DMAA / OxyElitePro - The Good, the Bad and the Downright Ugly - More Powerful (+180% Perf.) Than You'd Think, but ...

Back in the day, when the original Oxy-ELITE Pro was pulled from the market, people paid crazy amounts of money for the bottles that were left on Ebay - a big mistake! Not because it would fry your liver, but rather because it's 'stim' effects will - just as those of other DMAA products - turn against you, w/ chronic use. 

You may (rightly) be asking yourselves, why I am addressing an (albeit famous) supplement that is no longer on the market in 2016 blog post. Well, the answer is simple. I still see people whining about how "awesome" this product was all over the web. People who wish that DMAA and OxyElitePro would come back and people who would be willing to spend at least 5x the original price for the few (long expired) bottles that appear to be traded on the black market.

It's those people I want to advice: Even if you ascribe the liver damage as the result of stupid overdosing and acknowledge that other products appear to be far worse (García-Cortés. 2016 | FFT), don't waste your money on DMAA products, in general, and the original OxyElitePro (OEP), in particular. And here's why...

Unlike the average fat burner, OxyELITE was indeed more than just caffeine:

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Caffeine Resis- tance - Does It Even Exist?

The "why"s are based on a recent study from the Department of Physiological Sciences at the University of Espírito Santo (Zovico. 2016) in Brazil. The study was originally conducted to "to evaluate acute and chronic OEP affects, at controlled doses in Wistar rats, on physical performance, metabolic parameters, liver injury markers and oxidative stress markers and mitochondrial biogenesis in skeletal muscle. A study of which you'd guess that it would long have been done in view of the fact that serious adverse effects have been reported after OEP consumption, all over the web.

Figure 1: Photo of the original OxyELITE Pro bottle and supplement facts label (Google Image Search).

In said study, the rats were divided in control, 4.3 mg OEP/kg (1/2 cap in human equivalents, HED), 12.9 mg OEP/kg (~1 cap HED) and 25.8 mg OEP/kg (1.5-2 caps, HED). All groups were submitted to supplementation with OEP for 4 weeks and the experimental protocols were performed 30 min after the first OEP administration (acute response) and 30 min after the last OEP administration at the end of the fourth week (chronic response).

• The Good: OEP simply works -- If you are one of the previously referred to users of the product, you will probably remember your first training "on OEP". How would you describe it? Probably similar to the rodents in Zovico's study, who easily ran 2.6x and 2.8-fold further with the medium, respectively, the high dose of OPE in their blood.

  

  Figure 2: Effects of acute OEP supplementation at different dosages on running distance and time to exhaustion (Zovico. 2016) - based on data that is written out twice in the full-text of the study at hand, but has not been correctly plotted in the figure(s) from the original publication.

  Now, "awesome" would, in fact, be an appropriate word to describe the effects I've plotted for you in Figure 2 (note: the original figure in the study is messed up). In view of the fact that ...

  "[n]o effect was found in other analyses such as spontaneous physical activity, body weight, food and water intake, hepatic toxicity, cardiac oxidative stress and mitochondrial NA amount" (Zovico. 2016),

  ... you will now probably (and rightly so) ask yourselves: "So, what's 'the Bad', then, if it's not liver or heart damage as they both have been reported allegedly as a consequence of the (ab-)use of both, OxyElitePro and DMAA based products, in general?" 
• The Bad: No liver damage, but potentially impaired adaptation to training -- Ok, part of the previously discussed "good news" was that there was no measurable - or, I should say - no sign. changes in AST, ALT and GGT (liver health) and even small beneficial effects on TBARs, i.e. lipid oxidation in the group of rodents that received the medium dose of the supplement (see MDA levels in Figure 3).
  

  

  Figure 3: Oxidative stress measured in MDA per mg or protein (left) and mRNA activity PGC-1A, a primary
  marker of exercise-induced mitochondrial biogenesis (Zovico. 2016).

  On the other hand, the scientists also found a significant, albeit likewise dose-dependent decrease in PGC-1A in the high dose group (the high dose group also saw non-significant decreases in food intake and body weight). With the latter being an important regulator of (exercise-induced) mitochondrial biogenesis, one may speculate that at least part of the exercise-induced adaptational response may be blunted in response to the either DMAA or one of the other supplement ingredients, namely the undisclosed amounts of Bacopa Monnieri, Bauhinia Purpurea, Cirsium Oolygophyllum, or Yohimbe bark extract (cf. Figure 1 | note: we know from previous studies that the 100mg of caffeine can't be the problem).
  
  Since this occurs only with the high dose of the supplement, i.e. 25.8 mg/kg or ~1.5-2 caps for a human being. This effect is bad, but not downright ugly - speaking of which...
• The Ugly: OEP simply stops to work -- If you belong to the group of former OEP users I've previously alluded to and/or have used any other DMAA product more than once or twice, you will probably remember "the Ugly", anyway: After only a few workouts "on OEP" (or any other DMAA) products, the effects began to vanish.
  

  

  Figure 3: Relative endurance performance with acute and chronic (4 wks) supplementation (Zovico. 2016); all data expressed relative to the values of the control group on day 1 (cf. Figure 2).

  And as if that was not bad enough, the stimulant actually began to make you tired - as tired as it made the rodents in the study at hand, whose running performance decreased significantly (by up to 45% in the case of the running distance after high dose consumption) over the course of the 4-week supplementation period compared to the performance of the control group on day one (see Figure 3).
  
  Whether that's related to and/or a consequence of the previously discussed reduction in PGC-alpha expression in the chronically supplemented rodents would have to be investigated in future, studies - it does not seem unlikely, to say the least.

This study raises the question: Can you become caffeine-resistant, too? Learn the answer.

That your liver probably doesn't take a hit doesn't make OEP the hit: I guess that most of you will not even know where to get those expired bottles of OEP I mentioned in the introduction of this article. For those who do and those who contemplate buying one of the many illegal DMAA products you can still order on the Internet, the article at hand should be convincing enough to stay away: I mean, what's the use of a workout booster you can use only once or thrice before it backfires and the formerly ergogenic powder or tablets show their ugly ergolytic (=athletic performance decreasing) face? | Discuss your experience w/ this or other stims?

References:

• García-Cortés, Miren, et al. "Hepatotoxicity by Dietary Supplements: A Tabular Listing and Clinical Characteristics." International journal of molecular sciences 17.4 (2016): 537.
• Zovico, et al. "Effects of controlled doses of Oxyelite Pro on physical performance in rats." Nutrition & Metabolism201613:90 | DOI: 10.1186/s12986-016-0152-4 [ahead of print].

Potassium-Magnesium Aspartate, an Overlooked Endurance Enhancer? Acute 100% Increase in Time to Full Exhaustion

1952, Italian Fausto Coppi is drenched with water by a fan during the golden years of the Tour. Question: Can the topical application of K & Mg do the same magic? Answer: That's very unlikely, ...

What sounds like a supplement producer was trying to sell his product with a sponsored study is, in fact, the gist of a 1968 study from the Departments of Clinical Physiology and Internal Medicine at the venerable Karolinska Institute in Stockholm, Sweden (Ahlborg. 1968).

The authors' conclusion that "[a]fter administration of potassium-magnesium-aspartate [KMgA] the capacity for prolonged exercise increased about 50 per cent" (Ahlborg. 1968) can thus not be discarded as marketing babble. And, before we decide whether it's too good to be true, I'd suggest we take a closer look at the way the data was generated before we either (a) discard it as outdated or (b) get totally excited for nothing.

Mineral water will contain some K and Mg, too - and it will have other benefits:

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Mineral Water Supercharges 'ur Performance?!

Another ten years before Ahlborg et al. published their study, an effect of potassium and magnesium salts of aspartic acid on muscular fatigability has been demonstrated experimentally in animals by several independent research groups. Back in the 1960s, humans studies had yet only subjectively assessed the effects of KMgA on endurance performance in man. Ahlborg et al. were thus right to consider it... "to be of interest to investigate, whether a positive effect on the capacity for prolonged standardized physical exercise after oral administration of potassium-magnesium-aspartate can be objectively demonstrated" (Ahlberg. 1968).

Table 1: Some anthropometric and other data in the test subjects (Ahlborg. 1968).

The scientists recruited 6 out of a group of 300 military recruits who had been examined at the Military Medical Examination Centre at the Karolinska Institute back in the 1960s. All subjects were subjected to the following routine: On 4 consecutive days, which will be called day 1, 2, 3 and 4, prolonged exercise to exhaustion was performed every day beginning at 1 p.m. The subjects were not fasted.

To get the results they wanted and to make sure the subjects' performance was not thwarted, the scientists required all subjects to record all foods they'd been consuming for the 4 days of the test. This practice was meant to avoid interference with of high carbohydrate intakes of which people back in the day still knew and appreciated that they can "increase the capacity for prolonged exercise markedly" (Ahlborg. 1968).

Does this work for strength training as well? While it may help you up your workouts, a study by Consolazio et al. (1964) found  no measurable beneficial effects on muscle strength. This disappointing result was later confirmed by De Haan, et al. (1985). So, I'd venture the guess that - if KMgA is a thing at all - it's an endurance athletes' thing.

To test each subject against itself while still having averages to compare, the authors had all subjects perform the "W170", a bicycle ergometer ride at a pulse rate of 170 beats/min (duration ~90 minutes until physical exhaustion) on days 1, 2, 3 and four. And here's how the supplementation worked:

"Beginning at 6 p.m. on the day before day 1, 5 tablets were administered every sixth hrs. last 5 tablets were given 1 hr before the prolonged exercise test on day 4, see Fig. 1. All subjects were given placebo tablets before the tests on days 1, 2 and 4. Before day 3 active substance was given. The subjects were told that the tests were aimed at elucidating the influence of a vitamin tablet on maximal performance time. No information was given to the test supervisor (the same nurse on all days) or to the subjects as to when placebo or active substance was administered. The placebo and active tablets were identically looking" (Ahlborg. 1968)

This is admittedly not exactly standard procedure, and one could argue that what we are seeing here is a vitamin placebo effect, but the effect (a) appears to be a bit too large (see data in Figure 1) and you could (b) also argue that the previous two 170Ws may have had a negative effect on the subjects' performance during cycling to exhaustion.

Figure 1: Duration of prolonged exercise (y-axis) in the 6 test subjects after administration (x-axis) of placebo (striped area) and after administration of aspartate (black area) and individual data in the table (Ahlborg. 1968).

As you can see in Figure 1 the effect differed from subject to subject but was (a) highly significant in all of the 6 men and (b) doesn't have a residual effect. The latter suggests that the ~100% increase in time to exhaustion is not the result of K or Mg repletion, but an acute response to the KMgA supplement.

Research overview and supplement suggestion: In order to put the results into perspective I've curso-rily searched subsequent studies on aspartate bound minerals with the following results (in random order): [1] Sign. increased ergogenic effects in with 10 g of potassium-magnesium as-partate over a 24 hr in Wesson et al. (1988) in subjects cycling at 70% VO2Max; [2] no benefits in trained indiv. cycling at lower intensities in Hagan, et al. (1982); [3] no benefits were likewise seen, when the supplement was taken in lower amounts chronically, i.e. 5 weeks, only 2g/day (Consolazio. 1964) and / or when the supplement was controlled against equimolar amounts of "regular" (HCL) Mg + K (Maughan. 1983).

Overall, the research, there-fore, appears to suggest that athletes who perform high-intensity endurance exerci-ses could benefit most from the serial administration of a total of 10g/24h of Mg and K - not necessarily bound to aspartate, for which scien-tists have not conclusively proven benefits when it's taken on its own, either (Trudeau. 2008).

So what's triggering these benefits? As you will know I am not happy if I don't understand the cause-and-effect relationships in any field of research that does not belong to quantum sciences. Unfortunately, I have to admit that, in this particular case, where Heisenberg's uncertainty principle obviously doesn't apply, I still cannot explain exactly what the reason for the surprisingly pronounced ergogenic effects is.

What appears to be certain (also based on previous studies) is that the 100% increase is not a normal day-to-day performance variation. As Ahlborg et al. point out, the antifatigue effect in previous research in rodents was often interpreted as the result of an ATP and phosphocreatine sparing effect, i.e. a decreased consumption of ATP and phosphocreatine. The authors of the paper at hand, however, believe that it is "more likely that the resynthesis of the energy-rich phosphates ATP and phosphocreatine might be accelerated by potassium-magnesium-aspartate" - quite obviously, the net result will be the same, an increased available amount of energy-rich phosphates in the muscles. This, in turn, was suspected to be due to a glycogen sparing effect of the Mg and K esp. with a focus on aspartate co-administration ('cause Asp is a major source of gluconeogenesis during exercise). Since the latter has been refuted by Trudeau, et al. in 1993, we are thus stuck with hypothesis #2, i.e. a direct effect on the (accelerated) rate of resynthesis of phosphocreatine.

Well, back in the day Ahlborg et al. wrote that "investigations are in progress to evaluate these theories". Unfortunately, the final answer to the question "how does that work" has yet not been found (see box on the right). Increased heart rate, increased lipolysis and glucose oxidation as they have been observed in Wesson et al. who confirmed the benefits on endurance performance in 1988 are probably rather a consequence than the cause of the performance enhancement you may be able to see in the conditions I outlined in the box to the right | Comment!

References:

• Ahlborg, Björn. Capacity for exercise in man. Forsvarets sjukvardsstyrelse, 1967.
• Ahlborg, Bjorn, et al. "Human muscle glycogen content and capacity for prolonged exercise after different diets." Forsvarsmedicin 3.Suppl 1 (1967): 85ą89.
• Ahlborg, Björn, et al. "Muscle glycogen and muscle electrolytes during prolonged physical exercise1." Acta Physiologica Scandinavica 70.2 (1967): 129-142.
• Ahlborg, Björn, Lars‐Göran Ekelund, and Carl‐Gustaf Nilsson. "Effect of Potassium‐Magnesium‐Aspartate on the Capacity for Prolonged Exercise in Man." Acta Physiologica Scandinavica 74.1‐2 (1968): 238-245.
• Consolazio, C. Frank, et al. "Effects of aspartic acid salts (Mg and K) on physical performance of men." Journal of applied physiology 19.2 (1964): 257-261.
• Ekelund, Lars-Göran. "Circulatory and respiratory adaptation during prolonged exercise." Acta physiologica Scandinavica. Supplementum 292 (1967): 1.
• De Haan, A., J. E. Van Doorn, and H. G. Westra. "Effects of potassium+ magnesium aspartate on muscle metabolism and force development during short intensive static exercise." International journal of sports medicine 6.01 (1985): 44-49.
• Hagan, R. D., et al. "Absence of effect of potassium-magnesium aspartate on physiologic responses to prolonged work in aerobically trained men." International journal of sports medicine 3.03 (1982): 177-181.
• Maughan, R. J., and D. J. M. Sadler. "The effects of oral administration of salts of aspartic acid on the metabolic response to prolonged exhausting exercise in man." International journal of sports medicine 4.02 (1983): 119-123.
• Trudeau, François, and René Murphy. "Effects of potassium-aspartate salt administration on glycogen use in the rat during a swimming stress." Physiology & behavior 54.1 (1993): 7-12.
• Wesson, Matthew, et al. "Effects of oral administration of aspartic acid salts on the endurance capacity of trained athletes." Research Quarterly for Exercise and Sport 59.3 (1988): 234-239.

Cutting Carbs After PM HIIT Workouts Will Make You Cross the Finish Line Before Anyone Else: 3% Faster Time Trial, 9% More Power and Twice as Much Fat Mass Lost in 7 Days

Don't be a fool. Simply eating no carbs in the PM is not going to yield the same results. It's all about timing it correctly with your workouts... workouts? Yes, bad  news: you got to get off the couch, bro; workout daily: one light, one HIIT day.

I've written about the adaptational response to "training low", i.e. doing endurance training on a low carbohydrate diet previously. In January, this year, for example, I have reported the results of a study from the French National Institute of Sport that showed that strategically cutting carbs in the PM and thus "sleeping low" will trigger game-changing Performance gains in only 3 weeks (read the article).

Now, the scientists go one better: In their latest study, Laurie-Anne Marquet and colleagues investigated the effect on an even shorter timescale - a timescale that is short enough to consider "sleeping low" as a possible  pre-competition strategy... well, assuming that it would work its performance-enhancing magic within as little as the 7 days, during which the subjects' in Marquet's study followed the "no carbs after your workout" (="sleep low" | SL) prescription the researchers copied from their own previously discussed study.

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Overall, 21 endurance-trained male cyclists (mind the typo about the # in the abstract of the original study, in case you read it; the summary says 11, not 21, which is the correct number) volunteered to participate in the study. All were healthy, aged between 18 and 40 years, and training at least 12 h/week, having at least 3 years of prior training. Their mean (±SD) age was 31.2 ± 7.1 years, their mean body mass was 71.1 ± 5.6 kg, their mean maximal oxygen consumption (VO2max) was 64.2 ± 6.0 mL/min/kg, and their mean maximal aerobic power (MAP, W) was 342 ± 38.3 W.

To isolate the effects of the dietary / carbohydrate modulating intervention, the subjects who trained
according to their habitual training program, initially (1st week) ate according to their usual dietary habits, documenting their food intake via a daily food diary. These diaries were then compared to the prescribed carbohydrate pattern in the 2nd week, which set their CHO intake at 6 g/kg per day.

Figure 1: Graphical overview of the study design; CHO: carbohydrates; HIT: high‐intensity training session; LIT: light intensity training session; SL: Sleep‐Low; CON: Control; MAP: Maximal aerobic power (Marquet. 2016).

After the dietary standardization and the pre-test at the end of this period, the subjects were randomly assigned to two different groups undertaking the same one-week training program.

The study used pre-bed protein shakes, a strategy to build muscle.

Nightly protein shakes, glycogen depletion and lean muscle mass: In contrast to what some people may expect, the no-carbs before bed strategy did not lead to measurable decreases in lean mass. Whether and to which extent that was a result of the protein shake both groups consumed before bed cannot be answered without doing another study. What I can tell you based on previous research, however, is that this, i.e. having a protein shake "before" (not necessarily right before) bed, is a very promising strategy to maximize net protein retention (see "12-Week Study: 25g Bed-Time Protein Almost Doubles Size & Increases Strength Gains" | more).

The built-in and significant difference between the group can be found in the nutritional guidelines according to which all subjects consumed the same amount of 6g/kg CHO, in total, but periodized their carbohydrate intake differently over the day. Specifically,...

• the control group trained with a high CHO availability (control group, CON group, n = 9) with an even spread of CHO intake over the day and between training sessions,
• the "sleep low" (SL) group (n = 12 | mind the typo in the scientist' abstract) trained with a CHO intake that was periodized within the various days in a way that no CHO was consumed between the high-intensity interval training sessions (HIIT) held

Practically speaking: The subjects in the "sleep low" group were thus doing truly fasted or, rather, glycogen depleted low-intensity cardio in the morning of each of three of the six otherwise identical workout days.

Figure 2: 20km cylcling times and mean power output in pre- and post-test (Marquet. 2016).

Against that background, it is all-the-more surprising that the subjects saw both: significant reductions in their time-trial times (-3.32%) and improvements in their average power production during the workouts (+9.17%). What is not surprising is that the data in Figure 1 indicates that these power improvements occurred specifically in the latter part of the workout, i.e. when the glycogen stores are running out and the training effect from training low in the AM shows.

Table 1: Rating perception of effort (RPE) during the 20 km cycling time-trial every 5 km (Marquet. 2016).

In contrast to what you would expect, the scientists did not detect a significant difference between group and pre and post tests for the substrate oxidation, markers of lipid oxidation and stress markers - or, more specifically there was ...

• no decrease in CHO oxidation in the SL group and 
• no increase in FAT oxidation in the SL group
• no increased cellular damage in form of lipid oxidation, and
• no significant difference in the subjects' stress response (plasma catecholamines),

... in the high-performing "sleep low" aka "SL" group. Now, there's a (small) catch, though, that should be mentioned in spite of the lack of statistical significance: the scientists observed a small increase in the subjects' rate of perceived exertion during the light AM sessions (+13%), as well as the post-intervention time trial (+10%) in the "sleep low" group. Moreover, the last-mentioned increase is more or less identical to the increase in average power production during the post-test on day 7. Accordingly, it is questionable if one should call this already non-significant effect a "catch", at all.

Brad Schoenfeld's 2014 "Fasted Cardio"-study falsifies the myth of superior long-term (4 week) fat loss in non-glycogen-depleted non-athletes on a moderate energy deficit (more). It does not exclude, however, that the glycogen-depleted subjects of the study at hand could see increased fat loss in the short or long term.

"And the subjects got ripped, right?" Not exactly. While the statement from the headline is 100% accurate, the total fat loss was (and this is not surprising in view of the study duration) marginal: statistically significant −395 ± 491 g in the SL and statistically non-significant −151 ± 363 g in the control group.

The reason that it is still worth mentioning is that previous studies suggested that doing AM cardio on empty would not increase fat loss (even over longer periods of time). So, how can we consolidate these conflicting results? Well, while further research appears necessary, I could imagine that both, the advanced training status of the subjects' in the study at hand and the fact that they were actually glycogen-depleted and not, as the subjects' in Schoenfeld's seminal paper (Schoenfeld. 2014), "only fasted", so that, if anything, their liver glycogen may have been lowered | Comment!

References:

• Marquet, Laurie-Anne, et al. "Periodization of Carbohydrate Intake: Short-Term Effect on Performance." Nutrients 8.12 (2016): 755.
• Schoenfeld, Brad, et al. "Body composition changes associated with fasted versus non-fasted aerobic exercise." Journal of the International Society of Sports Nutrition 11.54 (2014). Previously discussed, here!

Not Getting into Ketosis? Try Plain Old Caffeine to Double Your AM Ketone Levels Regardless of High CHO Breakfast

Neither a ketogenic breakfast nor buttered coffee were necessary to double the subjects' ketone production.

Ok, I have to admit that the breakfast that was served in the latest study from the Research Center on Aging, Sherbrooke, CIUSSS de l’Estrie – CHUS and the Department of Pharmacology & Physiology, Université de Sherbrooke in Canada (Vandenberghe. 2016) is not exactly what anyone would recommend to people who are trying to get into full ketosis. This, however, does not make the scientists' observation that the addition of 3mg/kg and 5mg/kg of caffeine in form of cheap caffeine pills from the pharmacy will almost (moderate dose) and more than (high dose) double the subjects' ketone production, does not make the latest study from Camille Vandenberghe's lab less interesting.

You can learn more about coffee and caffeine at the SuppVersity

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But, let's tackle things one by one: With ketogenic diets getting more and more attention in mainstream dietary research, it is not exactly surprising to see a study that uses the potential therapeutic effects of ketones on aging-induced cognitive impairments in Alzheimer’s disease as a point of departure for their investigation of caffeine "as a potential ketogenic agent" (Vandenberghe. 2016) - or I guess whe should say "ketogenic facilitator".

Owing to its actions on  lipolysis/ lipid oxidation, the scientists expected that caffeine co-ingestion with breakfast would be ketogenic in healthy adult subjects. To test this hypothesis, the authors recruited a group of healthy adults (BMI 24kg/m² | previous daily caffeine intake < 300mg/day!) to evaluate their individual and average response to the acute ingestion of...

• 2.5 mg/kg caffeine (equiv. to ca. 1.5-3 cups of coffee w/ ~95 mg/cup)
• 5.0 mg/kg caffeine (equiv. to ca. 3-5 cups of coffee w/ ~95 mg/cup)

alongside the afore-hinted-at standardized breakfast that consisted of  two pieces of toast with raspberry jam, a piece of cheese, applesauce and 100 ml of juice - a breakfast that is, with its 85 grams of carbohydrate, only 9.5 g of fat and 14 g of protein, not exactly "ketogenic".

Figure 1: Ketone production and FFA levels in the control and caffeine 2.5 ad 5.0 mg/kg trials (Vandenberghe. 2016).

As you can see in Figure 1, the bolus of caffeine still elevated both, the concentrations of ketone bodies and free fatty acids in the subjects' blood. And what's even more exciting, the ketone advantage became significantly more (not less) pronounced over time (see Figure 2)

Yes, you remember that correctly: High FFA = lower insulin sensitivity - So eventually, you have to be careful with the caffeine for ketones approach if you consume high amounts of carbohydrates and/or are already having issues with glucose management. If that's not you, I'd like to remind you of the beneficial effects of caffeine on glycogen repletion, I discussed in "Post-Workout Coffee Boosts Glycogen Repletion by Up to 30% and May Even Have Sign. Glucose Partitioning Effects" | more.

This is an observation which would suggest that the breakfast coffee could be even more useful for ketogenic dieters who are intermittently fasting, as it would give them a headstart into full-blown ketosis in the time between breakfast and dinner.

Figure 2: Time course of the ketone response in the study subjects according to treatment (Vandenberghe. 2016).

The observation that caffeine enhances lipolysis and increases blood FFA levels, which in turn provide substrates for ketogenesis ad thus stimulate safe and mild ketonemia in healthy adults to a ketone level twice that seen after an overnight fast, has the authors speculate that regular caffeine consumption may be linked to the decreased risk of developing late-life cognitive decline, as it was observed by Panza, et al. only recently in what is one of the latest reviews on this topic, if not primarily, then at least also because of its effect on ketogenesis.

Eventually, we do yet still need evidence that the "trick" works with a ketogenic diet, as well. After all, the relative increase in the study at hand may be huge, the absolute levels of ketones in the blood, on the other hand, are small (compared to eating a 100% ketogenic diet (=nutritional ketosis), where levels will go up to 0.5 - 3.0 mmol/L), but still impressive in view of the fact that the caffeine was consumed with a high carbohydrate (high GI) breakfast.

Bulletproof coffee is a fad, but is it also bad for your blood lipids? Studies suggest that it's at least not the butter that elevates cholesterol | Learn more!

Bottom line: Yes, it's too early to get all-too-excited, but whence we have (a) the studies to evaluate caffeine’s long-term effect on ketonemia and the corresponding impact on brain function during aging, the authors ask for, as well as (b) insights into potential interactions with the composition of the meal it is co-ingested with, and all that confirms what the study at hand suggests, i.e. that caffeine can double the ketone production in healthy individuals, ketogenic dieters would have all-the-more reasons to cherish their large AM pot of coffee (not necessarily with butter, though; after all the trick works without sign. amounts MCTs and even in the presence of ~90g of carbohydrates) | Leave a comment on the SuppVersity Facebook Page!

References:

• Panza, Francesco, et al. "Coffee, tea, and caffeine consumption and prevention of late-life cognitive decline and dementia: a systematic review." The journal of nutrition, health & aging 19.3 (2015): 313-328.
• Vandenberghe, Camille, et al. "Caffeine intake increases plasma ketones: an acute metabolic study in humans." Canadian Journal of Physiology and Pharmacology (2016) [ahead of print].

Gain DXA-Confirmed 3% Lean Mass Within ~12h, Glycogen Loading Does the Trick | Plus: Training on 'The Pill' & More...

The first December 2016 research update with studies that are relevant for both, women and men. I mean, who wouldn't want to get sign. more muscular in hours? I guess those who know that this is just an often overlooked measuring error.

Have you ever wondered about the accuracy of your DXA data? It's supposed to be "the gold standard", but you've learned only recently in the SuppVersity Facebook News that this is only the case if you measure at the same time of the day, identical hydration and - as a more recent study shows - even identical glycogen stores. What? Yes, that's right! You can make DXA-confirmed 3% gains in lean mass within hours. Simply by glycogen loading.

You're not interested in body fat data? Well, this is your lucky day. Today's installment of the short news will also discuss the latest study on the interaction between oral contraceptive and the adaptive response to exercise (Schaumberg. 2016).

Looking for more cutting edge exercise and supplementation science?

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Pump Supps & Synephrine & X | ISSN'15 #2

High Protein, Body Comp & X | ISSN'15 #3

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The Misquantified Self & More | ISSN'15 #5

BCAA, Cholos-true, Probiotics & Co | ISSN'15 #6

That's still not for you? Well, there's also the interaction between glucose, fructose and gastric emptying, which is of "urgent" (keyword: diarrhea vs. fastest glucose uptake) importance for endurance athletes (Shi. 2016).

• Diarrhea vs. fastest glucose uptake - How the glucose / fructose ratio can make all the difference (Shi. 2016) -- In their latest study, scientists investigated the effect of beverage osmolalities, carbohydrate (CHO) type and CHO concentration on gastric emptying in euhydrated subjects at rest.
  
  To this ends, the scientists measured the gastric emptying of water (W), and compared it to four glucose beverages containing either 2, 4, 6, or 8% glucose (2G, 4G, 6G, and 8G, respectively) and four sucrose (= 50% glucose + 50% fructose) beverages containing identical percentages, i.e. 2, 4, 6, or 8% of sucrose (2S, 4S, 6S, and 8S) in eight healthy subjects using the modified George double-sampling technique (Beckers. 1988).
  

  

  Figure 1: Mean gastric residual volume and gastric emptying rate in with standardized drinks with different carbohydrate sources (glucose or sucrose = 1:1 glucose : fructose) and volume (Shi. 2016).

  The scientists did not find significant differences in the gastric secretion volume among beverages across time and practically less relevant differences for the gastric residual beverage (GRBV) volume. What is interesting for you, on the other hand, is the scientists' observation that the gastric emptying rate (GER) was negatively correlated to the calories emptied (r=0.84) - and that the effect was more pronounced for glucose than for sucrose.
  
  

  

  Bad Fructose? Increased Glycogen Synthesis, Reduced Glycemia, Higher Glucose Oxidation | more

  What does that mean? Well, the answer is simple. Shi et al. provide more evidence of and a "novel" mechanism for the superiority of glucose + fructose mixes as intra- and post-workout shakes. Especially at high energy content, i.e. high levels of glucose and fructose in the drink, they are simply processed faster. Accordingly, it is not surprising that studies show benefits, not detrimental effects of adding the allegedly bad fruit sugar to a sugary intra- or post-workout shake. You can learn more about this in "Bad Fructose? Increased Glycogen Synthesis, Reduced Glycemia, Higher Glucose Oxidation" (more) and "Post-Workout Glycogen Repletion - The Role of Protein, Leucine, Phenylalanine & Insulin" (more).
  
  On the other hand, the risk of getting diarrhea may increase with each extra-gram of fructose in your intra- or post-workout beverage. The "optimal" 2:1 ratio for glycogen recompensation, I discussed in the previously cited article from 2013.
• Manipulation of Muscle Creatine and Glycogen Changes DXA Estimates of Body Composition (Bone. 2016) -- As the authors of the previously referred to study say dual x-ray absorptiometry (DXA) protocols are thought to provide a reliable measurement of body composition. In fact, however, their study shows that the accuracy will largely depend on the muscle glycogen content upon measurement (not so much on the level of creatine, though).
  
  How do they know? Well, the researchers had eighteen well-trained male cyclists (the training status is important, because the results may well differ for untrained or only recreationally active subjects) participate in a parallel group application of creatine loading (n=9) (20 g/d for 5 d loading; 3 g/d maintenance) or placebo (n=9) with crossover application of glycogen loading (12 v 6 g/kg BM/d for 48 h) as part of a larger study involving a glycogen-depleting exercise protocol. Body composition, total body water, muscle glycogen and creatine content were assessed via DXA, bioelectrical impedance spectroscopy, and standard biopsy techniques.
  

  

  Figure 2: Percent changes in leg lean and fat mass vs. baseline following glycogen depletion and creatine and glycogen loading with and without creatine (Bone. 2016).

  Their results confirm glycogen, as the primary determinant of ostensible gains. In fact, glycogen loading, both with and without creatine loading, resulted in substantial increases in estimates of lean body mass (mean +/- SD; 3.0 +/- 0.7 % and 2.0 +/- 0.9 %) and leg lean mass (3.1 +/- 1.8 %and 2.6 +/- 1.0 %) respectively. Cool? Well, the only bad news is that the DXA scan's body fat analysis will be messed up even more (+4.5% of body weight for the whole body, albeit - due to interpersonal differences - not statistically significantly) - in the end, you would thus always be told that you failed to achieve lean gains.
• Oral Contraceptive Use Dampens Physiological Adaptations to Sprint Interval Training (Schaumberg. 2016) -- Dampens? Yes, this means "the pill" will impair your fitness gains - in this case maximal oxygen uptake (VO2peak) and peak cardiac output (Qpeak), but there is good news, too... before we get to that, however, we should take a brief look at the study design.
  
  The scientists studied women taking oral contraceptives (OC | n=25) or experiencing natural regular menstrual cycles (MC; n=16) who completed an incremental exercise test to assess VO2peak, PPO, and Qpeak before, immediately after, and four weeks following 12 sessions of SIT. The SIT consisted of 10, one-minute efforts at 100-120% PPO in a 1:2 work:rest ratio.
  Now, the bad news I've already revealed is that the OC group saw a significantly reduced increase in VO2peak (OC +8.5%; MC +13.0%; p=0.010) and Qpeak (OC +4.0%; MC +16.1%; p=0.013), but the good news is...
  • the peak power output (PPO) increased to a similar extent in both groups (OC +13.1%; MC +13.8%; NS), and
  • intriguingly, the OC group showed more sustained training effects in VO2peak (OC -4.0%; MC -7.7%; p=0.010) on the follow up 12 weeks later
  Eventually, SIT did thus (i) improve peak exercise responses in all recreationally-active women, with (ii) women on OC responding significantly worse, yet (ii) more sustained (when the women seized training) than those with natural menstrual cycles.
  
  Therefore, the authors conclusion that "OC use should be verified, controlled for, and considered when interpreting physiological adaptations to exercise training in women" (Schaumberg. 2016) is obviously right - during detraining, on the other hand, it could be an advantage to be on oral contraceptives (needless to say that the adaptation conserving effects would have to be proven in a future study in which MC women would be put on OC after SIT).

Yes, I do suggest that it may be beneficial to drink these two and another two cups of coffee w/ lots of sugar after your workout - if you are an athlete, at least -- "Post-Workout Coffee Boosts Glycogen Repletion by Up to 30% and May Even Have Sign. Glucose Partitioning Effects" | more

So what's the verdict here? I guess there's no clear verdict on the headliner study. We will need a follow up to investigate whether a woman's "gains" (in this case in the conditioning department) can be conserved if she starts taking oral contraceptives during de-training. What we do know without another study, however, is that taking oral contraceptives during a training period will impair the normal physiological adaptation to sprint training.

And what about the other studies? Well, I guess if you can stomach it (and as of now, nobody complained), the previously discussed 2:1 glucose:fructose ratio is probably the "optimal" natural sugar supplement for your workout.  And if you want to measure your results, you better make sure you did not change your carb intake or had a glycogen depleting workout before doing a DXA scan | Comment!

References:

• Beckers, E. J., et al. "Determination of total gastric volume, gastric secretion and residual meal using the double sampling technique of George." Gut 29.12 (1988): 1725-1729.
• Bone, et al. "Manipulation of Muscle Creatine and Glycogen Changes DXA Estimates of Body Composition." Medicine & Science in Sports & Exercise: Post Acceptance: November 28, 2016 - doi: 10.1249/MSS.0000000000001174.
• Schaumberg, et al. "Oral Contraceptive Use Dampens Physiological Adaptations to Sprint Interval Training." Medicine & Science in Sports & Exercise: Post Acceptance: November 28, 2016 - doi: 10.1249/MSS.0000000000001171.
• Shi et al. "Effect of Different Osmolalities, CHO Types, and [CHO] on Gastric Emptying in Humans." Medicine & Science in Sports & Exercise: Post Acceptance: November 28, 2016 -doi: 10.1249/MSS.0000000000001176.