A deep intelligence brief on NaHCO₃ — its mechanism, evidence base, key debates, unresolved questions, and what a sophisticated coaching program actually does with it. Includes analysis of Bob Bowman's practitioner critique.
Unlike most supplements, sodium bicarbonate has a well-characterized mechanism, a decade of consistent evidence at the category level, and IOC endorsement. It sits in a small group of legal ergogenic aids that have cleared the bar of scientific credibility.
The evidence says it works for 200m and 400m events. The question for a sophisticated program is not whether to consider it — it's whether a specific athlete, in a specific context, meets the conditions under which the average effect becomes a reliable individual benefit.
Think of bicarbonate as borrowing physiological capacity from before the race to spend during it. The pre-race alkalosis is the loan. The race is the expenditure. Like any leverage, it amplifies outcomes in both directions.
This clarifies when it makes sense: high-stakes competition, well-prepared athlete, validated individual response. It does not make sense for development training, athletes who haven't validated their response, or contexts where GI failure would be catastrophic.
Sports governance, policy analysis, and swimming industry insights — written for coaches, scientists, and anyone who thinks seriously about the sport.
Subscribe on Substack — it's freeA clear-eyed assessment of where the evidence is strong, where it's weak, and where it's been misread.
Evidence quality rated across key claims. The headline 1.3% figure is real but rests on a methodologically mixed literature. Confidence intervals narrow considerably when you restrict to elite athletes and competition conditions.
Click an event to see evidence summary
Most bicarbonate studies are nominally "double-blind" but functionally single-blind. Athletes frequently know they've received the active treatment due to GI sensations, taste, and physiological awareness. Expectancy alone can drive performance improvements of 1–2% — precisely the magnitude bicarbonate produces.
One recent study using an "ergolytic" framing showed expectancy substantially altered outcomes even when the substance was identical across conditions. The true pharmacological contribution may be materially smaller than reported literature suggests.
The characteristic bicarbonate study uses 6–10 participants. Meta-analyses pool these studies but don't solve the small-sample problem — they aggregate it. The 1.3% figure has the appearance of precision that its underlying data doesn't warrant.
Publication bias compounds this: null results are systematically less likely to be published. Funnel plot asymmetry in the meta-analyses suggests the true average effect size is smaller than what appears in the literature.
The entire evidence base is built on moderately trained athletes. Elite swimmers have spent years specifically developing the buffering systems bicarbonate is supposed to augment. Whether exogenous bicarbonate produces meaningful marginal gains on top of highly trained acid-base regulation is genuinely unknown.
Studies that do include elite athletes produce inconsistent results. The extrapolation from college-level time trials to Olympic-level competition is an inference the field makes with more confidence than the data supports.
The consensus story — H⁺ buffering delays acidosis-driven fatigue — is elegant but increasingly contested. Westerblad's muscle physiology work has demonstrated that inorganic phosphate accumulation and calcium handling disruption may be more important than H⁺ in contractile failure.
If the mechanism is wrong or incomplete, optimizing use based on the acid-base rationale is working from an incorrect map. Bicarbonate may work through partially different pathways than the field assumes — including central/perceptual effects that are almost entirely uninvestigated.
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Subscribe on Substack — it's freeEvidence-based guidance on dosing, timing, delivery, and the individualization process that separates sophisticated use from naive application.
* Calculator provides guidance estimates. Always validate with individual training trials before competition use.
The delivery format significantly affects GI tolerance without necessarily changing efficacy. Hover/click each option to see risk level.
The single most important insight from the research that most programs skip: individual time-to-peak blood bicarbonate varies from 60 to 180+ minutes. An athlete who peaks at 90 minutes and takes it 60 minutes before a race is competing in a declining alkalotic state, not a peak one.
Minimum protocol before any competition use: 3–5 training sessions at competition intensity using 0.3 g/kg, with varied ingestion timing (60, 90, 120 min), tracking both GI response and perceived exertion during the set. Establish individual peak window. Establish GI tolerance threshold. Only then commit to a competition timing.
This isn't optional refinement. It's the difference between using bicarbonate intelligently and using it naively.
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Subscribe on Substack — it's freeThe researchers and organizations whose work you'll encounter most in this literature — and what each actually argues.
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Subscribe on Substack — it's freeThe underexplored angles, systematic blind spots, and genuinely unresolved questions that sophisticated practitioners should hold.
Stress hormones differ in competition versus training. Motivational state affects pacing. The presence of competitors changes effort selection. Cortisol and adrenaline alter GI motility — precisely the mechanism by which bicarbonate causes problems. None of this is captured in existing research. The translation from laboratory to competition is an assumption, not a demonstrated fact. This is the deepest unresolved issue in the entire literature.
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Subscribe on Substack — it's freeWhat a sophisticated coaching program actually does — distilled from the full evidence base into actionable principles.
High-intensity swimming creates H⁺ faster than the body clears it. Bicarbonate buys clearance capacity. The evidence for 200–400m events is real but built on imperfect data. GI risk is the central practical problem, not a footnote. Individual response varies enormously and predicting who benefits remains unsolved. Competition-condition validity is assumed, not demonstrated. Sophisticated programs individualize timing, validate GI tolerance in training, and hold the expected benefit loosely — treating it as a tool that may help specific athletes in specific contexts, not a standard protocol for all middle-distance swimmers.
"The research says it works and it does. But it works with a specific dose for a specific physiology at an incredibly specific time before a specific event. Before we worry about sodium bicarb, how about make the intervals on your main set — or just show up to every practice."
// Bob Bowman — 38 Olympic medals, coach of Phelps · Marchand · McIntosh
Sports governance, policy analysis, and swimming industry insights — written for coaches, scientists, and anyone who thinks seriously about the sport.
Subscribe on Substack — it's freeTwo live models: the full physiological mechanism from ingestion to ion transport, and a lap-by-lap race simulator with configurable athlete parameters.
Four interactive layers — from ingestion to ion transport. Start at the top and go deeper, or jump to any layer. Each layer builds on the one above.
Sodium bicarbonate dissociates immediately in gastric fluid: NaHCO₃ → Na⁺ + HCO₃⁻. In the highly acidic stomach (pH ~1.5–3.5), bicarbonate is rapidly converted:
The CO₂ produced drives the bloating and belching characteristic of bicarbonate ingestion. Absorption of the remaining bicarbonate and sodium ions occurs primarily in the small intestine via active transport and passive diffusion. Peak plasma [HCO₃⁻] typically occurs 60–90 min post-ingestion in most individuals — but the range is 60–180 min, driven by differences in gastric emptying rate, gut motility, and baseline acid-base status.
Delivery format effects: Solution maximizes absorption rate but floods the GI tract with osmotic load. Capsules delay gastric emptying and distribute the bolus, reducing peak osmotic stress. Co-ingestion with a carbohydrate meal further slows absorption and reduces GI symptoms by diluting the bicarbonate bolus.
The clinically important implication: an athlete who takes bicarbonate 60 minutes before their event but peaks at 150 minutes is competing in a declining alkalotic state — potentially worse than no dose at all due to GI discomfort without physiological benefit.
Blood pH is governed by the Henderson-Hasselbalch equation:
During high-intensity exercise, glycolysis generates pyruvate faster than mitochondria can consume it. Pyruvate is converted to lactate, with co-release of H⁺. This H⁺ is initially buffered intracellularly (by phosphocreatine, inorganic phosphate, and proteins), then extracellularly by the bicarbonate system:
By pre-loading extracellular [HCO₃⁻] from ~24 to ~29 mmol/L, bicarbonate loading steepens the H⁺ concentration gradient between intracellular and extracellular compartments. This accelerates the efflux of H⁺ from contracting muscle via MCT (monocarboxylate transporter) co-transport, delaying intracellular acidosis.
The physiological fatigue threshold (pH ~7.0–7.10 in muscle) is not crossed as quickly, extending the time the athlete can sustain high glycolytic flux. This is the mechanistic basis of the performance benefit.
The muscle cell membrane is where the core mechanism operates. Hover each zone to explore the molecular events.
The key molecular actors are the MCT1 and MCT4 monocarboxylate transporters. MCT4 is the high-capacity efflux transporter in glycolytic (Type II) muscle fibers — the fibers that dominate energy production in 200–400m swimming. Its transport rate is directly proportional to the transmembrane H⁺ gradient.
Pre-exercise bicarbonate loading raises extracellular [HCO₃⁻] from ~24 to ~28–30 mmol/L. This alkalizes the extracellular space, increasing the chemical gradient that drives H⁺ efflux. The rate equation simplifies to:
By lowering extracellular [H⁺] (raising pH), the denominator decreases and net flux increases. The practical result: the muscle can sustain higher glycolytic rates for longer before reaching the intracellular pH threshold that impairs contractile function.
Intracellular buffering systems: Phosphocreatine (first line), bicarbonate (limited intracellular), protein histidine residues (carnosine), and inorganic phosphate all contribute. Bicarbonate loading augments only the extracellular component — it does not directly change intracellular buffer capacity. This is why it complements rather than replaces beta-alanine (which raises intracellular carnosine).
The bicarbonate consensus rests on the H⁺ fatigue hypothesis. Westerblad's work from Karolinska Institute challenges this at the mechanistic level.
The H⁺ fatigue hypothesis dates to classic work by Fabiato & Fabiato (1978) and Donaldson & Hermansen (1978), showing that acidified solutions impaired Ca²⁺ sensitivity of isolated myofibrils. These studies were done at 12–22°C.
Westerblad and colleagues showed that at physiological temperature (35–37°C), the inhibitory effect of H⁺ on Ca²⁺ sensitivity is substantially reduced. The crossbridge kinetics change: the Q10 (temperature coefficient) means that what is true at 15°C is not necessarily true at 37°C. This complicates the foundational mechanistic argument.
In contrast, inorganic phosphate — released during ATP hydrolysis and PCr degradation — does not show the same temperature-dependence. Pi inhibits crossbridge cycling and directly precipitates Ca²⁺ in the SR lumen. The Pi mechanism appears more robust across temperature ranges.
The current mechanistic picture: fatigue in high-intensity exercise is likely multifactorial. H⁺ contributes, but is not the sole or even dominant driver. Pi and Ca²⁺ handling are co-equal or superior mechanisms. Bicarbonate addresses the extracellular H⁺ component, which remains a real contributor — just perhaps not as primary as the original theory assumed.
Configure your athlete, select an event, then activate NaHCO₃ to see the lap-by-lap physiological and performance effect in real time.
| Lap | Stroke / Leg | Split — No NaHCO₃ | Split — With NaHCO₃ | Δ | Mechanism |
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