Carbohydrate Timing Boosts Training Effect: Cut Out Carbs After PM Glycogen Depleting HIT Workout ⇨ "Sleep Low" to Make Game-Changing Performance Gains in Only 3 Weeks

Carbohydrate Timing Boosts Training Effect: Cut Out Carbs After PM Glycogen Depleting HIT Workout ⇨ "Sleep Low" to Make Game-Changing Performance Gains in Only 3 Weeks

athletes carbohydrate timing CHO glycogen glycogen depletion high carbohydrate HIIT hit LISS LIT low carbohydrate performance triathlon

You are no triathlete or coach? That doesn't mean that this study isn't of interest for you. The figurative "extra wind" this training strategy can give you is relevant for almost every athlete.

In a recent study, scientists from the French National Institute of Sport investigated the effect of a chronic dietary periodization strategy in a group of twenty-one highly-trained male triathletes. Previous studies, in which "train-low" strategies, during which athletes are deliberately carbohydrate restricted over certain periods of their training cycle, have reported robust a up-regulation of selected markers of training adaptation (increased whole body fat oxidation, increased activities of oxidative enzymes) compared to training with normal glycogen stores and high CHO availability, however, the subjects experienced at best disappointing performance increases.

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Scientists have long speculated that the disconnect between the benefits "training low" offers on the level of cellular / mitochondrial adaptation, on the one hand, and the real-world performance increases, on the other hand, could be a consequence of the necessarily reduced high intensity training intensity during the low-carb phases (Yeo. 2008; Hulston. 2010). If we simply assume that this hypothesis is correct, the solution to the problem should be obvious: Train low when carbohydrates are not necessary and use them, whenever they promote maximal performance.

Marquet et al. implemented this principle in a way I tried to illustrated in Figure 1. More specifically, they tried to maximize the subjects' performance during PM high-intensity training (HIT) by providing copious amounts of carbohydrates before the session and restricted the carbohydrate intake to close to zero after this glycogen-depleting workout.To test the efficacy of this protocol, the scientists used a 2x3 week study design in which the first 3 weeks were used to standardize the volunteers training regimen (10-15 h·wk- 1 : 40% running, 35% cycling, 25% swimming), assess subjects' compliance to the study demands and ensure they all attained similar baseline fitness measures before study commencement.

Figure 1: Overview of important aspects of the dietary / supplemental aspects of the study.

During the decisive second 3-week phase, the subjects were instructed to follow identical diets (by prescribing exact menus, the scientists achieved a high degree of standardization) in combination with either the previously described "sleep low" carbohydrate intake strategy or their usual carbohydrate intake patterns. Unlike the diet / supplementation regimen, the training program the subjects followed was identical for all of them - it ...

Figure 2: Sample weekly protocol for training and CHO intake (g/kg) to achieve different CHO avail. around training (Marquet. 2016)

"consisted of six sessions over four consecutive days, including high intensity training (HIT) sessions in the afternoon and low intensity training (LIT) sessions the next morning. [...] LIT sessions consisted in 60 min cycling at 65% MAP (218.8 ± 20.4 W - 95% CI: 227.5 and 210.7), while HIT sessions consisted alternatively in 8 x 5 min cycling at 85% MAP (286 ± 26.7 W- 95% CI: 297.5 and 274.7) or 6x5 min running at their individual 10 km intensity with 1 min recovery between sets (37). [...] One LIT session per day was prescribed for the other days of the week for a total training volume of 10-15 h" (Marquet. 2016).

All subjects used their own training equipment to record their activity, the duration and intensity of exercise and heart rate. In conjunction with the volunteers' perceived exertion records, as well as VO2max tests, maximal and submaximal performance tests and the results of a simulation of the final leg of a triathlon race, the scientists got a pretty comprehensive set of data.

The effect of "training low" largely depends on the master regulator of mitochondrial adaptation PGC-1a. The latter is activated not just by the contraction induced calcium flux and exercise stress, but also by a lack of glycogen and increased levels of the (low) energy sensing protein AMPK.

How does "training low" work? By deliberately restricting the carbohydrate intake during certain phases of your training you will be able to train in a glyocogen-depleted state and thus with clearly suboptimal fuel availability. The lack of readily available glucose that can be derived from the glycogen stores in your muscle, whenever necessary, exerts profound effects on your overall resting fuel metabolism and patterns of fuel utilization during exercise and triggers acute regulatory processes underlying enzyme and gene expression, as well as cell signaling (signaling proteins, gene expression, transcription rate of several genes, enzymes activity) which regulate the adaptive response to exercise. The results are an increased capacity to oxidize fat, a reduced reliance on glucose as a preferred substrate, etc.

Data that tells us that the authors' hypothesis that they could get the benefits of training low while avoiding the negative sides by "sleeping low" was accurate:

• 

  Figure 3: Make no mistake about it! The total amount of CHO the subjects consumed was identical it was just timed differently. No difference existed for any of the other macronutrients, either (Marquet. 2016).

  There was a significant improvement in delta efficiency during submaximal cycling , i.e. the power output per calorie, a very important measure for endurance athletes, for the "sleep low" compared to the control group (CON: +1.4 ± 9.3 %, SL: +11 ± 15 %, P<0.05).
• A similarly pronounced, albeit due to inter-individual differences, which loom large in studies with relatively few participants, only borderline significant (P = 0.06) beneficial effect was observed during the supra-maximal cycling to exhaustion trial at 150% of peak aerobic power, where the control group saw improve-ments of only 1.63 ± 12.4 %, while the "sleep low" group improved by 12.5 ± 19.0 %.
• The "sleep low" protocol also triggered significantly higher (P < 0.05) improvements in 10k running performance, where the meager -0.10 ± 2.03 % increase in the control group was topped by a -2.9 ± 2.15 % performance increase in the "sleep low" group.

In the "sleep low" group, even the effects on the body composition were significantly more pronounced compared to the control group. To be precise, the subjects who "slept low" burned a whopping 8.7 ± 7.4 % body fat literally overnight, while the control group lost a likewise measurable, but significantly lower and overall non-significant -2.6 ± 7.4% of their body fat - don't be mislead by the size of the bars in Figure 4; the fat mass is on the right axis which starts at 8kg and ends at 10kg. So there was no significant inter-group difference at baseline. No significant inter-group differences were observed for the changes in lean and total mass, either.

Figure 4: Even if you're not training for performance, the improvements in body composition, or more specifically the significant reduction in body fat without sign. changes in lean or total mass, may be of interest for you | total and lean mass on the left axis, fat mass on the right axis; all values in kilograms; sign. changes in % above bars (Marquet. 2016).

Against that background, it is by no means an exaggeration to say that even in the short-term (and that's what I consider particularly impressive here) the "periodization of dietary CHO availability around selected training sessions" can promote "significant improvements" in several highly relevant performance marker of trained athletes" (Marquet. 2016).

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Drop the carbs pre-bed! No, that's not because carbohydrates in the evening would make you fat. As a SuppVersity reader you know that this is bogus (learn more). The reason why you should consider dropping carbs in the PM (or rather after intense workouts) is their "anti-adaptive" effect - an effect that occurs in response to their ability to replenish your glycogen-stores and thus shut down the "we need to adapt to use more fat" signal to your mitochondria...

Ok, that's not exactly the most scientific explanation (see red box for more), but it is one that highlights one of the most important and yet commonly overlooked principles of physiological adaptations: they occur in response to a need.

If you always provide more than enough carbohydrates, there's no need to increase your ability to use fat as a fuel. If, on the other hand, you (A) fuel yourself with carbs when your body really needs them (during HIT training) to perform at the crucial i + 1 level that will trigger an adaptive response at high intensities, and (B) cut yourself off of a readily available carbohydrate supply when you don't need them (during sleep and low intensity exercise) you maximize the adaptive response to both HIT and LIT (low intensity training) and boost your overall training results | Comment!

References:

• Hulston, Carl J., et al. "Training with low muscle glycogen enhances fat metabolism in well-trained cyclists." Medicine and science in sports and exercise 42 (2010): 2046-55.
• Marquet, et al. "Enhanced Endurance Performance by Periodization of CHO Intake: “Sleep Low” Strategy." Medicine & Science in Sports & Exercise (2015): Publish Ahead of Print.
• Yeo, Wee Kian, et al. "Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens." Journal of Applied Physiology 105.5 (2008): 1462-1470.

Alternate Day Fasting (ADF) Cuts 50% Body Fat and Boosts Lean Mass by 12-13% - In Fat Rodents on Low Fat ADF Diet

Alternate Day Fasting (ADF) Cuts 50% Body Fat and Boosts Lean Mass by 12-13% - In Fat Rodents on Low Fat ADF Diet

alternate day fasting fasting high fat IF intermittent fasting lose fat low fat

When you're alternate day fasting your plate will look as empty or almost as empty as this every other day.

In the scientific literature, the term "intermittent fasting" is used inconsistently. Often, however, it refers to an every-other-day-fasting-regimen, in which you eat on day A and don't eat (or eat almost nothing) on day B. This was also the case of Juliet D. Gotthardt's latest study, where "intermittent fasting" therefore meant eating an ad-libitum diet (eat as much as you want and when you want) on day 1 and starving on day 2 (Gotthardt. 2015). What the scientists from the State University of New Jersey already knew was that this would protect male C57BL/6 from weight gain, what they didn't know and wanted to find out was whether the macronutrient content of the diet would modulate this effect..

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Accordingly, 64 mice were purchased from The Jack son Laboratory (Bar Harbor, ME, USA) and fattened up on an ad libitum, high fat diet (HFD; 4.73 kcal/g, 45% fat, 20% protein, 35% carbohydrate; D12451) for 8 weeks (note: this means all mice were already overweight, when the actual "intermittent fasting" began).

Figure 1: Energy content (kcal/100g) of the high and low fat diets the rodents were fed over the course of the 4-week experimental phase either ad-libitum or on an every-other-day-fasting regimen (Gotthardt. 2015).

The mice were then equally divided by bodyweight and transitioned to one of four experimental groups:

• HFD - an ad libitum high fat diet 
• IMF-HFD - an every-other-day fasting high fat diet
• LFD - ad libitum low fat diet
• IMF-LFD - an every-other-day fasting low fat diet

The mice in the IMF group were food deprived every other 24-hour period beginning at 9:00 AM (fasting day), 2 hours into the light cycle. On fasting days, all animals were weighed, food in take was recorded, cages were changed.

The alternative-day fasting induced a sign. reduction in food intake.

What's the mechanism, here? As the food intake data on the left shows, the effect is at least partly mediated by a significant reduction in food intake. In other words, just as it has been observed in humans, there's no full compensation for the lack of energy intake on the fasting day. This is intriguing, because the increase in norepinephrine (NE | 50-60%) in the hypothalamus and the expression of NPY in the arcuate nucleus ( 65–75%) in both IMF groups would suggest that the rodents were not immune to the regular compensatory stress response to fasting.

After four weeks, the mice on the IMF-HFD ( 13%) and IMF-LFD ( 18%) had significantly lower body weights than those who continued on the HFD.

Figure 2: Body composition as assessed by EchoMRI in all groups at the end of 4 weeks of the diet intervention. Data are represented as means SEM. A: Fat mass (g). B: Lean body mass (g). *** indicates difference from HFD (P .001); * indicates difference (P < .05) from HFD; $ indicates difference (P < .05) from IMF-HFD (Gotthardt. 2015).

As you can see in Figure 2, the body fat of the mice was also significantly reduced - in all four groups by 40–52%. The significant lean mass increases I hinted at in the headline, however, were observed only in the intermediate fasting low fat diet group (IMF-LFD | 12–13%).

Figure 3: Oral glucose tolerance tests in all groups at the end of 4 weeks of the diet intervention. Data are represented as means SEM. A: Blood glucose (mg/dl) response to an oral bolus of glucose (2 g/kg) over 180 minutes. Values for IMF-HFD and LFD overlap. B: Area under the curve (AUC) of glucose tolerance test (Gotthardt. 2015).

As Figure 3 goes to show you, the low fat alternative-day fasting (IMF-LFD) group also had the highest oral glucose tolerance with almost no increase in glucose during the glucose tolerance test. Whether that's due to the increase in lean mass is yet as questionable due to the mere extent of the reduction in glucose AUC. If the latter was simply due to an increase in muscle mass, you'd furthermore expect that the insulin levels of the IMF-LFD rats would have been lower as well. Insulin, as well as leptin, however, decreased to a similar extent in all treatment groups (compared to the high fat diet, obviously).

Figure 4: Cause and consequences of the low-fat exclusive increase in dopamine (DA) in the anterior hypo-thalamus of the fasted rodents are two things researchers don't yet fully understand (Gotthardt. 2015).

What do we make of this study? While I have to admit that the headline suggests that the lean mass increase was a result of the reduced fat intake, a hypothesis that would explain why there should be a mechanistic link between alternate-day-fasting, low fat dieting and increases in lean mass is not in sight. That's disappointing, but with the low-fat exclusive significant increase in anterior hypothalamus dopamine expression (see Figure 4) and the previously mentioned extreme increase in glucose sensitivity (cf. Figure 3), Gotthardt's study provides starting points for future research and it confirms that alternate day fasting does not cost you muscle mass... in this respect previous human trials showed similar results, by the way.

One thing you have to keep in mind is that the high fat diet (HFD) in the study at hand was after high in fat, but it was not low in carbohydrates. Accordingly, it would be really interesting to see, how a true low-carb diet would have affected rodents - and obviously humans, of whom a 2013 human study by Klempel et al. that used a similarly messed up "high fat diet" (45% fat, 40% carbs, 15% protein) shows that they lose the same amount of weight and body fat on "high" and "low fat" diets. Whether that's a species-dependent difference to the study at hand or a result of "too much fat" in Klempel's diet (25% fat is significantly more than in the Gotthardt study) will yet have to be determined in future studies; studies that will hopefully also use an actual high fat alternate-day-fasting regimen instead of the the high fat + high carb Western diet clone that was used in both, the study at hand, and the previously cited human study by Klempel et al. | Comment!

References:

• Gotthardt, Juliet D., et al. "Intermittent Fasting Promotes Fat Loss with Lean Mass Retention, Increased Hypothalamic Norepinephrine Content, and Increased Neuropeptide Y Gene Expression in Diet-Induced Obese Male Mice." Endocrinology (2015): en-2015.
• Klempel, Monica C., Cynthia M. Kroeger, and Krista A. Varady. "Alternate day fasting (ADF) with a high-fat diet produces similar weight loss and cardio-protection as ADF with a low-fat diet." Metabolism 62.1 (2013): 137-143.

First Study to Provide Evidence Creatine HCL Could Beat Monohydrate as a Muscle Builder and Fat Shredder, BUT...

First Study to Provide Evidence Creatine HCL Could Beat Monohydrate as a Muscle Builder and Fat Shredder, BUT...

body composition build muscle creatine creatine HCL creatine monohydrate lose fat

"Dude, that better be creatine HCL in dat drink of yours, because..." - bullshit, no?

I have to admit that I still have my doubts about the reproducibility and practical significance of the results, but since the authors declare that they have no competing interests, I think it is worth taking a look at what is the first (and only) study to suggest that any of the bazillion allegedly "superior" forms of creatine are actually an improvement over good old plain creatine monohydrate.

You will probably have heard the yadiyada about how creatine doesn't dissolve properly and creatine HCL was 41 times more soluble in water than creatine monohydrate, would permeate the intestinal tract easier and would thus yield significantly better results than plain monohydrate... right?

Obviously you've heard that bullshit. "Bullshit"? Yes, it's bullshit, because as of now there has been ZERO experimental evidence that the last and most important claim that the increased solubility of the product would improve its effect is more than yet another marketing gag.

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With a recent study from Brazil, this evidence appears to be finally there. In the corresponding experiment, Elias de Franca et al. compared the effects of two different doses of creatine HCl (1.5 g and 5 g) with creatine monohydrate (or "monohidrate" as the scientists like to spell it ;-) on the strength (std. 1-RM testing) and body composition (skinfold method) of recreational weightlifters.

As the scientists point out, all subjects had their diet homogenized by the research team nutritionist. In addition, subjects who hadn't been "creatine free" for at least 2 months were excluded. Whey protein, ad other amino acid supplements were - that's my understanding of the full text - allowed, but "managed to fit in the protein amount of the diet" (Franca. 2015). How much of a standardization in terms supplementation existed, is yet by no means clear. What I can tell you is that all subjects received either placebo (CG | capsules with resistant starch), 5 g creatine monohydrate (CMG), 5g creatine HCL (HCl-1) or 1.5 g creatine HCL (HCl-2) for 28 days. In that, the dosage for the creatine monohydrate group was selected based on a study by Hultman et al. that shows that 5 g of CrM during 28 days, is enough to promote the ergogenic effects of the supplement. By choosing the same and a lower dose of creatine HCL of which the the manufacturer obviously claims that it has the same effect as 5 g of the real deal, Franca et al. were able to (a) verify / falsify the claim and (b) check whether increasing the dosage beyond those 1.5g that are supposedly equal to 5 g of creatine monohydrate would yield significant advantages..

Figure 1: Pre / post (and rel. change in % above post-bar) strength data (de Franca. 2015).

As you would expect it, the training alone produced some changes in the male and female subjects' strength parameters. Figure 1 displays how the 1RM strength on the leg and bench press developed over the course of the 28 days and 8 workouts that were completed in an AB, CD, AB, CD fashion, i.a. as a basic 2-way split with different exercises in weeks 1, 3 vs. 2, 4. All programs (full text lacks detailed information) were composed of four exercises of chest and back muscles, three to shoulder muscles, four to legs muscles, three to biceps and triceps, and two abdominal exercises, though; and subjects performed four sets of 10 to 12 reps (80% to 90% of 1 MR) of each exercise and with every set being executed until momentary exhaustion.

No significant inter-group differences = no true benefit! In contrast to what you will probably read elsewhere the study at hand did not really show that creatine HCL is superior to creatine monohydrate. It did, not even as the scientists rightly say "induce changes on body composition in recreational weightlifters" (de Franca. 2015) while creatine monohydrate did not. Why's that? Well, de Franca et al. have (deliberately or not) left out two words that are of utmost importance: statistically significant. These two words must go before the word "changes" and they tell you that the body composition changes in the creatine HCL group with their laughable N = 7 and N = 6 subjects were significant, while those in the monohydrate group (N = 8) were not. On average, however, both groups gained almost the same amount of muscle and lost almost the same amount of fat. Accordingly, there is no wonder that there is no significant inter-group difference... not even for the placebo group, by the way. To say that one, i.e. PLA, CreM or CreHCL has been shown to yield superior results would thus be simply lying (most likely to increase one's sale).

Interestingly, enough, the scientist analysis of the data shows that none of the (in absolute terms high) increases in bench press performance reached statistical significance. Similarly, the only 1-RM increase for the leg press was the one in the 5g creatine HCL group, where the probability p that the increase we see was coincidental is smaller than 5% (p < 0.05)

Figure 2: Pre / post (and rel. change in % above post-bar) body composition data (de Franca. 2015).

If we continue to look at statistical significant results, only, the data in Figure 2 is what will make snake oil vendors love and abuse this study: according to the researchers' statistics software, only the 8% reduction in body fat of the two creatine HCL groups and the 15% increase in lean mass in the 5g creatine HCL groups were statistically significant.

Now, malicious gossip has it that this wouldn't prove anything, because there is (a) no significant inter-group difference, and because (b) the absolute increase in lean mass in the creatine monohydrate group was greater than in any HCL group and that the subjects in the 8 subjects in the monohydrate group were much fatter (yes, not significantly, though) than the 13 men and women in the other two groups. Speaking of men and women,... I wonder why the authors don't disclose the number of each in the groups. They only say that there were 60-70% men, 30-40% women in both groups. Well, that's nice, but since de Franca et al. "lost" 13 of their 40 subjects along the way (the abstract says they had 40 subjects, but there are 6, 7, 6, and 8 subjects in the four groups), this only adds to the already existing doubts about the reliability, reproducibility and the foreseeable mainstream interpretation of this study.

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Bottom line: You may be asking yourselves why I am not all excited now. Well, I tell you what: The scientists write that they "hypothesized that, CrHCl im proves performance similarly to CrM, but promotes different results in body composition" (de Franca. 2015) - why on earth would they do that. If there was a science-based hypothesis to be made, it would be that creatine HCL would yield the same effects as creatine at lower dosages, because it dissolves better and is taken up faster (Gufford. 2010), so that less is necessary to saturate the muscle. To speculate that it would produce of all things what people are willing to pay for the most is... to say the least, a bit suspicious, don't you agree?

The same goes for the surprising "coincidence" that the researchers, who obviously couldn't afford reliable DXA scans (Pietrobelli. 1998) *cough*, were able to conclude, without reference to the conclusion being (a) based on the lack of statistical significance and (b) made in view of identical changes in body mass (within standard deviations), that their caliper data tells them "that CrHCl and CrM improve performance but only CrHCl induces changes on the body composition in recreational weightlifters" (de Franca. 2015).

Thus, I personally would suggest we all wait for independent, adequately powered research to (a) confirm the findings and (b) show that there is a significant inter-group difference with an advantage for creatine HCL. Until that study is done, peer-reviewed and published, I refuse to get all excited about yet another form of allegedly "superior creatine" companies use for the sole purpose of increasing the margins on products that would otherwise hardly have margin | Comment!

References:

• de França, Elias, et al. "Creatine HCl and Creatine Monohydrate Improve Strength but Only Creatine HCl Induced Changes on Body Composition in Recreational Weightlifters." Food and Nutrition Sciences 6.17 (2015): 1624.
• Gufford, Brandon T., et al. "Physicochemical characterization of creatine N-methylguanidinium salts." Journal of dietary supplements 7.3 (2010): 240-252.
• Pietrobelli, Angelo, et al. "Dual-energy X-ray absorptiometry: fat estimation errors due to variation in soft tissue hydration." American Journal of Physiology-Endocrinology And Metabolism 274.5 (1998): E808-E816.
• Wells, J. C. K., and M. S. Fewtrell. "Measuring body composition." Archives of Disease in Childhood 91.7 (2006): 612-617.

Is Lard More Fattening Than Hydrogenated Vegetable Oil!? 17% Extra Weight, 32% Extra Fat Gain + Increased Appetite

Is Lard More Fattening Than Hydrogenated Vegetable Oil!? 17% Extra Weight, 32% Extra Fat Gain + Increased Appetite

diabesity fat fats health homa-ir insulin lard obesity oil oils partially hydrogenated fats partially hydrogenized fats QUICKI shortening transfats vegetable oils

Not all fats are created equal and lard and hydrogenated vegetable oils are not on the top-list of "healthy fat choices".

Our perspective on fat has changed significantly over the last decade. While some people still propagate that "fat is bad" and "should be generally avoided", most experts have stopped bashing fat in general and are now focusing on saturated fats. Saturated fats as they occur in lard,.. but wait! If you take a closer look at the fatty acid composition of lard, it turns out that it contains "only" 39.2% saturated, but 45.1% mono- and 11.2% polyunsaturated fats. That's actually not too far off of the average vegetable shortening with a saturated to monounsaturated to polyunsaturated fat ratio of 25.0 / 41.2 / 28.1% (nutritiondata.com)

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In contrast to said even more dreaded partially hydrogenized vegetable fats, which contains a whopping 13.2g of transfats per 100g, lard is yet mostly trans-fat free. That's a good thing, right? After all, high trans-fat intakes have been associated with increased inflammation and cardiovascular disease  (Hu. 1997; Lopez-Garcia. 2005. Now, while experimental evidence confirming negative effects in humans is non-existent, negative effects have also been observed in controlled animal experiments. It is thus more than reasonable to assume that of two of the most commonly used fat sources for cooking, i.e. lard and hydrogenated vegetable-shortenings, the former, the trans-fat free 100% "natural" fat source should be the healthier one.

Figure 1: Fatty acid content (g) of the three test diets (Kubant. 2015)

To check the validity of this hypothesis, scientists from the University of Toronto fed male Wistar rats for 14 weeks diets which contained either (1) high vegetable fat (HVF, 60 kcal% from vegetable shortening) or (2) high lard fat (HLF, 60 kcal% from lard). A group of rats that received the normal-fat chow (NF, 16 kcal% from vegetable shortening) served as control (see Figure 1). Body weight, food intake, adipose tissue mass, serum 25[OH]D3, glucose, insulin and fatty acid composition of diets were the scientists' main outcome data - data that confirm that not everything we take for granted will actually stand the test of science.

Figure 2: Body weight and fat gain over 12 weeks on control (low fat) or high fat diets w/ lard (HLF) or hydrogenated vegetable oils (HVF) as main fat sources (Kubant. 2015).

In contrast to what common sense would dictate, the rodents in the lard group were not leaner and healthier. In fact, the data in Figure 2 tells you that the exact opposite was the case: The rodents on the high lard diet gained significantly more body weight and - more importantly - body fat and did not, as some may now speculate, simply store the extra energy away instead of having it float around in the blood and ruin their insulin sensitivity (see Figure 3).

Figure 3: Markers of glucose metabolism at the end of the study (data expressed relative to control | Kubant. 2015)

So, basically, the scientists, who had even speculated that lard, due to its naturally high vitamin D content "may act to reduce the metabolic consequences associated with obesity, as suggested by other investigators" (Kubant. 2015), had to realize that their prediction was wrong. Whether lard is simply unhealthier or whether the effect was a results of the comparably lower food intake of the vegetable shortening group is difficult to say. What we do know, however, is that the animals who were on the lard diet consumed more calories than the HVF group. That 1g/day of extra food, however, was enough to have the scientists conclude that the rats have a strong preference for the taste of fat sources containing long-chain fatty acids (that is, oleic and linoleic), but by no means enough, to fully explain the significant difference in weight and body fat gain.

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So lard is much worse than transfats? I wouldn't dare making a general statement about lard vs. vegetable shortenings based on this study. One thing I would like to remind every saturated animal fat worshipper of, however, is that his beloved "saturated fat sources" like lard are in fact hardly saturated at all. The common lard, the scientists used in the study at hand, for example, has higher amounts of polyunsaturated fatty acids in it than the average vegetable shortening. Its (by the saturated fat lovers dreaded) content of omega-6 fatty acids in the form of linoleic acid, which is currently everybody's favorite scapegoat for being obese, diabetic or whatnot, is even three times higher!

What we must not forget, either, are the divergent results about the fattening effects of transfats from monkey and rodent studies. While the one existing monkey study showed higher levels of intra-abdominal adiposity and insulin resistance in monkeys fed trans fatty acids (TFAs) for 6 years under a controlled feeding regimen (Kavanagh. 2007), a more recent study in rats found that dietary TFAs fed ad libitum (as much as the rodents wanted) did not influence food intake or body fat accumulation (Ochiai. 2013). Now, monkeys are more reliable than rats, right? Well, yes, but if the monkeys are on an energy restricted and the control diet was no lard diet, but rather the "perfect monkey diet", the rodent study with its realistic ad-libitum access to food and a diet composition that was more akin to what people eat these days becomes increasingly attractive. Overall, however, it doesn't really make sense to use any of these studies to speculate about the practical significance Kubant's rodent study has for men. If you asked me, it is not even relevant, anyways, because neither lard nor hydrogenated vegetable oils should be a regular part of your diet | Learn why in a previous SuppVersity Article or tell me what you think on Facebook!

References:

• Hu, Frank B., et al. "Dietary fat intake and the risk of coronary heart disease in women." New England Journal of Medicine 337.21 (1997): 1491-1499.
• Kavanagh, Kylie, et al. "Trans fat diet induces abdominal obesity and changes in insulin sensitivity in monkeys." Obesity 15.7 (2007): 1675-1684.
• Kubant, R., et al. "A comparison of effects of lard and hydrogenated vegetable shortening on the development of high-fat diet-induced obesity in rats." Nutrition & Diabetes 5.12 (2015): e188.
• Lopez-Garcia, Esther, et al. "Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction." The Journal of nutrition 135.3 (2005): 562-566.
• Ochiai, Masaru, et al. "Effects of dietary trans fatty acids on fat accumulation and metabolic rate in rat." Journal of oleo science 62.2 (2013): 57-64.

Alkaline Diet - 4-9 Days Suffice to Boost Urinary pH, Boost Time to Exhaustion (21%) + Fat Oxid. During Exercise (10%)

Alkaline Diet - 4-9 Days Suffice to Boost Urinary pH, Boost Time to Exhaustion (21%) + Fat Oxid. During Exercise (10%)

acidic acidity acidosis alkaline alkaline diet alkalosis bicarbonate fruits health performance sodium bicarbonate vegetables

Many of you may now shake their heads and say: Well I am already eating such a diet... even though, I didn't do it for its alkalizing effects. Good for you!

As a SuppVersity reader you're familiar with the multifaceted benefits of sodium bicarbonate. Evidence that it will improve your performance, even when taken chronically, however, is still lacking. With a recently published study by Susan L. Caciano and colleagues we do yet have more evidence that this could be the case even though, we're not talking about bicarbonate supplementation, technically: In her study, Caciano tried to experimentally confirm the previous cross-sectional findings (Niekamp. 2012) suggesting that even a short term (4-9 days) low-PRAL, i.e. highly alkaline diet, would result in a higher respiratory exchange ratio during maximal exercise as compared to the SAD acidic diet.

You can learn more about bicarbonate and pH-buffers at the SuppVersity

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Bicarb Buffers Creatine

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Now, this may initially sound like a disadvantage, but in view of the fact that the study showed that the exact opposite was the case and the alkaline diet reduced the ratio of glucose to fat Caciano's 18-60 year-old, healthy volunteers, who had been randomly assigned in a cross-over design (meaning all subjects performed the tests once on both diets) to a high or low PRAL diet, burned during...

• 

  You will probably remember that Serial loading helps avoid the gastro-intestinal side effects from consuming large amounts of sodium bicarbonate in one sitting. Eventually, however, it is a special way to alkalize your diet aggressively.

  [...] a graded exercise test that was initiated at a speed determined during warm-up to increase HR to ~70% of age-predicted maximal heart rate (HRmax) and a grade of 0% and then increased by 2 percentage points every 2 minutes until the subject could no longer continue due to fatigue, and 
• [...] an anaerobic exercise performance during which they had had to run to exhaustion on a treadmill with the speed set at the same speed used during the graded exercise test, albeit at a treadmill grade that was 2 percentage points steeper than that achieved during the last full stage of the graded exercise test

For each of the dietary interventions, the study dietitian provided the subjects with specific instructions on how to modify their habitual diets to achieve a low- or high PRAL diet.

Ketogenic diets, acidic and problematic? The standard versions of low-carb or ketogenic diets have been shown to trigger significant decreases in blood pH (Yancy. 2007), of which the study at hand shows that they could trigger relevant performance decreases. Since eating more fruit is not an option, though, your vegetable intake should be as high as possible. On the other hand, the standard Western Diet will have similar consequences and the effects observed in the study at hand, as well as in previous studies could be corollary to the alkalinity of the diet and in fact caused by a mere increase in polyphenols, vitamins, dietary nitrate and other potentially performance enhancing substances in fruits and vegetables.

The study dietitian was in contact with the participants (via telephone or email) every day during the dietary interventions to encourage compliance and to provide specific food suggestions as needed.

• The general strategy used for the low-PRAL diet was to increase the consumption of alkaline-promoting foods such as fruits and vegetables and to reduce the consumption of acid promoting foods such as meats, cheeses, and grains. More specifically, participants were instructed to consume 6-8 cups of vegetables and >4 servings of fruit each day. Because there is a tendency for lower energy intake with diets that are rich in fruits and vegetables, such as the low-PRAL diet, participants were instructed to eat frequently and consume energy dense foods during the low-PRAL trial, such as starchy vegetables (e.g. sweet potatoes), dried fruits (e.g. dates and raisins), and plant sources of fat (e.g. avocado, coconut, nuts, seeds). Foods with moderate PRAL values (e.g. legumes, yogurt, egg whites, quinoa) were allowed and were used to ensure that energy and macronutrient intakes were adequate. The participants were also advised to minimize the consumption of all meats, cheeses and common grains (most of which are high-PRAL) during the low-PRAL diet. 

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  Bicarbonate keeps muscle activity high - even during most intense workouts | more

  During the high-PRAL diet, participants were instructed to consume at least 3-4 servings of common grains (e.g. wheat, corn, and oats), 3 servings of meat, and 3 servings of cheese (especially hard cheeses such as parmesan) each day while minimizing the intakes of fruits and vegetables. Moderate PRAL foods were allowed as desired as long as it did not displace high PRAL foods from the diet. In general, the high-PRAL diet required less intensive counseling from the dietitian be cause it closely resembled the baseline diet of the participants.

Now, obviously even the most tightly controlled study will have confounding effects that may mess with the results. For the time being, however, we will simply assume that the only thing the diets did (and were intended to do) was to achieve a dietary PRAL of ≤-1 mEq/d during the low- and a PRAL ≥15 mEq/d during the high-PRAL diet phases (I will get back to the validity of this assumption in the bottom line). As the scientists point out, "these cut points were based on PRAL values of the high and low PRAL tertiles that were observed in our previous cross-sectional study on 57 middle-aged men and women (Niekamp et al., 2012)" (Caciano). Whether the subjects achieved the desired level of alkalinity was measure with pH stripes in their morning urine.

Figure 1: Fasted morning urine pH during the dietary intervention for the low- and high-PRAL interventions. The objective was to attain the pH goal in 4 days; however, up to 9 days were required for some participants. “Last day” indicates urine pH on the last day of the dietary intervention (i.e. 4 to 9 days), which was also the morning during which outcomes assessments were performed (Caciano. 2015); values are means, error bars are standard deviations.

As the data in Figure 1 tells you, the dietary intervention successfully changed the urinary pH levels of which most critics of the idea of an "alkaline diet" say that it was as irrelevant as the PRAL-value, i.e. the degree of alkalinity of acidity of your diet, itself.

Figure 2: Respiratory exchange ratio (RER | high = higher CHO/FAT oxidation) and performance time-to-exhaustion on the graded (left) and anaerobic (right) performance tests (Caciano. 2015).

If this assumption is correct, the significant increase in RER (=increase in fat oxidation during the graded performance test), as well as the borderline significant and significant performance increases on the graded and anaerobic performance (+21%) test in Figure 2 would have to be explained by ergogenic effects of certain polyphenols, vitamins or other ingredients of fruits and veggies. This is possible, but just as hypothetical as the assumption that the changes were observed in response to a dietary-induced increase in serum bicarbonate.

What about the conflict w/ previous observational data? Neither I nor the scientists have an explanation for the difference to the previously cited observational data by Niekamp et al who had found increased RER-values in individuals consuming a lower PRAL diet. One possibility is that the low PRAL diet was also lower in carbohydrates and thus triggered a decrease in RER. Another possibility the scientists plan to test in a future study is "that the shift in systemic pH altered the activity of enzymes that regulate lipid and carbohydrate oxidation [due to the pH-sensitivity] of carnitine acyl transferase-I, one of the rate limiting enzymes in lipid oxidation" (Caciano. 2015).

High Dietary Acid Load Doubles Risk of Type II Diabetes in Lean Individuals! Causative or Corollary? Plus: Are Grains, not Meats the Main Offenders in the Modern Diet? Learn more about the benefits of alkaline diets in this SV Classic!

Unlike the mere ingestion of increased amounts of fruits and veggies, the levels of bicarbonate in the blood has yet previously been shown to will trigger improvements in time-to-exhaustion from numerous studies on sodium bicarbonate. That the latter was in fact increased, even though the scientists measured only the urinary pH, which increased by by ~12%, can be assumed based on previous studies by Unwin and Capasso (2001); studies that confirm that the urinary pH is a reliable indicator of serum bicarbonate. Accordingly, Caciano et al.'s explanation that, both the performance increases and the borderline significant increase in VO2max (p = 0.08 | not shown in Figure 2) "could have resulted from an alkaline environment created by the consumption of low PRAL foods, and possibly by an increase in bicarbonate availability" (Caciano. 2015) is reasonable.

Plus, the authors are also right to point out that it is "generally accepted that bicarbonate loading improves anaerobic exercise performance by enhancing acid buffering capacity," and that it would be pretty awesome, if the same or at least similar benefits could be achieved without risking gastrointestinal distress, as it has been repeatedly observed in response to bicarbonate loading, high intakes of fruits and vegetables, which have the added benefits of being rich in phyto-chemicals, fiber, antioxidants, and other nutrients. Overall, the planned consumed of an alkalizing diet may thus, just like Caciano et al. say, "be an attractive alternative to bicarbonate loading for improving anaerobic exercise performance" (Caciano. 2015). It that's due to or rather corollary to its "alkalizing" effects, is yet open to debate...

For 66% of all athletes, sodium bicar-bonate will work; others get diarrhea.

Bottom line: I guess, the performance benefits of the low-PRAL diet are about as undebatable as the beneficial health effects of increased intakes of fruits and vegetables. Practically speaking, we do thus not really need to know why the performance of the subjects increased significantly on the low-PRAL diet. What is important, though, is that the performance did increase statistically significant and to an extent that is practically relevant for every athlete who performs in competitions that require one or several 1-5 minute bouts of high intensity exercise... what? Yeah, that's probably more than 50% of all athletes.

Addendum: For those who have been indoctrinated by self-proclaimed mythbusters and avengers of "the truth" or quacks who claim to be able to heal every ailment with certain dietary tweaks against or in favor of the benefits of "alkaline diets" here's an interesting overview (Schwalfenberg. 2011) of proven and unproven claims of what an "alkaline diet" may be good for | Comment!

References:

• Caciano, Susan L., et al. "Effects of Dietary Acid Load on Exercise Metabolism and Anaerobic Exercise Performance." Journal of sports science & medicine 14.2 (2015): 364.
• Niekamp, Katherine, et al. "Systemic acid load from the diet affects maximal exercise respiratory exchange ratio." Medicine and science in sports and exercise 44.4 (2012): 709.
• Schwalfenberg, Gerry K. "The alkaline diet: is there evidence that an alkaline pH diet benefits health?." Journal of Environmental and Public Health 2012 (2011).