage of another placebo or sodium bicarbonate noted that the 12.1% increase in time to exhaustion seen with beta-alanine and the 6.5% increase seen with sodium bicarbonate were somewhat additive, increasing time to exhaustion by 16.2% although this was not statistically significant. This additive effect has failed to be noted elsewhere (3.1+/-1.8% with sodium bicarbonate, 3.3+/-3.0% with the combination).
Both beta-alanine and sodium bicarbonate are somewhat effective at the same thing, but it's unclear if they're additive when used together.
Caffeine is a xanthine structure found most commonly in coffee. Due to its own performance enhancing effects and the inability of caffeine to modify the absorption of bicarbonate (as assessed by serum levels) they are sometimes used alongside each other
In a 3km cycling test trial in trained cyclists given either sodium bicarbonate (300mg/kg), caffeine (3mg/kg), or their combination noted that both supplements were approximately equally effective in improving power output (2.4-2.7%) and reducing time trial time (relative to control; 0.9-1.2%) and that they were not additive. The combination of these two supplements was not reported to be more adverse to intestinal comfort than either agent alone. Elsewhere, the combination was associated with a reduction in the rate of percieved exertion while no individual compound was in a 2k rowing test and one test that did not find any statistical differences between groups noted that more than half of the subjects reported their best times (200m freestyle swim) with combination therapy relative to either supplement alone or placebo.
Although a possible additive benefit may exist, currently the literature does not support this. Although combining these two agents can theoretically augment intestinal side-effects, this has also not been reported in the literature to a reliable degree
Insufficient evidence to support any interaction between these two supplements
When gastrointestinal symptoms do occur at the 300mg/kg dosage, they appear to be mostly related to the stomach (stomach bloating, stomach pain, and belching) at around 30 minutes with symptoms being attenuated but still present at 60 minutes.
Diarrhea has been reported at tim 90 minutes following ingestion to be more prominent than placebo, but was not present at 120 minutes. When reporting symptoms experienced over 24 hours after supplement ingestion, flatulence and diarrhea are both present.
Sodium bicarbonate has the potential to cause some stomach problems within 30-60 minutes of ingestion (aching and cramping, possibly nausea secondary to that) and after that it may cause diarrhea when it reaches the intestines and flatus appears to be more common than placebo. These symptoms are present, but somewhat minor-moderate in magnitude
Some studies have tested an association between symptoms and sports performance, and suggested that in the sodium bicarbonate groups the increase in gastrointestinal symptoms could be a limiting factor in the performance enhancement attained from supplementation.
Studies that divide the group into individual performance do note a high degree of variability despite similar serum increases in lactate and pH, so it is plausible to assume that gastrointestinal side-effects limit the efficacy of sodium bicarbonate supplementation in enhancing performance.
It is possible that sodium bicarbonate supplementation enhances performance more in persons with less gastrointestinal side effects, suggesting that supplementation regimens to minimize side-effects would indirectly improve the efficacy of supplementation
Due to the supplement being sodium bicarbonate and dissociating into free bicarbonate in serum this supplement can confer dietary sodium, which consists of 27.3% of sodium bicarbonate's total weight. An oral dose of 300mg/kg sodium bicarbonate would confer 82mg/kg dietary sodium, which is a nonlethal but quite high dosage. Although about a quarter (24+/-2%) of sodium is excreted within 210 minutes and controls the blood levels somewhat, the 300mg/kg dose still increases serum sodium by 2.9% (from 138.1 to 142.1mmol/L) within one dose; repeated doses over 5 days do not further increase sodium.
Due to this, sodium bicarbonate may not be advisable for persons with blood pressure issues that are deemed to be salt sensitive. Potassium bicarbonate can be used as an alterantive, but excessive potassium intake is associated with increased risk for cardiac arrythmia and doses of 300mg/kg have not been conclusively confirmed safe.
Dietary sodium bicarbonate, if taken in the active doses for performance enhancement, will increase dietary sodium intake quite a bit and thus may be inadvisable for persons on a sodium-restricted diet. Although about 25% of dietary sodium is rapidly excreted from sodium bicarbonate (due to elimination of bicarbonate also taking sodium) this still leaves approximately 62mg/kg bodyweight (75% of 82mg/kg; the sodium content of 300mg/kg sodium bicarbonate)
As mentioned more in depth in the pharmacology subsection 'Excretion', sodium bicarbonate supplementation results in an increased excretion of bicarbonate in order to regulate serum concentrations of this vital buffering agent (as too much can result in alkalosis); this increased excretion results in increased sodium excretion and the increased sodium excretion further results in increased potassium excretion. As sodium is ingested via sodium bicarbonate but potassium is not, chronic and excessive usage of sodium bicarbonate supplementation is a potential risk factor for reducing serum potassium concentrations.
Supplemental potassium bicarbonate (a generally recognized as safe compound albeit limited long-term toxicological information) appears to be safe in humans in short duration trials at 90mmol (9g) over 10 and 42 days or 64-67.5mmol (6.4-6.75g) daily for 4 months or 3 months.
Replacing a small (less than 9g) amount of sodium bicarbonate with potassium bicarbonate can possibly reduce dietary sodium load and increase potassium relative to that, but higher doses than 9g or supplementation periods for more than 3 months are not yet demonstrated safe (very high acute doses of potassium may cause heart arrythmia)
Alkalosis is the metabolic state of excessive alkalinity in the blood (a lack of acidity), which can be clinically induced with administration of high levels of buffering agents (although charcterized by high serum bicarbonate, it becomes clinically relevant when renal excretion of bicarbonate is suppressed as well). In general, persons with impaired renal function (such as chronic kidney disease) are at greater risk for alkalosis while sufficient renal function is usually met with an increase in bicarbonate excretion to regulate serum concentrations.
It is theoretically plausible that oral sodium bicarbonate (similar to infusions) can induce a state of metabolic alkalosis, which would be a potentially lethal situation. Due to this, the dosing recommendations given in the 'How to take' section should be adhered to and supplementation should never exceeed 500mg/kg daily (for non-obese persons, obese persons would need to calculate this in relation to a 'normal' BMI for their height)