IngredientesPyruvate (as the ionized anion) and its conjugate acid pyruvic acid are the same fundamental biochemical entity encountered under different physiological conditions. Pyruvic acid is a three-carbon alpha-keto acid with the molecular formula C₃H₄O₃, a central metabolite in biochemistry, particularly in cellular energy processes. Its systematic IUPAC name is 2-oxopropanoic acid, which precisely describes its structure, indicating a ketone group at the second carbon and a three-carbon chain with a carboxylic acid. Pyruvic acid was formerly called pyroracemic acid in older literature.
At room temperature, pure pyruvic acid is a colourless liquid with a pungent odour resembling that of acetic acid. On cooling, it forms crystals that melt at 13.6 °C, and the boiling point is 165 °C. It is completely miscible with water, facilitating its role in aqueous biological environments.
The Brønsted–Lowry conjugate base, CH₃COCOO⁻, is known as pyruvate, and is a key intersection in several metabolic pathways. It is also a breakdown product of certain amino acids, including alanine, glycine, cysteine, and serine.
In the supplement industry and in clinical research, pyruvate is sold and studied under several chemical forms:
Calcium and magnesium pyruvates, in particular, have become established as agents suitable for therapeutic purposes and as food supplements.
Pyruvate is a three-carbon ketoacid that occurs naturally in cells; it is produced through enzymatic reactions in the glycolytic pathway and plays a crucial role in energy metabolism. Pyruvate is not an essential nutrient, since the body makes all it needs.
Dietary sources of pyruvate include certain foods, though concentrations are modest. Pyruvate is present in red apples (approximately 450 mg), red wine and dark beer (approximately 75 mg), and cheeses. Due to the limited amounts available in food, therapeutic dosages typically require supplementation.
Unlike most botanical dietary supplements, pyruvate has no traditional herbal or folk medicine history. Its use as a supplement is rooted entirely in modern biochemistry and clinical research originating in the late 20th century.
In 1834, Théophile-Jules Pelouze distilled tartaric acid and isolated glutaric acid and another unknown organic acid. Jöns Jacob Berzelius characterized this other acid the following year and named pyruvic acid because it was distilled using heat. Pyruvic acid was first obtained by Jöns Jacob Berzelius in 1835 by the dry distillation of tartaric acid; the preparation of pyruvic acid in bulk amounts follows a similar principle: tartaric acid is heated with fused potassium hydrogen sulfate at 210–220 °C.
The name "pyruvic acid" is derived from the Greek word pyros, meaning "fire," and "acetic," as it was first discovered through the pyrolysis of tartaric acid.
The elucidation of its role in metabolism began in the early 20th century with the work of scientists such as Gustav Embden, Otto Meyerhof, and Jakub Karol Parnas, who mapped the glycolytic pathway. Their research demonstrated pyruvic acid as the end product of glycolysis, a discovery that was pivotal for unraveling the mechanisms of energy production in cells. The Krebs cycle, which uses pyruvate as a substrate, was subsequently elucidated by Hans Adolf Krebs, who shared the 1953 Nobel Prize in Physiology.
The commercial supplement era began in earnest in the early 1990s, largely driven by the clinical research of Ronald T. Stanko, MD, at the University of Pittsburgh Medical Center, who published a series of human trials on pyruvate supplementation for weight loss and exercise performance. Pyruvate is now sold as a dietary supplement for use in promoting weight loss and enhancing energy.
Pyruvic acid is a key component in the glycolytic pathway, acting as the final product of glycolysis and a precursor for the citric acid cycle. In glycolysis, one molecule of glucose, a sugar with six carbon atoms, is split into two molecules of pyruvate, a compound with three carbon atoms, and this reaction generates energy in the form of two ATP molecules.
Pyruvic acid supplies energy to living cells through the citric acid cycle (also known as the Krebs cycle) when oxygen is present (aerobic respiration); when oxygen is lacking, it ferments to produce lactic acid. This bifurcation makes pyruvate a central metabolic switch:
Pyruvate exhibits antioxidant activity and can affect the cellular redox state, and exogenous pyruvate can influence metabolism by affecting the acid-base balance of the blood.
The main mechanisms through which exogenous pyruvate exerts its beneficial effects include the neutralisation of reactive oxygen species, protection and stabilisation of mitochondria, maintenance of ATP levels, and inhibition of inflammatory signalling pathways, including the nuclear factor-kappa B (NF-κB) pathway.
Pyruvic acid treatment generally suppresses inflammation. Pyruvate treatment has been reported to inhibit the activation of p38 mitogen-activated protein kinase and NF-κB, two signaling pathways important for cytokine release.
The ester derivative ethyl pyruvate has been studied extensively as an anti-inflammatory compound in preclinical models. Ethyl pyruvate (EP) is a simple derivative of pyruvic acid that can scavenge reactive oxygen species (ROS). Treatment with EP is able to ameliorate systemic inflammation and multiple organ dysfunctions in multiple animal models, such as acute pancreatitis, alcoholic liver injury, acute respiratory distress syndrome (ARDS), acute viral myocarditis, acute kidney injury and sepsis.
It is unclear exactly how pyruvate works to promote weight loss, but in rats a lower respiratory exchange ratio has been demonstrated, indicating that there was increased utilization of fat and an elevation in resting metabolic rate. Because pyruvate may accelerate fatty acid synthesis through acetyl-CoA, excessive pyruvate intake may paradoxically be ineffective in promoting fat loss.
Recent studies have revealed that the mitochondrial pyruvate carrier (MPC), which transports pyruvate into the mitochondria, is reduced in failing human and mouse hearts. Pyruvate is handled differently in the failing heart, where a large proportion of it is reduced to lactate in the cytosol instead of being fully oxidised in the mitochondria. Several recent studies have found that MPC abundance was reduced in failing human and mouse hearts characterised by maladaptive hypertrophic growth.
Evidence strength: Weak to mixed. Small, often methodologically limited trials; a systematic review and meta-analysis found only a small, uncertain clinical effect.
The earliest human evidence came from inpatient metabolic ward studies conducted by Stanko and colleagues in the early 1990s. In one double-blind, placebo-controlled trial, 14 obese women housed in a metabolic ward consumed a 4.25-MJ/d liquid diet for 21 days with or without pyruvate (partially, isoenergetically substituted for glucose; n=7 per group). Subjects fed pyruvate showed a greater weight loss (5.9 ± 0.7 kg versus 4.3 ± 0.3 kg, P < 0.05) and fat loss (4.0 ± 0.5 kg versus 2.7 ± 0.2 kg, P < 0.05).
A companion study measured body composition, energy deficit, and nitrogen metabolism in 13 obese women housed in a metabolic ward consuming a 2.1-MJ diet for 21 days with the three-carbon compounds dihydroxyacetone and pyruvate (DHAP), partially and isocalorically substituted for glucose. Subjects fed dihydroxyacetone and pyruvate showed a greater weight loss (DHAP = 6.5 ± 0.3 kg, placebo = 5.6 ± 0.2 kg) and fat loss (DHAP = 4.3 ± 0.2 kg, placebo = 3.5 ± 0.1 kg).
A subsequent lower-dose study used pyruvate in a more ambulatory population. In a six-week, double-blind, placebo-controlled trial, 51 persons were given either pyruvate (6 g daily), placebo, or no treatment, and all participated in an exercise program. In the treated group, significant decreases in fat mass (2.1 kg) and percentage body fat (2.6%) were seen, along with a significant increase in muscle mass (1.5 kg).
Twenty-six healthy subjects (16 women, 10 men) with a BMI ≥ 25 participated in another study. The results demonstrated that supplementation of pyruvate results in a modest, but significant, decrease in body weight and body fat over a 6-week treatment period, consistent with previous work that utilized higher doses.
The aggregate picture from a formal systematic review is less optimistic. Nine trials were identified and 6 were included in the meta-analysis; all had methodological weaknesses. The meta-analysis revealed a statistically significant difference in body weight with pyruvate compared to placebo (MD: −0.72 kg; 95% CI: −1.24 to −0.20), but the magnitude of the effect is small and its clinical relevance is uncertain. The evidence from randomized clinical trials does not convincingly show that pyruvate is efficacious in reducing body weight.
A 2024 PMC review noted important nuances: Early studies used high doses of pyruvate (16–53 g/d) along with dihydroxyacetone and/or energy restriction. Subsequent studies examining lower doses (2–10 g/d) have found conflicting results. Two of the studies that found pyruvate supplementation to be ineffective involved trained athletes who had low body fat composition at the start of the study (15.7% for American football players and 8.8% for soccer players), and fat loss is unlikely to occur in such lean active people.
Evidence strength: Weak overall. Early positive studies used high doses in untrained subjects; subsequent well-controlled studies in trained athletes found no benefit at commonly used doses.
The earliest exercise studies by Stanko et al. used very high doses combined with dihydroxyacetone (DHAP) and found positive results. The first studies of pyruvate supplementation and exercise performance were conducted by Stanko et al., who found improvements in aerobic endurance capacity after pyruvate supplementation, possibly as a result of an increased rate of muscle glucose uptake and sparing of muscle glycogen. However, these studies involved untrained participants who consumed 25 g of pyruvate per day combined with 75 g dihydroxyacetone.
Later studies in trained athletes at more practical doses produced negative results. In one study, 5 weeks of pyruvate supplementation (0.22 g/kg/d) during the training program of American football players did not improve maximal strength, cycle ergometer peak power, or static vertical jump power output. Similarly, 2 weeks of pyruvate supplementation (8.1 g/d) did not improve the ability to maintain power output without fatigue (critical power). In another study, 1 week of pyruvate supplementation (7 g/d) did not influence the time to exhaustion during exercise performed at 75–80% VO₂max.
A study testing the hypothesis that pyruvate ingestion would enhance performance during intense aerobic exercise found that nine recreationally active subjects consuming 7, 15, and 25 g of pyruvate were monitored for a 4-hour period. Pyruvate consumption failed to significantly elevate blood pyruvate, and it had no effect on indexes of carbohydrate or lipid metabolism. The results of that study indicated that oral pyruvate supplementation does not increase blood pyruvate content and does not enhance performance during intense exercise in well-trained cyclists.
Despite promising early results, later well-controlled studies of physically active people have shown that pyruvate supplementation lasting more than 1 week has no ergogenic effects. However, some data suggest that ingested pyruvate may be preferentially metabolized without accumulation in the bloodstream.
Some research with creatine pyruvate has produced mixed findings. A double-blind, placebo-controlled, randomized study evaluated oral creatine pyruvate (Cr-Pyr, 5 g/d, n=16) or creatine citrate (Cr-Cit, 5 g/d, n=16) or placebo (5 g/d, n=17) supplementation for 28 days, assessing performance during intermittent handgrip exercise of maximal intensity. Subjects performed ten 15-second exercise intervals, each followed by 45-second rest periods. Cr-Pyr significantly increased mean power over all intervals. However, 7 days of 7 g per day Cr-Pyr supplementation did not beneficially impact endurance capacity or intermittent sprint performance in well-trained cyclists.
A 2022 randomized controlled trial examined the effect of sodium pyruvate specifically on sprint recovery. Sodium pyruvate has been reported to improve aerobic metabolism and attenuate metabolic acidosis; aerobic capacity and the ability to remove hydrogen ions affect the recovery from repeated high-intensity activities. This study explored the effects of pyruvate ingestion on repeated sprint exercise (RSE) ability and recovery. Fourteen male soccer athletes (aged 20 ± 2 years) participated in a double-blinded crossover study, completing two experimental sessions after randomized ingestion of either pyruvate or maltodextrin placebo for 1 week.
A recent study reported higher blood pH, bicarbonate level, and base excess, as well as improved performance during high-intensity interval exercise after pyruvate supplementation. The current state of understanding suggests that studies of the effects of pyruvate supplementation should prioritize investigating the timing of pyruvate intake.
Evidence strength: Preliminary. Mechanistically plausible based on metabolic research, but only a limited number of clinical trials have examined pyruvate therapy for cardiovascular conditions.
Although pyruvate has been repeatedly found beneficial in preclinical models of cardiovascular disease, only a limited number of clinical trials have examined pyruvate therapy for cardiovascular syndromes.
Research has established that mitochondrial pyruvate transport is critically relevant to cardiac function. Recent studies revealed that the mitochondrial pyruvate carrier (MPC), which transports pyruvate into the mitochondria, is reduced in failing human and mouse hearts. MPC abundance was reduced in failing hypertrophic human hearts, as well as the myocardium of mice induced to fail by angiotensin II or transverse-aortic constriction. Constitutive knockout of cardiomyocyte MPC1/2 in mice resulted in cardiac hypertrophy and reduced survival.
Early clinical research into sodium pyruvate intravenous infusion for alcohol-related liver disease and heart failure has shown some promise. Early research suggests that giving sodium pyruvate intravenously for 25 days improves measures of liver function in people with alcohol-related liver disease. Preliminary clinical studies in patients with heart failure or mitochondrial diseases have demonstrated safety and high tolerance of pyruvate with few side effects.
A published study on pyruvate supplementation in a hyperlipidemic population also investigated lipid effects. Stanko et al. studied pyruvate supplementation of a low-cholesterol, low-fat diet for its effects on plasma lipid concentrations and body composition in hyperlipidemic patients, published in the American Journal of Clinical Nutrition in 1994. Adverse events in the meta-analysis included gas, bloating, diarrhea, and an increase in low-density lipoprotein (LDL) cholesterol.
Evidence strength: Preliminary to limited. Some clinical observations for topical application in acne and hyperkeratotic disorders, but large controlled trials are lacking.
Pyruvate is used topically for scaly, flaky skin. Some people also apply pyruvic acid, a liquid form of pyruvate, to the skin to reduce wrinkles and other signs of aging. Applying a pyruvic acid skin peel might improve acne in some people.
Pyruvic acid seems to cause the outer layer of skin cells to slough off, functioning as a chemical exfoliant similar in mechanism to alpha-hydroxy acids. Historical clinical use of sodium pyruvate for hyperkeratotic (thickened, scaly) skin disorders was documented in the dermatological literature as far back as 1979. Topically applying pyruvic acid as a facial peel can cause an intense burning sensation.
Evidence strength: Preclinical and very preliminary clinical. Research is largely in vitro or animal-based; limited evidence of corneal penetration in humans.
Pyruvate has been explored for its potential benefits in skin health, mitochondrial diseases, heart health, and possibly as a supportive treatment for cataracts and cancer. Research published in Ophthalmologica in 2009 investigated the possibility of topical antioxidant treatment of cataracts and corneal penetration of pyruvate in humans, suggesting that topically applied pyruvate may reach the anterior segment of the eye.
Evidence strength: Preclinical only (animal and cell culture studies). No established human clinical evidence as of the available literature.
It is hypothesized that pyruvic acid has a protective effect against neuronal cell death induced by various stresses, such as ethanol toxicity or excessive release of Zn²⁺ as seen during stroke. Preliminary in vitro studies suggest the mechanism involves suppression of the mitochondrial injury caused by cytochrome c release.
Animal model studies have examined pyruvate in Alzheimer's disease models. Pyruvate has been shown in a mouse model to prevent the development of age-dependent cognitive deficits in a mouse model of Alzheimer's disease without reducing amyloid and tau pathology. These findings remain animal-only and have not been replicated in human clinical trials.
Evidence strength: Very preliminary. One small clinical study, no replication.
Inhaled sodium pyruvate may act as an anti-inflammatory agent to improve some chronic lung diseases, based on preliminary clinical trials. Research published in the Journal of Aerosol Medicine and Pulmonary Drug Delivery in 2008 reported that inhaled sodium pyruvate improved FEV1 and decreased expired breath levels of nitric oxide in patients with chronic obstructive pulmonary disease (COPD). This remains a single preliminary study.
Evidence strength: Primarily in vitro and animal. Mechanism is well-established biochemically but human clinical evidence is limited.
Exogenous pyruvate, for example in the form of sodium pyruvate or ethyl pyruvate, has potential therapeutic applications due to its antioxidant and anti-inflammatory properties. Reviews summarize cell culture and animal studies reporting the cytoprotective effects of exogenous pyruvate compounds during exposure to environmental pollutants, drugs, UV radiation, and burns.
Research has found that pyruvate exerts cytoprotective effects against vanadium-induced toxicity at least in part by decreasing ROS generation and preserving mitochondrial functions.
Pyruvate supplements are available in the following forms:
The dosages used across research studies span a wide range:
Limited evidence exists about the safety of pyruvate.
Adverse events documented in the systematic review included gas, bloating, diarrhea, and an increase in low-density lipoprotein (LDL) cholesterol. While generally deemed safe, some mild side effects such as stomach upset may occur. These gastrointestinal complaints appear to be dose-related, being more common at higher intake levels.
The systematic review and meta-analysis by Onakpoya et al. (2014) flagged an increase in LDL cholesterol as a documented adverse event across some trials, which warrants attention given that elevated LDL is a cardiovascular risk factor.
Topically applying pyruvic acid as a facial peel can cause an intense burning sensation. It should be applied in adequate ventilation because the vapors have been reported to cause respiratory irritation.
One child receiving intravenous pyruvate for restrictive cardiomyopathy died. This case, reported in The Lancet in 1991, involved a pyruvate loading test in a child with an underlying cardiac condition. This event is not directly applicable to oral or topical supplement use, but it flags the need for caution with parenteral administration in vulnerable populations, particularly those with underlying cardiac or mitochondrial disease.
It is advised to use high-quality products, as impurities could lead to adverse effects, especially given the high dosages involved.
Insufficient data exist about safety in pediatrics, pregnancy and lactation, and patients with liver and kidney disease.
Possible hypoglycemia via blood glucose extraction into muscle cells and decreased insulin resistance has been proposed as a mechanism of concern. Formal drug interaction data are largely absent from the published literature. There is insufficient reliable evidence about the effectiveness and interaction profiles of pyruvate for most proposed uses.
Pyruvate (pyruvic acid / calcium pyruvate) is a dietary supplement with published peer-reviewed studies involving approximately 160 participants, researched for weight management, exercise performance, fat oxidation, and additional areas. The overall body of clinical evidence is characterized by small sample sizes, short durations, and methodological weaknesses. Evidence to substantiate most of the claims about pyruvate is lacking, and many pyruvate studies are largely outdated or were conducted in animals.
Future trials involving the use of this supplement should be more rigorous and better reported. The biochemical role of pyruvate in energy metabolism is scientifically well-established, but the translation of this endogenous metabolic role into clinically meaningful effects of exogenous supplementation has not been convincingly demonstrated for most proposed uses.
Condiciones de salud que piruvato puede ayudar a apoyar.
Pyruvate is the end product of glycolysis and the central metabolite linking carbohydrate metabolism to mitochondrial energy production via the TCA cycle and oxidative phosphorylation. Supplemental pyruvate has been studied in multiple RCTs for effects on exercise capacity, fat oxidation, and energy endurance.
Sistemas corporales que piruvato puede ayudar a apoyar.
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