Adelfo Cerame - Finally a PRO: How I Won My IFBB Pro Card. Plus: SHR Audio Interview & All the Details About Adelfo's Nutrition & Training Regimen Before the Show

Adelfo at the NPC Sunshine Classic/Wheelchair Nationals '13

In case you missed the live show yesterday, you should by now have had the chance to listen to the podcast of yesterday's SuppVersity Science Round-Up Special in honor of Adelfo Cerame Jr.

If you did, you may have noticed that we talked a lot about the prep, about dieting and training in general, but did not really get to the contest itself... but hey, this is what the Science Round-Up "Seconds" are for and therefore I am now going to copy and paste the content of the latest blogpost Adelfo just shot me.

Before I do that, I do yet want to remind you of the SuppVersity Facebook Wall which holds, among other things news on

• the effects of grass and sand on your sprinting ability on different surfaces (read more), 
• the infection risk that comes with high glucose levels even in non-diabetic women (read more),
• Silvestrol, a natural anti-leukemia agent (read more),
• how low vitamin D levels could be a sign excessively high insulin levels (read more)

and much more... but for now, that's enough of abstract science. Let's get back to the real world and hear, or rather read how the last 4 days before the show went for your's truly Adelfo Cerame Jr.!

My last hours as an amateur and how I finally won the pro card

This is how the biggest winners look like, when they celebrate ;-)

I didn’t officially start my peak week until Wednesday, so prior to (Monday, Tuesday) everything pretty much stayed the same with regards to training and nutrition.

I felt pretty good going into my peak week. My food was high and energy levels were high as well. I was not dragging ass, hungry, or feeling miserable like some people do coming into the final week – I attribute this to starting my prep early and giving myself enough time to diet down (about 24 weeks). I did most of my intense digs with my diet early in my prep and was prepared or at least lean enough to the point where I was able to start slowly bringing food back up and recover metabolically almost 7-6 weeks out.

All I did from there was made tweaks and minor adjustments and improve, which I have summarized in the column on the right hand side of the following paragraphs.

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My numbers heading into peak week

• Energy: 2210kcal
• Fats: 50g
• Carbohydrates: 240g
• Protein: 200g

Wed: Start of Peak

• Energy: 3130kcal
• Fats: 70g
• Carbohydrates: 400g
• Protein: 225g

Wed: Training

• 2x horiz. row ex.
  4x6-8/8-10 @ 9 RPE
• 2x vert. row ex.
  4x10-12 @ 9 RPE
• Biceps curl ex.
  4x12-15 @ 9 RPE

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Thu: Nutrition

• Kcal: 2480
• Fats: 40g
• Carbohydrates: 350g
• Protein: 180g

Thu: Training

• 2 flat press ex.
  4x6-8/ 8-10 @ 9 RPE
• 2 vertical press ex.
  4x10-12 @ 9 RPE
• Biceps curl ex.
  4x12-15 @ 9 RPE

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Fri: Nutrition

• Kcal: 2370
• Fats: 50g
• Carbohydrates: 250g
• Protein: 180g

Fri: Training

• Horizontal row of choice 2x12-15 @ 9 RPE
• Flat press of choice
  2x12-15 @ 9 RPE
• Overhead press of choice 
  2x12-15 @ 9 RPE
• Biceps curls
  2x12-15 @ 9 RPE
• Lateral raise
  2x10-12 @ 9 RPE

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Sat: Nutrition

• Kcal: 3190
• Fats: 70g
• Carbohydrates: 460g
• Protein: 180g

Sat: Show Day - Fluids

• 20 oz water upon waking
• 16 oz. of water with / between meal

Sat: Show Day - Toolbox

• Morton’s lite salt
• Bagels
• Muffins
• Detour bars
• Rice cakes
• Goober PB&J
• Peanut butter cups
• Tuna pouches
• Beef jerky

Florida, I am on my way! I took the red eye flight (Thursday- midnight), so I basically slept during the flight since it was my habitual bedtime and touched down in Florida around 7 AM.  It was a direct flight that took about 4 ½ hours so it didn’t really affect me with regards to jet lag. Since I like keep things simple and as efficient as possible, I had packed a light bag with the bear necessities and decided that I would just do all the groceries, when I arrived at my destination.

Believe it or not, not one chicken breast was eaten during my travels ;-)

As for my protein sources, I stuck to whey protein sample packets, Quest bars, beef jerky, tuna packets and Greek yogurt, solely. While the carbs came from rice cakes, potatoes, bagels, fat free Pringles, cereal, apples and bananas. All that was topped off with some Goobers peanut butter & jelly, as well as coconut oil for the fats..

I arrived on Thursday, at 7 AM. What followed was the usual itinerary of checking in at the hotel, training, sending the latest photo updates to coach Alberto, shopping at at Walmart (I find it much easier to buy most of my foods when I arrive at my destination rather than packing everything all at once), practicing my poses and, not to forget, rest... what? Oh yeah, I almost forgot: Rest and EAT!

So from Wednesday through Friday I kept everything pretty much the same, the only difference was that my food was a lot higher and coach Alberto just made the adjustments with my food on the fly depending on how I looked with update pictures that I sent him throughout the day (again, you find the exact macros in the column on the right).

As you will see, the training volume was a lot higher, but the overall duration of the workouts was still short and the intensity was under tightly controlled via the RPE scale (if you want to learn more about the RPE scale, listen to yesterday's interview on the Science Round-Up Special).

My fluid and sodium intake was habitual – I probably drank a little bit more though than I did in the past Friday nights before the show (around 60-70 ounces more than I was use to)

Saturday, the big day has come

As the overview on the right is telling your my overall energy intake on the day of the show was pretty high. It was therefore all the more critical to time the meals appropriately.

• Pre-Judging AM 

• 6-7 hours out = 2 bananas, 2.6 oz. tuna, 2 tbsp. Goobers PB&J
• 4-5 hours out = detour protein bar + 5 oz. apple
• 60-90 minutes out = blueberry bagel, pumpkin pie pop-tart, 1 oz. beef jerky, and 1 tbsp. goobers PB&J
• 15-10 minutes out = 3g sodium + 1 peanut butter cup + big gulp of water

• Night show PM

• 6-7 hours out = 2 bananas, 2.6 oz. tuna, 2 tbsp. Goobers PB&J
• 4-5 hours out = detour protein bar + 5 oz. apple
• 60-90 minutes out = slice of pizza
• 15-10 minutes out = 3g sodium + big gulp of water

On show day I weighed in at 141 lb., so I came in 5 pounds heavier this year compared to last, which was something that really surprised me since I’m usually hovering around at 132-135lbs come show day but I’m not complaining ;-)

5lbs heavier, but still a lightweight compared to the mass monsters

When sizing up the competition, I had an idea of who the 2 main guys that I would probably face in the overalls, they both were in higher weight divisions and both were mass monsters, but I was very confident in my conditioning and overall package that I brought this year to be able to compete.

When I finally won the dang thing, it felt like more of a relief than anything and being able to finally get that monkey off my back!   

Lol. It was a surreal moment and it took a while to soak in but when it finally did; it felt great to know that I’m now considered a professional at what I love to do!

How I celebrated this victory? To be honest I really wasn’t craving much or felt the need to binge and stuff my face. I snacked on some of my rice cakes and beef jerky, then went out to the town and had two tall glasses of Guinness, and three slices of pizza and called it a night.

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Don't be worried, folks. We will find a good excuse to keep Adelfo "aboard" the SuppVersity! So this is certainly not the last post of Adelfo Cerame Jr, it may be the last of the "Amateur" Adelfo Cerame, but at the same time it's also the first or many posts of the IFBB Pro Adelfo Cerame ;-)

So what will the future bring? I jumped right back to my diet once I arrived back home on Monday evening. My appetite was pretty much under control and I attribute a lot of it to not depriving myself of anything during my whole contest prep, and I also had the advantage to be ready early or lean enough to where I was able to slowly start bringing my food back and recover metabolically.

As of now I plan on taking the whole year off for a long off-season in order for me to make the improvements I need to make in order to compete on the next level with the big boys! So, 2014 would probably be my pro debut.

Before I sign off; I would just like to thank all the SuppVersity readers for all the love and support you all have shown me throughout this journey, and I’m glad I was able to share it with you all.

Your's truly, Adelfo

Greater Strength Without Compromised Size Gains With Rest-Pause. Can Dietary Variety Contribute Cause Obesity? Catabolism & Anabolism Just 2 Sides of the Same Coin. GABA as a GH Promoting Brain Anabolic?

Can't squeeze out another rep? Not a problem have some intra-set rest and continue pumping thereafter.

I guess, I did this before, but I say it again: "Congratulations, Adelfo Cerame Jr.! You are the man." Obviously, we all knew he is, but as of now, even the judges have finally acknowledged that. Reason enough to do a Science Round-Up Special today, in the course of which Carl Lenore and me are going to pick Adelfo's brain and have him surrender all the secrets that made him finally achieve what he has been chasing for years, now: The status of a wheelchair pro bodybuilder.

Just like the regular show the live show will be kicking off at 1PM EST. If you miss it it's not a problem, there is also going to be a special edition of the "Seconds", tomorrow with Adelfo looking back at how the contest went and how he made sure to peak right on time (edit: you can download the podcast now).

And just to make sure that no one complains: I compiled a couple of news as a surrogate for the regular Science Round-Up, today (this was "last minute", so please ignore any typos and grammatical mistakes).  

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Rest-pause technique leads to greater strength w/ identical size gains (Oliver. 2013) -- The bad news first, I can't tell you exactly how long the 22 male subjects (25 +/- 5yrs, 179.71 +/- 5.0cm, 82.1 +/- 10.6kg, 13.6 +/- 4.3% fat, 6.5 +/- 4.5yrs training)  Jonathan Oliver recruited for the experiment he wrote his dissertation on actually rested withing (=intra) their sets. Usually you would expect something along the 10 deep breaths - just enough to get your game on, so to say.

Figure 1: 1-RM max and power on bench presses and squats before and after 12 weeks of classic (regular sets) and alternative intra-set rest interval (rest-pause) training in 22 young resistance trainees with >2y of training experience (Oliver. 2013)

You got to remember, though, that I cannot guarantee that the 10 deep breath version of the rest-pause technique will yield the same remarkable results you see in figure 1 until the embargo on the dissertation falls or a student of the Texas A&M who I believe should be able to peak into the actual full text gives me a hint on the details of the study protocol. In the mean time, take the increased strength gains (check the percentages above the bars in the post columns), as an incentive to (re-)incorporate rest-pause sets where you perform 2-5 reps, rack the weight, pause, pick it up again and perform another 2-5 reps with the same weight and so on until you hit your target rep range, e.g. 12 reps on the bench with 200lbs, where you usually cannot do more than 5, into your routine.

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Dietary variety does not protect us from from becoming fat (Vadiveloo. 2013) -- In a soon-to-be-published systematic review of epidemiological studies researchers from the Steinhardt School at the New York University report that dietary variety does not protect against obesity. In fact, the exact opposite can be the case if "your variety" is a variety of sugar + fat-laden junk foods. In that case you are even more likely to fall victim to the metabolic syndrome than someone who eats just Twinkies and does not switch to Dingdongs once in a while:

If you are interested in buying quality, you may want to revisit the post on pesticide residues in organic and regular produce (go back)

"The present review is an important first step in clarifying the associations between dietary variety and excess adiposity, which is currently limited by the methods used to assess variety.

In the present review, we found that (1) dietary variety within recommended and low-energy foods alone do not increase the odds of overweight and obesity, (2) greater variety within less healthful, energy-dense foods increases the odds of overweight and obesity and (3) the association between total dietary variety and adiposity is mixed and accurate evaluation of this association requires a consistent and theoretically valid measurement tool."

This is, allegedly not a really surprising finding, what may yet surprise you is that the scientists didn't find a positive association for a variety of healthy foods in the diet, either. Sounds like quality and quantity, but not diversity remain what determines our likelihood of becoming obese... but let's be honest, isn't eating - at least from time to time - so much more than just providing your body with the nutrients it needs?

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There is no protein synthesis without catabolism (Bentzinger. 2013) -- A very intriguing study that's about to be published in the next issue of Skeletal Muscle found that the constant and isolated expression of MTOR-1C in a rodent model leads to profound muscle catabolism and not as you may have expected exuberant muscle growth. The underlying reasons for this counter-intuitive effects are the m-TOR induced blockade of the p-AKT pathway which is also responsible of keeping the catabolic MuRF1 pathway in check:

The AMPK-mTOR seesaw

"Our study shows that the mTORC1- and the PKB/Akt-FoxO pathways are tightly interconnected and differentially regulated depending on the muscle type. These results indicate that long-term activation of the mTORC1 signaling axis is not a therapeutic option to promote muscle growth because of its strong feedback induction of the E3 ubiquitin ligases involved in protein degradation."

In view of the fact that few of you will be mutants with a constant (over-)expression of mTOR-1C the scientists most recent observation does actually have implications for you as a trainee. It does not only re-emphasize the importance of the cyclic nature and tight inter-regulation of protein synthesis and degradation, but should also remind you no to rely too heavily on studies measuring only increases in protein synthesis without accounting for the net protein retention.

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GABA exerts indirect "anabolic" effects on the brain (Thanapreedawat. 2013) -- In yet another advanced publication that happens to overlap with the sudden re-appearance of GABA supplementation within the health and fitness community, Thanapreedawat and colleagues report that the administration of gamma-amino-butyric in the drinking water (0.5% and 1.0%) of young rats lead to highly significant activation of the intra-cerebral mTOR pathway, a subsequent dose-dependent increase in S6K1 phosphorylation and corresponding increases in brain protein synthesis.

Figure 2: Relative changes (compared to control) in insulin, insulin-like growth factor (IGF-1) and growth hormone (GH) in response to 0.5% or 1.0% GABA in the drinking water of 3-week old Wistar rats (Thanapreedawat. 2013)

Now what's really interesting about the study is that these effects were not mediated centrally. In other words, the orally ingested GABA did not pass the blood brain barrier. That this was possible is sometimes touted by producers of respective supplements. Previous studies have yet conclusively shown that orally ingested GABA does not make it across an intact blood brain barrier in vivo, so that any effects GABA may have must originate in the periphery  and that's actually what the scientists believe happened here, as well.

The peripheral effects of the orally administered GABA, namely the pronounced increase in growth hormone (GH) (cf. figure 2), a molecule which has previously been shown to be able to cross the blood brain barrier (Bermann. 1994; Ohsumi. 2008) lead to an activation of the intra-cerebral mTOR cascade and the subsequent increase in protein synthesis. If you expand on that, you could even speculate about other GH mediated effect of GABA supplementation... I must yet forewarn you: GABA is not a proven ergogenic of any kind (doesn't build muscle, doesn't make you lean, etc.).

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Usually this would be the place to add some references to the latest Facebook news, but since the show is about to start in a couple of minutes (listen live), I'll just refer you directly to the SuppVersity Facebook Wall. With 6-9 studies you won't read about anywhere else every day, it's always worth visiting, anyway ;-) 

References: 

• Bentzinger CF, Lin S, Romanino K, Castets P, Guridi M, Summermatter S, Handschin C, Tintignac LA, Hall MN, Rüegg MA. Differential response of skeletal muscles to mTORC1 signaling during atrophy and hypertrophy. Skelet Muscle. 2013 Mar 6;3(1):6.
• Bermann M, Jaffe CA, Tsai W, DeMott-Friberg R, Barkan AL. Negative feedback regulation of pulsatile growth hormone secretion by insulin-like growth factor I. Involvement of hypothalamic somatostatin. J Clin Invest. 1994 Jul;94(1):138-45.
• Ohsumi M, Tujioka K, Hayase K, Nagata S, Yokogoshi H. The growth hormone affects the brain protein synthesis rate in hypophysectomized aged rats. J Nutr Sci Vitaminol (Tokyo). 2008 Feb;54(1):76-81.
• Oliver J. Intra-Set Rest Intervals in Hypertrophic Training: Effects on Hypertrophy, Strength, Power, and Myosin Heavy Chain Composition.Doctoral dissertation, Texas A&M University. 2013.
• Thanapreedawat P, Ohsumi M, Hayase K, Yoshizawa F, Yokogoshi H. Influence of GABA on Brain Protein Synthesis Mediated by the Mammalian Target on the Rapamycin Pathway. Biosci Biotechnol Biochem. 2013 Mar 7.
• Vadiveloo M, Dixon LB, Parekh N. Associations between dietary variety and measures of body adiposity: a systematic review of epidemiological studies. Br J Nutr. 2013 Feb 27:1-16.

Does Creatine Blunt Fat Loss? A Recent Study Supports Long-Standing Suspicions, But What Are the Implications?

Better  lean than strong? Why not both?

Anyone remember the allegedly not very popular post on the "anti-creatine" β-Guanidinopropionic Acid (GPA) and it's ability to increase AMPK, decreases blood glucose & insulin, induce weight loss without dieting, increase skeletal muscle oxidative capacity and delay the development of mammary cancer (read up on the news)? I thought so...

Even I had was just about to forget about it, when I stumbled upon a recently published Brazilian study which found that the "real" - not the anti-creatine - does in fact what you would expect from the "evil twin" of GPA: It blunts the exercise induced fat loss in highly trained amateur athletes (Manjarrez-Montes de Oca. 2013).

"What!? Creatine makes me fat?"

Now, before you start freaking out, let me say this: There are also studies which suggest that creatine supplementation does the exact opposite, i.e. that it can (combined with an intense exercise protocol) decrease body fat level (van Loon. 2003; Volek. 2004). If you dig deeper, you will yet find that most studies actually don't report any changes in the ratio of fat to total body mass most of you know as "body fat percentage" (Kreider. 1998; Volek. 1999; Becque. 2000).

Whatever the results of the individual experiments may be, in the end only studies like the one done by Jeff Volek et al. at the University of Connecticut or the study at hand, i.e. studies in the course of which the scientists actually measure/d the total amount of lean and fat mass can provide an adequate idea of what exactly supplemental creatine can do for our physiques. If the data includes only body fat percentages, maybe even measured with bio-impedance (→ yesterday's Facebook news on "losing" 1.4% of body fat in a single session), this does not suffice to say, whether the absolute amount of body fat changed. Or in other words, whether any observed increase / decrease in body fat (%) was simply a result of the fact that the ratio of lean to total body mass increased faster than the rate of fat to total body mass, wile the subjects abs still disappeared under a nasty layer of blubber.

Figure 1: Changes in body mass, bone free lean mass, fat mass and body fat percentage (left), as well as individual "fat gain" response to creatine supplementation in the 14 subjects (Manjarrez-Montes de Oca. 2013).

The study at hand is in fact a perfect example for the way body fat  levels alone can fool you. A brief glance at the data in figure 1 confirms that. While the body fat percentage says that the 12 non-smoking, non-vegetarian, red and black belt male recreational taekwandoo players must effectively have lost weight in the creatine phase of this, the total fat mass reveals that adding 50mg/kg creatine to their sports drink (30 g of sucrose, artificial flavor, 500ml) lead to an increase, the addition of the same amount of maltodextrin to a decrease in DEXA measured total body fat.

If it were not for the results of of 2002 paper by Huso, I guess, I would just tell you to simply forget about the hoopla and discard the notion that creatine would have any effect on body fat levels, at all (Huso. 2002). Huso et al. had investigated the influence of creatine supplementation (20 g/day for 4 days, then 2 g/day for 17 days) on substrate utilization during rest using a double-blind crossover design. To this ends the researchers recruited 10 active men who participated in a 12 wk resistance training protocol (3x /week full body resistance training; 3 sets, 10 reps) involving a placebo and a creatine trial that were separated by a 4-wk washout.

Figure 2: Changes in body composition (body mass, body fat and fat free mass) and 1RM strength on the bench press and leg press in the 12-week double-blind randomized cross over trial by Huso et al. (Huso. 2002)

Very similar to Manjarrez-Montes de Oca et al. in the study at hand,  Huso et al. observed a significant decrease in fat mass (-2.4kg) in the placebo trial, while there were no significant changes in either of the two parameters, when the subjects were "on creatine".

So how come that creatine does even have the ability to inhibit fat loss?

Just like the identical change in lean mass (in fact, only the strength increase speaks in favor of the creatine loading + maintenance regimen) the inhibition of the fat loss in the trial of the Huso study was actually only a "side finding". Originally, Huso et al. had set out to elucidate, whether the "anecdotal evidence of weight gain, including a lack of fat loss, in persons taking creatine" (Huso. 2002) could be brought about by creatine induced increases / decreases of the respiratory exchange ratio (RER = the ratio of carbohydrates to fats that are oxidized during a workout). And while the scientists state in their abstract that the "[c]hanges in substrate oxidation" they observed "may influence the inhibition of fat mass loss associated with creatine after weight training" (Huso. 2002), it is at least in my humble opinion not very likely that the small statistically only borderline significant shift from fat to carbohydrate oxidation (+/- 9%, respectively) alone can actually explain the >2kg difference in total fat mass loss. Still, this is exactly what Manjarrez-Montes de Oca et al. feel would be the most likely explanation for the observations they made 11 years later, as well:

I wonder if Usain Bolt consumes creatine supplements. Or is he on GPA, click here to learn what would be more likely.

"It has been suggested that the increase in carbohydrate utilization induced by Cr may be due to an activation of the enzyme phosphofructokinase, which produce an increase in glucose utilization, with elevation of malonyl-CoA and inhibition of carnitine palmitoyltransferase 1 (CPT1) system, which transports fatty acids into the mitochondria for oxidation (Huso. 2002).

If fatty acids are not transported into the mitochondria of skeletal muscle cells to be oxidized, they could be expected to be maintained in blood as triglycerides; and then stored in the adipose tissue.

We observed a higher concentration of triglycerides after Cr supplementation, and also found that subjects after Cr treatment gained fat mass whereas after placebo treatment fat was lost. Therefore, both findings could imply that fatty acid mitochondrial uptake has been inhibited by Cr ingestion, altering the normal fat loss produced by TKD training."

What you should keep in mind though, is that the dietary intake was not controlled for (what if increased glucose oxidation simply made the subjects hungrier?). In calorically restricted scenario the results could thus have been very different, so that it is overall not very likely that creatine would ruin your dieting efforts. Moreover, there is some, allegedly not very conclusive evidence that the addition of a reasonable amount of creatine to your diet could actually help you spare muscle tissue. The fact that the placebo-specific increase in protein oxidation from 11.6% to 15.3% was just as absent in the creatine group as the fat loss, is however hardly a convincing, let alone bullet-proof argument in favor of creatine as a dieting aid. After all the protein oxidation in the creatine group remained stable on the same high levels of roughly 15%.

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Bottom line: I don't feel that the evidence "against" taking reasonable amounts of creatine (2-3g per day) is conclusive enough to panic and give up on the possible beneficial effects on lean mass (Nissen. 2003; Poortmans. 2010). Still, if you really have good reason to believe that creatine may blunt your fat loss (it's not impossible, take a look at the "high responders" in figure 1, right), I don't see why you could not give it a try and simply stop taking your creatine for a months or so. If after an initial flattening effect you don't see any other changes in your physique you are at least sure that you don't belong to the unlucky few, for whom creatine monohydrate (not one of the sugar-laden combi products!) could maybe and due to whatever interaction of genes, diet and whatever other confounding factors, forestall fat loss.

References:

• Becque MD, Lochmann JD, Melrose DR. Effects of oral creatine supplementation on muscular strength and body composition. Med Sci Sports Exerc. 2000 Mar;32(3):654-8.
• Huso ME, Hampl JS, Johnston CS, Swan PD. Creatine supplementation influences substrate utilization at rest. J Appl Physiol. 2002 Dec;93(6):2018-22.
• Kreider RB, Ferreira M, Wilson M, Grindstaff P, Plisk S, Reinardy J, Cantler E, Almada AL. Effects of creatine supplementation on body composition, strength, and sprint performance. Med Sci Sports Exerc. 1998 Jan;30(1):73-82.
• Manjarrez-Montes de Oca R, Farfán-González F, Camarillo-Romero S, Tlatempa-Sotelo P, Francisco-Argüelles, Kormanowski A, González-Gallego J, Alvear-Ordenes I. Effects of creatine supplementation in taekwondo practitioners. Nutr Hosp. 2013;28(2):391-399.
• Meglasson MD, Wilson JM, Yu JH, Robinson DD, Wyse BM, de Souza CJ. Antihyperglycemic action of guanidinoalkanoic acids: 3-guanidinopropionic acid ameliorates hyperglycemia in diabetic KKAy and C57BL6Job/ob mice and increases glucose disappearance in rhesus monkeys. J Pharmacol Exp Ther. 1993 Sep;266(3):1454-62.
• Nissen SL, Sharp RL. Effect of dietary supplements on lean mass and strength gains with resistance exercise: a meta-analysis. J Appl Physiol. 2003 Feb;94(2):651-9. Epub 2002 Oct 25.
• Poortmans JR, Rawson ES, Burke LM, Stear SJ, Castell LM. A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance Part 11. Br J Sports Med. 2010 Aug;44(10):765-6.
• van Loon LJ, Oosterlaar AM, Hartgens F, Hesselink MK, Snow RJ, Wagenmakers AJ. Effects of creatine loading and prolonged creatine supplementation on body composition, fuel selection, sprint and endurance performance in humans. Clin Sci (Lond). 2003 Feb;104(2):153-62.
• Volek JS, Duncan ND, Mazzetti SA, Staron RS, Putukian M, Gómez AL, Pearson DR, Fink WJ, Kraemer WJ. Performance and muscle fiber adaptations to creatine supplementation and heavy resistance training. Med Sci Sports Exerc. 1999 Aug;31(8):1147-56.
• Volek JS, Ratamess NA, Rubin MR, Gómez AL, French DN, McGuigan MM, Scheett TP, Sharman MJ, Häkkinen K, Kraemer WJ. The effects of creatine supplementation on muscular performance and body composition responses to short-term resistance training overreaching. Eur J Appl Physiol. 2004 May;91(5-6):628-37.

Predictive Value of Equations to Calculate Your Resting Metabolic Rate (RMR) Flawed: Results Can Be 14-29% Off

Would she still look so happy, if she knew that thee treadmill just lied to her?

I have written, said and, in person, even shouted it out often enough: Once you start to rely on the figures certain formulas generate (and this includes what your treadmill, your heart rate monitor etc. will produce, 'cause they use the same flawed formulas), you are lost.

The message of today's SuppVersity article is therefore by no means a new one. What's pretty new, though, is the study by V. Bonghana and colleagues from University of Campinas who have compared five predictive equations that are supposed to predict your and everyone else's basal (=excluding physical activity) energy demands (Bonghana. 2013).

"Start with a 15% energy deficit" - based on what?

The above, i.e. to start dieting by consuming ~15% less energy than you usually do, is my usual suggestion for anyone who's not in the "so fat that your health is in danger" zone, someone like you, maybe - someone who wants get rid of his/ her belly to finally see a at least the uppermost portion of his / her abs.

Table 1: The five equations the researchers used to calculate the predicted resting metabolic rate (RMR) that was then compared to the measured RMR (indirect calorimetry by respiratory gas analysis) of the 43 participants (Bonganha. 2013)

Now, what do you think would happen if this person was a postmenopausal women (of whom many, as we all know, love to "diet" exactly as they are told to, counting calories and what not) who is too lazy to follow my even more important advice to track her caloric intake for 2 weeks in order to get a "baseline reading"? What would happen if this woman, instead of doing just that simply used one of the calculators on the Internet and build her diet right according to the number the machine vomits out?

Figure 1: Comparison of the predicted resting metabolic rates and the mean difference to the "real" (=measured) RMR of the 43 healthy postmenopausal women who participated in the study (Bonghana. 2013)

Actually a cursory look at the data in figure 1 should suffice to tell you what the result would be. If she was lucky and the calculator used the rather uncommon Mifflin-St Jeor equation she would not lose a single pound, because she would end up right at the 1,063 kcal/day she, a 52-year young women, who's 159cm small has a totally age-appropriate BMI of 25kg/m², but a slightly high body fat level of 33%, just like the "average subject" in our experiment, needs to fuel her most basic metabolic demands (measured those are 1063.8 kcal/day). The former obviously implies that she did also take into account that she spends a few extra calories, even when she does not exercise.

Use the WHO calculation and you are lost

Guess how she got in in shape? Right! The EDC Program (learn more)

If she was not just as lucky and used the WHO equation as a baseline, she would not only overestimate her basal energy requirements by more than 30%. No, even with the 15% reduction she would be continuously gaining gaining wait... now, imagine she had also started to work out and had for once heard received some good advice, which is not to freak out about the weight gain, because it's all muscle. What? Right, she would be working away instead of towards her goal to lose weight and fat, 'cause one thing is sure.

Unless you expend more energy than you eat it is almost impossible to get rid of the belly. Unfortunately, simplistic calories in vs. calories out calculations won't help you find out whether this is the case..

The notion that exercise "alone" can, especially for those who are pretty chubby to begin with, have a "repartitioning effect" may still hold here, but it is more  likely that our imaginary post-menopausal training rookie is - if anything - gaining more muscle than fat and that's certainly not going to give her the look she is aspiring. In fact the situation would probably not be much different from the one in the study I had in the Facebook News a couple of days ago (Tibana. 2013).

Adding exercise on top of a proven (your N=1 experience) obesogenic diet rarely helps

In the course of this 8-week intervention study, the subjects, a group of 14 middle-aged (33.9 ± 8.6 years) overweight/obese women (body mass index - BMI 29.6 ± 4.1 kg/m²) underwent 24 sessions (3 times per week) of a whole body RT program with 3 sets of 8–12 repetitions maximum (RM). Unfortunately, for them without any dietary advice / incentive to modify the baseline diets that were obviously to blame for the extra-weight they were carrying.

Figure 2: Body mass, waist, hip, neck circumference, body adiposity index and visceral fat volume in middle-aged women before and after an 8-week 3x/week full body weight training intervention (Tibana. 2013)

The net result of this "intervention" was thus by no means representative of what you can achieve, when you really commit. If you discard the diet component, or even worse, fall for the common idea that you've worked out for an hour and could thus "afford" that piece of pizza, pie or panacotta, you are effectively bulking. Therefore, you should thus not be surprised, if you got strong and bulky, but don't see improvements in your body fat level, your waist line and any of the biochemical variables, i.e. fasting glucose, HbAIc, insulin,  triglycerides, HDL, and the TG/HDL ratio (not shown in figure 2), your doctor will be eyeballing.

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Without taking a "baseline reading" and accessing where you want to go, you ain't going to succeed (read more)

Bottom line: In conjunction, the results of the Bonghana and Tibana papers only underline the necessity to (a) make a baseline assessment of your current, individual food quantity and quality(!), before you embark on any kind of diet and (b) that the notion of "exercising the fat away" is only useful when you are not making the mistake to chart your dietary intake up against whatever you believe your exercise induced energy expenditure would look like. Even if it's not pizza, pasta and panacotta you are thinking of, when you look at the figure your treadmill or heart rate monitor calculated based on similarly whacky formulas as those used for the RMR, you are still lost whenever you put more faith into a impersonal arithmetics than the signals of your own body... and this, gentleman, is true irrespective of your age and sex.

If you still insist on calculating something, you may also want to take a look at Part III / III of the Female(?) Athlete Triad Series, but please be aware that I am not liable for the damage this type of calorie counting is going to do to your physique and your psyche.

References:

• Bonganha V, Libardi CA, Santos CF, de Souza GV, Conceição MS, Chacon-Mikahil MP, Madruga VA. Predictive equations overestimate the resting metabolic rate in postmenopausal women. J Nutr Health Aging. 2013;17(3):211-4.
• Tibana RA, Navalta J, Bottaro M, Vieira D, Tajra V, Silva AD, de Farias DL, Pereira GB, de Souza JC, Balsamo S, Cavaglieri CR, Prestes J. Effects of eight weeks of resistance training on the risk factors of metabolic syndrome in overweight /obese women - "A Pilot Study". Diabetol Metab Syndr. 2013 Feb 28;5(1):11.

Carnitine as Repartitioning Agent? IGF-1, p-AKT & mTOR Up, Catabolic Proteins Down + 7% Improvement in Lean- to Total Mass Ratio W/ HED of 1-1.5 of Carnitine/Day

It won't spare you the sweat, but carnitine could make it even more worthwhile by ramping up the anabolic and shutting down the catabolic signals.

Until 2006 l-carnitine has been known as a fat-burner, an in-effective fat-burner and an expensive and pretty useless supplement (depending on whom you were asking). Then, in July 2006, Kraemer et al. published a paper (a human study, above all!) in the journal Medicine & Science in Sports and Exercise a consequential paper so to say; a paper in which the authors report that l-carnitine l-tartrate supplementation at a dosage of 2.933g/day (this amount of LCLT contains 2g of pure carnitine) led to a statistically significant increase in androgen receptors in the vastus lateralis after a heavy resistance training protocol in previously strength trained male subjects (Kraemer. 2006).

Still, the evidence has always been inconclusive to say the least

Despite the fact that the concomitantly elevated post-workout luteinizing hormone levels (+19%) Kreamer et al. observed would tell you that the testosterone that would have been necessary to activate those receptors was already on its way, I have never considered this study as convincing evidence of the anabolic prowess of l-carnitine. Plus, let's be honest, differences in whatever serum markers in response to an acute bout of resistance training have failed us way too often, not to look at studies like these with appropriate skepticism.

Do you remember the Ratames study from 2005? The one that showed that high volume training lowers the no. of androgen receptors on the trained muscles? This certainly makes l-carnitine sound like the perfect addition to high volume routines, right? (learn more)

That the same principle of "calm down and don't get too excited over the results of a single trial" does all the more apply to rodent studies should be self-evident and still, science is all about taking each and every experimental result into account to form a theory that can explain all of them, or, alternatively, is able to bust short-comings in previous studies that don't comply with the predictions of the respective theory.

Now, the soon-to-be-published paper by Janine Keller and her colleagues from the University of Giessen (Germany) certainly qualifies as part of the evidence we simply cannot ignore, when we are looking for evidence in support of the theory that l-carnitine could be an overlooked muscle builder or repartitioning agent.

After all, their observation of decreased levels of the proteolytic (=catabolic) MuRF1 protein, as well as the ubiquitin-protein conjugates, which are increased in catabolic states such as starvation and atrophy denervation (cf. Wing. 1995) , alone, would signify that l-carnitine could make a valuable addition to everybody's supplementation regimen.

Lower catabolism + increased anabolism = ???

There is more, however, the addition of 1250 mg L-carnitine/kg to a basally "low carnitine" vegetarian diet also led to significant increases in systemic IGF-1 concentrations in plasma and a local increase in the activity of the PI3K/Akt/FoXO-1 signalling pathway (see figure 1)

Figure 1: IGF-1 mRNA and serum levels, as well as the muscle specific expression and phosphorylation (ph) Akt, mTOR & co after four weeks on the low or high carnitine diets (Keller. 2013)

These results do yet not stand in isolation as the ones by Kraemer et al. still do. Other recent studies by the same research group in Giessen, as well as colleagues from the University of Barcelona have already confirmed the anti-catabolic effects of l-carnitine in piglets and a cancer cachexia model in rodents, respectively (Keller. 2013; Busquets. 2013).

"And you are telling me that works in humans, as well? "

What's the best form of carnitine to take to elicit these effects: I knew you would ask this, so I react to two facebook questions by adding this red box willingly admitting that I just cannot tell you what the best form of carnitine is. There simply is no study that would compare e.g. acetyl-l-carnitine (ALCAR) and l-carnitine l-tartrate (LCLT) in a scenario that would be relevant to the above question. What I can tell you though, is that it appears as if you were better off with LCLT than with ALCAR, if your goal is to top off your intra-muscular carnitine levels. That being said, even normal creatine can do that - you will just have to take more of it. If you are looking for more information you can check out the part of the Amino Acids for Super Humans Series that's dealing with "the carnitines", here.

In this context it does yet also have to be mentioned that the effects of l-carnitine are at least in part species specific. How we know that? Well, in contrast to the said study by Basquets et al. the provision of an carnitine to piglets (Keller. 2013) did not only reduce the MuRF-1 expression, but also the level of its likewise catabolic E3 ligase cousin atrogin-1.

"It has been shown that myofibrillar proteins, like myosin light chain proteins are the main targets of MuRF1for ubiquitination. Thus, carnitine might suppress particularly the degradation of myofibrillar proteins, which under physiological conditions comprise around 60% of total muscle proteins. In contrast to MuRF1, atrogin-1 tags primarily proteins for degradation which are important for controlling protein synthesis and myoblast differentiation, like myogenic factor MyoD, myogenin and the eukaryotic initiation factor of protein synthesis eIF3-f." (Keller. 2013)

With pigs usually being a superior model of the human physiology, this would suggest that the anti-catabolic effects l-carnitine could have on humans are probably more, not less pronounced than those that were observed in previous rodent studies.

Whether the same goes for the IGF-1 response cannot be said, but just like the anticatabolic effects, the pro-anabolic increase in IGF-1 has been observed in previous trials, including a human trial by Di Marzio et al. who observed a significant increase in IGF-1 in HIV patients in response to the provision of 3g/day of acetyl-l-carnitine (Di Marzio. 1999). In the absence of the existing evidence from animal studies, these results would yet have little significance for healthy human beings, whose growth hormone and IGF-1 levels are not rock bottom to begin with (Viganò. 2003).

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Bottom line: Irrespective of the absence of human data on the IGF-1 boosting effects from non-HIV patients - or even better in training scenarios - it would warrant future studies if an adequate amount of carnitine in the diet can exert beneficial effects in non-obese human beings. For the "sedentary", or let's rather say non-exercised rodents in the study at hand, the latter was a mere fat loss effect - despite the elevations in p-AKT, m-TOR, IGF-1 and the overall more "anabolic" state the rodents were in their lean body mass was not increased compared to their peers on the low carnitine diet.

"Just another set!" ... "I don't know man, we've already pumped away 100,000kg today... do you really believe that's productive, I mean, yeah, we are cuttin', but still" ...learn what this dialog is all about and whether and if / when "another set" is / isn't a good idea (read more)

The lean-to-total mass ratio of the rodents, on the other hand was ~7% higher in the rodents in the high carnitine group. If we do however take into consideration that most of you will not be vegetarians and thus not similarly carnitine deprived as the rodents in the control group on the <1mg/kg carnitine diets, it is highly questionable if the addition of the human equivalent of the 1.25g/kg chow, i.e. 15mg/kg body weight (HED) would actually yield any measurable benefit to non-vegetarians - irrespective of whether they train or not. After all, even the average omnivore human being consumes 100-300mg of carnitine per day (Broquist. 1994), so that the difference between your basal carnitine intake and the supplemental equivalent dose of 1050-1500mg/day is more than 100x lower than the exorbitant difference between the low (if not deficient) carnitine diet in Keller's rodent study at hand (remember: the basal diet had less than 1mg/kg chow; the supplemented diet hat 1250mg/kg diet!).

So what's the verdict then? I guess, I will leave the final words to Burke et al. who reviewed the usefulness of carnitine as an ergogenic aid in one of the first installments of the "A-Z Supplement Review" in the British Journal of Sports Medicine and wrote "future work with l-carnitine may also find some useful outcomes" (Burke. 2009) - needless, to say that the SuppVersity is going to be the place, where you will read about it first ;-)


References:

• Broquist HP. Carnitine. In Shils ME, Olson JA, Shike M (eds): "Modern Nutrition in Health and Disease." Malvern, PA: Lea & Febiger, 1994. 459– 465.
• Burke LM, Castell LM, Stear SJ, Rogers PJ, Blomstrand E, Gurr S, Mitchell N, Stephens FB, Greenhaff PL. BJSM reviews: A-Z of nutritional supplements: dietary supplements, sports nutrition foods and ergogenic aids for health and performance Part 4. Br J Sports Med. 2009 Dec;43(14):1088-90.
• Busquets S, Serpe R, Toledo M, Betancourt A, Marmonti E, Orpí M, Pin F, Capdevila E, Madeddu C, López-Soriano FJ, Mantovani G, Macciò A, Argilés JM:  l-Carnitine: An adequate supplement for a multi-targeted anti-wasting therapy in cancer.  Clin Nutr. 2013;31:889–895.
• Di Marzio L, Moretti S, D'Alò S, Zazzeroni F, Marcellini S, Smacchia C, Alesse E, Cifone MG, De Simone C. Acetyl-L-carnitine administration increases insulin-like growth factor 1 levels in asymptomatic HIV-1-infected subjects: correlation with its suppressive effect on lymphocyte apoptosis and ceramide generation. Clin Immunol. 1999 Jul;92(1):103-10.
• Glass DJ:  Signalling pathways that mediate skeletal muscle hypertrophy and atrophy. Nat Cell Biol. 2003; 5:87–90 .
• Kraemer WJ, Spiering BA, Volek JS, Ratamess NA, Sharman MJ, Rubin MR, French DN, Silvestre R, Hatfield DL, Van Heest JL, Vingren JL, Judelson DA, Deschenes MR, Maresh CM. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exerc. 2006 Jul;38(7):1288-96.
• Keller J, Ringseis R, Koc A, Lukas I, Kluge H, Eder K:  Supplementation with l-carnitine downregulates genes of the ubiquitin proteasome system in the skeletal muscle and liver of piglets. Animal. 2013;6:70–78.  
• Keller J, Couturie A, Haferkamp M, Most E, Eder K. Supplementation of carnitine leads to an activation of the IGF-1/PI3K/Akt signalling pathway and down regulates the E3 ligase MuRF1 in skeletal muscle of rats. Nutrition & Metabolism. 2013; 10:28. 
• Lösel D, Rehfeldt C. Effects of l-carnitine supplementation to suckling piglets on carcass and meat quality at market age. Animal. 2013 Mar 11:1-8.
• Salama AF, Kasem SM, Tousson E, Elsisy MK. Protective role of L-carnitine and vitamin E on the testis of atherosclerotic rats. Toxicol Ind Health. 2013 Feb 13.
• Viganò A, Mora S, Brambilla P, Schneider L, Merlo M, Monti LD, Manzoni P. Impaired growth hormone secretion correlates with visceral adiposity in highly active antiretroviral treated HIV-infected adolescents. AIDS. 2003 Jul 4;17(10):1435-41.
• Wing SS, Haas AL, Goldberg AL. Increase in ubiquitin-protein conjugates concomitant with the increase in proteolysis in rat skeletal muscle during starvation and atrophy denervation. Biochem J. 1995 May 1;307 ( Pt 3):639-45.

True or False? Caffeine is The Main Main Stroke Protectant in Tea & Coffee. High MCT Diets Are the Key to Longterm Fat Loss. Soybean Oil Makes You Fat not Heavy.

Adelfo Cerame Jr. after winning his weight class, the overall and the pro-card (leave him a message).

The first "True or False?" today, does not really pertain to diet and nutrition science, but it is still highly relevant for the SuppVersity:

Adelfo Cerame Jr. did eventually win his well deserved pro-card at the Wheelchair Nationals in Florida, yesterday. - True!

Ok, I have to admit that this may have been too easy with the picture of Adelfo holding the trophies for his weight class and the overall in his hands on the right, but it was the best way to include this important news "seamlessly" *rofl* into today's SuppVersity article.

You want some more difficult stuff? Well, let's see what you know about tea, coffee, MCTs and heated soy bean oil, then.

Caffeine (probably) is the main stroke protectant in coffee and tea

True. As a recent study from the Universidade Federal de Santa Maria in Brazil clearly indicates, the "bad" caffeine is at least one, if not the main anti-oxidants that's responsible for the neuroprotective effects of coffee, tea and co (Souza. 2013).

Caffeine is also part of the classic CCC fat loss stack (learn more)

According to the results of the paper MA Souza et al. are about to publish in one of the future issues of  Neurochemistry International, a 2-weeks front-load with 6mg/kg caffeine per day increases the glutathione (=master antioxidant of the mammalian body) levels in the brain and protects rats from the oxidative damage and subsequent seizures in response to the administration of pentylenetetrazol-induced seizures (pentylenetetrazol is a circulatory and respiratory stimulant that overtaxes the brain, when it is administered in high doses).

What you should keep in mind, though, is the fact that Souza et al. used a dosage that was way lower than the amount of caffeine the average stim-junkie is consuming. It is thus not unlikely (in fact it is quite the opposite ;-) that we are dealing with a hormetic effect that occurs at human equivalent doses of 0.97mg/kg (~1 small cup of coffee) and turn against you when you escalate the doses to four or five MonterBullDrinks(TM) per day... I mean, the mere willingness of spending money on products like this goes to show you that drinking them compromises people's brain function, doesn't it? No, well I guess you have to reread the "Fat Content Per Energy Drink 0g. Fat Gain Per Energy Drink Drink 18g Study", then (reread it).

Most recent epidemiological human data supports these findings

And in case you don't believe this was relevant, check out the latest study in Stroke, in which Kokubo et al. which does not only confirm the stroke protective effects of green tea and coffee (Kokubo. 2013), but also yields some insights into what may be the "optimal" intake. After all, it takes 2x more green tea to achieve the effect you get from >2x cups of coffee per day, which is another hint at caffeine as the major driving force behind the anti-stroke effects of tea and coffee. Why? Well a large cup of Starbucks' green tea has 80mg of caffeine, the same amount of their regular coffee has roughly 290mg of caffeine in it.

Figure 1: Age and multivariable-adjusted hazard ratios of cardiovascular disease and its subtypes according to coffee (left) and green tea consumption in 82 369 Japanese (aged 45-74 years; without cardiovascular disease [CVD] or cancer in 1995 and 1998 for Cohort I and II, respectively) who received 13 years of mean follow-up through the end of 2007 (Kokubo. 2013)

Yet despite the validity of the "more caffeine = more brain protection" eqation the catecholamine surge of high amounts of green tea, but even more so coffee is not what you would call "heart healthy" (see figure 1; I would love to tell you the caffeine equivalents, but the scientist don't disclose the serving size). Just another reason to take it easy on stims in pill and drink form and keep your daily caffeine intake in the < 400 mg range (suggested read especially for the smokers: "Putting an "N" as in "nicotine" into "EC" amplifies the negative effects of ephedrine and caffeine on your heart";  read more)

Eating tons of medium chain triglycerides (MCTs) will make you lean

Are we, or rather you, my American friend eating too much fat or simply the wrong type of fats? According to a study that was in the SuppVersity news in Nov. 2013, it's the latter the "SAD Diet Has the Optimal Ratio to Induce Diabesity" (learn more)

It depends. While it may be that you can derive certain benefits by kicking out junkfood from your diet and replacing it with MCTs the "fat-burning" effects of medium chain triglycerides (MCTs) wear off after one to two weeks (White. 1999). Unfortunately, this is way longer than the usually cited studies on the direct metabolic effects lasted, so that a cursory look at the research easily fools you to believe that you could effectively burn fat by simply using MCT oils instead of whatever "bad" fat you had been using before.

Moreover, in the aforementioned study that was published in the American Jorunal of Nutrition roughly 14 years ago the postprandial total energy expenditure was already only 3% higher after the MCT meal in the first week. And it's not only that this advantage disappeared within the next 7 days, the respiratory ratio, a measure of the ratio of carbohydrate to fat oxidation, total fatty acid oxidation and carbohydrate oxidation were also identical in the  32% MCT and 32% LCT diets (both diets contained additional 8% of fat from other sources).

But what about all the other research?

While the transient benefits of the MCT feeding on energy expenditure alone are unlikely to have practical relevance there are a good handful of trials, which show some real world benefits in various dieting scenarios. Unfortunately, they are usually too short (Alexandrou. 2007), compare MCTs to beef tallow & co only diets, observe increases in fatty oxidation, which don't translate into changes in body composition (St-Onge. 2003), or have the subjects in the control group use relatively fragile control oils, such as olive oil for frying and cooking (St-Onge. 2008).

Accordingly, you should not be too surprised that the latest review of the effects of dietary intake of medium chain triglycerides on body composition, energy expenditure and satiety concludes: "

Curried Carrot Soup w/ coconut oil certainly qualifies as a good food choice, also bc. it's made with coconut oil, not plain MCTs (more).

"In the present review it was possible to verify that data related to increased satiety after consumption of MCT are quite controversial. Most studies showed no significant difference as to increased satiety and/or satiation related to lipid consumption. [...] A relevant fact in the lack of consensus among the studies concerns the large variation in the amount of MCT provided in different studies due to lack of reference values for a minimum, ideal and maximum consumption in literature. Moreover, there isn’t enough to long-term studies to identify either beneficial effects or potential harmful effects." (Souza. 2013)

If you go through the list of studies included in the review there are a couple other interesting patterns emerging: (a) the effects - if there were any - originated from the gut (mostly greater satiety effects), (b) if there were effects on body composition those often reached statistical significance in the obese individuals, only, (c) the benefits were more pronounced the less the subjects ate (esp. on those 800kcal hunger diets), (d) when the control was not nasty corn oil, or saturated long chain triglycerides (Atkins diet style), the effects were non-existent.

So, if your are lean, your current diet is balanced and your main fat source is neither corn oil nor beef tallow, the chances that you will be better off with expensive MCT oils than with a couple of spoons of coconut oil in your diet probably border zero. You see, it's just as so often not so much about "adding something in", as it is about leaving something else out / replacing it with a better food choice.

Soy bean oil offers a shortcut to metabolic disease even in the absence of obesity

True. I guess that this "true or false" item was actually way too easy to answer, but the recently published study by Potu et al. is simply too intriguing not to add it to the huge heap of existing evidence that the overabundance of "healthy" polyunsaturated fats from purportedly healthy plant oils is a major contributer to the fat mess we are dealing with.

Figure 2: Effects of 16 weeks on non-heated and heated soybean oil diets rodent food intake, weight gain and body fat (EWAT & IWAT) levels (Penumetcha. 2013)

Now, pro-obesity and pro-diabetic effects of corn oil, soy oil & co are actually no news. Penumetcha et al. do yet emphasize that they are the first to observe that soybean oil which has been heated on a hot plate at 190°C for 3 hours (think of the huge pots, frying pans & co that are used to produce convenient and fast foods) before it was added to the rodent chow has the unique ability to increase its consumers body fat levels without increasing their total body weight. Excellent, right?

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Thats it for today! Ok, I guess that was too easy, as well. Still, it's true and I hope you enjoyed the last week and are already looking forward to the next week of exercise and nutrition science news here at the SuppVersity.

In the mean time you can kill some time by surfing over to the Suppversity Facebook Wall, where you will find news such as

• 

  Even if you align them like that, it is at least debatable whether capped fish oil is much more natural than the structurally modified 16 -carbon saturated fatty acid tetradecylthioacetic acid (TTA). And the usefulness of the longterm use of both remains questionable (learn more). 

  Beware of omega-3s unless you have the right genes -- New Inuit study confirms: If n-3 fatty acids are good or bad for you is in your genes (read more)

• Muscular imbalances commonly overlooked factor in lower extremity sports injuries -- Scientists observe significant relationship of the coordination between muscle strength (ankle plantar flexor/ dorsi flexor), (hip addactor/abdactor), (knee flexor/ extensor) with muscle injuries (read more)

• Arteriosclerosis is not a "neolithic" disease that occurred with the advent of agriculture -- Lancet paper debunks the myth of the "agricultural origin" of atherosclerosis (read more)

and when you are at it, don't forget to congratulate the one and only Adelfo Cerame Jr for finally bringing home those two small muscular statues you see in the image on the top of the page.

References:

• Alexandrou E, Herzberg GR, White MD. High-level medium-chain triglyceride feeding and energy expenditure in normal-weight women. Can J Physiol Pharmacol. 2007 May;85(5):507-13.
• Kokubo Y, Iso H, Saito I, Yamagishi K, Yatsuya H, Ishihara J, Inoue M, Tsugane S. The Impact of Green Tea and Coffee Consumption on the Reduced Risk of Stroke Incidence in Japanese Population: The Japan Public Health Center-Based Study Cohort. Stroke. 2013 Mar 14.
• Rego Costa AC, Rosado EL, Soares-Mota M. Influence of the dietary intake of medium chain triglycerides on body composition, energy expenditure and satiety: a systematic review. Nutr Hosp. 2013 Jan-Feb;27(1):103-8. 
• Souza MA, Mota BC, Gerbatin RR, Rodrigues FS, Castro M, Fighera MR, Royes LF. Antioxidant activity elicited by low dose of caffeine attenuates pentylenetetrazol-induced seizures and oxidative damage in rats. Neurochem Int. 2013 Feb 26.
• St-Onge MP, Bourque C, Jones PJ, Ross R, Parsons WE. Medium- versus long-chain triglycerides for 27 days increases fat oxidation and energy expenditure without resulting in changes in body composition in overweight women. Int J Obes Relat Metab Disord. 2003 Jan;27(1):95-102.
• St-Onge MP, Bosarge A. Weight-loss diet that includes consumption of medium-chain triacylglycerol oil leads to a greater rate of weight and fat mass loss than does olive oil. Am J Clin Nutr. 2008 Mar;87(3):621-6.
• White MD, Papamandjaris AA, Jones PJ. Enhanced postprandial energy expenditure with medium-chain fatty acid feeding is attenuated after 14 d in premenopausal women. Am J Clin Nutr. 1999 May;69(5):883-9.

Selenium & Skin Cancer. ALA, Inflammation & Muscular Adaptations. Eccentric Training & Oxidative Muscle Fibers. Tip of the Day: Have Plenty & Regular Sex For Your Brain

Certain "behaviors" during spring break can give your brain a neuro-anabolic break.

13% and 15% that's the number of Canadian University Students who claim to do what it takes to keep their brain volume at least stable over the spring break. 13% of the female and 15% of the male student and female students, respectively, that's also the SuppVersity Figure of the Week and at the same time the relative number of students who openly declared that they were about / had previously engaged in "casual sexual activity" on the upcoming / past spring break trip to Daytona Beach, Florida (Maticka-Tyndale. 1998)

Who said our youth did not know what's good for them?

Since the pertinent study preceded the Glasper study addressed in the current installment of on short notice by 15 years, these results just go to show you that we know instinctively what's necessary to counter the effects of the alcohol over spring-break ;-)

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Selenium and skin cancer (Cassidy. 2013) -- I guess you will remember the debate that arose after the data from the selenium + vitamin E large scale trial hit the mainstream media news. Hell broke lose and people did (unfortunately) not only start questioning the usefulness, but also the safety of all vitamin supplements - and that quite frantically (cf. "Ask Dr. Andro, Are Vitamin Pills Bad for Me?").

The results of a recently published study by scientists from the Huntsmen Cancer Institute (no that's not "Paleo" ;-) in Salt Lake city could shed at least some new insights into the very mixed results we are seeing in the studies on vitamins and/or minerals with anti-oxidant prowess:

"Taking A Multivitamin is a Question of Faith", above all (read more)

"We studied the effects of Se in vitro on UV-induced oxidative stress in melanocytes, and on apoptosis and cell cycle progression in melanoma cells. In vivo, we used the HGF transgenic mouse model of UV-induced melanoma to demonstrate that topical treatment with l-selenomethionine results in a significant delay in the time required for UV-induced melanoma development, but also increases the rate of growth of those tumors once they appear. In a second mouse model, we found that oral administration of high dose methylseleninic acid significantly decreases the size of human melanoma xenografts." (Cassidy. 2013)

In other words, in as much as they are able to postpone / prevent the occurrence of cancer by protecting the healthy cells, their protective effect is not tissue specific and will - once the bad guys have appeared on the scene protect the cancer from your bodies own, as well as the pharmacological inflammatory anti-cancer machinery.

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Alpha lipoic acid does not hamper exercise induced intramuscular ROS production & DNA damage (Fogarty. 2013) -- I know this does not really sound like good news to some of you, but you will be surprised that even the authors of the study at hand feel that it is.

While this is not directly related to the intramitochondrial ROS production, I still reccomend, you read my previous article on the purported "nutrient partitioning effects" of ALA before you go and buy a year's supply. (learn more)

The scientists from the University of Ulster recruited 12 of this in the world of scientific paper "rare specimen" of healthy male study participants (age 28 + 10 years, stature 177 +/-12 cm and body mass 81 +/-15 kg) and had them take either 2x1,000mg of regular alpha lipoic acid twice a day or placebo.

Wouldn't it be better to use R-ALA? I am telling you this now for the 1124th time: There is no reliable evidence for the superiority of R-ALA over regular ALA, the majority of the studies showing benefits of ALA supplementation has been conducted with the 50% r-enantiomer and 50% s-enantiomer version and if you have ever heard of the hormesis hypothesis (=low (eu-)stress induces beneficial adaptation) you would rather ask, "isn't it likely that taking R-ALA would not have yielded the same beneficial effects?"

The caps were to be taken in addition to the regular diet, the young men were following and were supposed to build up a protective anti-oxidant belt against the exercise induced oxidative assault of 100 isolated and continuous maximal knee extensions in the non-dominant leg after 14 days of supplementation.

"[The ALA preload] increase[d] plasma antioxidant status and attenuates lipid peroxidation and DNA damage following maximal, eccentric muscle contractions[, but] had no protective effect on muscle mitochondrial DNA damage."

Now this is actually awesome news, because it shows that ALA blunts the systemic oxidative damage only, while leaving the local intra-muscular oxidative damage of which the researchers rightly point out that "a substantial body of literature documents" the beneficial effects of ROS on "cell adaptation associated with exercise training" (Fogarty. 2013). In other words: It's unlikely ALA will hamper your gains.

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Eccentric training for bigger stronger muscles? (Hody. 2013) -- At first sight the conclusion of a soon-to-be-published study from the University of Liège in Belgium, which says:

"Our data suggest that the eccentrically biased contractions in mice induced specific adaptations in protein expression and muscle fiber composition which may reflect a more oxidative muscle phenotype." (Hody. 2013)

appears to suggest that the longstanding wisdom that eccentric reps are (given you get adequate rest) profoundly anabolic was inaccurate. If you use your knowledge about the enormous degree of type I fiber hypertrophy in bodybuilders (cf. fig.1 here), however, the information that eccentric training causes a shift in the muscular phenotype towards a predominantly oxidative slow-twitch fiber make-up, would at least the part about the muscles becoming "bigger" will remain intact.

Figure 1: Effect of five training sessions of variable duration (75-135 min / increasing from session to session) with 48h breaks between sessions on the muscle fiber make-up of mice (Hody. 2013)

Now, don't be afraid that your eccentric biceps curls could eventually make you weak. There are some "on the other hands" attached to the study results. The first and most important one of these is the mere fact that the largest increase occurred in type IIa fibers which are also often referred to as "oxidative" muscle fibers, but are actually more of an "jack-of-all-traits" fiber type, which happen to do most of the work in the BB-relevant 6-15 rep range. Secondly, the training downhill-running protocol the adult C57BL6 mice were exposed to. Downhill-running, may be eccentric, but it is also an endurance and no strength training regimen, and will thus have a tendency to promote the

No pain inflammatory signaling, no gain? In the long(er) run this could in fact be true (learn more). And what would be more fitting to induce the former if not eccentric training?

That being said, it is only logical that whatever growth / genera adaptation mechanism a given exercise regimen may be triggering, the trained muscle group and in this case also the trained fiber-type will benefit the most. Moreover, scientists and laymen tend have a very different understanding of a "shift in fiber type composition" by which the former don't imply loss of any fibers, while the latter misunderstand the ratios for absolute values and fool themselves to believe that results like the ones of the study at hand were about "losing precious type II" (=fast twitch, glycolytic, "lift heavy, but short") muscle fibers. What they are really about, is yet the accentuated ability of the highly stressing eccentric reps to induce more than just a "balooning up" of the muscles and induce profound structural adaptations, the importance of which I have highlighted only a couple of days ago in the context of my post on satellite cells (read up on that one).

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Only regular sexual intercourse keeps your brain healthy and in shape (Glasper. 2013) -- No, I am not going to start this comment with a reference to certain old men who met a couple of days ago in Rome. I will rather stick to the relevant facts and inform you that you better make sure you get laid this weekend. Why? Easy, a recent study by scientists from the University of Maryland and Princton University shows quite impressively that our body notices that we are useless once we give up reproducing. So useless, in fact, that he even does not bother to repair our brains any longer:

In a past installment of On Short Notice you have already learned what the female orgasm could be for, remember? Which brings up the question will the women benefit, as well? Likely.

"Sexual experience enhanced the number of newly generated neurons in the dentate gyrus with both single and repeated exposures in middle-aged rats. Following continuous long-term exposure to sexual experience, cognitive function was improved. How-ever, when a prolonged withdrawal period was introduced between the final mating experience and behavioral testing, the improvements in cognitive function were lost despite the presence of more new neurons." (Glasper. 2013)

You want a bottom line? Well, let's make it fast, I feel I got to do something for my brain, now! Have sex, have it regular and have plenty of it (the rodents did it at least once a day) and when the new pope calls, tell him it's just for your brain health ;-)

Note: Although I deliberately wrote this part of On Short Notice, I hope that you are all old enough to know that getting drunk and having unprotected sexual intercourse with the next best person you can find "spring break style" is an absolute no-go. Not just for Catholics, but for any sane human being who has not already drowned his last neuron in alcohol.

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That's it for today, and I guess with the Glasper study in the back of your head, I don't have to tell you that there are other things than hanging out in front of the computer, TV or even the gym that can be done on the weekend, right? Enjoy!


References:

• Cassidy PB, Fain HD, Cassidy JP, Tran SM, Moos PJ, Boucher KM, Gerads R, Florell SR, Grossman D, Leachman SA. Selenium for the prevention of cutaneous melanoma. Nutrients. 2013 Mar 7;5(3):725-49.
• Fogarty MC, Devito G, Hughes CM, Burke G, Brown JC, McEneny J, Brown D, McClean C, Davison GW. Effects of α-Lipoic Acid on mtDNA Damage following Isolated Muscle Contractions. Med Sci Sports Exerc. 2013 Mar 6.
• Gasper ER, Gould E. Sexual Experience Restores Age-Related Decline in Adult Neurogenesis
  and Hippocampal Function. Hippocampus. 2013 [Epub ahead of print]
• Hody S, Lacrosse Z, Leprince P, Collodoro M, Croisier JL, Rogister B. Effects of Eccentrically and Concentrically Biased Training on Mouse Muscle Phenotype. Med Sci Sports Exerc. 2013 Feb 22. 
• Maticka-Tyndale E, Herold ES, Mewhinney D. Casual sex on spring break: Intentions and behaviors of canadian students. Journal of Sex Research. 1998; 35:3.