Removal of Amalgam Fillings Associated With Reductions in Memory Loss, Fatigue, Anxiety, Confusion & Other Health Problems, Observational Study from Canda Shows

Amalgam removed = health restored?

While there is little doubt that mercury vapor poses a known health risk, there is neither a clearly established safe level of exposure, nor evidence that similar ill health effects can occur with chronic low grade exposure to mercury vapor from dental amalgam fillings.

As you may know amalgam is not 100% but "only" 50% mercury, but is that enough to represent a significant health risk? The objective of a recent study from the University of Calgary was "to determine if mercury exposure from amalgam fillings is associated with risk of adverse health effects" (Zwicker. 2014).

Mercury is among the reasons fish should not be your exclusive protein source

Salmon Better Than Whey?

Cod protein for recovery

Krill = Super Protein?

Farmed vs. Wild-Caught Fish

Fast vs. slow protein

5x More Than FDA Allows

To this ends, Zwicker et al. conducted a large longitudinal non-blinded study involving participants from a preventative health program in Calgary, Canada. The goal was to assess whether (a) there was an association between having amalgam fillings, the amount of mercury in the urine and reported health issues and (b) whether the 14 previously self-reported health symptoms would improve in a sample of persons who had their fillings removed compared to a sample of persons who had not had their fillings removed.

Figure 1: Summary data for study sample with urine mercury measures (Zwicker. 2014)

A brief glimpse at the baseline data reveals that the presence of 18.4 and 23.7 amalgam fillings on the tooth surfaces of the subjects in the treatment (amalgam fillings will be removed) and the amalgam control group (amalgam fillings will not be removed) have higher amounts of mercury in their urine.

What do previous studies say? Oskarsson et al. (1996) fount that mercury from amalgam fillings was the main source of mercury in milk. In fact, the amount of mercury babies were exposed to from breast milk ranged up to 0.3 μg/kg/d, of which approximately one-half was inorganic mercury and which corresponds to approximately one-half the tolerable daily intake for adults recommended by the World Health Organization (Oskarsson. 1996). Other studies present opposing results, though, and claim that fish, not amalgam fillings was the major source of mercury in breast milk (Drexler. 1998). Still, evidence from other studies, such as Nylander (1987), which report mercury vapor from amalgam fillings to be the major source of mercury in the organs of human subjects, support the notion that at least the "first generation" amalgam fillings are a major source of human mercury exposure. The correlation with subjective health symptoms, on the other hand, is less obvious. Studies like Ahlqwist et al. (1988) and a twin study by Björkman et al (1996) clearly refute the existence of a significant correlation.

What is interesting, but not actually what the scientists wanted to investigate is the fact that the mercury levels in women are generally higher (may be a result of a comparatively lower body size and mass and similar mercury exposure).

What do you think happened one year after the fillings were removed?

Well, let's see. As the data in Figure 2 indicates, the mercury levels in both amalgam groups declined in comparison to the baseline measure (follow up data for the amalgam free group is not available)

Figure 2: Changes in mean urinary mercury level after one year after the amalgam fillings
were removed / not removed (Zwicker. 2014)

The effects are, I guess you will agree with me on that one, not exactly impressive. Against that background the obvious question is: "Are the self-reported measured improvements in headache, memory loss, depression, fatigue, anxiety & co a result of a placebo effect?" I mean, the subjects obviously knew that their amalgam fillings were removed (remember: it's a non-blinded study!) and you bet that they've read some of the horror stories about mercury on the Internet.

Table 1: One year odds of symptom improvement and worsening in the group of subjects who had the amalgam fillings removed, controlled for age and sex | Odds ratio coefficients are the odds of change in treatment group relative to the positive amalgam group. {P values}; * indicates coefficient is different from 1 at size 0.05; ^ represents statistical significance at size 0.10 (Zwicker. 2014).

So, can we tell whether the "improvements" you see in Table 1 are actually brought about by the removal of the amalgam fillings or simply by the subjects psyche? I would say we can't and that's why I have my doubts about the validity of the researchers conclusion that "that mercury exposure from amalgam fillings adversely impact health and therefore are a health risk" (Zwicker. 2014) - not necessarily because I believe they are harmless, but rather because the data the scientists evaluated does not prove this claim.

If avoiding mercury from fish is a good thing, avoiding mercury exposure from amalgam fillings is a good thing, too. Irrespective of the fact that the study at hand provides only insufficient evidence of its ill health effects.

Bottom line: I personally had my one filling removed back in the day, but rather the necessary result of the fact that it was in a baby tooth ;-)

That being said, I still subscribe to the researchers assertion that "a safer alternative materials for dental fillings should be encouraged to avoid the increased risk of health deterioration associated with unnecessary exposure to mercury" (Zwicker. 2014), yet not because of the data in the study at hand, though, but rather based on the notion that you would want to limit any unnecessary exposure to heavy metals, no matter how small the amount that's leeching from the amalgam fillings may be, though.

On a side note: A study investigating the commonly heard claim that the removal of amalgam would only increase the load of mercury (at least temporarily) indicates that - if it's done properly - "[t]he uptake of amalgam mercury in the GI tract in conjunction with removal of amalgam fillings seems to be low" (Björkman. 1997). So if you are considering this procedure, it's unlikely that it will make whatever symptoms you believe to have as a consequence of having amalgam fillings more severe | Comment on Facebook!

References:

• Ahlqwist, Margareta, et al. "Number of amalgam tooth fillings in relation to subjectively experienced symptoms in a study of Swedish women." Community dentistry and oral epidemiology 16.4 (1988): 227-231. 
• Björkman, Lars, Nancy L. Pedersen, and Paul Lichtenstein. "Physical and mental health related to dental amalgam fillings in Swedish twins." Community dentistry and oral epidemiology 24.4 (1996): 260-267.
• Drexler, Hans, and Karl-Heinz Schaller. "The mercury concentration in breast milk resulting from amalgam fillings and dietary habits." Environmental research 77.2 (1998): 124-129. 
• Oskarsson, Agneta, et al. "Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women." Archives of Environmental Health: An International Journal 51.3 (1996): 234-241.
• Nylander, Magnus, Lars Friberg, and Birger Lind. "Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings." Swedish dental journal 11.5 (1986): 179-187.
• Zwicker, Jennifer D., Daniel J. Dutton, and John Charles Emery. "Longitudinal analysis of the association between removal of dental amalgam, urine mercury and 14 self-reported health symptoms." Environmental Health 13.1 (2014): 95.

Health & Exercise Quickie: Vitamin D Deficiency, Taurine & Glycine. Multiple Sclerosis & Epstein-Barr. Paracetamol & Muscle Gains. Gender & Fatigue from Workouts. HIIT, LISS & Appetite. Plus: Scientists Debate: Light vs. Heavy Weights

While there is a positive trend in the percentage of US adults who meet the 2008 federal physical activity guidelines according to which they have to "devote at least 150 minutes/week to moderate, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination", the number of people who have gotten the message that a combination of both strength and aerobic training (red line) is much more efficient than doing just aerobics (blue line) remains the same (CDC. 2012)

48%! That's the SuppVersity figure of the week and the percentage of US adults aged 18 and over who met the 2008 federal physical activity guidelines for aerobic activity in 2012 - that's 5% more than in 1997. It would be better to see it up in the 75%+ region, but it's nice to see that more and more people are devoting at least 150min/week to moderate intensity exercise, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination.

What's not so nice is that people are still way too focused on aerobics and the number of US citizens that's combining resistance and aerobic training to reach their exercise goals is stagnating below 20%. Moreover, best-agers and baby boomers, who would probably benefit even more from some weight lifting than the 36% of the young men (age 18-24) who make up the lion's share of the 'real' physical culturists who know about the importance of both, 'weights' and 'cardio', are - if they work out at all - still sticking to the tried and disproven LISS only regimen.

On Short Notice, today: A Health & Exercise Quickie

Apropos "LISS" as the headline of today's On Short Notice news quickie already gave away, light intensity steady state aerobic training aka LISS is one of the exercise related topics today. We will however start out with the health related news... and don't wonder that the first post is about polar bear health. I promise you will be intrigued, when you've read it ;-)

• 'Westernized' polar bears' bones look as if they would need vitamin D supplements, in reality all they are probably missing is sufficient taurine in their diet. I don't know but maybe you've asked yourself before: "How on earth can a white bear survive in the Arctic, when his nose is the only part of his skin that's exposed to the sun and would thus be able to produce vitamin?" (Please mind that this is not a serious question ;-) He eats his vitamin D!
  
  

  

  Scientists speculate: Their cousins in captivity suffer from rickets and fractures due to secondary vitamin D deficiency in consequence of insufficient taurine intake.

  Ok, first question first answer, but what about question #2: "How come that the clubs of his brethren and cousins in captivity get rickets and fractures as if they were vitamin D deficient, although they get the exact same amount of vitamin D from mother's milk and their later diet (sometimes the latter is even supplemented) as their wild counterparts?" Answer? No idea? Well, if you ask the researchers from the The University of Tennessee Health Science Center the answer is (Cheesney. 2009): A lack of taurine in the diet.
  
  Taurine plays a fundamentally important role in the conjugation of ursodeoxycholic acid to TUDCA and facilitates the uptake of fatty acids and fat soluble vitamins. With insufficient taurine in the diet polar beers (and human beings) can probably drink as much vitamin D in olive oil or whatever other fat base they deem more appropriate then dry tabs without any effects on their 25-OHD => calcitonin levels and consequently bone health (suggested read "Fat D-Ficiency! Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat").
  
  Moreover, a recent guinea pig study from Department of Internal Medicine at the Medical College of the National Cheng Kung University suggests that glycine could be another 'pro vitamin D amino acid' due to its beneficial effect on the liver and subsequent protection of disturbances in vitamin D metabolism and low 25-OHD levels (Chen. 2008) - now, what if any of these, i.e. taurine or glycine, or simply insufficient bile acid, which incidentally depends on the consumption of the "bad, bad" cholesterol (cf. Kern. 1994), is the actual reason of the rampant vitamin D deficiency in our meat-, fat- and cholesterol-o-phobic societies?
• "Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years." (Décard. 2012) Usually I don't simply copy the study titles, but this one says it all. Even before the first symptoms of multiple sclerosis occur, i.e. in the so-called pre-CIS (=clinically isolated syndrome) interval, patients with quiescent multiple sclerosis have 50% lower 25OHD levels than their healthy peers and - what could actually be the causal factor, here - three times higher Epstein-Barr specific IgG levels (EBNA1). Can these observations a group of scientists from the Department of Neurology at the St. Josef-Hospital of the Ruhr-University Bochum in Bochum, German, really be mere coincidence?
  
  

  

  Figure 1: While it would be best never to be infected with Epstein-Barr your risk of EP-related MS is more than twice as high if you are exposed late (Ascherio. 2010)

  At least as far as the Epstein-Barr relation goes the answer of a 2010 review of the literature would be 'no, probably no coincidence' (Ascherio. 2010). It appears to be established that Epstein-Barr (EB) plays a pivotal role in the etiology of MS. Based on the observation that people without EB are virtually MS free, and the fact that their own previous research has clearly shown that late infections with EP increase your risk to develop MS by more than 2x (compared to people who have been exposed in childhood; see figure 1), Ascherio et al. argue that it is very unlikely that EP is not at least the trigger, if not the ultimate cause of MS.
  
  The scientists also refer to the hygiene hypothesis which has been advanced by other authors before, unfortunately, however, getting rid of the 'cleanliness' and exposing your immune system to the training it needs by exposing yourself to the virus at an earlier age, is of little use, if not totally stupid. After all it would only reduce your risk to develop MS to a level that's still more than 1,000% higher than in people who have never been exposed to the virus in the first place (see figure 1).
  
  Due to the inconclusive data on the long and short term effects of Epstein-Barr infections on the B-cell and T lymphocyte response, the Ascherio et al. are not yet sure about the exact mechanism by which EP stimulates, triggers or drives the development of MS. All that can be said with relative certainty is that Epstein-Bar infections contribute to the increase in multiple sclerosis. Aside from the previously mentioned correlations the mere fact that those regions of the world where Epstein-Barr is quasi non-existent are virtually MS free is probably the best evidence of its involvement in autoimmune attacks on your brain. So if you want to protect yourself you better make sure you don't get infected!  Since EP is part of the herpes family and transmitted via saliva this is unfortunately not exactly easy...

• 

  Figure 2: Overall there is no statistical significant downside to chronic paracetamol supplementation, but there is a slight advantage for the NSAID free group in term of increases in lower body strength - the time course (not shown) of the strength gains was by the way identical for both groups, as well (Jankowski. 2012)

  Paracetamol does not interfere with muscle gains in elderly men. The issue whether or not NSAIDs will interfere with resistance training induced gains in skeletal muscle is certainly relevant for everyone. If there is one group of people for whom it could be of paramount importance, though, this would be the men and women in their best ages (>50 years) who have finally realized that muscle is not just metabolic currency, but a true life insurance.
  
  Against that background the most recent results from the College of Nursing at the University of Colorado Anschutz Medical Campus may be important news (Jankowski. 2012). I mean, if the use of N-acetyl-4-amniphenol (ACET) aka paracetamol would hamper or even forestall muscle gains, the training efforts of the men and women who take ACET would be to no avail.
  
  Now the good news is that the chronic use of paracetamol at a daily dose of 1,000mg did not reduce the lean mass gains in the 17 men (age >50y) who actually participated (instead of giving up) in all of the 3-5 days A/B resistance training sessions
  
  • workout A: R three sets of lateral pull down, bench ress, hip abduction and adduction, biceps curls, seated row, and ssisted chin ups
  • workout B: overhead press, leg press, triceps xtension, knee extension and flexion, heel raise, and shoulder external rotation
  • warm up / cool down: 10 min warm-up on the treadmill, a stair climing intermezzo after the first warm up sets and another 10 min cool down
  that were performed with at 80% of the 1-RM and with at least 1 day off in-between over a period of 16 weeks.
  
  
  The chronic ingestion of paracetamol is not advisable regardless of its negligible detrimental effects on skeletal muscle gain. Only recently, Kane et al. have shown that older people in are particularly prone to the hepatoxic effects of this (imho falsely OTC available) NSAID (Kane. 2012). If there is no way around it, because you cannot stand the pain, a safer (at least for the liver) and more effective medical approach could be the combination of tramadol (75 mg), a weak opioid analgesic, with low dose of paracetamol (325-650mg, max!; cf. Pergollizzi. 2012).
  In as much as the nonexistent negative effects are good news, they are likewise strange news, because according to the expression of proteins involved in the protein synthetic response to exercise, it should actually have hampered the gains:
  

  "[...] in the ACET group that the expressions of the anabolic gene p70S6K and the catabolic gene MAFbx were significantly reduced at week 16 of PRT. Given that the increases in FFM in response to PRT were not significantly different between the groups, it is possible that the suppression of catabolic signaling was sufficient to offset reductions in anabolic signaling in the ACET group." (Jankowski. 2012)

  As the authors point out future studies will have to elucidate the exact mechanism this at first sight contradictory results.
  
  In the mean time Jankowski et al. do yet speculate that the loss of prostaglandin signalling and supsequent increases in p70S6K, the protein that's responsible for muscle protein synthesis may be countered by the normalizing effects paracetamol exerts on the expression of Akt, the ameliorative effect on the overexpression of nitric oxide synthase (iNOS) and the reduction of the age-relatedly increased myocyte apoptosis.
  

• 

  Compared to Hope Solo or Serena Williams Olympian Brian Lochte, is probably a weakling - of course only as far as the fatigabilty of his skeletal muscle is concerned - as far as the risk do develop the Athlete's Triad is concerned, this may yet be advantage.

  Men and women tire differently - men (once more ;-) the weaker sex Let's face it guys,  we are weaklings. At least this is what Beth W. Glace and her colleagues from the Nicholas Institute of Sports Medicine and Athletic Trauma at the Lenox Hill Hospital in New York report in their latest paper. Other than the quadriceps muscles of our significant others, our muscles fatigue after 2h of cycling with intermittent one minute sprints every 20 minutes.
  
  In women, in this particular case just like their male counterparts trained cyclists or triathletes with a training load of at least 100km per week, on the other hand, it's solely the central nervous system fatigue that will keep them from cycling 'forever'. Unfair, right? Us men have to battle both, central as well as local muscular (=peripheral) fatigue.
  
  Now what seems nothing but advantageous can however turn against you. In a way the low fatigability of female muscle is also part of the reason why are way more susceptible to the athlete's triad (click here to learn more) than men: They are simply able to work their CNS into the ground, because their peripheral musculature is less prone to exhaustion.
• Recent study puts question mark behind assumed appetite reducing benefit of HIIT sprints vs. classic aerobics - but does that mean that aerobics is the way to go? Not yet in press, but already intriguing are the results of a recent study by  Kevin Deighton et al. from the School of Sport at the Loughborough University who say that they found that ...
  

  "[a]n acute bout of endurance exercise resulted in lower appetite perceptions in the hours after exercise than sprint interval exercise and induced a greater 24 h energy deficit due to higher energy expenditure during exercise" (Deighton. 2012)

  

  Figure 3: Intentionally or not, based on the conclusion of the abstract you would probably not have expected to see these results (data adapted from Deighton. 2012)

  Now this sentence from the abstract certainly suggests that sprinting would have nothing but negative effects. The actual data you see in figure 3 does yet tell you something different. The sprinters may have had increased ghrelin and lower PYY levels with the expected downstream effects on perceived hunger, but this did not translate into significant differences in food intake. In other words, even longish sprint exercises like the ones in the study at hand won't put you at danger of overeating - despite transient increases in ghrelin levels.
  
  In fact, the increased ghrelin amplitude can actually be an advantage (see August 04, 2012) and the calories in vs. out calculation the scientists do is so irrelevant to the real world health and body composition effects of exercise that I refuse to repeat it here ("No, you cannot eat that extra piece of layer cake because you ran on the treadmill earlier today" ;-)
  
  In the end, comparisons like this always suggest you had to choose between doing one or another mode of "cardio", when a combination of both, i.e. cycling HIIT and LISS, yet not both in one session, would be the most productive way to go. And no, Mr. Taubes, none of them is "just going to make you hungry" (see "Every Dog Has His Day: Dr. Oz Was Right, Exercise Does Not "Just Make You Hungry", But Reduces Energy Intake!")
  
• Researchers debate the "low vs. high weight" conundrum. In the editorial to the next issue of the Journal of Applied Physiology Mark D. Schuenke, Jennifer Herman, and Robert S. Staron reject the criticism they received from Nicolas Burd et al. for the pro heavy weights arguments they put forward in their recently published study on the effects of high vs. low weight training (Schuenke. 2012a; covered on the SuppVersity on October 01, 2012). Now while this back and forth between the two groups does not deliver any new data, I believe that it is still interesting and highly educative to see how science is actually a matter of negotiated not set truths. So, let's see how Schuenke et al. respond to Burd's assertion that ...
  

  

  Figure 4: Changes in body composition (left) and changes in muscle fiber cross-sectional area in response do different training regimen (Schuenke. 2012a; this study was discussed here on the SuppVersity on October 01, 2012)

  "[t]he authors’ views continue to contribute to a resistance training doctrine that is incorrect, most notably the belief that heavier weights are better concept. This conclusion is likely due to the relative dearth of quality studies assessing the hypertrophy potential of lower load resistance training paradigms, in contrast to the large number of studies employing ‘traditional’ resistance training intensities (*70 % of maximal strength).

  Clearly, evidence exists to support the concept that light(er) loads can support training-induced muscle hypertrophy both independently and by comparison to heavy loads. We would propose that so long as the stimulus is an overload, performed with high effort (fatigue), and progressive then even the most seasoned lifters would see progression,  at the very least no regression, in strength or muscle mass." (Burd. 2012)

  I will briefly summarize the most important points the researchers from the University of New England College of Osteopathic bring forward to defend their "go heavy or go home" argumentation:
  
  • The list of previous studies which confirm the the efficacy of training with high(er) weight for "optimal" gains in hypertrophy and strength is extensive.
  • Low load training is not as Burd et al. suggest "simply a milder form of low-load blood flow restrictive exercise", of which the researchers state that it is "interesting".
  • Schuenke et al. specifically refer to a Y2k study by Takadara et al. which shows that without the cuffs light loads don't build anything (Takadara. 2000).
  • The researchers point out that the claim by Burd et al. that "maximal muscle fiber activation can be achieved in any circumstance as long as the effort is to failure is unwarranted and unsubstantiated".
  • The study by Mitchel et al. Bird et al. cite to prove their hypothesis may not report significant differences between knee extensions performed at 30 % of 1RM for 3 sets, 80 % of 1RM for 1 set, or 80 % of 1RM for 3 sets as far as the isometric strength and hypertrophy between the three types of training are concerned, but
    

    "[t]his result is not surprising considering the following: (1) no control group was used, (2) each subject trained each limb using a different protocol (cross-over effect), (3) only one single-joint exercise was used (low volume versus a much higher volume of training used, for example, in Schuenke et al.: 3 sets each of leg press, squat, and knee extension), and (4) only fiber types I and II were delineated (severely limiting interpretation of the results).

    In that the last parentheses is obviously another direct criticism of what Schuenke would probably call "cherry picking" studies and specific results to support an unwarranted hypothesis.
  Based on this line of argumentation, Schuenke et al. conclude their deliberations on the note:
  

  

  One should not forget that it's not only about light vs. heavy, but in as much about appropriate and inappropriate weights. If you go by the quantity of the evidence there is however no debating that those weights are too light - probably even for a Lady in her best years.

  "Low-load training appears to have some merit. How-ever, our data support the use of high-load, high-intensity resistance training to maximize fiber hypertrophy and strength. In addition, heavy loading of the muscle has an impact on bone and other connective tissues which are minimized/lacking using low-load training. Finally, Burd et al. appear to oversimplify the field of exercise physiol-ogy. To claim that any training load (light or heavy) con-fers the same physiological adaptations as long as the end point is volitional failure is shortsighted and similar to claiming that running for any distance or time will elicit the same effects as long as fatigue is reached." (Schuenke. 2012)

  If you asked me, both are right. While I personally tend to agree with Schuenke, the main reason that I do is that the heavy weights approach is tried and proven, while - just as Burd says - the sceintific evidence pertaining to low weights is scarce and ambiguous and the anecdotal evidence from 'big guys' is non-existent. I am still curious about the next move(s) on both sides of this divide. And by the way, conflicts like these have always been among the driving forces of scientific progress, so I am pretty sure that we as trainees can only benefit from this debate as well as potential follow-up studies, both groups will feel inclined to conduct in order to 'prove' their point.

That's all for today! I hope you enjoyed the stay, all have electricity and an intact water supply ... I mean it's nice if you have a fully charged iPhone to get your daily dose of SuppVersity news, but even I have to concede that some other things in live are way more elementary.

References

• Ascherio A, Munger KL. Epstein-barr virus infection and multiple sclerosis: a review. J Neuroimmune Pharmacol. 2010 Sep;5(3):271-7.
• Burd NA, Moore DR, Mitchell CJ, Phillips SM. Big claims for big weights but with little evidence. Eur J Appl Physiol. 2012 Oct 20. 
• CDC. Early Release of Selected Estimates Based on Data From the January–March 2012 National Health Interview Survey. September 2012
• Chen CY, Wang BT, Wu ZC, Yu WT, Lin PJ, Tsai WL, Shiesh SC. Glycine ameliorates liver injury and vitamin D deficiency induced by bile duct ligation. Clin Chim Acta. 2012 Oct 23-
• Chesney RW, Hedberg GE, Rogers QR, Dierenfeld ES, Hollis BE, Derocher A, Andersen M. Does taurine deficiency cause metabolic bone disease and rickets in polar bear cubs raised in captivity? Adv Exp Med Biol. 2009;643:325-31.
• Deighton K, Barry R, Connon CE, Stensel DJ. Appetite, gut hormone and energy intake responses to low volume sprint interval and traditional endurance exercise. Eur J Appl Physiol. 2012 Oct 31.
• Décard BF, von Ahsen N, Grunwald T, Streit F, Stroet A, Niggemeier P, Schottstedt V, Riggert J, Gold R, Chan A. Low vitamin D and elevated immunoreactivity against Epstein-Barr virus before first clinical manifestation of multiple sclerosis. J Neurol Neurosurg Psychiatry. 2012 Aug 11.
• Kane A, Mitchell SJ, Carroll PR, Matthews S, Hilmer SN. Characteristics of older and younger patients with suspected paracetamol toxicity. Australas J Ageing. 2012 Sep;31(3):190-3.
• Kern F Jr. Effects of dietary cholesterol on cholesterol and bile acid homeostasis in patients with cholesterol gallstones. J Clin Invest. 1994 Mar;93(3):1186-94.
• Kappenstein O, Vieth B, Luch A, Pfaff K. Toxicologically relevant phthalates in food. EXS. 2012;101:87-106.
• Pergolizzi JV Jr, van de Laar M, Langford R, Mellinghoff HU, Merchante IM, Nalamachu S, O'Brien J, Perrot S, Raffa RB. Tramadol/paracetamol fixed-dose combination in the treatment of moderate to severe pain. J Pain Res. 2012;5:327-46.
• Schuenke MD, Herman JR, Gliders RM, Hagerman FC, Hikida RS, Rana SR, Ragg KE, Staron RS. Early-phase muscular adaptations in response to slow-speed versus traditional resistance-training regimens. Eur J Appl Physiol. 2012a Oct;112(10):3585-95.
• Schuenke MD, Herman J, Staron RS. Preponderance of evidence proves "big" weights optimize hypertrophic and strength adaptations. Eur J Appl Physiol. 2012b Oct 25.
• Sioen I, Fierens T, Van Holderbeke M, Geerts L, Bellemans M, De Maeyer M, Servaes K, Vanermen G, Boon PE, De Henauw S. Phthalates dietary exposure and food sources for Belgian preschool children and adults. Environ Int. 2012 Nov 1;48:102-8.
• Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol. 2000; 88:2097–2106.

Pyruvate Supplements - Useless as Ergogenic, Surprisingly Effective as Dieting Aid & Body Recompositioning Agent

Pyruvate = Recomp agent, not performance enhancer?

I am not sure if you even remember that pyruvate, which is made from glucose through glycolysis, and can be converted back to carbohydrates (such as glucose) via gluconeogenesis, or to fatty acids through acetyl-CoA, has once been touted as (yet another) "next big thing" by parts of the supplement industry.

The idea was that pyruvic acid could supply energy to working muscles through the citric acid cycle (also known as the Krebs cycle) when oxygen is present (aerobic respiration), and alternatively ferment to produce lactate when oxygen is lacking (fermentation) - this would make it the perfect workout fuel for high intensity exercise, but theory and practice are two very different animals.

The best way to shape your body? Build muscle, Ladies & Gents!

Tri- or Multi-Set Training for Body Recomp.?

Alternating Squat & Blood Pressure - Productive?

Hula Hoop Yourself to a Slim Waist!

Full ROM ➯ Full Gains - Form Counts!

Battle the Rope to Get Ripped & Strong

Study Indicates Cut the Volume Make the Gains!

Past studies investigating its efficacy have however yielded mixed results. In the year 2000, Michael A. Morrison , Lawrence L. Spriet , David J. Dyck reported that "oral pyruvate supplementation does not increase blood pyruvate content and does not enhance performance during intense exercise in well-trained cyclists." (Dyck. 2000)

Similarly disappointing results have been reported by Ebersole et al., likewise in the year 2000 for improvements in critical power (there were none) and stand in contrast to observations by JL Ivy who found that pyruvate, when "provided as an oral supplement for several days", whill "enhance aerobic endurance capacity" in rodents (Ivy. 1998) or Stanko et al. who found back in 1990 that feeding  dihydroxyacetone and pyruvate for 7 days  increased  arm  muscle  glucose  extraction  before  and  during exercise,  thereby  enhancing  submaximal  arm  endurance  capacity of (albeit) untrained men.

Weight & amp;fat loss(kg)/4.25-MJ deficit (Stanko. 1995) ➽ Pyuruvate makes dieting more effective.

Previous studies show that Pyruvate propels weight and fat loss: On a standardized 1.015kcal per day diet, subjects lost significantly more weight and body fat, when they received 30 grams of mixed sodium + calcium pyruvate per day. Plus: The pyruvate supplement had protein sparing effects, as well. In spite of the fact that the difference was not statistically significant, the subjects in the pyruvate group lost 5% less lean mass (relative to the total weight loss) than their peers in the placebo group.

Olek, et al. the authors of the most recent pyruvate paper in the open access journal nutrients, were well aware of the fact that pyruvate (PYR), in spite of its importance in energy metabolism, has not been shown to have ergogenic effects after prolonged supplementation. In view of the fact that Morrison et al. indicated that acute oral intake of calcium PYR (Calcium Pyruvate), even at a dose of 25 g, did not modify the PYR concentration in the whole blood or in the plasma, while Olek et al. have previously shown that a single dose of sodium PYR (NaP) does, the researchers from the Gdansk University ofPhysical Education and Sport in Poland decided to re-examine the effect of a single NaP ingestion on blood acid-base status and the exercise metabolism markers.

"Since 0.1 g of sodium bicarbonate per kg of body mass induces metabolic alkalosis 60 min following ingestion [14,15], we hypothesized that a similar NaP treatment before commencing the high intensity physical exertion may change the exercise metabolism." (Olek. 2014)

Nine active, but non-specifically trained, malesubjects (mean ± SEM: 23 ± 1 year old, 1.75 ± 0.02 m height, 72 ± 2 kg body mass) participated in the double-blind, placebo-controlled, crossover study.

"On separate days, the subjects reported to the laboratory in the morning, then rested for 30 min and then ingested placebo or NaP in a random order. In the previous studies the subjects consumed PYR in the amount of ~0.07–0.08 g/kg body mass;  therefore, the subjects in our study ingested NaP in a single dose of 0.1 g/kg body mass (which is ~0.08 g of PYR per kg body mass). " (Olek. 2014)

An hour following the ingestion, the subjects performed the physical exertion. The exercise protocol consisted of 2 min at a power output of 50 W and then for 6 min at a constant power output, corresponding to ~90% O2max. To determine  O2max, participants performed a graded cycle ergometry test on an electromagnetically-braked, cycle ergometer. After an initial warm-up period, the work rate was increased by 25 W/min until volitional exhaustion was achieved.

Figure 1: Lactic acid and blood pH during the placebo (•) and (o) pyruvate trial (Olek. 2014)

As you can see in Figure 1 the lactic acid concentration after the workout was significantly higher in the dotted pyruvate trial. Interestingly, though, the pH and thus the acidity of the blood was only marginally elevated - a clears sign that the buffering function of sodium pyruave Olek et al. had speculated about is real.

Pyruvate as a PGC-alpha driven metabolic engine builder: In view of the fact that high pyruvate levels would usually occur during intense exercise it's no wonder that researchers from Novartis Institutes for BioMedical Research in Cambridge have found that it increases mitochondrial biogenesis in rodent muscle (Wilson. 2007)

Table 1: Gas exchange, ventilation and heart rate responses during and after severe-intensity exercise following placebo and sodium pyruvat eingestion. Values are the means ± SEM (Olek. 2014) | As you can see, there are no asterisks (*) which means: None of the differences reached statistical significance.

A brief glimpse at the measured differences in O2 uptake, CO2 output, minute ventilation, respiratory exchange ratio, and heart rate (see Table 1) does yet reveal that the study at hand generally confirms what previous studies by Ebersole et al (2000) and Morrison et al. (2000)  suggested: In spite of the fact that it would be 100% logical, if we saw performance improvements with pyruvate supplementation, the parameters Olek et al. recorded do not suggest that there were any.

And even when it was administered as creatine pyruvate, Van Schuylenbergh et al. did not find any benefits on cycling performance in a 2003 study.

Bottom line: In spite of the fact that it's physiological function would suggest that supplemental pyruvate should increase exercise performance, there is as of now no good evidence that it will actually do that.

Figure 2: Pyruvate may not improve performance, but it promotes improvements in body composition in dieting overweight men and women (Kalman. 1998).

Against that background you may be interested to hear that several studies suggest that it may not improve performance, but could help you lose weight. The ingestion of pyruvate 6 g/d for 6 weeks, along with regular exercise, for example, has been shown to reduce body fat, increase lean body mass, and improve fatigue and vigor scores in a 6-week, double-masked, placebo-controlled study that was conducted by Douglas Kalman et al. in 1998 to determine the effects of pyruvate supplementation on body weight, body composition, and vigor and fatigue levels in overweight men and women. Quite an impressive result. Specifically if you take into consideration that there were no changes in body composition in the placebo group who followed the same diet and training regimen.

Similar, albeit slightly less pronounced effects have been observed in the absence of dietary restrictions by Koh-Banerjee et al. (2005) and in a low energy + no exercise context by Stanko et al. (1992). Unfortunately, the mechanism(s) remain unclear. As Kalman et al. point out, previous rodent studies would suggest that an increase in insulin sensitivity and glycogen storage and decrease in fatty acid synthesis in fat cells may be at the heart of the effects the researchers observed 15 years ago | Comment on Facebook.

References:

• Ebersole, Kyle T., et al. "The Effect Of Pyruvate Supplementation On Critical Power." The Journal Of Strength & Conditioning Research 14.2 (2000): 132-134.
• Ivy, John L. "Effect of pyruvate and dihydroxyacetone on metabolism and aerobic endurance capacity." Medicine and science in sports and exercise 30.6 (1998): 837-843.
• Kalman, Douglas, et al. "Effect of pyruvate supplementation on body composition and mood." Current Therapeutic Research 59.11 (1998): 793-802.
• Koh-Banerjee, Pauline K., et al. "Effects of calcium pyruvate supplementation during training on body composition, exercise capacity, and metabolic responses to exercise." Nutrition 21.3 (2005): 312-319.
• Morrison, Michael A., Lawrence L. Spriet, and David J. Dyck. "Pyruvate ingestion for 7 days does not improve aerobic performance in well-trained individuals." Journal of Applied Physiology 89.2 (2000): 549-556.
• Stanko, Ronald T., Denise L. Tietze, and Judith E. Arch. "Body composition, energy utilization, and nitrogen metabolism with a 4.25-MJ/d low-energy diet supplemented with pyruvate." The American journal of clinical nutrition 56.4 (1992): 630-635.
• Van Schuylenbergh, Reinout, Marc Van Leemputte, and Peter Hespel. "Effects of oral creatine-pyruvate supplementation in cycling performance." International journal of sports medicine 24.02 (2003): 144-150. 
• Wilson, Leanne, et al. "Pyruvate induces mitochondrial biogenesis by a PGC-1 α-independent mechanism." American Journal of Physiology-Cell Physiology 292.5 (2007): C1599-C1605.

Creatine + Sodium Bicarbonate: Two New Studies Show You Can Make the Most-Researched Ergogenic Even Better W/ a Few Grams of Baking Soda - Sign. & Non-Sign. Benefits

The benefits of bicarbonate show on the finish line, not the starting block.

As a true students of the SuppVersity you will know that you can "Supercharge Your Creatine W/ Baking Soda" (learn more) and thus build your own "buffered creatine product". What you probably didn't know yet, though, is that there is evidence to prove that the increased stability and bioavailability will actually translate to performance gains.

You don't believe a word? Well, scientists from the Sheffield Hallam University (Griffen. 2014) and the Human Performance Laboratory at the University San Luis Obispo (Barber. 2013).

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

Griffen et al. (2014) investigated the effects of creatine and sodium bicarbonate co-ingestion on mechanical power during repeated sprints.

Their subjects, nine well-trained men (age = 21.6 ± 0.9 yr, stature = 1.82 ± 0.05 m, body mass = 80.1 ± 12.8 kg) performed six 10-s repeated Wingate tests in a double-blind, placebo controlled, counterbalanced, crossover study. Before the exercise tests, the oarticipants supplemented with either

• creatine and sodium bicarbonate contained 20 g/d of creatine monohydrate (Myprotein Inc., Northwich, UK), 0.3 g/kg of sodium bicarbonate (Buy Whole Foods Online, Canterbury, UK) and 0.5 g/kg of maltodextrin (Myprotein Inc., Northwich, UK). 
• creatine alone, i.e. of 20 g/d of creatine monohydrate and 0.5 g/kg of maltodextrin, 
• sodium bicarbonate alone, i.e. 0.3 g/kg of sodium bicarbonate and 0.5 g/kg of maltodextrin, or
•  the placebo which contained only 0.5 g/kg maltodextrin. 

for one week. On the day of the exercise tests, however, no supplement was ingested (probably do exclude acute beneficial effects of bicarbonate). As far as the specifics of the dosing regimen are concerned, the scientists point out that the maltodextrin was added to to all conditions to maintain the volume consistency and to facilitate creatine uptake (Green et al., 1996).

The split-dose strategy, on the other hand, was employed to reduce side effects from sodium bicarbonate supplementation (Burke & Pyne, 2007) - something you've read here at the SuppVersity before (Bicarbonate Serial Loading | learn more).

"Supplements were split into four equal dose to be consumed at 9 am, 12 pm, 5 pm and 9 pm. Participants were also instructed to ingest each supplement sachet with 330 ml of water diluted with 40 ml of orange cordial." (Griffen. 2014)

The degree of compliance reported was 86 ± 7% for co-ingestion of creatine and sodium bicarbonate, 89 ± 7% for creatine alone, 90 ± 7% for sodium bicarbonate alone and 93 ± 4% for the placebo. Participants were instructed to maintain their habitual diet and abstain from strenuous exercise, caffeine and alcohol 24 h prior to each trial.

Avoid gastrointestinal distress and still get all the benefits from bicarbonate supplementation by using a serial-loading protocol, as I described it in "The Latest on Sodium Bicarbonate: Serial Loading Almost as Effective as Acute Loading and Free of Gastrointestinal Side Effects. Plus: Can You Use Potassium Bicarbonate Instead?" | learn more.

The trials that were performed on a magnetically braked ergometer, began with a warm up at 50 RPM against a resistance of 0.5 kg for 5 min, with one 5 s sprint against a resistance of 7.5% of the participant’s body-mass after 2.5 min. Participants then completed six 10-s sprints using a standardised resistance equating to 7.5% body mass. One min of active recovery at 50 RPM was provided between each test. Participants were asked to cycle at a cadence of 50 RPM until the start signal to ensure the inertia of the system was not overcome by standardising the angular momentum of the flywheel (Winter & Fowler, 2009).

Figure 1: Changes in peak, mean and rel. power, total work and fatique index (W/s) relative to baseline (Griffen. 2014)

The results were somewhat disappointing, though, while both creatine (effect size (ES) = 0.37-0.83) and sodium bicarbonate (ES = 0.22-0.46) alone led to meaningful improvements on indices of mechanical power output, the co-ingestion of both provided performance increases that were not significant compared to creatine, alone (see yellow vs. gray bars in Figure 1).

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." (SIDS. 2002) And thirdly, there is more and more evidence that suggests that the chloride rather than the sodium content of common table salt (NaCl = Natrium Chloride) is the root cause of "sodium induced hypertension" in "sodium sensitive" individuals / animal models.

Only recently, a study for the Schmidlin et al. showed that chloride loading induced hypertension in the stroke-prone spontaneously hypertensive rat despite profound sodium depletion (Schmidlin. 2002). 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)

That's in contrast to another recently published study by from the the Human Performance Laboratory at the University San Luis Obispo (Barber. 2013).

Figure 2: Unlike Griffen, Barber et al. (2013) measured significant increases in rel. peak power.

As you can see in Figure 2, Barber et al. who compared the effects of (a) Placebo (Pl; 20 g maltodextrin + 0.5 g/ kg 21 maltodextrin), (b) Creatine (Cr; 20 g + 0.5 g /kg 21 maltodextrin), and (c) Creatine plus sodium bicarbonate (Cr + Sb; 20 g + 0.5 g /kg 21 sodium bicarbonate) on the performance of thirteen healthy, trained men (21.1 years, 23.5 kg /m²) in a double-blinded, crossover fashion:

"Each condition consisted of supplementation for 2 days followed by a 3-week washout. Peak power, mean power, relative peak power, and bicarbonate concentrations were assessed during six 10-second repeated Wingate sprint tests on a cycle ergometer with a 60-second rest period between each sprint." (Barber. 2013)

In contrast to Griffen, et al. (2014), the researchers from St. Lois found a 3% greater increase in relative peak power with Cr + Sb (7%) compared to creatine alone.

What may be of even greater practical relevance is the absence of performance decreases during sprint tests 4–6, compared with that in sprint 1, in both the placebo and creatine trial, respectively their absence in the Cr + Sb trials, where the sprint performance decreased only on spring #6!
This effect is probably directly related to the blood bicarbonate pre- and post-Wingate bicarbonate concentrations which were significantly higher in Cr + Sb (10%), compared with the Pl and Cr.

22g Baking Soda 60min Before a Old-School 4 x 12RM Leg Workout Allow for Significant 22 Rep Volume Increase | learn more

So what's the meaningful difference between the studies that explains the discrepant results? The age of the subjects was identical, both were trained, lean men in their early twenties (no detailed information in the Griffin study, but the subjects in the Barber study, were really fit and performed a high level of aerobic exercise training >5h/week and were accustomed to high intensity exercise >2h / week). The exercise test, a Wingate test with with 6x10s sprints was more or less identical, and the amounts of creatine and sodium bicarbonate that were ingested in four equal doses were not different, either... well, aside from the addition of maltodextrin which was present in all supplements only in the study by Griffin et al. (no effect).

The most significant difference, however, are allegedly minute differences in the supplementation and study protocol. For one, the supplements in the Barber study were ingested for only 2 days prior to the tests - in the Griffin study, it were 7 days. In contrast to the supplementation period, the wash-out period in the Griffin study was shorter. Only 7 days compared to 21 days in the Barber study. Both of these differences could explain the different outcomes.

In that, difference #1 (duration of the supplementation period) would make the bioavailability increase due to the addition of sodium bicarbonate to creatine more important, while difference #2 (different washout periods) is nothing but a methodological shortcoming, due to which the later trials would still be influenced by residual effects from previous supplementation periods (recent studies show that this could be specifically the case for creatine) | Comment on Facebook!

References:

• Barber, James J., et al. "Effects of combined creatine and sodium bicarbonate supplementation on repeated sprint performance in trained men." The Journal of Strength & Conditioning Research 27.1 (2013): 252-258.
• Griffen, C., et al. "Effects of Creatine and Sodium Bicarbonate Co-Ingestion on Multiple Indices of Mechanical Power Output During Repeated Wingate Tests in Trained Men." International journal of sport nutrition and exercise metabolism (2014). 
• Luft, Friedrich C., et al. "Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man." Journal of hypertension 8.7 (1990): 663-670.
• Schmidlin, Olga, et al. "Selective chloride loading is pressor in the stroke-prone spontaneously hypertensive rat despite hydrochlorothiazide-induced natriuresis." Journal of hypertension 28.1 (2010): 87.
• SIDS, OECD. "Sodium Bicarbonate." (2002).

Glutamine or BCAA, Which is the Better Fatique Buffer? 18g GLU Suprisingly Effective, 9.5g BCAAs (Un-)Surprisingly Useless as Blood Fatigue Factors & Cytokine Buffers

Rowing is an excellent cardio exercise for wanna be bodyuilders, by the way!

I am not really a fan of glutamine, but unlike BCAAs that are still hyped all over the Internet, the conditionally essential amino acid which is the most abundant of all amino acids in human blood is at least not falsely heralded as a potent catabolic, anabolic, weight loss adjuvant and what not, any longer.

Against that background I have to admit that I am not exactly unhappy to tell you that Ga Hee Koo, Jin Hee Woo, Sung Whun Kang, and Ki Ok Sjin who work at the Dong-A University and the Republic of Korea Airforce Academy, have recently observed that BCAAs have absolutely no, glutamine at least a minimal impact on the blood fatigue factor response of juvenile athletes in response to a 2,000 m all out rowing challenge w/ placebo, BCAA or glutamine supps.

Learn more about glutamine and BCAAs at the SuppVersity

Glutamine Helps W/ Diabetes

Whey + Casein Beat GLU + BCAA

Alanyl-Glutamine is it any good?

GLU for Glycogen Repletion?

GLU as Intra-Workout BV?

BCAAs deplete neurotransmitters

In the corresponding experiment, the scientists from the College of Sports Science at the Dong-A University had five male juvenile elite rowing athletes perform the same 2,000m rowing test at maximal intensity after having received a placebo, BCAA, or glutamine for 7 days before
the test. The specific supplementation regimen included:

• BCAA (Spomax, Seoul, Republic of Korea) was given three times a day (25% valine, 50% leucine, 25% isoleucine, 3.15 g/day).
• L-glutamine (Optimum Nutrition, Aurora, IL, USA, 6 g/day) was given three times a day.

Blood samples were collected from the antecubital vein on the day of testing while resting before the test, immediately at the end of test, and 30 min after the test. All tests were conducted with a 1-week interval to eliminate the potential effects from potentially longer-lasting effects of the previously administered supplement.

Which parameters did the researchers test and why? Koo et al. tested lactate, the accumulation of which will eventually impair ATP synthesis and lead to muscular fatigue. They tested the accumulation and clearance of ammonia, which can trigger central fatigue, when the levels increase rapidly during high intensity exercise. And they tested creatine kinase (CK) which is a classic marker of muscle damage and IL-8 and IL-15, two cytokines that will be elevated, when the activity of the immune system is not sufficient to deal with exercise induced stressors.

The actual test was conducted with an indoor rowing machine (Concept², Morrisville, VT, USA) two times each for supplementation with the placebo, BCAA, and glutamine. All the subjects performed a 2,000 m (Olympic single scull race) race at their own individual maximum paces (42–45 pace for 0m~250m, 40 pace for 250m~500m, 36–38 pace for 500m~1,500 m, and over 42 pace for 1,500 m~2,000 m)

Figure 1: Serum markers of fatigue and muscle damage, expressed relative to placebo (Koo. 2014)

There were no significant differences in lactate levels; a significant phopshorus-sparing effect from BCAAs (small effect size) and glutamine (large effect size) of which the scientists believe that it was mediated by the use of the amino acids to maintain adequate muscular ATP levels; and there was a non-significantly elevated level of ammonia in the glutamine group (some arginine could help clear those | learn more) that returned to normal 30 min after the test.

The dosages are not the same! That's unfair! No, it's not necessarily unfair, but it would still have been better to test 18g of glutamine vs. 18g of BCAAs. There is after all one thing both have in common: They both can be used as workout fuel in the muscle, so the advantage of glutamine may have become smaller (maybe even non-significant), if both had been administered at the same amounts.

The creatine kinase levels (a marker of muscle damage) and the levels of interleukin-8 and interleukin-15, however, were significantly lower in the glutamine than they were in either the BCAA or placebo group. This is a result of which the authors of the study believe that, it may...

"[...]represent the effects of energy supplementation from glutamine supply, which activated as a fuel in the muscle and as a nitrogen precursor for nucleotide synthesis" (Koo. 2014). 

An alternative explanation would be that glutamine (probably via its connection to glutathione; see Roth. 2002) had a direct protive effect on the skeletal muscle tissue during the workouts.

Figure 2: Serum levels of inflammatory cytokines expressed relative to placebo (Koo. 2014)

This hypothesis would also be supported by the changes in interleukin expression. i.e. the blunted increase of interleukin-8. IL-8 is an inflammatory cytokine that serves as a chemical signal which attracts neutrophils at the site of inflammation. The corresponding increase in IL-15, which was likewise reduced in response to sub-chronic glutamine supplementation, on the other hand, indicates a reduced production (not activity!) of natural killer cells.

Table 1: Intense exercise is not the only condition / disease that's associated  with low blood glutamine levels (Roth. 2002)

In that, it is crucial to understand that the authors (imho reasonably) believe that the increase in IL-8 & IL-15 is a compensatory mechanism which is initiated to counter the reduced immune function that occurs, when the amount of glutamine in the blood and skeletal tissue drops. We do after all know for sure that the this will result in a significant decrease in the cell proliferation rate of lymphocytes, the amount of antioxidants, peptides, amino sugars related to cell resistance against apoptotic processes, purines, as well as the synthesis of key molecules such as pyrimidines which are all involved in redox reactions (Roth. 2002).

Whether supplementation is warranted with low(er) intensity exercise, as well, is however questionable. Previous research by Ostrowski et al. (2001), who had their subjects exercise at significantly lower intensities, did not find comparable increases in IL-8. This difference is probably due to a comparably lower amount of exercise induced stress that corresponds to the reduced intensity. In this context it's also worth mentioning that Fischer et al. (2006) report that the blood chemokine concentrations would increase little or remain stagnant unless a sufficient muscle mass is mobilized and maintained at a certain level of intensity sufficiently... now, everyone who has ever done an all-out rowing time trial will confirm: This is (a) intense and will (b) involve almost every muscle in your body.

If maximal muscle hypertrophy, not performance increases in all-out (aerobic) exercise and protecting your immune function is your goal, buy some whey + casein and stay away from glutamine & BCAAs unless you insist on wasting money on hitherto unproven promises of strength & size gains | learn more

Bottom line: In contrast to BCAAs which will "only" blunt the increase in debilitating phosphorus in the blood,  "glutamine supplementation could be helpful for enhancement of immune function and the defensive inflammatory reaction after exercise." (Koo. 2014)

The results of the study at hand do thus confirm an older piece of broscience, i.e. the importance and efficiency of adequate amounts of glutamine (15g or more per day!) for recovery and immune function. They do yet also put another question mark behind the ergogenic potential of brach-chained amino acids about which I have written repeatedly in previous articles here at the SuppVersity (in other contexts, BCAAs may well be superior to glutamine, but long-term studies to prove any of the claimed benefits are missing, as well).

Whether the results from the study at hand warrant the consumption of 18g of glutamine per day for all of us, is still questionable. If you are in a phase of your training that requires a lot of all-out exercise and already feel that your immune defenses are dwindling, it probably won't hurt to buy a cheap 500g bag of glutamine from the bulk supplier you trust. Don't expect instant results of illusive tingles as you'll get them with certain other supplements. If there are benefits they will only be visible over time and will include faster / more complete recovery, reduced rates of infection and overall fatigue. Eventually, these would help you to make faster gains in strength and size, though | Comment on Facebook.

References:

• Fischer, Christian P. "Interleukin-6 in acute exercise and training: what is the biological relevance." Exerc Immunol Rev 12.6-33 (2006): 41.
• Koo, Ga Hee, et al. "Effects of Supplementation with BCAA and L-glutamine on Blood Fatigue Factors and Cytokines in Juvenile Athletes Submitted to Maximal Intensity Rowing Performance." Journal of Physical Therapy Science 26.8 (2014): 1241-1246.
• Ostrowski, Kenneth, et al. "Chemokines are elevated in plasma after strenuous exercise in humans." European journal of applied physiology 84.3 (2001): 244-245.
• Roth, Erich, et al. "Regulative potential of glutamine—relation to glutathione metabolism." Nutrition 18.3 (2002): 217-221.