Sodium Bicarbonate commonly known as household baking soda or less commonly as saleratus is a chemical consisting of NaHCO3 (Sodium, Hydrogen and Carbon Tri-oxide). Its pH is weakly alkaline. It is commonly used to counter acid reactions. It is often added to coffee or tomato sauce to reduce acidity. It acts as an excellent deodorizer against acidic scent molecules. This natural ability to neutralize acidic environments is exactly the reason it makes a good performance ergogenic. Sodium Bicarbonate is claimed to be a good ergogenic aid to reduce Lactic Acid build-up in the muscle cells and bloodstream.
One of the most common terms used improperly by athletes and health professionals alike is “Lactic Acid Production”. The production of Lactic Acid is known to be one of the rate limiting factors in short intense athletic performances. Its generic reference as “lactic acid” and its effects are often misquoted in an attempt to understand the overall result of the buildup of hydrogen (H+) atoms in the muscle cells and lactate (the dissociated acid-free version of Lactic Acid) in the blood system.
The misconception that fatigue is caused by a buildup of Lactic Acid was due to the fact that when Lactate was found in high concentrations in the blood, it was a good indication of the amount of acid in the muscle. As such, when blood lactate rises, there is an associated rise in acid accumulating in the muscle. The thought was that the lactic acid in the muscle was the performance limiting factor, but in reality it was the dissociated acid (H+) that was causing the problem.
It is now known that the dissociated Lactate is used as fuel by the muscles and is converted to carbon compounds in the liver and recirculated for energy production (the Cory Cycle). Conversely, the dissociated Hydrogen ions accumulate in the muscle cells block the ability for calcium to bind to troponin. When calcium is not present the muscle fibers are unable to contract and relax.
Further research and hypothesis exists that provides evidence that acidosis is not even caused by Lactic Acid but by the proton released from the uncoupling of the phosphorus atom during the use of ATP in the glycolysis and the phosphagen system. ATP from nonmitochondrial sources is used continued muscle contraction releasing H+ and causing acidosis from intense exercise. It is theorized that Lactate production increases as a result of high intensity movements in order to prevent pyruvate accumulation and make sure that ample supplies of NAD(+) are available for the second phase of glycolysis. Thus Lactate production auto-correlates with cellular acidosis but may not be a causal factor but rather an indirect marker for metabolic cellular conditions that induce metabolic acidosis. Without Lactate, acidosis and muscle fatigue would accumulate more quickly impairing performance even faster.
Am J Physiol Regul Integr Comp Physiol. 2004 Sep;287(3):R502-16
Robergs RA Ghiasvand F Parker D.
Exercise Science Program, Department of Physical Performance and Development, Johnson Center, Rm. B143, The University of New Mexico, Albuquerque, NM 87131-1258, USA
In 1977, South African biochemist Wieland Gevers proved that the reaction that produces lactate actually consumes a pair of free protons. As such the production of Lactate appears to be a protective mechanism to slow down or retard metabolic cell acidosis.
Improvement in the performance of any high intensity exercise is enhanced by delaying what has been commonly referred to as the lactic acid threshold. More properly this is the point of accumulation in the muscle cells of H+ so that the crossbridge cycle of skeletal muscle is unable to be completed and performance stops.
There are many natural mechanisms that are thought to contribute to the redux of Hydrogen that enables an athlete to train at harder more intense levels over time. The conversion of lactate back to a fuel source through the liver and muscle cells along with the removal of the dissociated Hydrogen atoms is part of what contributes to the elevated post exercise metabolic burn rate or postexercise oxygen consumption (EPOC). But during a high intensity performance, the muscle cells must learn to reduce the levels of acid very quickly so as not to shut down the creation of muscle contracting forces. These natural mechanisms are still not entirely understood.
One of the more controversial theories on the body’s process for dealing with Lactic Acid accumulation is the Lactic Shuttle Theory put forth by Dr. George Brooks Professor ; Director, Exercise Physiology Laboratory at The University of California – Berkeley. He claims that Lactic Acid is oxidized within the mitochondria. The opposing debate to this theory suggests that this would cause the environment between the Cytosol and inner mitochondria to be the same thereby eroding the pH gradient that drives energy production. In addition the speed at which lactate dissociates from Lactic Acid and exits the cell could make this almost impossible. Although, if indeed acid is caused by other factors such as proton released from the uncoupling of the phosphorus atom during the use of ATP in the glycolysis and the phosphagen system, this theory appears more plausible.
Brook’s most recent research suggests that bathing the cell in high levels of lactate during intense exercise may stimulate the production of free radicals that “upregulate” a variety of genes. These genes govern mitochondrial biogenesis causing the muscle cell to produce more mitochondria, thus enhancing an athlete’s ability to burn lactate in future workouts. This would begin to explain the training adaptations that occur that produce increased anaerobic threshold levels.
The more widely recognized mechanism for buffering this intracellular acid production is through a gradient diffusion process whereby the load of buffer outside the muscle exceeds that inside the muscle causing the Hydrogen atoms to be pulled out of the cell and into the bloodstream. Normal cellular processes allow for carbon dioxide waste product to be transported away from the cell as bicarbonate ions. (bicarbonate-CO2 System) It combines with water (H2O) in the blood to form Carbonic Acid (H2CO3). Carbonic acid can be converted to Hydrogen (H+) and Bicarbonate (HCO3-) and or back to Carbonic acid in a reverse process. As such bicarbonate acts as a buffer for picking up Hydrogen atoms and creating Carbonic Acid. A third transformation of these molecules can be formed into CO2 + H2O thereby neutralizing the acid and allowing the CO2 to be eliminated through expiration. In addition buffers in the intracellular and extracellular fluids including the bone (calcium carbonate) as well as excretion from the kidneys allow for rapid adjustment of blood pH and elimination of H+.
CO2 + H2OH2CO3H+ + HCO3-
When Sodium Bicarbonate dissociates in the blood stream into Na+ and HCO3- the Sodium acts as a transport mechanism for exchange of bicarbonate and H+ in the cells (Na+ / H+ exchanger) This exchange is one for one and is electrically neutral. Helping to draw the acid out of the cell and into the bloodstream, the bicarbonate can now react with the Hydrogen in one of the bicarbonate-CO2 sytsems described above. In addition, sodium dependent exchangers, help to move bicarbonate in and out of the cell to regulate pH as well.
Having established the human physiological chemistry for creating and removing acids or more properly Hydrogen ions (H+) from the cells and blood system, we can begin to understand the basis for sodium bicarbonate loading for performance. Regardless of the mechanism that creates the H+, it exists and the only question left is weather its effects on the cellular level contribute to muscle fatigue and if so then sodium bicarbonate should benefit the high intensity short duration efforts of athletic endeavors. Several if not the majority of studies seem to show some ergogenic benefit of bicarbonate loading.
Sodium Bicarbonate Supplementation Protocols
What is commonly referred to as “soda loading” or “bicarbonate loading” is a 70 year old practice. Its common form of ingestion is 300mg per kg of body mass 1-2 hours prior to performance in the form of household bicarbonate soda mixed with water or other flavored drink or as pharmaceutical urinary alkalinisers such as Ural. (The equivalent of 4-5 teaspoons of bicarbonate powder). The ingestion of this product is not considered to pose any kind of potential health risk although gastrointestinal distress such as cramping or diarrhoea is common. Excess water consumption can alleviate the symptoms of diarrhoea.
Bicarbonate loading is not considered a banned practice for human performances. Even if it were it would be very hard to detect as dietary practices cause a wide variance in urinary pH. It is best used in short duration 1-7 minute high intensity exercises (MMA, Wrestling, 400-1500 meter run, 100-400 meter swim, rowing and track and field events). Team sports that require repeated anaerobic bursts, may benefit from bicarbonate loading. Its repeated use after a performance in anticipation for another one may not be recommended due to gastrointestinal discomfort.
McNaughton and colleagues studied the effect 500 mg/kg/day, spread into four doses for 5–6 days of bicarbonate supplementation (McNaughton et al. 1999a; McNaughton & Thompson 2001). This protocol resulted in an increase in plasma base excess, and was sustained for the entire time of the bicarbonate intake. It was found to enhance the performance of a prolonged sprint performed 1–2 days after the bicarbonate supplementation ceased compared to the pre-trial performance (McNaughton & Thompson 2001). The persistence of blood levels of bicarbonate may be a desirable outcome for sports involving a series of competition events. Alternatively, the athlete can terminate their intake of bicarbonate (along with the risk of gastrointestinal side effects) 24 hours prior to their competition, yet still maintain the benefits to their performance.
Matson & Tran 1993 performed a meta-analysis of the general research literature on bicarbonate loading and concluded that in 29 randomized double-blind crossover investigations the ingestion of sodium bicarbonate has a moderate positive effect on exercise performance, with a weighted effect size of 0.44 The mean performance of the bicarbonate trial was, on average, 0.44 standard deviations better than the placebo trial. Their findings suggested a weak relationship between the increased blood alkalinity (increase in pH and bicarbonate) achieved in the bicarbonate trial and the performance outcome. Ergogenic effects were related to the level of metabolic acidosis during exercise suggesting the need to reach optimal cell membrane pH diffusion gradient. The tests also showed significant individualization in the reported outcomes due to varied bicarbonate ingestion. As such, it may be that a certain level of intensity for a certain period of time in a certain level of conditioned athlete may benefit most from the ergogenic effects. As discussed it is thought to be best in short duration, 1-7 minutes and extreme high intensity efforts.
In a further review of the research literature, 13 of 18 studies showed a statistically significant effect of bicarbonate loading during both short and longer term high intensity endurance activities. In all but one study where the ergogenic effect was not measured, the bicarbonate was taken less than 2 hours prior to an event. All other studies where the effect was not measured, the bicarbonate was taken more than 2 hours prior to an event except for the case of one study where it was consumed 1 hour before the event.
Study Performance Enhancement
Stephens et al. (2002) No
Schabort et al. (2000) No
McNaughton et al. (1999b) Yes
Potteiger et al. (1996a) Yes
Van Montfoort et al. (2004) Yes
Oopik et al. (2003) Yes
Shave et al. (2001) Yes
Potteiger et al. (1996b) No
Tiryaki and Atterbom (1995) No
Bird et al. (1995) Yes
Goldfinch et al. (1988) Yes
Wilkes et al. (1983) Yes
Mero et al. (2004) Yes
Pierce et al. (1992) No
Gao et al. (1988) Yes
McNaughton and Cedaro (1991) Yes
Bishop and Claudius (2005) Yes
Price et al. (2003) Yes
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