Intra-Workout Supplementation: Increased Carbohydrate Oxidation with L-Arginine, Lower Fat Oxidation with Glucose & Lowest Rate of Perceived Exertion with Plain Water

Image 1: This bird certainly knows about the importance of adequate hydration ;-)

Have you been at the gym today? If so, what kind of beverage have you been sipping in the rest-periods between your sets, your sprints or during your regenerative (not fat burning ;-) "classic" cardio exercise? Was it Funky XYZ the latest and greatest intra-workout product on the market? If so, you better check out its ingredients, who knows maybe the "latest and greatest" turns out to be quite counterproductive towards the goals you have been setting after reading one of the last two installments of the Intermittent Thoughts? Let's assume you are the "Peter Griffin"-type of chubby - in that case, I hope that your Funky XYZ did not contain glucose, maltodextrin, waxy maize, or any other of the sugars of which the supp companies are going to tell you that they "superior" to the white poison your granny uses in her delicious muffins. Why? Well, according to a soon to be published study by scientists from the Massey University in Wellington, New Zealand, as little as 12g of glucose will reduce the amount of endogenous fatty acid (i.e. the stuff your body is using to hide your abs ;-) oxidation by -22%! Sounds terrible, doesn't it? Well, let's look at some details to decide whether those -22% will really make a difference and what effects the presence of l-arginine and l-glutamine in your intra-workout supplement could have had.

150 min @ 177 Watt + Glucose + (Glutamine or L-Arginine) = ???

Figure 1: Composition of the intra-workout supplement; sodium citrate base + 12g glucose (glucose) and additional 1g l-glutamine (Glu + L-Glutamine) or 0.1g l-arginine (Glu + L-arginine)

It stands out of question that adequate hydration is of utmost importance, when it comes to maximizing athletic performance (incidentally, the same is true, when it comes to "burning fat"). What athletes should drink before (pre-hydration), during (hydration) and after your workouts (re-hydration) is thusly one of the classic topics of exercise science and the recent study by D.S. Rowlands et al. is thusly probably #1001 on the never-ending list of investigations into the optimal mineral and nutrient composition of intra-workout drinks. For us, it is of interest, because it is one of the few which investigated the differential effect of the amino acids l-arginine and l-glutamine on substrate utilization, plasma glucose, lactate and sodium levels and rates of perceived exhaustion in eight male cyclists and triathletes during 150min (!) of cycling at 50% of the individually predetermined peak power (this is noteworthy, because 50% of their peak power equalled 177 W, which is not exactly "light" exercise), in the course of which the athletes consume 150ml of a fluid containing a 0.95g sodium base and either 12g of glucose alone or a combination of glucose and either 1g of l-glutamine or 0.1g of l-arginine (cf. figure 1).

Figure 2: Oxygen consumption (L/min) and substrate utilization (g/min) in 8 trained cyclists / triathletes during 150 min of cycling at 177W with 150ml of four different intra-workout drinks (data adapted from Rowlands. 2011)

As a seasoned student of the SuppVersity, it should not surprise you that the exogenous (i.e. from the outside) supply of glucose produced a -22% shift in substrate oxidation from fatty acids to the now more readily available carbohydrates (cf. figure 2). What you have probably not expected, though, is that the addition of the minuscule amount of l-arginine (which is btw. about what you will get with many of the proprietary blends in the still incredibly popular "NO-boosters") would promote this shift by increasing the total amount of oxidized carbohydrates by another ~10% over the 12g glucose solution alone.

Figure 3: Comparison of total / relative substrate utilization for the 12g glucose + 0.1g arginine, the 12g glucose and the water + sodium citrate groups (data adapted from Rowlands. 2011)

Now you are stunned, hah? So after all it is yet not your fault that you cannot see your abs. It's your NO-suppement! Well, not exactly. I mean take a look at the way I arranged the data in figure 3. You will probably acknowledge that the 12g glucose + 0.1g l-arginine group "burned" more energy - if you want it in calories (remember this is stupid ;-) 0.68kcal/min or 102kcal during the whole session and then come back to the -22% reduced fatty acid oxidation and lament: "But Dr. Andro, they burned 22% less fat than the water-only group! Now I know why I don't get lean." If that is your train of thought, I would invite you to continue the idiotic kcal number crunching and calculate on how much fat the poor l-arginine group would have missed to burn... well, it's the "exorbitant" amount of 170mg/min or - for the whole session 25.5g! While this may be more than one tablespoon of coconut oil, I guess you will probably admit that this probably is not the reason your abs are still covered by a thick layer of flabby adipose tissue, won't you?

Arginine reduces oxygen cost at the expense of glucose

Now, the real interesting findings of the studies are thusly not the changes in substrate utilization but rather the profound impact the addition of the two amino acids had on the lactate levels during the 150min of cycling (cf. figure 4) and the rates of perceived exertion (RPE).

Figure 4: Plasma lactate levels (mmol/L) in 8 trained cyclists / triathletes during 150 min of cycling at 177W with 150ml of four different intra-workout drinks (data adapted from Rowlands. 2011)

The latter (RPE), and this is actually quite surprising, were minimal in the water + sodium citrate group and maximal in the 12g glucose + 1g l-glutamine group (0.8 pts greater on a 0-7 scale). The RPE values of the arginine group, on the other hand, were only marginally elevated and that despite the significant increase in glucose clearance, which, by the way, has also been observed by McConell et al. (McConell. 2006) and Linden et al. (Linden. 2010). 

In view of recent studies such as Greer et al. (Greer. 2011), who observed a small, but statistically significant decreases in endurance during a strength training circuit in response to Arginine-Alpha-Keto-Glutarate (AAKG) supplementation, it is yet very unlikely that the observed effects of an arginine-enriched glucose containing intra-workout supplement observed in this study "have the potential to benefit endurance exercise performance" (which is what the scientists, much to my surprise, conclude). Another thing is yet more than likely, I would even say it is 100% certain: Neither the results of this nor of any future study will change the sales ranks on Bodybuilding.com & Co., where the purported NO-Boosters (and factual stimulants) still are the front-runners of the "TOP 10 selling products" ;-)

Low Sodium Intake for Athletes? Good for Your Health, or Ergolytic Bogus & Hazardous Bullshit? 30g/Day Sodium Loss in "Hard Sweating" Athletes Speak for Themselves

Salt reduction is for "hard-sweating" athletes not.

Whenever I am browsing the latest studies, I see at least one of those hilarious "salt kills" papers citing official recommendations to reduce sodium intake, in order to lower your risk for hypertension, diabetes, stroke and what not. So, if everyone recommends it and scientists write about, it must be true, right? Well, I guess after reading today's SuppVersity article, you may question the way the average Westerner thinks: What the government suggests you should do is not always good for you.

You, a decently lean & insulin sensitive individual who works out at least thrice a week, and someone who takes the stairs instead of the elevator at least every other day, may in fact put himself / herself at risk of hampering your workout performance and eventually even your health if you reduce your salt intake too much.

Normal salt and sodium bicarbonate are not bad for athletes:

The Hazards of Acidosis

Build Bigger Legs W/ Bicarbonate

HIIT it Hard W/ NaCHO3

BA + Bicarb are Synergists

Bicarb Buffers Creatine

Creatine + Baking Soda = 2x Win!

And even if you weren't lean and athletic, it's questionable, whether you'd benefit. The latest Cochraine Review of the effects of reductions in dietary salt intake on the prevention of cardiovascular disease, for example says:

"Despite collating more event data than previous systematic reviews of RCTs (665 deaths in some 6,250 participants) there is still insufficient power to exclude clinically important effects of reduced dietary salt on mortality or CVD morbidity. Our estimates of benefits from dietary salt restriction are consistent with the predicted small effects on clinical events attributable to the small BP reduction achieved." (Taylor. 2011)

And there is more, as I've previously reported the low chloride intake that comes hand in hand with a reduction in dietary salt intake has been associated with +21% increased mortality risk.

Figure 1: Associations of serum chloride, natrium, potassium and HCO2 with systolic and diastolic blood pressure as well as risk of all-cause, cardiovascular disease, ischemic heart disease, stroke and non-CVD mortality risk (McCallum. 2013)

Scientists from the Incorporated Administrative Agency of Health and Nutrition a Japanese government institution that claims to have made "numerous contributions to improve nutrition and dietary habit and to advance the knowledge of health and nutrition science for the public," (Institute Website), say: "Low dietary Na may [...] be a risk factor for maintaining positive balances of Ca and Mg" (Nishimuta. 2005).

Figure 2: If exercising individuals follow the WHO recommendation for salt intakes, they will put themselves at risk of having negative magnesium and calcium balances (based on data from Nishimuta. 2005)

Nishimuta et al. base their assessment on analyses of the content of calcium (Ca) and magnesium (Mg) in sweat during exercise, which is considerably higher during a relatively low intake of sodium (Na) of 100 mmol/d than with an intake of 170 mmol/d. As the scientists point out in their 2005 paper, this is the reason that their subjects developed a negative calcium and magnesium balance, when their sodium intakes were below 61mg and 63mg per day, respectively.

Salt Reduction Kills! New Studies Suggest Cutting Back Below 3-5g Could Do More Harm Than Good! Scientists Say: Minimum Intake is Physiologically Set (King. 2014) -- Too much sodium remains a valid concern, but are current targets too low for optimal health?

Healthy salt intake physiologically determined - don't restrict, if you crave.

New research moves beyond sodium’s effect on the surrogate marker of blood pressure to examine the relation between sodium intake and cardiovascular morbidity and mortality. Results show that sodium intakes both less than and greater than ~3000–5000 mg/d increase the risk of negative health outcomes. Additionally, newly compiled sodium intake data across populations show a uniformity that suggests that intake is physiologically set. Perhaps not coincidentally, the observed intakes fall within the range related to lowest risk.

These findings are highly relevant to current efforts to achieve low sodium intakes across populations, because the data suggest that the efforts will be unsuccessful for healthy people and may cause harm to vulnerable populations. Remaining mindful of risks associated with both excessive and inadequate intakes is imperative with all nutrients, and sodium is no exception. Avoiding too much, and too little, sodium may be the best advice for Americans.

At first it may sound strange that a reduced salt intake would increase the calcium and magnesium loss during exercise, but when you look at it from a biochemical point of view you will realize that in the absence of sodium, other cations (like magnesium or calcium) will have to bind to the lactic acid molecule to form lactate and postpone the development of subchronic metabolic acidosis (Robergs. 2004).

Cramps could be a sign of severe sodium deficiency

The role of sodium during exercise takes us to another thing you should consider before you start restricting your sodium intake. If there is any mineral that is associated with exercise related cramping, it's not, as many people believe, magnesium or potassium, it's sodium! In his 2007 paper in Sports Medicine, Eichner points out that (Eichner. 2007)...

• heat cramping in industrial workers is alleviated by saline, and in a self-experiment, salt depletion provoked muscle cramping
• in tennis and football alike, heat-crampers tend to be salty sweaters
• triathletes who cramp may lose more salt during the race than peers who do not cramp
• practical experience with therapy and prevention indicates that untravenous saline can reverse heat cramping, and
• lastly, more salt in the diet and in sports drinks can help prevent heat cramping

All this evidence clearly indicates that the most prevalent reason for cramping is a lack / loss of sodium, not magnesium of which you've just learned that it's excreted in your sweet in significant amounts only if you don't consume enough salt.

Salt is essential and covering your needs will reduce, not increase water retention: Salt is 40% sodium and 60% chloride and both are important for athletes. Sodium is the major cation of the extracellular fluidandone of its primary functions is to maintain fluid equilibrium in the body. Sodium is a criticalnutrient in the maintenance of normal physiologic function and optimal exercise performance (Valentine. 2007). Although the typical American diet often contains more sodium than is needed, this may not be true for the athlete. Significant sodium and water losses can occur during exercise, exceeding the dietary intake and adversely affecting the fluid balance.

Very low sodium can impair glucose uptake (learn more)

In that, sodium is particularly important because sodium is needed in the rehydration process. The ingestion of plain water causes a rapid fallin plasma sodium concentration and osmolarity, leading to decreased aldosterone and vasopressin production; this increases urine output.... in the short run. Chronic low salt and high water intakes will yet have the opposite effects. As previously discussed, studies by Luther et al. (2011) even suggest that reducing sodium too much will not just increase water retention, the consequent increase in aldosterone may even impair your glucose sensitivity (see Figure on the left).

Acute high sodium intakes, on the other hand, have no effect on the water retention in healthy individuals, where an increase in serum renin (increases sodium excretion) and urinary aldosterone excretion (lowers water retention) nullified the effects of high salt intakes on body water - without the need to increase the potassium intake, by the way (Kirkendall. 1976).

In 2005 Stofan et al. published a paper that investigated the correlation between sodium loss during exercise and the occurrence of heat cramps in NCAA football players. What they found was that sweat potassium was similar between groups, but the sodium loss in the sweat of those NCAA players who had cramps was two times higher than it was in the controls (54.6 ± 16.2 vs. 25.3 ± 10.0 mmol/L). As Stofan et al. point out, "[l]arge acute sodium and fluid losses (in sweat) may thus be a characteristic of football players with a history of heat cramping." (Stofan. 2005)

Figure 3: Football players may be the best studies, but they are certainly not the only athletes who lose tons of salt during an intense training session (data in the figure based on (Fowkes Godek. 2010)

Only recently, E. Randy Eichner, who has long been arguing that "salt is simplest, most effective antidote" against heat cramps in athletes (Eichner. 1999), highlighted in an article in Current Sports Medicine Reports that the current momentum of those who argue that we all need to drastically reduce our sodium intake could hurt those who would do better if they even increased their intakes: Athletes (Eichner. 2014).

I am not giving a one size fits it all recipe, but what I can do is to cite the following considerations from Valentine (2007): "An athlete exercising 4 hours a day who has a sweat rate of 3.0L/h with a sweat sodium concentration of 80mmol/L will lose 12 L of fluid and 960 mmol of sodium in 1 day. This equates to over 22 g of sodium or over 55 g of salt." I guess that's impressive enough to make you reconsider any efforts to reduce sodium - specifically in view of the fact that chronic low sodium can cause, not prevent water retentions in athletes due to its effects on aldosterone. And as I have pointed out previously, this will even worsen whole body glucose uptake.

Bottom line: I am not sure if you consider the previously presented evidence convincing, but if you want to give salt a try, I'd suggest you simply follow your appetite. Studies like the one Wald & Lesham conducted in 2003 clearly suggest that your appetite for salty foods after a workout will increase, if your salt stores are depleted (Wald. 2003). In view of the fact that Walt & Lesham found that this increase is astonishingly proportional to the amount of salt their subjects lost during a 90 minute workout, the average gymrat (not the ultramarthoner, though) will just have to follow his appetite for salt to make sure that a lack of sodium won't impair his performance and / or overall health.

Against that background and in view of the large inter-individual differences (Bergeron. 2003), the differences between different types of sports, exercise intensities and, of course, the environmental conditions, I am not stupid enough to try and make a general recommendation other than the aforementioned advise to simply follow your bodies lead - trust it, it knows it, when he needs salt | Comment on Facebook!

References:

• Bergeron, M. F. "Heat cramps: fluid and electrolyte challenges during tennis in the heat." Journal of science and medicine in sport 6.1 (2003): 19-27.
• Eichner, E. R. "Heat cramps: salt is simplest, most effective antidote." Sports Med Digest 21.8 (1999): 88. 
• Eichner, E. Randy. "The role of sodium in ‘heat cramping’." Sports Medicine 37.4-5 (2007): 368-370.
• Eichner, E. Randy. "The Salt Paradox for Athletes." Current sports medicine reports 13.4 (2014): 197-198.
• Fowkes Godek, Sandra, et al. "Sweat rates, sweat sodium concentrations, and sodium losses in 3 groups of professional football players." Journal of athletic training 45.4 (2010): 364. 
• King, Janet C., and Kristin J. Reimers. "Beyond Blood Pressure: New Paradigms in Sodium Intake Reduction and Health Outcomes." Advances in Nutrition: An International Review Journal 5.5 (2014): 550-552.
• Kirkendall, Walter M., et al. "The effect of dietary sodium chloride on blood pressure, body fluids, electrolytes, renal function, and serum lipids of normotensive man." J Lab Clin Med 87.3 (1976): 411-434.
• Luther JM, Brown NJ. The renin-angiotensin-aldosterone system and glucose homeostasis. Trends Pharmacol Sci. 2011 Dec;32(12):734-9.
• McCallum L, Jeemon P, Hastie CE, Patel RK, Williamson C, Redzuan AM, Dawson J, Sloan W, Muir S, Morrison D, McInnes GT, Freel EM, Walters M, Dominiczak AF, Sattar N, Padmanabhan S. Serum Chloride Is an Independent Predictor of Mortality in Hypertensive Patients. Hypertension. 2013 Aug 26.
• Nishimuta, Mamoru, et al. "Positive correlation between dietary intake of sodium and balances of calcium and magnesium in young Japanese adults--low sodium intake is a risk factor for loss of calcium and magnesium--." Journal of nutritional science and vitaminology 51.4 (2005): 265-270.
• Palacios, C., et al. "Sweat mineral loss from whole body, patch and arm bag in white and black girls." Nutrition Research 23.3 (2003): 401-411.
• Stofan, John R., et al. "Sweat and sodium losses in NCAA football players: a precursor to heat cramps?." International journal of sport nutrition and exercise metabolism 15.6 (2005): 641.
• Taylor, Rod S., et al. "Reduced dietary salt for the prevention of cardiovascular disease: a meta-analysis of randomized controlled trials (Cochrane review)." American journal of hypertension 24.8 (2011): 843-853. 
• Valentine, Verle. "The importance of salt in the athlete’s diet." Current sports medicine reports 6.4 (2007): 237-240.
• Wald, N., and M. Leshem. "Salt conditions a flavor preference or aversion after exercise depending on NaCl dose and sweat loss." Appetite 40.3 (2003): 277-284.

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.

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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.

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.

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  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.

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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

Hydrated or Dumb: Dehydration Affects Brain, Muscle and Other Vital Organs - Plus: 15+ Causes of Dehydration + Can the Color of Your Urine Tell You if You Drink Enough?

If you want to stay smart, you should join hands w/ water!

Those of you who are following the 10+ SuppVersity Facebook news on a daily basis, will remember my post about the recent paper - co-authored by Brad Schoenfeld (Ribeiro. 2014) - about the significant "water gain" after workouts. I wrote about that myself, a couple of weeks before in "Cell Swelling Keeps Muscles "Pumped" For More Than 52h. Size Increases of Up to 16% After a Single Leg Workout!" | read more, and mentioned that the intra-muscular swelling is probably a necessary prerequisite, if not driver of skeletal muscle growth.

In today's SuppVersity article, I will now take a step back, away from the musclehead's only interest and peek at other health aspects that are influenced by the hydration status not just of your muscles, but of your whole body.

Hydration Tip of the Century: Many of you will accidentally (or because they read it here, at the SuppVersity, before) already follow this advice, but I still would like to emphasize that the dairy protein you're probably consuming after your workout is not only going to boost your muscle, but also your "water" (=positive hydration) gains. In 2010 James et al. were able to show just that: A post-workout beverage with 40 g/l carbohydrate + 25 g/l milk protein are more effective at augmenting fluid retention than 65g of pure carbs carbohydrate (James, 2010).

In one of the most recent papers on this issue, Natalie A. Masento and her colleagues from the University of Reading reviewed the surprisingly profound effect of dehydration on cognition and mood, of which Masento et al. write that it is "particularly relevant for those with poor fluid regulation, such as the elderly and children" (Masento. 2014).

"With evidence to suggest that individuals are routinely at a risk of mild dehydration day to day (Greenleaf. 1965), particularly vulnerable populations such as children and older adults, there has been an increased interest in studying whether additional water consumption might benefit cognitive performance. The small collection of published water intervention studies involving either young adults or school children report consistent positive effects of water intervention on particular cognitive abilities" (Masento. 2014)

If you take a look at the overview, the researchers compiled (it's too long and eventually repetitive to post it here), you will find studies everything from self-reported fatigue, tiredness and headaches to objectively measured declines in cognitive performance, eye-hand coordination, word recognition, visual attention and - as mentioned in the previously cited article physical performance markers, such as grip strength.

How come? I mean, why does dehydration have such a profound impact?

The above, probably is the question that's preying on your mind right now and I have to admit, I have - just like the researchers from the University of Reading - no conclusive, water-tight *pun intended* answer to that question.

"Despite the expansion of this research area, we still do not have a clear understanding as to how acute water intervention may influence mental performance and its associated neural activity. Researchers have suggested psychological mechanisms related to limited attentional resources during thirst. However, evidence has also highlighted the  importance of physiological mechanisms, with findings that the expectancy of water alone does not influence cognitive performance." (Masento. 2014)

Hitherto proposed mechanisms include references to the Global Workspace Model (Baars. 1993) and being distracted by the often subconscious thought "Where do I find water".

Gray matter activation clusters in dehydration (Streibürger. 2012).

Of potentially greater interest (at least to me) are theories that involve physiological mechanisms, such as the already confirmed...

• shrinkage of total brain volume shrinkage (Streitbürger. 2012; Kempton. 2011) and 
• over-recruitment of specific brain areas during cognitively demanding tasks,

as well as other significant changes at the neural level which contribute to the previously mentioned decline in cognitive performance and awareness (Kempton. 2011).

Luckily, these changes can be reversed by the provision of water in minutes, as long as the subjects are only mildly dehydrated. In view of the

"lack of data related to baseline hydration states of individuals and no further published work using imaging techniques to examine hydration state" (Masento. 2014) 

We do yet once more have to acknowledge that "we know that we know nothing" or, put differently, that these proposed mechanisms are merely speculative.

Potential causes of dehydration: It's not just working out in the heat or simply forgetting to drink (very common in the elderly), there is a multitude of other things that promote dehydration and here are a couple of examples: ✋Low sodium + chloride (can't store water), ✋high calcium, magnesium, zinc, chromium intake, ✋ extreme high sodium or potassium intake, ✋low phosphor intake; ✋high vitamin D, pantothenic acid (B5), pyridoxine (B6) intake; ✋low adrenal output; ✋high protein intakes (esp. when protein is abused as energy source); ✋laxatives, diuretics or other meds or supps -- One thing, however, does not cause dehydration: ☕ Coffee!

Another physiological mechanism that has been suggested is the albeit age-dependent reaction of the central nervous system in response to the ingestion of significant (500ml) amounts of water, of wich May & Jordan found that it causes

• a significant drop in heart rate and an increase in vasodilation in young adults (May. 2011), and the opposite effects, i.e.
• a significant increase in blood pressure in the healthy old subjects in a 2002 study by Schroeder et al. (Schroeder. 2002)

- whether this difference may be brought about by different baseline hydration status, is not clear. What is obvious, though, is that the cardiovascular reactivity promotes cerebral blood flow, which, in turn, will encourage the circulation of substances such as oxygen and glucose that are known to stimulate neural activity and associated behavioural performance (Gold. .1995) in healthy, non-diabetic individuals.

If you think about this hypothesis, i.e. the beneficial effects of water-induced increases, and the detrimental effects of reductions in glucose and oxygen availability in the brain and other organs that would occur, even upon mild dehydration, it seems perfectly logical, a mechanism similar to that has after all been proposed to account for the improved cognitive function due to physical exercise (Kashihara. 2009).

The urine color chart is a valuable tool to judge your hydration status (Wakefield. 2002)

"So how much water to I need?" -- I know. I am mean... the question that's been preying on your mind ever since the introduction. I still did not answer it - right?

Well, you can find the answer in your toilet bowel (see color chart on the right for a guide). You just have to check the color of your urine to know if you're drinking enough... well, at least if you didn't have beets, which will turn it red-brown or red, blackberries, which will give it a red tinge, carrots, which will produce a rusty yellow, paprika, which will make it look orange, rhubarb, which turns it re-brown, then orange, sometimes even yellow-pink, rusty or yellow-brown... and of course the nasty neon-green that's caused by the tons of useless riboflavin (aka vitamin B2) in your urine.

References:

• Baars, Bernard J. "How does a serial, integrated and very limited stream of consciousness emerge from a nervous system that is mostly unconscious, distributed, parallel and of." Experimental and theoretical studies of consciousness 174 (1993): 282.
• Greenleaf, John E., and Frederick Sargent. "Voluntary dehydration in man." Journal of Applied Physiology 20.4 (1965): 719-724.
• Kempton, Matthew J., et al. "Dehydration affects brain structure and function in healthy adolescents." Human brain mapping 32.1 (2011): 71-79. 
• Masento et al. "Effects of hydration status on cognitive performance and mood". British Journal of Nutrition (2014) [ahead of print].
• Ribeiro, Alex S., et al. "Resistance training promotes increase in intracellular hydration in men and women." European Journal of Sport Science ahead-of-print (2014): 1-8.
• Schroeder, Christoph, et al. "Water drinking acutely improves orthostatic tolerance in healthy subjects." Circulation 106.22 (2002): 2806-2811.
• Streitbürger, Daniel-Paolo, et al. "Investigating structural brain changes of dehydration using voxel-based morphometry." PloS one 7.8 (2012): e44195.
• Wakefield, Bonnie, et al. "Monitoring hydration status in elderly veterans." Western Journal of Nursing Research 24.2 (2002): 132-142.