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.

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 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 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 amino acid and BCAA supplements at the SuppVersity

Glutamine Helps W/ Diabetes

Whey + C Kicks BCAA Ass

Alanyl-Glutamine is it any good?

Glutamine Insted of CHO?

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.

Caffeine Works - Study Leaves No Doubt About It! Approx. 400mg of Caffeine Get You Going, Even After 32h Without Sleep - So Why Doesn't It Work for You Anymore?

The answer to post-positioned question in the headline of today's SuppVersity article is not easy to find. Therefore I will start with the facts. Facts, researchers from the University of Sfax present in their latest paper in the peer-reviewed scientific journal Psychology & Behavior; facts that leave little doubt that 5 mg/kg of caffeine could counteract the negative effect of 36 h of total-sleep deprivation on physical and cognitive performances, if your body would still react to stimulus - in other words: If your body still reacted like the bodies of the 13 healthy male habitual caffeine-not-abusing physical education students (age: 21.1 ± 1.1 years; body mass: 77.1 ± 7.2 kg; height: 1.77 ± 0.06 m) who volunteered to participate in the present study, it would get you going - seriously!

The students had exactly the same time schedule at the university from sunrise to sunset under the control of the experimental team. Participants had taken part in various recreational low-intensity physical activities such us walking, jogging, or aerobics in our university.

No time to sleep, do your "cardio" HIIT style instead of steady state for hours

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

Triple Your Energy Exp.

The participants were prescribed with standard isocaloric meals to consume, with breakfast at 07:30 h, lunch at 12:00 h, and dinner at 20:00 h. Only water was allowed ad libitum between meals. They were requested to maintain their habitual physical activity throughout the experimental period and to avoid strenuous activity before each test session. The overall daily energy intake goal was set at 10.5 MJ (2500 kcal) per capita/day.

Figure 1: Caffeine affects both body temperature and physical performance during sleep deprivation (Souissi. 2014)

During the experimental period, medications, which are expected to affect physical performance, were prohibited, more importantly, though:

"Participants were selected according to their usual consumption of caffeine and on the basis of their answers to the Horne and Ösberg Self-Assessment Questionnaire (Horne. 1979) (i.e., to have a group without “extreme type” (i.e., participants were selected as “neither type”)). This second criterion resulted in a sample of participants who shared the same timing in terms of rising times (06:30 ± 00:30 h) and bedtimes (23:00 ± 00:30 h). Participants reported no sleep disorder, are non-smokers, and do not consume caffeine or any alcoholic beverages."

After four consecutive nights of sleep in the laboratory (sleep adaptation: between 22:30 and 07:00 h), in a randomized order, participants performed four test sessions: after placebo or 5 mg/kg of caffeine ingestion during a baseline night (RN) or a night of 36 h of total sleep deprivation (TSD).

Does this look remotely familiar? If it does, you are already "tolerant".

Is caffeine tolerance even real? Scientists say: Yes! In 1992 Suzette M. Evans and Roland R. Griffiths conducted a study with 32 "healthy subjects with histories of moderate caffeine consumption" who had to abstain from their favorite beverage throughout the study (Evans. 1992). The subjects were stratified into two groups based on several factors including caffeine preference, which was assessed using a caffeine versus placebo choice procedure. Subsequently, subjects received either caffeine (300 mg t.i.d.) or placebo (placebo t.i.d.) for 18 consecutive days, and thereafter were exposed again to a caffeine versus placebo choice procedure. And the result?

"The study documented tolerance development to the subjective effects of caffeine: after chronic dosing, administration of caffeine produced significant subjective effects in the chronic placebo group but not in the chronic caffeine group." The study also provided indirect evidence for tolerance development: during chronic dosing, the chronic caffeine and placebo groups did not differ meaningfully on ratings of mood and subjective effect. That's important, because it means that not all benefits are lost; plus, it explains why you still don't quit drinking your coffee ;-)

During the run-in, participants were synchronized with a nocturnal sleep from 22:30 to 07:00 h. During the TSD-phase, they were not allowed to sleep and were kept awake by passive means such us watching TV.

Figure 2: Caffeine boosts cognitive performance during sleep deprivation (Souissi. 2014)

During each test session, after 10 min of rest in a sitting position, participants ingested the caffeine or the placebo dose; then they had to remain in a sitting position for 60 min. After the 60 min, they performed

• the reaction time, 
• the squat jump (SJ), and 
• the Wingate tests at 18:00 h with 15 min of recovery in-between 

All test sessions took place in similar conditions of temperature and relative humidity (27–28 °C and 63–66%, respectively).  The physical tests were complemented by a simple choice-reaction test and a profile of mood state evaluation - which yielded an impressive reduction of the depression and confusion the subjects felt after the 32h without sleep (see Figure 3)

Figure 3: Results of the profile of mood test w/ & w/out caffeine before and after TSD (Souissi. 2014)

In conjunction with the increase in vigor, decrease in anxiety and fatigue this alone would warrant the use, but not abuse of caffeine after sleepless nights. The latter, i.e. habituation to high doses of caffeine as they are really common in the pre-workout guzzling world of physical culturists, could potentially nullify the results.

So what? To withdraw, or not? In my humble opinion, caffeine junkies like us just have to live with the fact that the psychological and physiolo- gical effects even high doses of caffeine have are negligible. Caffeine or rather coffee is healthy, but it's only healthy if you consume it regularly; and the lack of effects on the central nervous system in the "habitual consumer" will actually protect your nervous and cardiovascular system. So, just stick to whatever you can still get out of caffeine, but do never increase your intake beyond 800mg per day on a chronic basis - if even that does no longer effect you, you've been overtraining + abusing for years.

Bottom line: We all know that caffeine works. At least for those 95% of us who don't belong to the caffeine hypermetabolizer, there is this memory somewhere deep inside our heads. A memory of our first "high dose caffeine, tear down the gym"-experience. It's a memory that's burried deep below memories of years of daily caffeine abuse and the knowledge that the only way to get anywhere close to the caffeine naive state we were in back in the day is withdrawal...

Yeah, I know that's hard to imagine and actually, there is no evidence that would suggest that withdrawal and resensitization would be necessary to get the dozens of health benefits I have written about in the past. In fact, you could rather argue that 400mg+ doses of caffeine are going to have a negative effect on your health, as long as they still 'cause an increase in Central Nervous System (CNS) activity as it was observed in the study at hand. I mean, what would you expect the health consequences of having one of these "high dose caffeine, tear down the gym"-experiences every (other) day? This can hardly be good for your heart and brain, can it?

References:

• Evans, Suzette M., and Roland R. Griffiths. "Caffeine tolerance and choice in humans." Psychopharmacology 108.1-2 (1992): 51-59.
• Horne, John A., and Olov Ostberg. "A self-assessment questionnaire to determine morningness-eveningness in human circadian rhythms." International journal of chronobiology 4.2 (1976): 97. 
• Souissi, Makram  et al."The effects of caffeine ingestion on the reaction time and short-term maximal performance after 36h of sleep deprivation." Physiology & Behavior 131 (2014): 1-6.