Lactic acid

Lactic Acid (2-Hydroxypropanoic Acid)

1. Identity: Chemical Names, Natural Sources, and Common Forms

Chemical Identity

Lactic acid is an organic acid with the molecular formula C₃H₆O₃. Its IUPAC name is 2-hydroxypropanoic acid. It is also known informally as "milk acid" because it was first isolated from sour milk. Lactic acid is an alpha-hydroxy acid (AHA) due to the presence of a hydroxyl group adjacent to the carboxyl group. The conjugate base of lactic acid is called lactate (or the lactate anion). In solution, it can ionize by loss of a proton to produce the lactate ion CH₃CH(OH)CO₂⁻, also known as 2-hydroxypropanoate.

Lactic acid is a chiral molecule with two optical isomers: L-lactic acid and D-lactic acid. Bio-based lactic acid is optically active; the production of either L-(+) or D-(−) lactic acid can be directed using bioengineered microorganisms. The L-isomer predominates in mammalian metabolism and is the form produced by most lactic acid bacteria; the D-isomer is produced by some bacterial species and is less efficiently metabolized by human enzymes.

In its solid state, lactic acid is white; when dissolved, it forms a colorless solution. Pure lactic acid, rarely prepared, is a colorless, crystalline substance that melts at 18 °C (64 °F); it rapidly absorbs moisture from the atmosphere.

Natural Sources

Lactic acid is an organic compound belonging to the family of carboxylic acids, present in certain plant juices, in the blood and muscles of animals, and in the soil. It is the commonest acidic constituent of fermented milk products such as sour milk. Lactic acid is a natural organic acid found not only in milk but also in other food products such as meat and beer. Lactic acid (2-hydroxypropanoic acid) is generated from pyruvic acid under anaerobic conditions in skeletal muscles, brain, red blood cells, and kidney.

Commercial Production and Common Forms

Lactic acid is produced commercially by fermentation of carbohydrates such as glucose, sucrose, or lactose, or by chemical synthesis; carbohydrate sources include corn, beets, and cane sugar. The carbohydrates are hydrolyzed into monosaccharides and then fermented under the absence of oxygen by microorganisms into lactic acid. Lactic acid is an organic compound produced via fermentation by different microorganisms; lactic acid bacteria are the main bacteria used to produce it, and among these, Lactobacillus spp. have shown interesting fermentation capacities.

Lactic acid is manufactured by the fermentation of molasses, starch, or whey in the presence of alkaline substances such as lime or calcium carbonate; it is available as aqueous solutions of various concentrations, usually 22–85 percent, and degrees of purity. USP grade is available for pharmaceutical applications, meeting strict purity standards. Common preparations encountered in commerce and research include aqueous solutions of lactic acid itself, calcium lactate, sodium lactate, and potassium lactate salts; topical formulations (creams, serums, chemical peels); and intravaginal gels.

As a food additive it is approved for use in the EU, United States, and Australia and New Zealand (listed as E270 or INS 270); lactic acid is used as a food preservative, curing agent, and flavoring agent.

2. Traditional and Historical Use

Discovery and Early History

Since its discovery in 1780 by Carl Wilhelm Scheele, lactate was often mistaken for a mere hypoxic waste product as a consequence of oxygen deprivation during muscle contractions. Scheele isolated the compound from sour milk, establishing its dairy connection. The biochemical understanding of lactic acid's role evolved dramatically over the following two centuries.

Fermented Foods Across Cultures

Lactic acid bacteria have been used in food production for thousands of years. Throughout history numerous civilizations have harnessed the power of lactic acid fermentation for foods that are now staples in the diet; nomadic people in Central Asia and the Caucasus were among the first to transform milk into yogurt and kefir, while the ancient Greeks and Romans refined cheese and yogurt-making techniques.

Lactic acid-fermented cabbage was consumed around the ancient world: in the Roman Empire as sauerkraut; in Asia as Chinese PaoCai; in the Himalayas or in Korea as kimchi. To preserve meat for the winter, Romans used the methods of the Gauls and Celts. The history of kimchi is around 3,000 years; it is now an emblematic health-promoting product of the Korean diet and, since 2013, has been acknowledged as a Korean heritage culture product.

In the 18th century, Commodore John Byron and Captain James Cook, among others, found that vitamin C-rich sauerkraut was an effective antiscorbutic agent of great value for lengthy sea voyages.

In many cultures, lactic acid fermentation shows a long history with a wide variety of fermented liquid and semi-liquid traditional foods being produced from cereals, legumes, and tubers. Food fermentation using lactic acid bacteria is an ancient technique deemed a simple and economical way to modify the nutritional contents of plant-based foods.

Even though until recently LAB fermentation capacity was mainly associated with dairy products, data have proved that LABs have a crucial role in the preparation of dozens of traditional cereal-based foods worldwide. In Latin America, Latin American countries have a long history of people who have elaborated fermented foods and beverages over the years from typical ingredients of the continent; according to some authors, a large variety of fermented foods and beverages in Latin America come from native inhabitants that traditionally elaborated these kinds of products using empirical information. Among these populations, fermentation was and is still used mainly as a food preservation method.

Early Therapeutic and Dermatological Use

Lactate was first reported to be used in a moisturizer as a treatment for ichthyosis in 1946. The use by dermatologists of alpha-hydroxy acids at doses of 30 to 70% is a very old practice for reducing deep scars. In 1989, dermatologist Gary Monheit worked with salicylic acid, resorcinol, and lactic acid, followed by trichloroacetic acid, with great results in treating various skin conditions. Lactic acid's role as a food acidulant and preservative has also been documented for centuries within cheesemaking and pickling traditions globally.

3. Key Constituents, Active Compounds, and Mechanisms of Action

Endogenous Biochemistry and the Lactate Shuttle

Since its discovery in 1780, lactate was often mistaken for a mere hypoxic waste product. The "low O₂ induces high lactate" paradigm led to the simplistic conclusion that "high lactate means low O₂." It was not until the 1980s, when shuttle transfer of lactate between cells was introduced, that a paradigm shift in the understanding of the role of lactate in metabolism occurred.

By shuttling between producer (driver) and consumer (recipient) cells, lactate fulfills at least three purposes: (1) a major energy source for mitochondrial respiration; (2) the major gluconeogenic precursor; and (3) a signaling molecule. Working by mass action, cell redox regulation, allosteric binding, and reprogramming of chromatin by lactylation of lysine residues on histones, lactate has major influences on energy substrate partitioning.

In terms of the organization of energy substrate partitioning in humans and other mammals, lactate is at the fulcrum of intermediary metabolism; lactate is the inevitable product of glycolysis. When cell work rate is high, lactate produced by driver cells is secreted into the interstitium and circulation, from where it can reach a variety of recipient cells such as those in the heart, liver, kidneys, and brain.

Lactate released into the blood reaches white adipose tissue, and by binding to HCAR-1, lactate acts to inhibit lipolysis via a cyclic adenosine monophosphate-dependent pathway (CREB), which limits subsequent release of fatty acids into blood. Second, lactate produces an abundance of mitochondrial acetyl-CoA that gives rise to malonyl-CoA, which in turn inhibits carnitine palmitoyl transporter-1 (CPT-1) and blocks mitochondrial free fatty acid uptake.

Catalyzed by the near-equilibrium enzyme lactate dehydrogenase (LDH), the reduction of pyruvate to lactate serves to regenerate the NAD⁺ necessary for continued glycolytic flux. Lactate in normal human subjects is cleared very quickly at a rate of 320 mmol/L/hr, mostly by liver metabolism and re-conversion of lactate back to pyruvate.

Mechanisms in the Skin

Lactate serves as a natural moisturizing factor (NMF) essential for maintaining skin hydration. In keratinocytes, lactate enhances filaggrin gene transcription by stabilizing HIF-1α. Lactate also upregulates SMPD-1 expression or activity via pH regulation, facilitating ceramide synthesis.

L-lactic acid and D,L-lactic acid appear to work by stimulating the synthesis of ceramides in the stratum corneum. Topical application of lactic acid modulates the secretion of cytokines by keratinocytes, and this regulation might represent a mechanism contributing to therapeutic effects such as addressing photoaging.

At 5% to 20% concentrations, lactic acid causes corneocyte detachment and desquamation of the lower, newly forming stratum corneum. Lactic acid peel is a superficial alpha-hydroxy peel with a large molecular size, making it less penetrable, thereby providing extra advantage of being more hydrating and soothing compared to smaller AHA molecules such as glycolic acid.

Antimicrobial Mechanisms

As a weak acid, lactate inhibits the growth of S. aureus and C. acnes. Only recently has lactic acid, at physiological concentrations, been shown to be highly potent at killing BV-associated bacteria — all 17 of the most abundant BV-associated species are potently inactivated at pH 4.5 with 55–111 mM racemic DL-lactic acid.

Mechanisms in Fermented Foods

During fermentation, lactic acid bacteria produce a variety of bioactive metabolites, including organic acids, antimicrobial compounds, exopolysaccharides, enzymes, and vitamins, which enhance food safety, shelf life, nutritional quality, and health-promoting potential. Nutritionally relevant benefits of the fermentation process include accumulation of bioactive compounds (exopolysaccharides, short-chain fatty acids, bioactive peptides), degradation of antinutritional factors, and improved bioavailability of essential nutrients (amino acids, minerals, vitamins).

4. Scientific Evidence by Area of Use

4.1 Skin Hydration and Natural Moisturizing Factor (NMF)

Other constituents of NMF include lactic acid, urea, and inorganic ions such as sodium, potassium, calcium, and chloride, all of which contribute to epidermal hydration. The NMF is composed principally of free amino acids, and various derivatives such as PCA, urocanic acid, and inorganic salts, sugars, as well as lactic acid and urea. NMF components are packaged within the corneocytes, making up approximately 10 percent of the corneocyte mass and 20 percent to 30 percent of the dry weight of the stratum corneum.

Lactate was first reported to be used in a moisturizer as a treatment for ichthyosis in 1946, and it has been shown to improve and prevent the reappearance of symptoms of dry skin compared with lactate-free moisturizers. Studies have confirmed that AHAs exert pronounced efficacy in alleviating skin xerosis, indicating that AHAs possess moisturizing activity; the moisturizing effect of AHAs is primarily attributed to their hydroxyl groups, which are endowed with robust water-binding capacities.

Evidence strength: The role of lactic acid/lactate as an endogenous component of the NMF is biochemically well established. Clinical evidence for topically applied lactate improving skin hydration is supported by decades of use and controlled studies in xerotic and ichthyotic skin, though much of this earlier literature predates modern rigorous RCT standards.

4.2 Keratolysis, Exfoliation, and Acne

Alpha-hydroxy acids (AHAs), including lactic acid, are widely used as first-line agents, as they promote exfoliation, hydration, and normalization of keratinization; these agents have been employed to alleviate follicular plugging and smooth the stratum corneum, yet the evidence base supporting their relative effectiveness remains scattered across small trials and observational studies.

These mechanisms provide a strong rationale for topical keratolytic therapy in conditions such as keratosis pilaris (KP), which aims to reduce corneocyte cohesion, facilitate desquamation, soften keratin plugs, and improve hydration of the stratum corneum. Topical keratolytics remain reasonable first-line, symptom-directed options for KP, with AHAs demonstrating potential benefit; however, the overall evidence base is constrained by small sample sizes, heterogeneous outcome measures, limited blinding, and short follow-up.

Existing clinical studies support improvement in texture and roughness with acids (e.g., lactic acid, salicylic acid, glycolic acid) and urea-based regimens, but designs often involve small sample sizes, short follow-up, limited blinding, and variable outcome measures, making cross-study comparisons difficult.

Chemical peeling causes a manageable injury to the skin, resulting in subsequent regeneration of a new epidermal layer. Injury depth is determined by the concentration of acid used, the type of vehicle, buffering, and duration of skin contact. Although often used to treat acne, chemical peeling is also widely used for melasma, photoaging, and lentigines. There is an emerging trend of using a combination of peeling agents; for instance, Vitalize Peel contains both salicylic acid and lactic acid for treating acne vulgaris. However, only one RCT was found comparing a chemical peeling agent with placebo for acne vulgaris, despite more than 10 chemical peeling agents actually being applied in practice; further well-designed RCTs comparing other chemical peels with placebo are needed.

Evidence strength: Mechanistic and in-vitro data are solid, and clinical use of lactic acid as a keratolytic in acne, KP, and dry skin is well established. High-quality RCT data specifically for lactic acid monotherapy remain limited, with most evidence derived from small or uncontrolled trials or studies using combinations with other agents.

4.3 Photoaging, Hyperpigmentation, and Melasma

AHAs are indicated for use in many in-home and dermatologist cosmetic and medical products for skin moisturization, wrinkle and pigment reduction, and chemical peeling. More recently, lactic acid has emerged as a safer alternative to the gold-standard glycolic acid without compromising efficacy.

Research has found that a TCA-lactic acid peel strongly inhibits tyrosinase, collagenase, and elastase — enzymes responsible for the production of melanin pigment and degradation of collagen and elastin, respectively. Chemical peeling is usually performed by dermatologists, plastic surgeons, and aestheticians for the treatment of photo-aged skin, dyspigmented skin, skin prone to acne eruption, and pre-cancerous skin lesions.

In a study of epidermal melasma, there is a paucity of controlled trials showing effectiveness and safety of pyruvic acid peel in melasma, and to the best of the investigators' knowledge, there are no controlled trials comparing the safety and effectiveness of pyruvic acid and lactic acid peel in melasma. In an in-vitro study in 2003 on melanoma cells, glycolic acid and lactic acid showed tyrosinase inhibition, demonstrating that these acids do more than just smooth the skin.

Evidence strength: In-vitro evidence for mechanisms involving collagenase inhibition, tyrosinase suppression, and ceramide stimulation is compelling. Clinical evidence for lactic acid peel in photoaging and hyperpigmentation is preliminary and largely based on small, uncontrolled or combination-therapy trials. Head-to-head RCTs comparing lactic acid alone to placebo or standard of care are sparse.

4.4 Vaginal Health and Bacterial Vaginosis (BV)

The vaginal microbiota in bacterial vaginosis (BV) typically has low abundance of lactic acid-producing lactobacilli. Lactic acid has properties that may make it effective for treating BV and/or restoring an optimal Lactobacillus-dominated vaginal microbiota.

Vaginal lactobacilli produce the metabolite lactic acid (LA), which is a bioactive that acidifies the vagina to a pH ranging from 3.2 to 4.2. Both low pH and lactic acid-producing Lactobacillus are correlated with beneficial reproductive outcomes and lowered STI infections; lactic acid has been shown to inactivate BV-associated bacteria and pathogens such as C. trachomatis, HIV-1, and N. gonorrhoeae.

Lactic acid has been put forward as a potential treatment or prophylaxis for BV due to its ability to restore the imbalance of the vaginal microbiota and to promote the disruption of vaginal pathogenic bacterial biofilms, which might trigger BV recurrence; a systematic literature review evaluated the clinical evidence regarding the efficacy and prophylactic potential of lactic acid in BV.

The recurrence of BV remains a considerable challenge given that about 60% of women experience BV relapse within six months after initial treatment. In vitro data suggest that lactic acid may be effective for BV treatment; however, high-quality evidence supporting the use of lactic acid-containing products for BV and modification of the vaginal microbiota is lacking. Large, rigorous randomized trials of lactic acid-containing products that have been carefully evaluated with respect to pH, lactic acid concentration, L-/D-isomer ratio and osmolality are needed. Future studies should include standardized clinical endpoints, standardized timing of endpoint measurement, assessment of adverse events, and long-term follow-up.

Evidence strength: In-vitro data and mechanistic rationale for lactic acid in vaginal health are strong. Clinical evidence is preliminary. Systematic reviews conclude that high-quality RCT evidence is currently lacking and that well-designed clinical trials are urgently needed before firm recommendations can be made.

4.5 Exercise Performance and Oral Lactate Supplementation

The Lactate Shuttle theory is applicable to diverse fields such as sports nutrition and hydration, resuscitation from acidosis, treatment of traumatic brain injury, maintenance of glycemia, reduction of inflammation, cardiac support in heart failure and following myocardial infarction, and to improve cognition.

A 2024 randomized crossover study investigated oral lactate supplementation for exercise performance: sixteen endurance-trained male cyclists (VO₂max 59 ± 7 mL·kg⁻¹·min⁻¹) consumed 120 mg·kg⁻¹ body mass of lactate or a placebo 70 min prior to a high-intensity interval cycling test. Blood acid-base balance, heart rate, perceived exertion, and gastrointestinal tolerance were assessed. There was no effect of lactate supplementation on exercise performance (p = 0.320), despite a reduction in RPE (p = 0.012) and increases in strong ion difference and bicarbonate (p = 0.026 and p = 0.041, respectively). In addition, gastrointestinal side effects were observed, but there was no effect on heart rate. Lactate supplementation did not improve exercise performance, despite positive changes in acid-base balance and RPE.

Earlier work in cyclists reached similar null conclusions: neither sodium bicarbonate nor lactate supplementation appeared to improve 40-km cycling time trial performance; however, the potential benefits of lactate supplementation regarding perceived exertion were noted as requiring further research.

Evidence strength: The theoretical basis for oral lactate supplementation as an ergogenic aid is scientifically interesting, but the available controlled human trials have not demonstrated significant improvement in exercise performance. Current evidence does not support oral lactic acid/lactate as an ergogenic supplement based on available RCTs.

4.6 Food Preservation and Antimicrobial Applications

In meat products, lactic acid can be used as an antimicrobial agent. Lactic acid is used as a flavoring agent and preservative in processed cheese, salad dressings, pickles, and carbonated beverages, and as a raw material or a catalyst in numerous chemical processes. These uses are well documented and approved by major regulatory bodies; they fall outside the realm of dietary supplementation per se but illustrate lactic acid's broad functional role in human food systems.

4.7 Emerging and Investigational Areas

Dysregulated lactate shuttling disrupts metabolic flexibility and, worse, supports oncogenesis. Lactate production in cancer (the Warburg effect) is involved in all main sequelae of carcinogenesis: angiogenesis, immune escape, cell migration, metastasis, and self-sufficient metabolism. This area is under intensive basic science and translational investigation; no human therapeutic interventions using exogenous lactic acid for cancer prevention or treatment have been established.

Poly-lactic acids have been clinically utilized to address skin aging, with poly-D,L-lactic acid (PDLLA) shown to stimulate collagen synthesis and even promote angiogenesis in the skin of aged mouse models. Injectable poly-L-lactic acid (PLLA) as a dermal filler is an approved clinical use, though distinct from dietary supplementation.

5. Body Systems Associated with Lactic Acid

• Musculoskeletal / Energy Metabolism: Challenges to adenosine triphosphate (ATP) supply stimulate lactate production, leading to immediate, short- and long-term cellular adaptions to support ATP homeostasis. Lactic acid is a central metabolite of anaerobic and aerobic glycolysis in skeletal muscle.
• Liver and Kidneys: Lactate in normal human subjects is cleared very quickly at a rate of 320 mmol/L/hr, mostly by liver metabolism and re-conversion of lactate back to pyruvate.
• Skin / Integumentary System: Lactic acid functions as an endogenous NMF component, a keratolytic agent, and a modulator of ceramide synthesis and cytokine secretion.
• Reproductive / Vaginal Microbiome: Vaginal lactobacilli producing lactic acid are central to maintaining low pH and protection against BV and sexually transmitted infections.
• Gastrointestinal System: Lactic acid is present in the gut and blood and is a product of colonic fermentation by commensal bacteria.
• Cardiovascular / Brain: The Lactate Shuttle theory is applicable to cardiac support in heart failure and following myocardial infarction, and to improve cognition.
• Immune / Inflammatory System: Many lactic acid bacteria species function as probiotics that support gut health, improve digestion, and strengthen the immune system; LAB contribute to many other health benefits, including enhancing nutrient absorption, reducing food allergenicity, and providing antioxidant effects. (These effects relate to the bacterial producers of lactic acid rather than to lactic acid as an isolated supplement.)

6. Dosage Forms and Dosages Reported in Studies

Topical Dermatological Use

• A controlled clinical study has evaluated 10% lactic acid and 5% salicylic acid with instrumental assessment in keratosis pilaris.
• Clinical studies have investigated 2% lactic acid-containing skincare products (e.g., cleansers, toners, and creams) for 12 weeks for acne management.
• 5% to 20% concentrations of lactic acid cause corneocyte detachment and desquamation of the lower, newly forming stratum corneum.
• Alpha-hydroxy acids at doses of 30 to 70% have been used by dermatologists for reducing deep scars.
• One study evaluated the therapeutic efficacy and safety of lactic acid peel at 90% for epidermal melasma; lactic acid peel at this concentration is a superficial AHA peel with a large molecular size, making it less penetrable and thereby providing extra advantage of being more hydrating and soothing.
• Recommended pH of dermatological preparations is 3.5 to 7.5; acid content varies from 1 to 20%, and compositions can be a mixture of water and alcohol or a suitable ointment.

Oral Supplementation (Sports/Exercise)

• Sixteen endurance-trained male cyclists consumed 120 mg·kg⁻¹ body mass of lactate (as calcium lactate) or a placebo 70 min prior to a cycling performance test.

Intravaginal Products

• Treatment of BV with 5 g of lactic acid gel has been studied in clinical trials in comparison with metronidazole. Large trials evaluating lactic acid-containing products should carefully control pH, lactic acid concentration, L-/D-isomer ratio, and osmolality.

Food Additive

• Lactates have been reported to have low oral toxicity, with a lack of adverse effects in feeding studies in rats, in which up to 3,900 mg/kg body weight/day was administered for 2 years.

7. Safety Considerations and Interactions

Regulatory Safety Status

L-Lactic acid is classified by the Food and Drug Administration (FDA) as generally recognized as safe (GRAS) for use in food (21 CFR 180.1061). In reviewing the safety of lactic acid and its sodium, potassium, and calcium salts, the Joint FAO/WHO Expert Committee on Food Additives (JECFA, 1974) concluded that it was "unnecessary to set ADI limits" for these additives since lactic acid is a normal constituent of food and a normal intermediary metabolite in humans.

Oral and Systemic Safety

Lactates have been reported to have low oral toxicity, with a lack of adverse effects in feeding studies in rats, in which up to 3,900 mg/kg body weight/day was administered for 2 years. Acute toxicity studies for oral, dermal, inhalation, dermal irritation, and skin sensitization demonstrate the low toxicity potential of L-lactic acid at use concentrations appropriate to food and cosmetic applications.

Measurement of lactate level in serum is required for the differential diagnosis and medical management of hyperlactatemia, cardiac arrest and resuscitation, sepsis, reduced renal excretion, hypoxia-induced cancer, decreased extra-hepatic metabolism, intestinal infarction, and lactic acidosis. Lactic acidosis is a serious clinical condition distinct from the physiological production of lactic acid during exercise or the intake of lactic acid from food or supplements.

Concentrated Solutions and Topical Irritation

Lactic acid is generally recognized as safe for food applications but can irritate the skin, eyes, and respiratory system in concentrated forms. While not classified as a carcinogen and considered relatively safe compared to other acids, it is mildly corrosive in concentrated solutions and may cause burns with prolonged exposure. L-Lactic acid has a very low pH (<1 at high concentrations) and is classified as a severe irritant; acute toxicity studies were limited by the fact that the 80% L-Lactic Acid test substance is a very low pH, severe irritant.

Alpha-hydroxy acids, whilst conferring a beneficial effect on the skin, may cause local irritation when applied to sensitive areas of the skin, in particular the face. There are possibilities of post-inflammatory hyperpigmentation and acid burn; therefore, chemical peeling should be performed by a trained professional or physician.

Infant Formula Restriction

Lactic acid is established as GRAS at 21 CFR 184.1061 and sodium lactate is affirmed as GRAS at 21 CFR 184.1768 for use in food; however, the FDA does not authorize the use of sodium lactate in infant foods and formulas.

Gastrointestinal Effects with Oral Supplementation

In the crossover cycling study investigating 120 mg·kg⁻¹ body mass oral lactate, gastrointestinal side effects were observed in some participants, which is a notable adverse effect consideration for high-dose oral lactate supplementation in athletes.

Photosensitivity Concerns

AHAs including lactic acid are known to increase skin photosensitivity due to exfoliation of the outermost stratum corneum, which reduces the skin's natural UV protection. This is a well-recognized clinical consideration when using AHA-containing products topically, particularly at higher concentrations or with professional peels. There are possibilities of post-inflammatory hyperpigmentation with chemical peels; peeling should be performed by a trained professional or physician.

Drug Interactions

No specific clinically documented pharmacokinetic drug-drug interactions between exogenous lactic acid (as a dietary supplement or topical agent) and pharmaceutical drugs have been identified in the sources reviewed. The primary clinical concern regarding elevated blood lactate in a pharmacological context relates to drugs such as metformin or nucleoside reverse transcriptase inhibitors, which can impair mitochondrial function and cause lactic acidosis — a mechanism entirely separate from dietary or topical lactic acid exposure.

References

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