11% Increase in Type I Fiber Cross Sectional Area During 12 Weeks of KHCO3 Supplementation: Are Alkali Supplements Fiber-Type Specific Anabolics W/ Add. Metabolic Benefits?

Muscle toning with bicarbonate? Without weight gain? For some women probably a dream come true ;-)

I guess, you will be hard-pressed to find another website with a similar amount of information the effects of alakali (mostly sodium bicarbonate) supplementation on exercise performance and metabolism as the SuppVersity. Irrespective of the previous posts on "baking soda" or the recent elaborations on the importance of a well-controlled acid base ratio (learn more), I am quite sure that the results of a recently published study from the Tufts Medical Center and the Bone Metabolism Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University will come as a surprise even for the most regular visitors among you - to be honest, I was and am still surprised myself ;-)

So what's the surprise?

In their 12-week rodent study that was devised to elucidate whether the addition of a neutralizing amount of potassium bicarbonate (KHCO3) to purified diet designed to match the standard acid forming Western way of eating would ameliorate the urinary nitrogen loss and affect the muscle fiber size and number, as well as the levels of circulating and muscle-specific IGF-1 in thirty-six vitamin D sufficient or deficient, 20-month-old, Fischer rats, Lisa Ceglia and her colleagues did not only observe (relative changes in brackets are expressed for vitamin D sufficient / insufficient animals)...

• higher urinary pH (33% / 34%, after only 6 weeks),
• lower urinary nitrogen losses (-28% / -42%) and
• increased circulating 25OHD levels (3% and 15%);

they also observed significant increases in the cross-sectional area of the soleus muscles of the animals that did not depend on the vitamin D status of the animals.

Figure 1: Vitamin D levels, 24h urinary Nitrogen / Creatine ratio, cross sectional area of soleus (type I fibers; CSA1) and extensor digitorum longus (EDL; type II fibers, CSA2) after 12 weeks in rodents on KHCO3 supplemented diets with / without adequate vitamin D, data expressed relative to unsupplemented control (Ceglia. 2013)

As the data in figure 1 goes to show you, this effect was fiber-type specific and was not observed in the extensor digitorum longus (EDL), which is - contrary to the soleus - type II (fast twitch, glycolytic; learn more) fiber dominant. What is surprising though is the fact that the researchers did not observe corresponding increases in muscle weights (p > 0.05).

Unfortunately, the scientists don't address the "growth vs. weight" discrepancy in the discussion of the results, so that we are left to come up with our own hypotheses to explain why this may have been the case. We know that it cannot be the mere result of decreased food intakes or total body weight - both were virtually identical in all groups (just a note: the muscle weight per total body weight did not differ either). Moreover, the scientists explicitly state that "the lower UNi/Cr could be considered an indicator of reduced muscle proteolysis" - so that common sense would dictate an increase in muscle size and mass as it was in fact observed in previous human studies from the same laboratory:

"In a 6-week study in 19 healthy adults (average age 62 years), KHCO3 supplementation attenuated a protein-induced rise in UNi/Cr excretion by over 50 % compared to placebo (Ceglia. 2009). A larger study in 162 adults (average age 62 years) given a lower bicarbonate supplement dose or no bicarbonate, also demonstrated a 6 % decline in UNi/Cr excretion (Dawson-Hughes. 2009)." (Ceglia. 2013)

In fact, the provision of the bicarbonate supplement in the latter of the two studies did also increase the lower extremity power of the healthy older women who participated in the study by 13%; an observation that speaks in favor of the practical relevance of bicarbonate supplements - at least in the context of a normal / low vegetable and correspondingly low dietary alkali intake and that irrespective of the presence / absence of increases in skeletal muscle mass.

So what's the general mechanism here?

What about the muscle fiber specificity? The scientists speculate that the difference may simply be mediated by the "size difference of type II fiber subtypes (IIa, IIb, IIx) in rat EDL muscle and an inadequate [study] duration to detect a significant fiber size effect." This alone would, warrant a "larger and longer-term" at the end of which it may be possible to "fully characterize effects of this dietary
intervention on muscle morphology." (Ceglia. 2013)

If we simply discard the (as of now inexplicable) absence of increases in muscle weight and focus on the increases in muscle cross-sectional area it would in fact appear as if the alkali-induced improvements in nitrogen retention are the primary cause for the "muscle building" effects, the New Yorker researchers observed.

The latter appears all the more likely, in view of the fact that neither the provision of vitamin D nor the addition of bicarbonate (or a combination of both) resulted in significant reductions in the catabolic signaling molecules E3 ubiquitin ligases, MURF1 and MAFbx. Still, if we don't assume that the rodents expended much more energy and simply burned off the extra protein it must have gone somewhere, so that the most likely explanation for the inconsistencies would actually be the time-point at which the signaling molecules were measured. After all, a pre- vs. post comparison doesn't tell us what happened during the 12-week supplementation period. Neither do we know whether the acid-base balance does not target a completely different set of anabolic molecules than exercise or protein nutrition so that the scientists may simply have missed measuring the "correct" markers of anabolism / catabolism to be able to fully explain their observations.

---

Bottom line: There is still much to be learned about the effects and detailed mechanisms of alkali supplementation. So much, in fact, that the addition of large boluses of potassium bicarbonate to a whole foods diet that includes large amounts of net alkalizing vegetables and fruits (funny how difficult it was to write that this way around and not "fruits and vegetables" ;-) as a means to increase your gains appears to be unwarranted or at least unnecessary at the moment.

Latent acidoses can set you up to become obese (learn more)

For someone following a typical Western and or high meat + fat / high grain or otherwise acid forming diet without adequate "vegetable buffer" a medium dose alkali supplement providing ~67.5 mmol of bicarbonate (~647mg of KHCO3 or 800mg NaHCO3/baking soda, which was the dose that has been used in the previously mentioned human study by Dawson-Hughes et al.) ingested twice a day, could yield all sorts of metabolic benefits, of which you have learned in previous posts on sodium bicarbonate and the acid base balance here at the SuppVersity that they go way beyond increases in muscle strength and cross-sectional area and reach into the realms of metabolic disease and even cancer.

Suggested reads:

• Calcium, Magnesium, Potassium & Co in Food, Water & Supps - Getting Enough is Easy, Knowing How Much Is Not! (read more)
• SuppVersity Science Round-Up on Sodium, Potassium, Alkalinity & Co (listen now)
• Science Round-Up Seconds: The Macro-Mineral Alphabet & the Potential Health Hazards of Diet-Induced Latent Acidosis (read more)
• Previous SuppVersity posts on sodium bicarbonate (browse all)

References:

• Bailey JL, Zheng B, Hu Z, Price SR, Mitch WE. Chronic kidney disease causes defects in signaling through the insulin receptor substrate/phosphatidylinositol 3-kinase/Akt pathway: implications for muscle atrophy. J Am Soc Nephrol. 2006 May;17(5):1388-94. Epub 2006 Apr 12.
• Ceglia L, Harris SS, Abrams SA, Rasmussen HM, Dallal GE, Dawson-Hughes B. Potassium bicarbonate attenuates the urinary nitrogen excretion that accompanies an increase in dietary protein and may promote calcium absorption. J Clin Endocrinol Metab. 2009 Feb;94(2):645-53. 
• Ceglia L, Rivas DA, Pojednic RM, Price LL, Harris SS, Smith D, Fielding RA, Dawson-Hughes B. Effects of alkali supplementation and vitamin D insufficiency on rat skeletal muscle. Endocrine. 2013 May 11. 
• Dawson-Hughes B, Castaneda-Sceppa C, Harris SS, Palermo NJ, Cloutier G, Ceglia L, Dallal GE. Impact of supplementation with bicarbonate on lower-extremity muscle performance in older men and women. Osteoporos Int. 2010 Jul;21(7):1171-9.

Science Round-Up Seconds: The Macro-Mineral Alphabet & the Potential Health Hazards of Diet-Induced Latent Acidosis

You lose 600x more sodium than magnesium during a workout. The RDA is yet only ~3-4x higher (Montane. 2007).

If you already listened to the podcast of yesterday's installment of the SuppVersity Science Round Up (if you have not already done so, you can dowload the podcast, here), you may have noticed that I confused the minimal potassium (K) to sodium ratio (Na), which is probably ~1:1, and the "original" K:Na ratio in the "paleo diet".

According to Sebastian et al. (2002) the latter is ~8-9:1 in other words: 8-9 mols of potassium per mol of sodium. That's miles apart from the 1:2-3 ratio the average Westerner (the exact ratio varies depending on which study you refer to) uses as a springboard to hypertension ;-)

The (un-)definite mineral synergism/antagonism chart

Another thing you may have noticed with yesterday's show is the fact that the show was pretty "topic centered". My personal feeling is that it has a much better flow this way and that not despite, but because Carl and I did not cover such a broad range of topics. I cherish the hopefully non-futile hope that you feel the same but am obviously open for any constructive criticism from your side

The SuppVersity macro mineral chart provides a general overview of the complex interactions that exist between calcium, phosphorus, magnesium, sodium, chloride, and potassium (compiled based on various sources)

. This, by the way, does also apply to the corresponding installment of the Seconds, of which you will soon realize that it is not a non-related add-on, but will expand, explain and summarize interesting aspects we've covered in the live show (note: from next week on the Science Round-Up will air at 12 PM EST, the same URL as usual).

On that note, let's start with an "expansion" I already promised to deliver towards the end of the show: some information on the synergism and antagonism of the macro minerals. It's a pretty complex matter and the following illustration is based on generalizations. Some of them, like the low-level exception to the antagonism between calcium and magnesium, of which I believe that it is important to know are explicitly mentioned, others are not.

A very good example of the former, i.e. the important second order interactions is the influence sodium has on the antagonism between potassium and magnesium. The latter disappears, when sodium levels are high and magnesium is needed as a sodium antagonist. Similarly, the often-touted antagonism between magnesium and calcium is actually a co-factor relation, where any "antagonism" is only the result of imbalances between the two.

The good, the bad and the ugly: Just a question of the "wrong" perspective

One thing that should actually be obvious, but is often ignored in all the hoopla about the "good" and "bad" guys among the macro-minerals is that "antagonisms" do not contradict the essential nature of all of the electrolytes, which are - antagonistic or not - in the end, all actors in the same metabolic play.

Figure 1: Average ratio of mineral content (new:old) of 20 vegetables and 20 fruit: data based on comparison of  UK Government’s Composition of Foodsdata at two-time points separated by approximately 50 years (Mayer. 1997)

I mean, take calcium and phosphorus as an example, they are both essential for the structural integrity of your bone and the fact that calcium has a reputation of being the "good guy", while phosphorus is the "bad guy" is just a necessary consequence of the overabundance of the latter, i.e. phosphorus from grains, soft drinks, dairy products, meats, fish, seeds, nuts, eggs and due to the change in mineral ratios (cf. figure 1) even most fruits and vegetables in the food chain of Mr. Joe Average, these days.

According to a 2009 paper by Dana Cordell et al. this may well change in the not all too distant future, after all "the quality of remaining phosphate rock is decreasing and production costs are increasing" (Cordell. 2009). With estimates saying that the demand for phosphorus is going to double within the next 40 years, it stands to reason that the decried overabundance of phosphorus, which is, among other things, also responsible for lowering the zinc content of the produce (cf. Peck. 1980) may be partly reversed within the next decades... I mean, we all know that nothing is as "convincing" as with financial interests, right?

The strong ion difference determines your pH levels

What's the difference between macro-minerals and their "little brothers" the trace minerals? Calcium, sodium, potassium, phosphorus, magnesium, chloride and sulfur are macro-minerals because you need them in amounts that are greater than 100mg per day. Of the trace minerals, on the other hand, you need less (in most cases much less) than 100mg per day. That does not mean though that Iron, zinc, copper, chromium, fluoride, manganese, iodine, molybdenum and selenium were less important - it's merely a quantitative distinction.

While it stands to reason that there is a reason, calcium, sodium, magnesium, and potassium are also called "electrolytes", astonishingly few people can actually give an ad hoc explanation why this is the case - and that despite the fact that their lives depend... no, not on the answer, but on the existence and physiological function of electrolytes ;-)

If you have listened closely to your physics teacher, you will yet probably be aware that an "electrolyte" (electro- ~ charge, -lyte ~ carrier) is a positively or negatively charged molecule (ion) and nothing out of the ordinary in nature.

In your body electrolytes are used to establish ionically charged gradients, similar to the gradient that exists between the positive and negative pole of a battery. These gradients are situated on the cell membranes in excitable tissues, such as muscle and verve, where they facilitate or hinder the influx/efflux of other charged particles.

One of these gradients, in fact probably the physiologically most significant one, by the way, is established by positive sodium (Na+) and potassium (K+) ions and their negative counterpart chloride (Cl-) - exactly those electrolytes you've heard about in yesterday's show (remember: whenever you hear "salt" it actually means Na + Cl).

The electrolytes are not the only charged particles ...

From your chemistry lessons, you may remember that there are not just ionic atoms, but also ionic molecules and that the electron configuration of these particles will determine how they bind, interact and react. But I guess, we have had more than enough complicated theory for today, so if you want to know how the anions and how the strong ion difference (SID) is calculated, check out this brief overview over at acid-base.com.

Rather than going into the details of the mechanism, I decided that it would probably of greater value to wrap the Seconds up with a brief overwiev of the downstream effects of a metabolic state, of which Pizzorno, Frassetto and Katzinger point out that it is not necessarily characterized by acedemia, i.e. pH levels below the "magic" (if we were honest, we'd you'd have to write arbitrary, here) cut-off limit of pH 7.35:

High intensity exercise can also lower your blood pH, an effect you can counter with sodium bicarbonate

"Acidosis only becomes acidaemia when compensatory measures to correct it fail. To illustrate the difference between acidosis and acidaemia, take the following example: two processes occurring simultaneously in the same individual, such as a respiratory acidosis combined with a metabolic alkalosis. In this case, if the respiratory trend toward acidosis is greater than the metabolic trend, a pH of less than 7·35 may be reached, and would be considered acidaemia, despite the presence of a metabolic alkalosis. The intensity of each ‘process’ will determine the pH, but the terms themselves (acidosis, alkalosis) do not indicate a certain pH." (Pizzorno. 2009)

In other words, you don't have to suffer from diabetic or otherwise pathogenic "acidosis", to suffer from one of the following ill health-consequences:

• 

  Hip fracture incidence per 100,000 study participants; aggregated data from cohorts from 33 countries (Frassetto. 2001)

  Calcium loss, bone loss, osteoporosis - Unfortunately, this is not only the best-known side effect of "being too acidic", it's also the only one people take seriously. In that, scientists and lay press alike have zoned in on the high intake of animal proteins as the main confounding factor. But despite the fact that the high sulfur content (methionine, cysteine & co) does certainly contribute to the problem, the data in the figure at the right should make it quite clear that the stuff we eat and don't eat with our meats is at least as much to blame for the misery. In view of the fact that
  

  "[...] cereal grains themselves are net acid-producing and alone accounted for 38% of the acid load yielded by the combined net acid-producing food groups in the contemporary diet" (Sebastian. 2002)

  the average (processed) grain addicted US citizen with his/her quasi-non-existent vegetable intake would end up way on the left side of the x-axis of the graph on the right-hand side, even if he ate not a single gram of animal protein - we would just have to relabel the axis to vegetable/acidd forming food intake (including grains!)".
• Increased renal nitrogen excretion and hampered protein synthesis - One of the less known effects of an increased acid/base ratio is an increase in nitrogen excretion that will obviously not simply hamper your gains, but can also set you up to sarcopenia (age-induced muscle loss).
  
  

  

  Correcting a diet-induced low grade metabolic acidosis with K-bicarbonate reduces the nitrogen loss of 750mg - 1000mg per day (per 60kg BW) in post- menopausal women (Frassetto. 1997)

  In the end, the excretion of nitrogen is nothing, but an adaptive mechanism and a consequence of the catabolism of tissue protein. It is, if you will, a basic necessity for your body to rob your muscle and other tissue of glutamine and all other amino acids, that can be convert to glutamine in the liver, from where it is delivered to the kidney where it's used to synthesize ammonia and excrete the potentially toxic acid load. This will obviously mitigate the severity of the acidosis, it does yet also entail a net loss in muscle and organ protein that cannot be compensated for by an increase in acid forming protein in your diet.
  
  As the data in the figure to the right goes to show you this is a process that's regulated on a day to day basis and the relief in nitrogen loss (data in mg/day/60kg) provided by bicarbonate supplementation (days 0-18) is transient and disappears as soon as you return to your regular low-base, high acid diet (days 19-30).
• Impairments of the growth hormone / IGF-1 axes - Brunnger et al. tested in 1997 whether experimental acidosis would have an effect on the growth hormone / IGF-1 axis and observed a "significant decrease in serum IGF-1 concentration without a demonstrable effect on IGF binding protein 3", which points towards an acid induced "primary defect in the growth hormone/IGF-1 axis" that occurs "via an impaired IGF-1 response to circulating growth hormone with consequent diminution of normal negative feedback inhibition of IGF-1 on growth hormone" (Brunger. 1997). Interestingly, Mahlbacher et al. were able to show that the administration of IGF-1 can in turn ameliorate acidosis and thus correct the previously discussed nitrogen wasting (Mahlbacher. 1999).
  
  

  

  Learn more about the effects of GH, IGF1 and it's splice variants MGF & co and their influence on skeletal muscle hypertrophy in the respective part of the Intermittent Thoughts on Building Muscle (go to the overview).

  In fact, potential physiological effects of the acid-induced impairment of the GH / IGF-1 axes had been observed much earlier, already. McSherry et al. for example report in a 1978 article in the Journal of Clinical Investigations that children with short stature and classic renal tubular acidosis developed normally, when they were treated with adequate amounts of alkalizing agents.
  
  That similar negative effects can be observed even in the presence of "low-grade 'tonic' background metabolic acidosis" was confirmed by Frassetto et al. who observed statistically significant increases (+11%) in 24-hour mean growth hormone secretion in post-menopausal women with diet-induced low-grade metabolic acidosis, when their dietary acid load was neutralized with adequate amounts of potassium bicarbonate (Frassetto. 1997).
  
  In a subsequently published study the scientists argue that the concomitantly observed increases in osteocalcin and bone metabolism would confirm the physiological significance of these changes (Frassetto. 2001). The effects on bone add to the well-known beneficial metabolic effects of growth hormone ( and line up with the recently reported association between low growth hormone levels and memory impairments (Wass. 2010).
  
  In view of the bad press GH and IGF1 are getting, it is important to point out that we are talking about a normalization of the GH/IGF-1 axis, here. It is therefore unlikely that the restoration of a normal acid-base balance will have any of the anti-longevity and pro-cancerous (see next bulletin point) effects of growth hormone and IGF-1 you may have read about in the pertinent literature.
• Potential protective / anti-cancer effects - While conclusive scientific evidence for the involvement of low-grade acidemia in the etiology of cancer is still missing, it has long been speculated that the genetic and epigenetic perturbations, which will turn normal cells into cancer cells may be triggered (among other factors) by disturbances in the acid-base equilibrium. As Ian Forrest Robey points out in his 2012 review of the literature, a diet induced
  

  "[a]cid-base disequilibrium has has been shown to modulate molecular activity including adrenal glucocorticoid, insulin growth factor (IGF-1), and adipocyte cytokine signaling, dysregulated cellular metabolism, and osteoclast activation, which may serve as intermediary or downstream effectors of carcinogenesis or tumor promotion." (Robey. 2012)

  If you want to learn more about the "state of the art research" on the potential link between latent dietary acidosis and the development of cancer, I suggest you simply read the free fulltext of the paper on PubMed. 

I guess, now that you've learned about some of the intricacies of adequate mineral intakes and balances, the acid / base balance, nitrogen and bone loss, growth hormone and cancer, and listened to the interactions of sodium blood pressure, blood glucose and insulin on yesterday's show, it's about time to come back to the simple things that work - the bottom line, so to say...

"What was that about the nutrient sufficiency of the vegetarian / vegan diet, you said on the air?" The above figure shows the % of omnivores, vegans and vegetarians who meet the RDAs  for protein and fiber and selected vitamins and minerals (DiMarino. 2013)

Bottom line: A whole foods convenient-"food" free with the right balance of vegetables, protein, and a reasonable amount of complex largely unprocessed carbohydrates, fats and fruits - call it "ancestral" or "paleo", if you will - is going to provide you with all the minerals you need, it will contain them in the right ratios and supply your body with all the co-factors it needs to use them. It will stabilize your pH levels, normalize your growth hormone / IGF-1 axis and is beyond any doubt the most effective way to get and stay in shape, to reduce your cancer risk, ward off diabetes and lead a life that's not simply long, but also worth living.

If you adhere to these simple rules, there is no reason to be worried about "not getting your minerals" and other essential nutrients. After all, this is what distinguishes you from the "average" western omnivore, vegetarian or vegan who fails to meet most of his or her nutrient requirements.

References:

• Brungger M, Hulter HN, Krapf R. Effect of chronic metabolic acidosis on the growth hormone/IGF-1 endocrine axis: new cause of growth hormone in sensitivity in humans. Kidney Int. 1997; 51:216–221
• Cordell D, Drangert J-, White S. The story of phosphorus: Global food security and food for thought. Global Environ Change. 2009;19(2):292-305.  
• DiMarino A. A Comparison Of Vegetarian Diets And The Standard Westernized Diet In Nutrient Adequacy And Weight Status. The Ohio State University. A Thesis Presented in Partial Fulfillment of the Requirements for Graduation with Distinction from the School of Health and Rehabilitation Sciences of The Ohio State University. 2013. 
• Frassetto L, Morris RC, Jr., Sebastian A. Potassium bicarbonate reduces urinary nitrogen excretion in post-menopausal women. J Clin Endocrinol Metab. 1997: 82:254–259.
• Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian A. Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Eur J Nutr. 2001 Oct;40(5):200-13.
• Mahlbacher K, Sicuro A, Gerber H, Hulter HN, Krapf R. Growth hormone corrects acidosis-induced renal nitrogen wasting and renal phosphate depletion and attenuates renal magnesium wasting in humans. Metabolism. 1999; 48:763–770
• May RC, Kelly RA, Mitch WE. Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism. J Clin Invest. 1986. 77:614–621.
• Mayer AM. Historical changes in the mineral content of fruits and vegetables. British Food Journal. 1997; 99(6):207 - 211
• McSherry E, Morris RC, Jr. At tainment and maintenance of normal stature with alkali therapy in infants and children with classic renal tubular acidosis. J Clin Invest. 1978; 61:509–527. 
• Montain SJ, Cheuvront SN, Lukaski HC. Sweat mineral-element responses during 7 h of exercise-heat stress. Int J Sport Nutr Exerc Metab. 2007 Dec;17(6):574-82.
• Peck NH, Grunes DL, Welch RM, MacDonald GE. Nutritional Quality of Vegetable Crops as Affected by Phosphorus and Zinc Fertilizers Agron. J. 1980; 72: 528–534.
• Pizzorno J, Frassetto LA, Katzinger J. Diet-induced acidosis: is it real and clinically relevant? Br J Nutr. 2010 Apr;103(8):1185-94.
• Sebastian A, Frassetto LA, Sellmeyer DE, Merriam RL, Morris RC Jr. Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors. Am J Clin Nutr. 2002 Dec;76(6):1308-16.
• Wass JA, Reddy R. Growth hormone and memory. J Endocrinol. 2010 Nov;207(2):125-6.
• Williams B, Layward E, Walls J. Skeletal muscle degradation and nitrogen wasting in rats with chronic metabolic acidosis. Clin Sci. 1991; 80:457–462

Supercharging Creatine With Baking Soda: Study Shows Increased Peak Power and Endurance - Plus: How Bicarbonate Could Help You Lose Fat & Build Muscle

The pH of your urine is not a reliable measure of your bodies acid base-status

I have written about the "love affair" of creatine and baking soda before. Once, in the "The Pharmacokinetics of Creatine" series (Part I, Part II), where I outlined how you can "brew" your own KreAlkalyn replacement using creatine and NaHCO3, and another time back in 2010, when I discussed the data from a dissertation by James J Barber, who had conducted a preliminary investigation into the joint ergogenic effects of N-Amidinosarkosin (creatine) and NaHCO3 (baking soda) on the repeated sprint performance of recreational athletes.

You can learn more about beta alanine & bicarbonate at the SuppVersity

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

BA + Bicarb are Synergists

Bicarb Buffers Creatine

Beta Alanine Fails to HIIT Back

The complete results of a follow up investigation by Barber, who now works at the Human Performance Laboratory at the California Polytech State University, are going to be published in the next issue of the Journal of Strength and Conditioning Research (Barber. 2012); and they underline what you, as a diligent student of the SuppVersity, knew all along: Baking soda is not only cheaper than 99% of the commercially available supplements, it is also more ergogenic than the average junk the guy at GNC is trying to sell to you.

Soda? But that must be bad for you?! False!

For their study, the researchers recruited a group of 13 healthy previously trained (>5h of aerobic and >2h of HIT per week) young men (age 21.1 ± 0.6 yrs, BMI 23.5 ± 0.5 kg/m²; VO2Max 66.7 ± 5.7 ml/kg-min). In a double-blinded crossover fashion (meaning that each participant had to complete every condition, i.e. "crossover", and neither he, nor the researchers knew whether he had been given the active or the placebo treatment, i.e. "double-blinded"), the men had to consume a supplement containing either

• placebo: 20g maltodextrin + 0.5g/kg maltodextrin,
   
• creatine (only): 20g creatine + 0.5g/kg maltodextrin, or
   
• creatine + NaHCO3: 20g creatine + 0.5g/kg baking soda*
  
  * for all supplement the total dosage was divided into four smaller doses, which were to be taken at 9:00 a.m., 12:00 p.m., 6:00 p.m., and 10:00 p.m.; the subjects also completed a 48h dietary recall and were asked to consume identical foods during each condition

before their peak power, mean power, relative peak power, and bicarbonate concentrations were assessed during six subsequent 10-second repeated Wingate sprint tests on a cycle ergometer with 60s rest periods between each sprint. To preclude any carry-over effects from previous tests, or rather supplementation, each experiment was followed by a three-week washout period.

Figure 1: Total and relative peak power output (left) and relative peak power output in the individual trials (right; data adapted from Barber. 2012)

As you can see in figure 1, Barber et al. were able to confirm his initial results. Interestingly, only the creatine + NaHCO3, yet not the creatine only regimen elicited statistically significant increases in both the relative power output (in W/kg; p < 0.05 for both) and the total power output (p < 0.05 only in the creatine + NaHCO3 trial; cf. figure 1, left). Moreover, the creatine + NaHCO3 supplementation lead to "the greatest attenuation of decline in relative peak power over the 6 repeated sprints." (cf. figure 1, right).

Creatine + baking soda: Additive or synergistic effects

An interesting question the scientists probably ignored, because their GNC guy did not yet tell them about the "extraordinary superiority of buffered creatine", is whether the ~37g of sodium bicarbonate the subjects ingested simply added to the beneficial effects the 20g of creatine had on the repeated sprint performance of the athletes, or whether the baking soda also decreased the breakdown and facilitated the uptake of creatine (cf. figure 2)

Figure 2: Relative increase in creatine in dry muscle mass of horses, after supplementation with creatine monohydrate, Kre-Alkalyn or Gastner's patented creatine + sodium carbonate +sodium hydrogen carbonate formula (posted first in "The Pharmacokinetics of Creatine: Part 1/2" based on Gastner. 2010)

And while it may not be important for your HIIT sessions, whether the mechanism behind the performance increase is additive of synergistic, it could well make the one-rep difference on a deadlift or bench press competition, in the course of which each additional phosphocreatine molecule counts.

"Cholesterol is the devil and sodium is his little brother!" Everyone who still believes everything the medical orthodoxy says, please raise your hands!

A note on the dangers of "salt": Firstly, baking soda is "only" ~28% sodium, which means that for every 4 grams you ingest you get roughly 1 g of sodium. Secondly, it is arguable how much of the sodium is effectively taken up and will be floating around in your blood. As T. Lakhanisky points out in his dossier for the Belgian government: "The uptake of sodium, via exposure to sodium carbonate, is much less than the uptake of sodium via food. Therefore, sodium carbonate is not expected to be systemically available in the body." (Lakhanisky. 2002) And thirdly, there is more and more evidence that suggests that the chloride rather than the sodium content of common table salt (NaCl = NatriumChloride) is the root cause of "sodium induced hypertension" in "sodium sensitive" individuals / animal models. Only recently, a study by Schmidlin et al. showed that chloride loading induced hypertension in the stroke-prone spontaneously hypertensive rat despite profound sodium depletion (Schmidlin. 2010). So, if you asked me, rather than pointing at salt as the #2 on the list of greatest evils (obviously cholesterol is still #1, here) the medical orthodoxy would be better advised to address the imbalances between sodium and potassium, which are so characteristic of the western diet, instead of painting yet another black and white picture where sodium is the bad guy and potassium the dangerous mineral that cannot be sold OTC in dosages >80mg.... but hey, this would be the topic for a whole new blogpost and as gross as it may sound, the chance that you get diarrhea from the baking soda is probably 1000x higher than the remote possibility of increases in blood pressure. A 1990 study by Luft et al. even found that the blood pressure of 10 mildly hypertensive and normal subjects decreased by 5mmHg after 7 days in the course of which they drank 3 liters of sodium bicarbonate containing water per day (Luft. 1990)

If you add to that all the previously reported benefits you can derive from a few tablespoons of baking soda

• +34% time to exhaustion and +91% total work during HIIT (Feb 29, 2012)
• synergistic and superior effects compared to beta alanine (Feb 20, 2012)
• protection against stress induced oxidative damage to white blood cells (Nov 28, 2011)
• increased performance in tennis players (Nov 4, 2010)

and obviously Barber's own previously reported results, you may understand why I urged our common friend Adelfo Cerame Jr to supplement with bicarbonate throughout his whole contest prep.

Latent metabolic acidosis hampers weight loss and muscle gains

Figure 3: The contribution of latent acidoses to the obesity epidemic and maybe even your inability to build muscle and/or lose weight
(based on Berkemeyer. 2009)

And even when you are not interested in your performance, a 2009 paper by Shoma Berkemeyer is by no means the only, nor the first article that linking an increased hydrogen ion concentrations (latent acidity, which can be countered by dietary bicarbonate) to weight gain and the obesity epidemic (Berkemeyer. 2009, cf. my summary in figure 3).

In view of the fact that even a latent H+ surplus could apparently compromise your efforts to lose fat and build muscle, it should be obvious that you better make sure to have enough alkalizing greens (and optional supplemental bicarbonate; not necessarily 30g, though ;-) in your diet - no matter if the whole acid/base balance issue, esp. the role of a high protein intake, is still very controversial.

More scientific evidence for the combination of bicarbonate & creatine in a more recent article | read it!

Practically speaking, what do I do? Since loading is not necessary unless you have a competition right ahead and this is the first time you take creatine you just take 3-5g of creatine monohydrate with approximately the same amount of sodium bicarbonate per day.

Larger doses of sodium bicarbonate as they would be used for acute performance enhancing effects are (almost certainly) not necessary to increase the efficacy of creatine. If you want the acute benefits, but get diarrhea from 15-20g of bicarbonate, I suggest you try to serial load.