To Spit or to Swallow - That is the Question! Carbohydrate Mouthrinse May Be Better Than Water, Yet Still Not an Option for Performance Oriented Athletes

Image 1: "You need carbs to fuel your workouts!" You know the whole litany... what may be news to you is that scientists are speculating that "intra workout carbs" do not necessarily have to be ingested to do their ergogenic magic.

Those of you, who already "friended" me on Facebook and are following what is going on on the SuppVersity Facebook page (just want to remind you that Facebook has now an option that allows you to be informed, whenever something new is posted), will probably remember the discussion revolving around "carbohydrate mouthrinsing" and whether or not it may be even more beneficial to spit and not to drink your Gatorade... now, all the health benefits of low-carbohydrate (when I am talking "low" I am not talking of Atkins type <80g) diets aside, it does seem pretty counter-intuitive that just swishing one of those carbohydrate-laden electrolyte drinks in between your teeth for a few seconds, to then spit it out again could actually have any merit. Yet, science, or I should say a handful of studies, do suggest otherwise.

As part of their recently published study into the effects of carbohydrate mouthrinsing on exercise capacity in the pre- and postprandial state (Fares. 2011), Elie-J. M. Fares and Bengt Kayser have compiled a list of the 8 hitherto published peer-reviewed papers on that subject. And if you just went by the column "increased perfomance", "yes or no", it appears like it was an established fact that carbohydrate mouthrinsing was highly ergogenic. After all, six out of the eight studies are marked with the tag "increased performance".

Figure 1: Performance increases and standard deviations of the respective measures from studies on the advantage of carbohydrate vs. artificially sweetened or plain water mouthrinse (data calculated based on summary in table 2 of (Fares. 2011)

If we do yet have a look at the quantity of those performance increases and the individual standard deviations (I compiled the respective data for you in figure 1), things begin to look less conclusive. I mean, there is obviously a standard deviation for both arms of each study and there also is a mean improvement (or decrease in performance), but if the "performance increment" is smaller than the standard deviation, for all but one study, this does make me feel uncomfortable with the statement that I would see "scientific evidence", let alone "conclusive scientific evidence" in support of carbohydrate mouth-rinses.

Mouthrinse vs. placebo = minimal (if any advantage), but what about vs. ingestion?

Regardless of what you think about the real world significance of an average performance increase of 1% (calculated based on the data from figure 1), for the small fraction of athletes for whom these minimal performance increases would actually count, i.e. high intensity endurance athletes, like time-trial Tour de France cyclists, the "control", or I should say the "benchmark" should not be plain or sweetened water, but rather one of these crab-, ah... pardon me, carb-loaden sugary electrolyte drinks these athletes are habitually consuming. I was thusly happy to see that Catherine Moss, a student of Sports and Exercise Sciences at the Massey University in Auckland, New Zealand has recently conducted an experiment for her thesis that has much more practical relevance for the high achieving athletes (Moss. 2011).

Table 1: Composition of the placebo and CHO supplement in the Moss study (adopted from Moss. 2011)

In a randomized, counter-balanced, double-blind study, Moss had eight recreationally trained cyclists perform a time trial (with a predetermined amount of work) in the course of which the cyclists ingested or rinsed (swirling 0.33ml/kg body weight of the solution for 8s) with either a placebo solution or a carbohydrate drink, whenever another 12.5% of the total work was done. In that it is worth mentioning that the composition of the CHO solutions differed for the one that was meant to be ingested and the one that was intended to be swished. With the former containing 7.5% and the latter 15% carbs, Moss mimicked solutions that had been used "successfully" previous studies. I do yet no idea, why the placebo did not contain electrolytes, as this could obviously have made a difference at least in the ingestion trials... I guess this is what distinguishes a thesis like this from a study that is worth being published in a peer-reviewed journal ;-)

Figure 2: Mean power output (in Watts) at different time points during time trial (data adapted from Moss. 2011).

As the performance data in figure 2 goes to show, only the ingestion of the carbohydrate led to significant improvements in mean power output, specifically at the later stages of the time trial. This "breakdown" may be explained by the "glycogen reduction exercise protocol" all participants had conducted the day before the time trial. So that after a "low carbohydrate" dinner, the participants were supposed to be glycogen depleted when they performed the time-trial on the subsequent morning.

Figure 3: Total time (in s) during time trial (data adapted from Moss. 2011).

In a way this is an unfair advantage, for the carb ingestion, which accordingly elicited way better time trial times. It does yet not lessen the significance of data on carbohydrate vs. water mouth rinse, which shows pretty conclusively that in a glycogen depleted state both forms of mouthrinsing (plain water or a 15% carbohydrate solution) are equally ineffective, when it comes to actual performance increases.

Figure 4: Pleasure / displeasure feeling during time trial (data adapted from Moss. 2011).

If you do however look at the pleasure/displeasure feeling scale data in figure 4, I would speculate that in a non-glycogen depleted state the carbohydrate-rinsers would have performed significantly better... I mean, without gas in the tank a car won't work even if it "wanted". In view of the fact that the carbohydrate ingestion group did yet pedal at a higher intensity, this would warrant further investigation.

Figure 5: Respiratory exchange ratio (higher values = higher carbohydrate oxidation) during time trial (data adapted from Moss. 2011).

That being said, there was what I consider an interesting effect of carbohydrate rinsing on the respiratory exchange ratio (remember higher values = higher carb oxidation), which would suggest that the theory Fares and Kayser propose (Fares. 2011), according to which the activation of sweetness taste receptors cells (T1R2 and T1R3) in the mouth would explain the previously cited performance "increases" in other studies, may have its merits. What else than the sensation of incoming carbs could explain that the cyclists burned more carbs in the carb mouthrinse compared to the placebo mouthrinse trial (cf. figure 5) - and that in the absence of significant differences in blood glucose or insulin levels?

Spit it or suck it? What's right for you?

While we do not know whether it would make sense to mouthrinse in a glycogen repleted state (yeah, I know +1% ;-), for any athlete interested in maximal performance, simply ingesting his carb + electrolyte drink would certainly be the best option. The (intermittendly) fasting dieter, who wants to maximize his fatty acid oxidation in the course of say his "morning cardio", on the other hand, would be best off with a non-carby electrolyte drink that helps him avoid dehydration and does not compromise (even if the effect is minimal) fatty acid oxidation... what? You want to know who would  benefit from spitting his carbs out? Well, at least based on the current data, mostly the cleaning contractors of your local gym - after all, they would have to work overtime (and be paid overtime) to clean up the mess ;-)

No Pump + Insulin Resistant? Maybe It's Your Healthy Low Salt Diet. Low Sodium Induced Increase in Aldosterone Has Direct Negative Impact on GLUT4 Mediated Glucose Uptake

A single Triple Whopper or about six whole steaks, what do you chose to get >75% of the 2g/sodium per day the feds are telling you you should maximally consume on a daily basis?

Today I felt kind of bored with covering only the latest studies. So I dug up one from 1999 that deals with the effects of dietary salt restriction on endothelial vasodilation (increased blood flow in the arteries) and insulin sensitivity by Ross D. Feldman and Nancy D. Schmidt. Yeah, the study is 14 years old, but when you've read today's SuppVersity article you'll probably still have learned something new - at least about "common wisdom".

If you also listen to the SuppVersity Science Round-Up on the Super Human Radio Network, you should be aware that very different rules apply with respect to salt consumption for athletes and physical culturists on a whole foods diet and the average sedentary inhabitant of the Western obesity belt (check out past episodes of the Science Round-Up).

Suggested Read: On "Clean Eating" being a myth - "A Tale of Macro- & Micro-Nutrient Modifi-cations" | read more

Talking about the ScienceRound-Up: In today's installment Carl and I will be talking about the latest meta-analysis on dairy and diabetes risk and how it's possible that only low fat dairy reduces the risk of diabetes. We will discuss how this relates to the differences in the fatty acid composition of milk which in turn depend on the feed the animals receive and whether there is in fact so much estrogen in milk that it can delay menopause. From there we will segue right into a discussion of the latest study on statins showing that they make you fat and diabetic and tell you which of the statins does what. If all works well, we will close the show by addressing Sarah M. Davis' question about a recently published and heavily discussed article that's titled "Why 'Clean Eating' is a Myth" (read it). I mean, is it really? Turn in live! at 12PM EST

What some of you may yet still not have on their radar is the fat that the "common wisdom" about salt being the root cause of all evil does not even apply to the majority of those guys and girls of whom you would expect they may in fact see benefits from a reduced salt consumption.

"Salt is bad, no matter what!"

In fact, Feldman & Schmidt were able to show that the provision of either normal or salt reduced diets to subjects aged 25 to 40 year.

Figure 1: Increased aldosterone levels during salt restriction will not only make you retain salt, but also reduce glucose uptake (Luther. 2011; my edits)

"Subjects were given a standardized diet that contained 75 mmol/L sodium chloride, 60 mmol/L potassium, and 20 mmol/L calcium for 14 days. Diets contained 16% protein, 54% carbohydrate, and 35% fat. Caloric intake was 2800 kcal/day. Subjects were advised to drink approximately 2L of water/day.

To assess the effects of dietary salt restriction independent of other dietary changes, subjects were randomized on a double blind cross-over basis to a daily supplement of 16 tablets of slow release sodium (Novartis, Mississauga, Ontario; 10 mmol/L sodium chloride/tablet) or matching placebo. Each were administered for 7 days." (Feldmann. 1999)

All of the participants had normal blood glucose levels, and were free of other abnormalities on history and physical examination. They did not smoke and their blood pressures levels ranged from normotensive to high normal/borderline. So, what would happen to the poor wretches consuming the additional sodium chloride tablets? Common wisdom tells us, their blood pressure will increase and they will develop metabolic abnormalities. Truth is (I quote from the study; Feldmann. 1999, my emphases), almost the exact opposite happened:

• Did you know? Aldosterone increases are caused by falling blood pressure, increased potassium levels, a higher blood acidity and decreased sodium concentrations in the blood trigger, decreases occur when your blood pressure drops, the potassium levels get low and/or the sodium levels are high.
  Dietary sodium restriction was associated with a significant decrease in 24-h urinary sodium excretion. However, blood pressure (based on the average 24-h automatic ambulatory measurements) was not significantly decreased with dietary salt restriction.
• Moderate salt restriction was associated with a significant increase in plasma norepinephrine concentrations. Dietary salt restriction was associated with a significant decrease in the glucose-to-insulin ratio, suggesting increased systemic insulin resistance. This decrease was primarily accounted for by an increase in plasma insulin concentration.

At the same time the researchers observed a significantly reduced effect of the vasculature to the insulin-mediated increase in blood flow, of which Hornstra et al. have shown only recently that it correlates negatively with blood pressure in overweight, but insulin sensitive individuals and may be the reason why those people don't suffer from the usual obesity related increases in blood pressure as well as its cardiovascular and renal consequences (Hornstra . 2013).

---

Most of you will remember the recent post about the ability of salt to block the negative effects of high intensity exercise on the cellular integrity of your heart and kidneys don't you?

Bottom line: If you are working out and sweating, even if it's not like a pig, SALT is the last thing to fear. In fact you can even increase your heart disease risk due to the negative impact on blood lipids (+10% total +12% LDL cholesterol in salt-sensitive and unsensitive normotensive subjects; Ruppert. 1991).

Now it is important to point out that it is not clear whether these effects are transient and a response to the abrupt changes in dietary salt in take that are characteristic of these short term intervention studies.

I am certainly not recommending you copy the salt intake of the average junk-food fanatic!

But let's be realistic, here: How much salt do you actually consume on a daily basis if you follow my advice and leave as much of the processed pre-packaged junk as you can right in the supermarket!? This will leave you with actually having to put salt on your foods and there really is no good reason for the average physical culturist not to so in a way that it's tasty and supplies you with one of the most important minerals in your body.

Suggest figure: Only obese people have increased risk of CVD with increasing sodium consumption | check it out the SuppVersity Facebook Wall

Reference:

• Egan BM, Lackland DT. Biochemical and metabolic effects of very-low-salt diets. Am J Med Sci. 2000 Oct;320(4):233-9. Review.
• Hornstra JM, Serné EH, Eringa EC, Wijnker MC, de Boer MP, Yudkin JS, Smulders YM. Insulin's microvascular vasodilatory effects are inversely related to peripheral vascular resistance in overweight, but insulin-sensitive subjects. Obesity (Silver Spring). 2013 Mar 20.
• Luther JM, Brown NJ. The renin-angiotensin-aldosterone system and glucose homeostasis. Trends Pharmacol Sci. 2011 Dec;32(12):734-9.
• Ruppert M, Diehl J, Kolloch R, Overlack A, Kraft K, Göbel B, Hittel N, Stumpe KO. Short-term dietary sodium restriction increases serum lipids and insulin in salt-sensitive and salt-resistant normotensive adults. Klin Wochenschr. 1991;69 Suppl 25:51-7.

Calcium, Magnesium, Potassium & Co in Food, Water & Supps - Getting Enough is Easy, Knowing How Much Is Not!

Image 1: "Minerals? Yeah that's the stuff you need to avoid cramping" While this is certainly true, the mineral loss during "normal" workouts is largely overblown, the most important and actually only necessary ingredients in respective drinks, even for Ironman Triathletes, are salt, water and sugar and what's worse this prejudice conceals the importance of electrolytes for our general health.

While it is Thursday, it is plain to see that this is not Adelfo Cerame's weekly SuppVersity post. There have been a couple of issues with the promised workout videos and neither I nor Adelfo wanted to postpone them yet another week so that we decided to rather publish videos + Adelfo's weekly update tomorrow instead of a reduced snippet today. To make sure you have more than enough food for thought to bridge the time, I applied a coupe of tweaks to a longer snipped from the next installment of On Short News that dealt with the protective effects of high(er) intakes of calcium, magnesium and potassium on the incidence of vascular dementia (=dementia in response to low blood flow to / oxygenation of the brain) and Alzheimer's dementia (=dementia due to the build up of plaque in the brain). As you may already have seen, the result got somewhat epic, so let's not waste anymore time and get straight into the original data before it's too late and we have already become demented ;-)

Don't forget your minerals or they'll soon be just one of the many things you tend to forget

While the studies and reviews on the effects of minerals, especially calcium (and as of late also magnesium), on cardiovascular health is about as abundant as the assessments of their individual and joint benefits and / or pitfalls, their role in the etiology of another, quieter, but not less prevalent pandemic is still insufficiently studied. Against that background, the results Ozawa et al. present in a recently published paper in the Journal of the American Geriatric Society could well provide some novel insights on whether or not forgetting to keep an eye on your mineral intake now will make you forget more than just a couple of minerals in the more or less distant future - and that even if none of the 1081 community dwelling elderly (>60y) Japanese the scientists followed up for 17 years is even remotely related to you ;-)

Figure 1: Hazard ratios for all-cause, vascular and Alzheimer's dementia for patients in the lowest to highest quartiles of potassium (≤1,856 / 1,857–2,149 / 2,150–2,559 / ≥2,560), calcium (≤431 / 432–531 / 532–638 / ≥638) and magnesium (≤147 / 148–169 / 170–195 / ≥196) intake in mg/day (top) and difference in intake of selected foods in the highest vs. lowest quantile of overall mineral intake (bottom; all calculated based on Ozawa. 2012)

Aside from the general association of higher potassium, calcium, and magnesium intake with lower incidence of dementia, which was - given the overall low median intake - more or less to be expected, there are a couple of other very noteworthy things I want you to take note of (see figure 1; data adjusted for age; sex; low education; history of stroke; hypertension; diabetes mellitus; total cholesterol; body mass index; smoking; alcohol intake; regular exercise; and energy, vitamin C, cholesterol, saturated fatty acid, monounsaturated fatty acid, and polyunsaturated fatty acid intake):

• a higher mineral intake was had a more pronounced beneficial impact on vascular compared to Alzheimer's dementia (-77% vs. -46% max. reduction)
• for potassium and calcium the general rule of thumb is "the more, the better" (the deviation from that rule in the individual analysis for Alzheimer's is statistically nonsignificant), but I don't this is mediated by the overall low intake of both and thus only valid within the given range of ~700-900mg of calcium and ~2600-3000mg of potassium - intakes you can by the way easily get from your diets alone
• aside from the usual suspects, i.e. (green) vegetables, fruits and fish, dairy is among the most important source of minerals and high dairy eaters tend to be high mineral consumers, while low / no dairy eaters tend to be in the lowest quartiles of overall mineral intake

as well as a couple of things you cannot read off the graphs, e.g.:

• women had  significantly higher mineral intakes than men, i.e. 68.3% of the persons in Q4 for overall mineral intake were women
• age had no effect whatsoever on the overall intake of potassium, calcium and magnesium
• a low(er) education (<6 years of schooling) was a good predictor of low total mineral intakes, just as it is by the way in view of an overall worse diet quality (this is however less pronounced than conventional wisdom would suggest)
  
• intriguingly, people with diabetes had on average higher mineral intakes than people without diabetes, almost certainly a non-causative relationship that is probably mediated by supplements and nutritional counseling the diabetics received
• contrary to the US, there was no association between high salt and low Ca, Mg, or K intakes, this is also surprising because the "average" middle aged Japanese consumes way more than 5g of salt (Nagata. 2004) and thus 2x more than the US "tolerable upper intake level" of 2300 mg (Cogswell. 2012)

Apropos US, in view of a couple of other studies that have only recently provided support for the widely held, but in fact rarely scrutinized believe that, the lack of adequate amounts of potassium and magnesium, in particular, is associated not only with the age-related cognitive decline and even dementia, but also with such profane things as "simple" obesity, e.g. ...

• Donfrancesco et al. report higher potassium and magnesium intakes were associated with lower BMIs in 1168 men and 1112 women aged 35-79 yrs from 12 Italian regions (Donfrancesco. 2012)
• almost identical results in a study by Shay et al. that found associations with lower BMIs for potassium and magnesium 1794 men and women (ages 40-59 y) from 8 US population samples (Shay. 2012)

... it would unquestionably make sense to eventually stop bashing on sodium and start promoting the consumption of magnesium- and potassium-rich foods, instead.

Figure 2: Percentage of the population mineral intakes below the EAR for individuals aged ≥2y (data from NHANES 2003–2006; n = 16,110; Fulgoni. 2011).

Did you know that according to latest data from the CDC (Cogswell. 2012) less than 2% of US adults meet the dietary recommendations for potassium (≥4700 mg K/d) and that the lack of potassium was even more pronounced in the elderly (0.5% of the >72y-old US citizens meet the dietary requirements) and obese (0.7% meet the recommendations. With two out of five Americans also failing to meet even the required amount of magnesium in the diet, it appears more than questionable why the good-meaning (I don't doubt they are but too often they are mislead of have the good of the wrong people in mind) policy makers don't put magnesium and potassium into the water supply instead of toxic junk such as chlorine and fluoride...

I mean, you will probably remember from "On Short News on July 28, 2012" that each milligram of magnesium per liter drinking water could decrease the heart disease risk of people with an unbalanced mineral intake by 5%! But, alas, who am I to make such bold suggestions?

Now, while the importance of watching your dietary magnesium and potassium are pretty obvious and probably nothing you have not heard before, there is still one question left to be answered - a question that will point us away from RDAs and EARs and back to foods, which never contain only one of the aforementioned minerals in isolation. So here is the question: What do we make of calcium? In the Ozawa study it appeared to be clearly useful, but that was with intakes of >638mg/day in the highest quintile of the study population! The average European citizen, on the other hand, consumes roughly 1g = 1,000mg, i.e. 36% more than the Japanese and still we (us Europeans) are about as sick, if not sicker than the average Japanese? How come?  

Potassium, check; magnesium, check; calcium, ... wait a minute! What about phosphorus? 

Aside from the mere possibility that we could already be consuming way too much calcium (which is not supported by science as long as those 1,000mg come from your diet and not from supplements; cf. "Higher Calcium Intake Greater Fatty Acid Oxidation"), the most straight forward explanation would be an imbalanced intake of phosphorus. For the average European the latter is at about 1,675mg/day (mostly from dairy, cereals and meats - 27.9, 23.4, 17.4.% of daily intake, respectively) and thus clearly twice the amount our (the European) version of the well-meaning policy makers are telling us each and every one of us should be consuming on a daily basis.

Figure 4: Relative potassium intake in European countries according to source; note: with 4,110mg/day the average potassium intake in the Euopean Union is much higher than in the US, highest intakes were observed in Spain, lowest in Germany (Welch. 2009)

Did you know that the average magnesium intake in Europe (409mg/day) is much higher than in the US? And guess what, the usual suspects, i.e. dairy and cereals aside, non-alcoholic beverages are the #2 source (19% of total mg intake) of dietary magnesium in Europe! I would, an observation Welch et al. attribute just like the almost "optimal" (wrt to the US recommendations) average potassium intake of 4,110mg/day to the high quality tap and bottled mineral water, and other non-alcoholic beverages (and certainly not to reverse osmosis or the consumption of mineral-free distilled water, which is something you can use to satisfy the water requirements of your radiator or  iron, but not those of your body ;-).

Figure 3: Hazard risk analysis based on the Cholesterol and Recurrent Events (CARE) study (n = 4127; Tonelli. 2005)

In fact, we have broached on another of these imbalances in the context of the effects that were observed with higher magnesium : calcium ratios in drinking water (cf. red box above + "On Short News on July 28, 2012"), before. With phosphor we have yet another "antagonistic partner" of calcium, of which Ritz et al. have only recently argued that its increasing use as a food additive (check out the label of whatever processed food you buy, chances you find a XZY-phosphate on it are >50%) poses a serious health risk. To support their argument, the researchers cite data from a 2005 study by Tonelli et al. that indicates that even serum phosphor levels that are well within the normal range (2.0-4.0mg/dl) were associated with significantly increased CVD risks (cf. figure 3; suggested read: "Does Low Vitamin D Protect Us From Dietary Phoshporus Overload?").

These are only two selected examples of the available evidence that suggests that we are still totally underestimating the effects of "electrolytes", in general, and their ratios, in particular, on our neurological and metabolic health - and, even worse, doctors, policy makers, experts and gurus keep making mostly unwarranted recommendations to increase our intake of one and decrease the intake of another mineral, when in fact the lack of synergists (e.g. normal amounts of dietary magnesium to complement calcium) and absence or abundance of antagonists (e.g. potassium and magnesium for salt and calcium, magnesium and potassium for phosphorus) are the actual problems we are dealing with.

Figure 5: Don't forget that there are personal, regional and historical difference in total and relative mineral intakes and never supplement, high amounts of isolated minerals simply because Mr or Mrs average would benefit, without checking how "average" you actually are in terms of your solid, fluid and supplemental mineral intake (data for image based on Crawford. 1971; data on US water hardness according to the Water Research Center)

Implications: I guess based on all the information on the allegedly complicated interactions between the different minerals, you will by now have realized that statements like "everybody will benefit from taking 300mg of supplemental magnesium" let alone "everybody must take at least 300mg of supplemental magnesium" are about as useful as the constant advice to cut your salt, cut your fat and cut your calories people are confronted with on a daily basis. The chances that person X may benefit are probably high, but they are certainly much lower than the chances that you will survive the sting of a bee - and even that will still kill 53 US citizens per year.

Individualization, evaluation are therefore obligatory steps which must necessarily come before supplementation, which would - as some of the data in the figure 4 did already suggest - rarely be necessary, if the average inhabitant of the Western hemisphere did not top his sugary, salty and phosphate-laden fast-food diet with beverages that are either devoid of any minerals or will simply exasperate the existing imbalances.

Too many people (and I believe this is particularly true for the US) seem to have forgotten that we have not always been forced to filter all the minerals out of our water just to make the chlorinate, fluorinated, and "estrogenated" sludge that streams out of the faucet suitable for human consumption. Think of that and the data in figure 5, the next time the as of late often second-guessed recommendation that you got to have "at least X cups of water per day" resurfaces and of how little use each of them is, when it does not contain any of the electrolytes your body needs to handle the water appropriately.

References:

• Cogswell ME, Zhang Z, Carriquiry AL, Gunn JP, Kuklina EV, Saydah SH, Yang Q, Moshfegh AJ. Sodium and potassium intakes among US adults: NHANES 2003-2008. Am J Clin Nutr. 2012 Aug 1. 
• Crawford MD, Gardner MJ, Morris JN. Cardiovascular Disease and the Mineral Content of Drinking Water. Br. Med, Bull. 1971; 27,1: 21-24.
• Donfrancesco C, Ippolito R, Lo Noce C, Palmieri L, Iacone R, Russo O, Vanuzzo D, Galletti F, Galeone D, Giampaoli S, Strazzullo P. Excess dietary sodium and inadequate potassium intake in Italy: Results of the MINISAL study. Nutr Metab Cardiovasc Dis. 2012 Jul 24.
• Fulgoni VL 3rd, Keast DR, Bailey RL, Dwyer J. Foods, fortificants, and supplements: Where do Americans get their nutrients? J Nutr. 2011 Oct;141(10):1847-54.
• Ozawa M, Ninomiya T, Ohara T, Hirakawa Y, Doi Y, Hata J, Uchida K, Shirota T, Kitazono T, Kiyohara Y. Self-Reported Dietary Intake of Potassium, Calcium, and Magnesium and Risk of Dementia in the Japanese: The Hisayama Study. J Am Geriatr Soc. 2012 Aug 2. 
• Ritz E, Hahn K, Ketteler M, Kuhlmann MK, Mann J. Phosphate additives in food--a health risk. Dtsch Arztebl Int. 2012 Jan;109(4):49-55. Epub 2012 Jan 27. 
• Shay CM, Van Horn L, Stamler J, Dyer AR, Brown IJ, Chan Q, Miura K, Zhao L, Okuda N, Daviglus ML, Elliott P; for the INTERMAP Research Group. Food and nutrient intakes and their associations with lower BMI in middle-aged US adults:  the International Study of Macro-/Micronutrients and Blood Pressure (INTERMAP). Am J Clin Nutr. 2012 Aug 1. 
• Tonelli M, Sacks F, Pfeffer M, Gao Z, Curhan G; Cholesterol And Recurrent  Events Trial Investigators. Relation between serum phosphate level and cardiovascular event rate in people with coronary disease. Circulation. 2005 Oct 25;112(17):2627-33. 
• Water Research Center. Hard Water  Hardness Calcium Magnesium - Water Corrosion Mineral Scale. < http://www.water-research.net/hardness.htm > retrieved Aug 16, 2012.
• Welch AA, Fransen H, Jenab M, Boutron-Ruault MC, Tumino R, Agnoli C, Ericson U, Johansson I, Ferrari P, Engeset D, Lund E, Lentjes M, Key T, Touvier M, Niravong M, Larrañaga N, Rodríguez L, Ocké MC, Peeters PH, Tjønneland A, Bjerregaard L, Vasilopoulou E, Dilis V, Linseisen J, Nöthlings U, Riboli E, Slimani N, Bingham S. Variation in intakes of calcium, phosphorus, magnesium, iron and potassium in 10 countries in the European Prospective Investigation into Cancer and Nutrition study. Eur J Clin Nutr. 2009 Nov;63 Suppl 4:S101-21.

Electrolyte Supplement Blocks Exercise Induced Elevations in LDH, Urea, Leucocyte Infiltration into the Heart & the Congestion of Renal Blood Vessels

For the average gymrat it is probably not a question of life or death, but an increase in recovery due to a decrease in detrimental muscle damage in response to dehydration should be an very good argument to get some salt and glucose in after / around your workouts.

Electrolytes have been at the heart of several SuppVersity articles as of late (check them out). Few of them did however have a direct link to exercise. Reason enough to discuss the results of a pertinent paper that was published by two scientists from Cairo University (Osman. 2013). At first sight, the study Hala F. Osman and  Azza M. Atya conducted does not appear to be very exciting. After all, the effects of electrolyte supplements on re-hydration after a workout are nothing that would not have been analyzed in previous studies. Moreover, the study at hand, which has been published in the latest issue of the World of Applied Sciences Journal, is a rodent study and the results would actually be pretty boring if the poor critters had not been sacrificed right after a lengthy HIIT session comprising 5x4 min intervals at 25m/min with 2min break in between, in order to beyond the conventional blood analyses and take a look at their hearts and kidneys.

Rodents don't complain

Now based on human studies we already know what happens in the blood, when we exercise vigorously, CK rises, LDH rises, the serum electrolyte levels get messed up, etc.

Figure 1: Changes in serum electrolyte levels (chloride, magnesium, calcium, phoporus, potassium, natrium) after the HIIT-esque workout w/ or w/out electrolyte supplementation (Osman. 2013)

The exercise induced changes in the electrolyte levels Osman & Atya observed in the rodents were in fact very similar to those that have been reported in human studies. What's more important, though is the fact that they persisted only those rats that did not receive the Rehydran-N solution daily for 45 days + immediately after the workout (see figure 1).

"[...] sodium ions decreased significantly  (P 0.05) after exercised while after  supplementation  by  Rehydran-n  and  Rehydran-n+ (Mg+Ca) citrate in group III and IV the level of sodium ion restored near to the control value. While  potassium ions level increased significantly (P 0.05) in exercised group. The supplementation by Rehydran-n and Rehydran  n+ (Mg+Ca) citrate in group III and IV not affected on the level of potassium and not return the value near to control value." (Osman. 2013)

One thing that is at odds with previous research in humans, is the acute -18.6% drop in magnesium levels. Interestingly, this drop was blunted even when the rodents received the magnesium free NaCl + K electrolyte supplement. The immediate provision of magnesium in the Rehydran-n + Mg + Ca arm of the study, on the other hand, raised the Mg2+ levels by +18% and did thus also result in a transient electrolyte imbalance.

Rehydration prevents organ stress

As I already hinted at in the introduction, having slightly screwed electrolyte levels, as well as elevated amounts of creatine kinase, lactate dehydrogenase and urea in the blood are more or less negligible problems compared to any direct ill health effects the dehydration and the corresponding loss of electrolytes could have on the structural integrity and health of your heart and kidneys. Effects such as those Osman and Atya saw when they analyzed the organs of the animals who did not compensate for the electrolyte loss by the immediate provision of adequate amounts of salt after a workout:

Figure 2: Sections of heart tissue after the workout (Osman. 2013)

"Figure [2] microscopic sections of heart from exercised group [2b] showed leucocytic cells infiltration in cardiac myocytes. Whereas other sections from Rehydran-n treatment  group [2c]  revealed  few  focal intermuscular  inflammatory  cells  infiltration.  While  Rehydran-n+  (Mg+Ca)citrate  treatment  group [2d] showing  no  histopathological  changeslike  those  in control group [2a]." (Osman. 2013)

Kidney sections of rat from control group revealed no histopathological changes. While in  prolonged exercising group showing hyalinosis [=degeneration] of  glomerular tufts. Moreover in Rehydran-n group vacuolations of epithelial lining renal tubules [=accumulation of waste that will be flushed out later on]. Rehydran  n+ (Mg+Ca) citrate treatment group congestion of renal blood vessel was observed [=one reason the better stick to salt, only].

Now, these results certainly sound more frightening than they actually are. Our bodies are (just like those of rodents, by the way) well equipped to handle the occasional cell / organ damage. And the heart is - believe it or not - "only" a muscle. It works slightly different, but can take at least as much beatings as our skeletal muscle tissue. Beatings of which the creatine kinase (CK) and lactate dehydrogenase (LDH) levels in the supplemented groups clearly show that they are are ameliorated by the the provision of electrolytes.

Figure 3: Creatine kinase (CPK), lactate dehydrogenase (LDH) and urea elevations (in %) after 5x4min treadmill runs with 2 min rest in-between (Osman. 2013)

"The present results are in accordance with the exhausted exercised rats resulted in an increased growth in serum CPK activity. This increase, however was markedly reduced in the rats after administration of antioxidant. For instance, 16h exercise in rats caused a marked rise in  activity levels of serum LDH. Increase in serum LDH  activity is mainly due to release from heart and skeletal muscles into blood stream. [...] Different  types  of  stressors  cause  an  increase in activities of serum creatine phosphokinase and lactate dehydrogenase in humans and animals which is an indication of tissue damage." (Osman. 2013)

Now you may be asking yourselves, whether similar effects can be expected in human beings!? Well, the answer should be obvious: "Similar", yes. 100% identical, no. Maughn et al., for example, demonstrated similar (re-)hydration benefits in human subjects in the 1994 - it should be obvious thought that they refrained from cutting their subjects open and checking what happened to their hearts so that we can only speculate about the extend of cellular / structural damage and the corresponding compensatory effects in humans.

Table 1: Ingredients of a single sachet of Rehydran-N which was bought by the reaserchers at a local pharmacy - no sponsorship involved

What can be said for with some certainty, though, is that it is unlikely that you would need more than one sachet of the electrolyte formula with its 0.3g K, 0.7g NaCl, 0.58g tri-sodium citrate and 4g glucose to achieve similar effects. After all, Osman & Atya modeled the amount of electrolytes the rodents received to what human beings would get from one serving of Rehydran-N. It is thus for once not necessary to calculate a human equivalent dose of the electrolytes in the water of the lab animals.

No glucose no effective rehydration

What is however necessary is the inclusion of the sugar or rather glucose in the rehydration formula, because the latter increases the efficacy of the formula significantly.

"The discovery that sodium transport and glucose transport are coupled in the small intestine so that glucose accelerates absorption of solute and water was potentially the most important medical advance this century."(Anonymous in Lancet. 1978)

So don't skip on the miniscule amount of glucose - even if you are suffering from carbophobia and believe that any amount of carbohydrates is going to make you hold water. Trust me, if anything will make you hold water its their absence and the suboptimal uptake of the electrolytes in the absence of glucose that will make you look like a watery version of the Michelin Man.

---

NaHCO3 loading increases performance & decrease LDH activity.

Bottom line: Despite the fact that they may have been derived in a rodent study, the results Osman and Atya present in their most recent paper re-emphasis the need for adequate (re-)hydration before, during and even more so after workouts. In the vicinity of a workout, the latter is best achieved, using a simple salt + glucose mixture that can, but does not necessarily have to include ~360mg magnesium- and ~800mg calcium-citrate. You should yet keep in mind that the the increased levels of Mg2+ and Ca2+ can become burden on your kidney, although they appear to have beneficial effects on the heart (see figure 2).

And as far as the ostensibly beneficial decrease in LDH in the Rehydran-N + Mg + Ca group is concerned, this may well be a simple result of the alkalizing effect of magnesium and calcium ions. Assuming this is correct, similar benefits should occur in response to sodium bicarbonate, aka baking soda supplementation (learn more). The latter is after all part of the standard anti-rhabdomyolysis (=rapid breakdown of damaged skeletal muscle tissue) protocol where it does prevent both, further damage to the musculature and permanent damage to the kidneys (Vanholder. 2000).

References: 

• Anonymous. Water with sugar and salt. Lancet. 1978 Aug 5;2(8084):300-1.
• Maughan RJ, Owen JH, Shirreffs SM, Leiper JB. Post-exercise rehydration in man: effects of electrolyte addition to ingested fluids. Eur J. Appl. Physiol. Occup Physiol., 69: 209-15.
• Vanholder R, Sever MS, Erek E, Lameire N. Rhabdomyolysis. J Am Soc Nephrol. 2000 Aug;11(8):1553-61. Review.

Magnesium Round-Up: Know If You Are Deficient, Whether You Need More, Where to Find It, How Dietary Mg Contents Changed & How Magnesium Interacts W/ Vitamin D

24%, 23% and 22% of the DV for magnesium that's what you can find in one serving of sunflower seeds (0.25cup), halibut (4oz) and a large(r) banana - now you tell me it was impossible to get your magnesium from dietary sources.

After having handled half of the Science Round-Up from Thursday yesterday, yesterday, there is still something left to serve: seconds to the seconds, if you will and probably not so "new" as the average SuppVersity news. In order not to bore you, I will yet refrain from telling you how important magnesium is and how it is involved in thousands of enzymatic reactions ... you know the whole magnesium-guru-spiel all too well, anyway. I mean, anyone doing a cursory Google search will have to conclude that there is nothing magnesium cannot cure, right?. Whatever you may suffer from, someone has already found out that it must be related to magnesium deficiency or, even more profitable, taking the wrong form of magnesium supplements.

Apropos deficiency: How do you even know you are deficient?

What sounds like a question that could be answered in one, at best two sentences turns out to be one of the root causes of the whole confusion about magnesium. Based on a standard blood test you can only exclude that your levels are (a) so high or (b) so low that you better head straight to the emergency room. Magnesium is, just as the other electrolytes, simply too important for your body to have them drop below a certain margin in which your heart works optimally. So if there is not enough magnesium around, your body will tap into tissue stores the status of which is obviously not identical to the serum levels on a standard lab test.

Table 1:The lion's share of magnesium to replete your serum levels is not coming from your red blood cells and therefore RBC levels are only a proxy and not a 100% reliable marker of total body mg status (data based on Elin. 1987)

According to Maurice J. Arnaud who wrote a review with the telling title "Update on the assessment of magnesium status" in 2008, the most reliable method to assess the whole body magnesium status would be a metabolic ward study in the course of which a so-called "loading test" would be performed, But...

"[b]alance studies are time consuming, labour intensive and need well trained staff. They are often performed in a metabolic unit and require complete urine and faecal collections; therefore it is not a method that can be applied as a routine test for the evaluation of Mg status. Loading tests are simplified balance studies where absorption is supposed not to be disturbed when Mg is given orally so that body retention is calculated from urine elimination. Mg administration during a loading test can be either oral or intravenous and it is important that the subjects have normal kidney function. Urine is collected for 24 hours following administration of the Mg load as Mg excretion by the kidney has been shown to have a circadian rhythm . Under these conditions, the loading test is supposed to be a reliable indicator of Mg status." (Arnaud. 2008)

With the erythrocyte (red blood cell) test for magnesium, there is however an alternative available, which may not be just as reliable but appears to show a relatively high correlation with whole body magnesium levels in many, but not all studies (Malon. 2004).

How likely is it that you are deficient?

Honestly, I would hope that it is unlikely, because if that is the case for someone who is not taking supplemental magnesium you can almost be sure that her or she is following a healthy whole foods diet.

Table 2: Overview of age groups with more than 5 % of intakes below the lowest recommended intake levels in 7 European countries; T, toddlers (1–3 years (both sexes)); C, children (4–10 years); Y, youth (11–17 years); A, adults (18–60 years); S, seniors (.60 years); capitals, both sexes; lower case, women only; lower case italic, men only (Mensik. 2013)

If you take a look at table 2 you will see that even the average German gets enough magnesium in his diet, irrespective of his age, and much contrary to our neighbors in the East, West and Northwest (I could not resist to mark zinc another of those purported minerals of which conventional wisdom tells you that you simply cannot get enough from your diet).

Knowing that most of you are probably Americans, I can calm you down. You are not worse than your British friends. In fact, the NHANES data from 1999-2000 suggests that the average American Caucasian and Mexican man below 50 gets enough magnesium from his food only! Unfortunately, the same cannot be said for the women, and both male and female African Americans who have trouble meeting their requirements even if one accounts for the additional magnesium from supplements (NHANES).

Magnesium and the athlete

A note on magnesium and cramps: While there is evidence that altered serum osmolality and altered serum electrolyte concentrations, notably hypochloraemia, hyponatraemia, and hypocalcaemia (=not hypomagnesaemia) can cause generalized skeletal muscle cramping at rest in specific clinical settings, "data from well-conducted prospective cohort studies show that athletes with acute EAMC are not hyponatraemic, hypochloraemic, or hypocalcaemic and do not have an abnormal serum osmolality." (Schwellnus. 2008).

For the average athlete, a low magnesium intake is yet rather the exception and can even be problematic for athletes with a high anaerobic-to-aerobic ratio who suffer from increases in blood mg due to an overall reduction on blood volume after intense workouts, anyway (Cordova. 1992; Joborn. 1985; Monteiro. 2005; Monteiro. 2006). It is thus no wonder that not magnesium deficiencies, but high magensium levels are a problem that is commonly observed in athletes. I mean, what are you supposed to do, when even your mother "lies" to you about cramps being caused by magnesium deficiency?

"The most common alterations were higher serum phosphate (29/61, 47%) and magnesium concentrations (28/61, 46%). Abnormalities of serum phosphorus and magnesium concentrations were detected in almost half of the athletes. Hyperphosphataemia and hypermagnesaemia were the most common abnormalities." (Malliaropoulos. 2012)

The data Malliaropoulos et al. analyzed came from 130 elite track and field athletes (65 males and 65 females, age range 20-30 years) from the National Athletics Sports Medicine Center database in Thessaloniki, Greece. And maybe some of them were even on the proven non-ergogenic ZMA (zinc + magnesium + vitamin B6; cf. Wilborn. 2004).

So where do you get your supplemental magnesium from and how much?

I am not going to tell you to stop supplementing with magnesium if you feel that this has done you good in the past. It is after all an important mineral. What I want to remind you of is yet the fact that taking 100% of the RDA is imho the absolute maximum. Even if you don't end up with high levels due to supplementing more and don't care about wasting money, there is one thing that's commonly overlooked about human physiology and that is how the intake and excretion of nutrients are highly inter-related. In other words, if your body switches into a "get rid of magnesium" mode it is likely you are loosing other electrolytes you do not supplement in copious amounts (e.g. salt ;-), as well.

Figure 1: Plasma an bone (primary axis) as well as red blood cell (RBC; 2ndary axis(!)) content after 14 days of supplementation with identical amounts of magnesium in different organic and inorganic forms (Coudray. 2005)

As far as the best forms are concerned the number of studies comparing multiple forms to each other is limited and the inter-comparison of different studies not really legit. Therefore I have simply copied + pasted the figure that went with a previous article on the matter - as you can see, you can generally use whatever form of magnesium you want - even the cheap oxides, which worked wonders for anxiety ridden ladies in a study by De Souza et al. that was published in the Journal of Women's Health & Gender-Based Medicine in March 2000. As long as you take your magnesium supplements in reasonably low doses - the dose in the De Souza study for example was 200mg + 50mg B6 - and over a long enough period, they are going to bring your levels back up - if not sooner, then later.

Magnesium depletion of our foods

A note on topical Epsom salt from the early 20th century: While I did tell you on the show that I could not find peer-reviewed adequately powered studies on the topical absorption of magnesium in the for of mg oil or Epsom salt, I found a comment in a 1915 paper on the potential harm caused by cosmetics quite enlightening, esp. the part on the economic value of respective products, where Martin I. Wilber writes that the ability of respective products to penetrate the "unbroken skin has as yet not been demonstrated" and cautions against the sue "of the now widely advertised lotions containing magnesium sulphate or Epsom salt", of which "the latter preparations serve very well to show the gullability of that portion of the public that is desirous of improving its facial appearance. As Epsom salt, magnesium sulphate can usually be purchased for 5 cents a pound, while in the form of any one of the popular skin or wrinkle lotions it is sold at the rate of from $2 to $4 a pound." (Wilbert. 1915) You see, there were snake,... ah I mean mg oil vendors all over the place even 100 years ago ;-)

Aside from the almost cult-like worship of epsom salt baths and topical ng oils, the notion of a general depletion of mg in the foods we eat is one of the favorites among the bazillion of websites run by people who hoax you to believe they were concerned with your physical health, when all they are concerned with is their own financial health.

Figure 2: Changes in mineral content of selected food types from 1940-2002 (Thomas. 2007)

It is, as the data in figure 2 goes to show you true that the amount of magnesium in many of the foods we consume is lower these days than it was amidst WW2. The mg loss in meats, for example, is  driven by the processing, while corned beef has lost almost 50% of its "original" mg content, the amount of mg in roast beef and steaks is still the same, the one in turkey is even up by ~30% and for chicken it remained 100% stable (Thomas. 2007). It is also a very intriguing coincidence that the same websites will usually also tell you how we are all not just magnesium deficient, but also copper toxic. Strange in view of the fact that the average reduction in copper is -62% and thus >2x higher than that of magnesium.

Magnesium supplementation for special conditions

Before closing this round-up with a bottom line, I am briefly listing a couple of things related to magnesium or rather a deficiency in this important mineral that could be solved by simply upping your dietary and/or supplemental magnesium intake.

• 

  Higher vitamin D levels increase MG uptake from the gut and supplementation with VD has been shown to increase mg in obese, yet not in normal individuals (Farhanghi. 2009). On the other hand, mg has recently been found to be necessary for the production of calcitriol from 25OHD (Matsuzaki. 2013)

  anxiety - mg is the gate-keeper at the NMDA receptor and interacts with the GABA receptors; a deficiency can cause anxiety, the use of extra magnesium will yet not automatically solve the problem if you are not low to begin with
• depression - low cellular mg levels can precipitate if not cause depression(-like) symptoms, 150-300mg of magnesium glycinate or better taurinate can help (Eby. 2006)
• low vitamin D - while it is not yet sure if it helps with upping the storage form of vitamin D (25OHD), it has been recently established that magnesium is necessary for the production of calcitriol the active form of vitamin D; adequate levels of D also facilitate mg absorption very high levels of vitamin D, on the other hand, have been associated with low / imbalanced mg levels - probably due to their effects on calcium homestasis
• constant stress / burnout - initially low mg levels will lead to a hyper activity of the stress-axis within the HPTA; the constantly overtaxed CNS will then give in and you will end up totally burned out (Sartori. 2011); this state cannot be reversed by magnesium supplementation, alone, but it can aid the recovery process which is largely based on taking off of everything that stresses you

Whether or not simply eating more high magnesium foods will be enough or whether you actually have to buy supplements to work on these and other issues will also depend on whether

• you can digest / absorb it, which would be hampered due to vomiting, diarrhea, bowel resection, intestinal and biliary fistulas or hemorrhagic pancreatitis
• lose too much mg over the kidneys, due to chronic parental fluid therapy, osmotic diuiresis, hypercalcemia, diuretics, aminoglycosides, amphotericin B, pentamidine, cisplatin, cyclosporine, alcohol metabolic acidosis (ketosis, starvation, alcoholism), renal diseases, or
• suffer from endocrine disorders like primary or secondary aldosteronism, diabetes, hyperthyroidism or hyperparathyroidism

If anything of these sounds familiar, I would certainly consider testing my mg levels (erythrocyte test) before and while I was supplementing and that's not about wasting money on potentially unnecessary supplements, but much more about making sure that you actually get, absorb and retain enough magnesium.

---

Bottom line: Magnesium is certainly an important mineral, but its effects must not be seen in isolation, it should not be supplemented in copious amounts in isolation without medical indication and it may not be misunderstood as a natural pharmacological agent - it works by (a) replacing a deficiency or (b) countering an imbalance. Plus: It is not generally impossible to get your 300-400mg of magnesium from your diet.

References:

• Arnaud MJ. Update on the assessment of magnesium status. Br J Nutr. 2008 Jun;99 Suppl 3:S24-36.  
• Bohl CH, Volpe SL. Magnesium and exercise. Crit Rev Food Sci Nutr. 2002;42(6):533-63. Review.
• Cordova A. Changes on plasmatic and erythrocytic magnesium levels after high-intensity exercises in men. Physiol Behav1992; 52: 819-21.
• Eby GA, Eby KL. Rapid recovery from major depression using magnesium treatment. Med Hypotheses. 2006;67(2):362-70. 
• Elin RJ. Assessment of magnesium status. Clin Chem. 1987 Nov;33(11):1965-70. Review.
• Farhanghi MA, Mahboob S, Ostadrahimi A. Obesity induced magnesium deficiency can be treated by vitamin D supplementation. J Pak Med Assoc. 2009 Apr;59(4):258-61. 
• Joborn H, Akerstrom G, Ljunghall S. Effects of exogenous catecholamines and exercise on plasma magnesium concentrations. Clin Endocrinol (Oxf)1985; 23: 219-26; (Oxf).
• Malliaropoulos N, Tsitas K, Porfiriadou A, Papalada A, R Ames P, Del Buono A, Lippi G, Maffulli N. Blood phosphorus and magnesium levels in 130 elite track and field athletes. Asian J Sports Med. 2013 Mar;4(1):49-53.
• Malon A, Brockmann C, Fijalkowska-Morawska J, Rob P, Maj-Zurawska M. Ionized magnesium in erythrocytes--the best magnesium parameter to observe hypo- or hypermagnesemia. Clin Chim Acta. 2004 Nov;349(1-2):67-73.  
• Matsuzaki H, Katsumata S, Kajita Y, Miwa M. Magnesium deficiency regulates vitamin D metabolizing enzymes and type II sodium-phosphate cotransporter mRNA expression in rats. Magnes Res. 2013 May 1;26(2):83-6.
• Mensink GB, Fletcher R, Gurinovic M, Huybrechts I, Lafay L, Serra-Majem L, Szponar L, Tetens I, Verkaik-Kloosterman J, Baka A, Stephen AM. Mapping low intake of micronutrients across Europe. Br J Nutr. 2013 Aug;110(4):755-73.   
• Miriam C. De Souza, Ann F. Walker, Paul A. Robinson, and Kim Bolland. Journal of Women's Health & Gender-Based Medicine. March 2000, 9(2): 131-139.  
• Monteiro CP. Equilíbrio Oxirredutor: um estudo em nadadores e em não atletas, em repouso e em resposta ao exercício [PhD]. Lisboa: Faculdade de Motricidada Humana, Universidade Técnica de Lisboa, 2005.
• Monteiro CP, Santa Clara H, Raposo MF,et al. Effect of training and exercise intensity on magnesium status. In: Alpoim C, Vasconcelos Morais P, Santos MA, Cristóvão AJ,
  Centeno JA, Collery P, eds.Metal Ions in Biology and Medicine. Paris: John Libbey Eurotext, 2006: 546-52 
• Sartori SB, Whittle N, Hetzenauer A, Singewald N. Magnesium deficiency induces anxiety and HPA axis dysregulation: modulation by therapeutic drug treatment. Neuropharmacology. 2012 Jan;62(1):304-12. doi: 10.1016/j.neuropharm.2011.07.027. Epub 2011 Aug 4.
• Schwellnus MP. Cause of exercise associated muscle cramps (EAMC)--altered neuromuscular control, dehydration or electrolyte depletion? Br J Sports Med. 2009 Jun;43(6):401-8. 
• Thomas D. The mineral depletion of foods available to us as a nation (1940-2002)--a review of the 6th Edition of McCance and Widdowson. Nutr Health. 2007;19(1-2):21-55. Review.
• Wilbert MI. Cosmetics as Drugs: A Review of Some of the Reported Harmful Effects of the Ordinary
  Constituents of Widely Used Cosmetics. Public Health Reports. 1896-1970; 30(42): Oct. 15, 1915. 3059-3066.
• Wilborn CD, Kerksick CM, Campbell BI, Taylor LW, Marcello BM, Rasmussen CJ, Greenwood MC, Almada A, Kreider RB. Effects of Zinc Magnesium Aspartate (ZMA) Supplementation on Training Adaptations and Markers of Anabolism and Catabolism. J Int Soc Sports Nutr. 2004 Dec 31;1(2):12-20.

Deep Mineral Water Maximizes Recovery After Dehydrating Exercise: Significant Effects Within the First 4h, Measurable Effects Even 24h Post - Mechanism Not Clear

Thirsty? Drink mineral water and recover faster!

If you have seen the FIFA World Cup quarter finals, France vs. Germany, you will be aware that the Germans could use a supplement that speeds up regeneration after dehydrating physical activity in the heat. Interestingly enough, a "supplement" like that has been identified only recently by Loreta Stasiule and her colleagues from the Lithuanian Sports University (Stasiule. 2014).

In the corresponding paper, which has been published in the Journal of the International Society of Sports Nutrition roughly a week ago, the researchers report the results of a randomized, double-blind, placebo-controlled crossover human study to evaluate the effect of ingestion of natural mineral water extracted from a depth of 689 m on recovery from prolonged fatiguing aerobic running conducted at 30°C.

You can still drink your protein shake just add the water on top!

Are You Protein Wheysting?

Blends over Isolates!

Protein requ. of athletes

High EAA protein for fat loss

Fast vs. slow protein

5x More Than FDA Allows

"689 m?" - if that's what you're thinking right now, just forget this hilarious detail and think of it as mineral water - I seriously doubt that the exact depth is relevant by any means. What really counts, is the mineral composition of the mineral and regular waters the subjects consumed after running on a motorized treadmill at 40% of their VO2max at a room temperature  of 30°C until a 3% decline in body mass was observed. The total amount of water the subjects had to consume was standardized and amounted to 1.5 times their body mass loss.

Table 1: Concentrations of the minerals and trace elements in drinks used inthe study (Stasiule. 2014)

The water supplements were evenly divided into five equal parts and were ingested at 30 min intervals. To compare their effects, measures of physical performance (aerobic power and lower-body muscle power) and blood CK activity were assessed at 4, 24, and 48 h during the recovery period. To control for possible confounding effects of individual variation, a randomized, double-blind crossover design was used with trials spaced 7 days apart.

Figure 1: VO2max and VO2Max Pulse changes (%) during the post-exercise period (Stasiule. 2014).

If you take a look at the outcome of these trials (Figure 1), its hard to deny that the effects are significant, but irrelevant for the German national soccer team. The next match, the semi finals, is on Tuesday, next week and that's way beyond those 48h where the advantage of mineral over regular water vanishes. The same is true for the accelerated recovery of muscle strength (not shown in Figure 1), which would be particularly useful in dead-ball situations ;-)

You can also use whey while rehydrating: A recent study in the peer-reviewed scientific journal Amino Acids shows that the provision of extra protein "neither enhances nor inhibits post-exercise rehy- dration, when a volume equivalent to 150 % of sweat losses is ingested in 1 h" (James. 2014). In other words: You don't have to drink only mineral water, you can add some whey protein on top of it - and if you're supersmart, you use mineral water to prepare that shake.

Bottom line: Ok, deep mineral water works but why is that the case? Honestly, I don't have a definite answer. One possible explanation the authors have to offer is "that stroke volume recovered better in the DMW trial and that this led to a faster and better recovery of VO2max." As they point out, the expansion of the plasma volume is a well-recognized early response to endurance training and is observed even as an acute response to a single bout of intense exercise. The onset of the phenomenon is extremely rapid and the consequent hypervolemia can improve performance by inducing better muscle perfusion and by increasing stroke volume and maximal cardiac output.

In view of the beneficial effects of the sulfur amino acid taurine, the sulfur and, via a totally different mechanism, the total electrolyte and trace mineral content could and certainly do figure as well. In fact, the latter, i.e. the high comparatively high amount of electrolytes may eventually facilitate the aforementioned maintenance / recovery of an optimal plasma volume and the observed improvements in muscle power recovery which depend on optimal electrolyte levels as well.

Reference:

• James, Lewis J., et al. "Effect of whey protein isolate on rehydration after exercise." Amino acids 46.5 (2014): 1217-1224. 
• Stasiule, Loreta, et al. "Deep mineral water accelerates recovery after dehydrating aerobic exercise: a randomized, double-blind, placebo-controlled crossover study." Journal of the International Society of Sports Nutrition 11.1 (2014): 34.

Science Round-Up Seconds: A Focus on Intra-/Post Workout Stims, Carbs & Protein and Their Effects on Performance, Hydration, GH, Cortisol, Testosterone & Fatty Acid Oxidation

As mentioned on yesterday's show, small 100kcal packets are as much of a problem as large dinner plates and XXL meals (data based on Coelho do Vale. 2008)

I want to start today's Seconds with a question: How did you like that Carl and I did not rush through the news-lineup as it was the case in previous episodes, but simply took our time to discuss the topics in depth an breadth, yesterday?

Personally, I believe that this is much better than the accumulation of "buzzword" the show had become in the previous weeks due to my "study hunter and gatherer" drive - or, in other words, the mere mass of studies I wanted to pack into the show and Carl's desperate effort to cover them all.

Would you agree? And what other changes / improvements would you like to see in the future? We are open for constructive criticism. You can't improve your game without it.

Let's get to what did not fit into the show, then...

The net result of the spending more time on each and every of the single items, or, to say it in the spirit of yesterday's show, a bit more mindfulness was obviously a much larger amount of Seconds for you to devour today. So, let's not waste any time and get right down to business:

• Is 200mg of caffeine the optimum!?A 2008 study by Beavan et al., which involved 24 professional rugby players who were randomly assigned to receive 0, 200, 400 or 800mg of caffeine 1h before performing a standardized resistance training protocol (Beavan. 2008), found that contrary to what bro-science has been suggesting for years, the ingestion of the high amounts of caffeine (800mg) lead to a profound drop in the testosterone-to-cortisol ratio, while the lower doses of 200mg and 400mg of caffeine only blunted the performance hampering decline of cortisol half-way into the workout, while increasing the testosterone levels by 15%
  Caffeine or pseudoephedrine for performance enhancement? As far as improving you game is concerned, a recent study from the School of Sports Science at the department of Exercise and Health of the University of Western Australia was able to show that you are only wasting your time an money, if you are trying to up your cycling-time trial and thus probably every other HIT performance by ingesting the purported CNS stimulant pseudoephedrine (not to be confused with the "real deal"; cf Spence. 2013).
  
  Contrary to the comparatively low amount of 200mg caffeine, which allowed the 10 well-trained cyclists and triathletes who participated in the study improve their TT times in trial 2 of 3, all of which were performed on th same day, by statistically significant 57s, the ingestion of the WADA banned substance pseudoephedrine at a dosage of 180g would have cost them their license for nothing.

  ---

  Bottom line: Spare yourselves pseudoephedrine and other nasal/sinus decongestant belonging to the the class of phenethylamines and amphetamines (e.g. geranium). Even if others worked (for 1,3-dimethylamine this has never been proven in isolation), the long(er)-term detrimental effects they'll have on your central nervous system really isn't worth it.

• Protein-enhanced Gatorade ain't worth your money -- If you are no ultra-endurance runner or at least marathon runner, you don't need, because you don't benefit intra-workout carbohydrate + electrolyte + protein (CEP) drinks for hydration.
  
  The results of a recent study from the Chinese University of Hong Kong show: A CEP solution containing 42g/L carbohydrate, 21g/L whey protein and 15.3 mmol/L sodium and 2.3 mmol/L potassium does not show "extra benefits for the maintenance of hydration status during 60 min cycling" (Sun. 2013)

• Carbohydrate + protein drinks maximizes GH response to exercise -- Now that you know that it's not worth to guzzle on carbohydrate + electrolyte + protein drinks during a workout for hydration purposes, I guess I should tell you that doing the same (w/out the electrolytes, though), may still provide an athletic / anabolic edge. After all, another recently published study that was conducted at the School of Sport at the Department of Exercise and Health Sciences of the Loughborough University in Leicestershire, U.K (Betts.  2013) shows that the ingestion of a carbohydrate + protein mixture (CHO+PRO: 0.8 g sucrose per kg bod weight per hour + 0.3 g/kg/h whey protein isolate) in the 4h recovery period between two exhaustive treadmill runs at the same intensity augmented the growth hormone response by 60%(!) compared to the ingestion carbohydrate only (0.8 or 1.1g of sucrose /kg per hour).
  

  

  Figure 1: Growth hormone (GH) and cortisol response to 2nd bout of exhaustive treadmill running with either 0.8 or 1.1g of sucrose /kg per hour (CHO, CHO-CHO) or  0.8 g/kg/h sucrose per kg bod weight per hour + 0.3 g/kg/h whey protein isolate (CHO+PRO; cf.

  As the data in figure 1 goes to show you this increase in GH was accompanied by a 23% reduction in cortisol. With both, GH and cortisol being released in response to the depletion of muscle glycogen and impeding low blood glucose levels (Galbo. 1977), you could thus argue that protein (probably by its glucagon promting effects; cf. Claessens. 2008) programs the "anabolic glucose procurement plan".
  

  ---

  Bottom line: Yet another reason for the often touted, yet tried and proven "Bananas + whey" = WIN! And that's not true wrt to the protein anabolic response after a workout, but also in view of the "anabolic" or I should probably say generally more favorable way of glucose procurement during subsequent workouts.

• 

  No, no and no! The ingestion of carbs before a HIIT workout will only increase, not blunt the fatty acid oxidation in the post-workout period.

  Pre-workout carb ingestion does not blunt, but promote fatty acid oxidation after the workout -- In as much as this result may go against common bro-science that you must never consume any carbs before your workout if you are trying to lose body fat, it is actually in line with what I have been preaching before. The beneficial effects of AMPK come with the depletion of ATP and the rise in ADP (~used ATP), not with the constantly depleted ATP stores of a no-carbohydrate + protein only starvation diet. Or put more simply - a constant over-expression of AMPK negates all the benefits of it's cyclic up and down (cf. "The mTOR/AMPK Seesaw"; read more)
  
  While the scientists from the Department of Nutrition & Metabolism at the Faculty of Health and Medical Sciences of the University of Surrey in Guildford, UK, did not observe statistically significant improvements in fatty oxidation due to the small study size (10 healthy untrained females; age 18–22 yr; BMI 22kg/m²), the pronounced decrease in RQ after 8-10x 60 second cycling bouts at 95 % VO2peak separated by 90 seconds recovery at 50 watts in 9 out of 10 participants (see figure 2) does speak itself: "In women, consuming carbohydrate before exercise may potentially be more beneficial for fat oxidation than consuming carbohydrate post-exercise" (Honnor. 2013).
  

  ---

  Bottom line: The results of the study at hand, which stand in line with previous research by Fuchs et al. who presented their research in the Proceedings of the Nutrition Society one year before, re-emphasis the fallacious over-reliance of high fatty oxidation rates during a workout. The max. 60-90min in which you may burn slightly more fat, are simply negligible compared to the much longer post-workout period, where the ingestion of 59 g CHO before a HIIT workout did not blunt but promote fatty acid oxidation.

---

Believe it or not, but that's it for today! If you are hungry for more, I suggest you either go to the SuppVersity Facebook Wall or listen to Casual Friday later today... actually, I found Gabriel's name, i.e.  "The Alisa Profumo Show", for the Friday edition of Super Human Radio show quite fitting ;-)

References:

• Beaven CM, Hopkins WG, Hansen KT, Wood MR, Cronin JB, Lowe TE. Dose effect of caffeine on testosterone and cortisol responses to resistance exercise. Int J Sport Nutr Exerc Metab. 2008
  Apr;18(2):131-41.
• Betts JA, Stokes KA, Toone RJ, Williams C. Growth Hormone Responses to Consecutive Exercise Bouts with Ingestion of Carbohydrate plus Protein. Int J Sport Nutr Exerc Metab. 2013 April. 
• Claessens M, Saris WH, van Baak MA. Glucagon and insulin responses after ingestion of different amounts of intact and hydrolysed proteins. Br J Nutr. 2008 Jul;100(1):61-9.
• Coelho do Vale R, Pieters R, Zeelenberg. Flying under the Radar: Perverse Package Size Effects on Consumption Self‐Regulation. Journal of Consumer Research. 2008; 35(3):380-39.
• Fuchs, A. & Young, H. Investigation into gender differences in the effects of feeding around exercise on exercise performance, energy expenditure and substrate utilisation. Proceedings of the Nutrition Society. 2011; 70 (OCE6), E380.
• Galbo H, Richter EA, Hilsted J, Holst JJ, Christensen NJ, Henriksson J. Hormonal regulation during prolonged exercise. Ann N Y Acad Sci. 1977;301:72-80. Review.
• Honnor M, Herdsman M, Collins AL.The effect of food timing on fat oxidation during exercise and resting recovery. Proceedings of the Nutrition Society. 2012; 71 (OCE3), E236 
• Spence A, Sim M, Landers G, Peeling P. A Comparison of Caffeine versus Pseudoephedrine on Cycling Time-Trial Performance. Int J Sport Nutr Exerc Metab. 2013 Apr 9. 
• Sun, F; Li, L; O’Reilly, J; Wong, SH. Effect of carbohydrate-electrolyte-protein solution on hydration. International Journal of Sport Nutrition and Exercise Metabolism. 2013; 23: S1-S15