Science Round-Up Seconds: Stevia, Cancer & Fertility. What is the Verdict? Exercise, Hunger & GLP-1. Can a Workout Fill You Up? Postactivation Potentiation & Personal Bests. 8% More Maximal Power After 5s Max. Voluntary Contraction?

Other news: Classic cardio ramps up GLP-1 and "posing" increases your maxes by up to 8%.

If you have already downloaded and listened to yesterday's installment of the SuppVersity Science Round-Up, you will probably be aware that the first thing I am going to do in today's Seconds is to (re-)address the stevia issue (read up on previous stories about Stevia here at the SuppVersity).

If I recall that correctly, I did in fact forget to mention something that's actually important if you want to get the whole picture - the gut microbiome! But before we tackle this one, let's not forget that there are a couple of other news stories which did not make it into the 60min show, news on the effects of LISS on GLP-1 and the potentiation of the post-activation potentiation effect. Sounds interesting, then let''s go for it!

Is stevia toxic, does it cause cancer and infertility? 

Let me start with the bottom line first. The currently available scientific evidence clearly suggest that stevia is safe to consume. Or, as "real" scientists (not that I would not consider myself a scientist, but without a single published paper in this domain of science, I am certainly not an authority ;-) write in their papers:

What was that about the microbiome? I forgot to mention that the "bad" aglycol aka "steviol" is also produced from the benign and usually not even absorbed pure steviosides and is thus not something you'll find only in "natural" stevia products. That being said, Wingard et al. observed in 1980 already that steviol is readily excreted via the billary pathway in the feces (Wingard. 1980; confirmed by Nakayama. 1986). You may thus be exposed to small amounts of steviol no matter what, but that's nothing your body cannot dispose of.

"The recent suggestions that steviol glycosides present a muta-genic – and therefore carcinogenic – risk to consumers are not sup-ported by actual test results. The paper making this claim by Matsui et al. (1996a) was published prior to most of the papers assessing the genotoxic risk of steviol glycosides as well as several expert panel reports and a review by Brusick in 2008. The database of genotoxicity studies for steviol glycosides and steviol as it currently stands, combined with a lack of evidence for neoplasm development in rat bioassays (Aze et al., 1991; Xili et al., 1992; Toyoda et al., 1997; reviewed by Carakostas et al., 2008, 2013; EFSA, 2010), is adequate to establish the safety of these food ingredients with respect to their genetic/carcinogenic potential." (Urban. 2013)

And with respect to the infertility claim, Geuns et al. write in their very detailed review from 2003:

"The results of a decrease of live birth rate in rats (Planas and Kuæ, 1968) by Stevia decoctions were refuted by Shiotsu (1996) who did more reliable experiments with many more animals using methods as similar as possible to the methods used by Planas and Kuc. No effect on general condition, body weight, water consumption, live birth rate or litter size was found. No effects of stevioside were found on fertility or reproduction in mice (Akashi and Yokoyama, 1975), rats ( Mori et al., 1981, Xili et al., 1992 and Sinchomi and Marcorities, 1989) or hamsters (Yodyingyuad and Bunyawong, 1991).

No significant effect was found on spermatogenesis, nor on the interstitial cell proliferation and tumor formation in the testes of F344 rats fed a ration containing up to 1% stevioside (95.2% purity) for 22 months (Yamada et al., 1985).

If you are either a newcomer to the SuppVersity or simply cannot remember the summary of selected stevia research from September last year, I suggest you go back in the archives and read up on "More Than Super Sweet: More Scientific Evidence, More Potential Implications for Weight Loss & -Maintenance, Anti-Diabetic & -Autoimmune and Even Pro-Anabolic Effects" (learn more) Some of the benefits are btw. mediated by the same stuff that's toxic in in-vitro studies...hormesis, you know ;-)

Whereas Melis (1999) suggested a possible decrease of the fertility of male rats by a very high dose of Stevia extract, Oliveira-Filho et al. (1989) who administered extracts with similar stevioside content stated that there is certainly not an effect on male fertility. It is not sure that the observed effects were due to the stevioside present in the extract. It should also be mentioned that the used extract concentrations were extremely high, at the start of the experiments even 5.34% of the body weight (or around 5.3 g stevioside/kg bw). For an adult person of 65 kg this means 3.47 kg of dry Stevia leaves or about 34.7 kg fresh leaves/day, i.e. more than 50% of the body weight! The significance of such experiments where only one extremely high concentration was tested, should be questioned. Melis' results are also in contradiction with the above and below cited studies that could not reveal any effect on fertility of male or female animals." (Geuns. 2003; my emphases)

Much ado about nothing? Well, in the end it may seem so and the preponderance about freakin' out over every potential and 0.5% marginal possibility that something you do or eat could be wrong or toxic certainly ain't healthy. On the other hand, it's always good to exhibit a certain degree  of suspiciousness - just do me favor: Do that towards both the good and the bad news!

Scheduled news that did not make it into the live show

The fat burning benefits of hydroxypropyl-distarch phosphate from waxy maize starch  (WMHDP) are - at least in part - also mediated by increases in GLP-1 production (read more)

Short and long-term effects of exercise on appetite and metabolism regulating hormones -- (Ueda. 2013) As a SuppVersity reader and SHR listener, you are no stranger to the acronym GLP-1 and the effects the "satiety hormone" it stands for has on your desire to eat and, more importantly, your metabolisms willingness to use not store the energy from the food you consume (learn more).

In a soon to be published paper, Shin-ya Ueda and colleagues report that chronic exercise, in this case 3x/week 60min of light intensit (65% of VO2max) cardio on a treadmill and/or cycle ergometer results in a statistically highly significant increase in GLP-1 in response to exercise.

Usually I don't like to repeat myself, but I would probably have missed the main important message here, if I were just skimming the above: The 20 healthy middle-aged women who participated in the 12-week experiment did not simply have higher GLP-1 levels after a meal. No, the post-exercise levels of GLP-1 and the other satiety hormone PYY increased hours before the ladies even got their next meal.

Figure 1: GLP-1 (pmol/ml; left) and PYY (pmol/ml; right) response to exercise before and after (0, 30, 60 min) a 80min (60 min effective training + 20min warm-up, cool-down etc.) supervised workout before (untrained) the 12-week exercise intervention and after (trained) the 12-week exercise intervention (Ueda. 2013)

In conjunction with the significant correlation of GLP-1 with the reduction in body weight the study participants achieved over the course of the course of the 12x3 = 36 supervised exercise session, this was reason enough for the scientists to hypothesize that...

"[...] that the ability of exercise training to create a negative energy balance relies not only directly on its impact on energy expenditure, but also indirectly on its potential to modulate energy intake." (Ueda. 2013)

So, does exercise "just make you hungry". No, it turns you into a satisfied fat burning machine - and that even if it's just 3x60min of LISS per week.

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Training increases the efficacy of 5-6s maximal contractions to before a maximal voluntary effort (Miyamoto. 2013) I guess you will be aware that Superman usually does a 5-6s maximal voluntary contraction (MVC) while checking out if everybody is watching before he eventually does the deed and lifts the car that has just overrun the beautiful blond bombshell with a "single-armed deadlift", right? Good, because if you know that, I don't have to explain why the scientists from the Waseda University in Japan 21 healthy male subjects perform a 5s MVC before they did their maximal voluntary concentric knee extensions 1, 3 and 5 minutes, thereafter.

Figure 2: Voluntary concentric torque on knee extensions after previous peak contractions before (left) and after (right) in the trained and untrained study participants.

What I probably still have to tell you though is that the "after" values you see in figure 2 were taken after 12-weeks of doing 5x 8 reps with 80% of the one-repetition max in a standard knee extension machine. Ok, I have to admit that the actual training effect is not really impressive, but since most of you have it already built in (after all, you probably train for more than 12-weeks already, right?) doing a single 5s maximal voluntary contraction before a max-effort trial is an easy and time-efficient (1 min!) way to increase your performance by superman-like 8%! What this funky technique is called like? Postactivation Potentiation - nice alliteration, isn't it?

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That is it, for the day - at least for the Seconds. If you don't know what to do before the weekend begins, browse over to the SuppVersity Facebook Wall and check out news on

• 

  If you have not done so, already, click here and teach yourself "How to Make the Correct Fish choices"? There is luckily way more swimming around in our oceans than farmed salmon with it's more than 4x elevated n6:n3 ratio (compared to wild salmon, learn more)

  Salmon in the vicious cycle of soy supplementation - Scientists try to come up with a certain bacteria that could protect farmed salmon from the junk, ah... soy it's fed (read more)

• Alpha lipoic acid (ALA) helps otherwise healthy schizophrenics on heavy anti-histamine regimen to lose weight - 2x 1gram of regular ALA does the trick (read more) 

• People who were breastfed as kids have healthier eating habits in their adulthood - Interestingly, this effect did not depend on social class at birth or later in life and occurred irrespective of smoking status, alcohol intake or reported physical activity.

Once you've done that, you first make sure that you did not miss part three of my interview with Sean Casey and then get off the screen and into the night, family or whatever real life, I'd hope you did not give up on after you bought your latest iPhone ;-)


References:

• Akashi H, Yokoyama Y. Security of dried-leaf extracts of Stevia. Toxicological tests. Food Industry. 1975; 18:34–43.
• Aze Y, Toyoda K, Imaida K, Hayashi S, Imazawa T, Hayashi Y, Takahashi M. [Subchronic oral toxicity study of stevioside in F344 rats]. Eisei Shikenjo Hokoku. 1991;(109):48-54.
• Carakostas MC, Curry LL, Boileau AC, Brusick DJ. Overview: the history, technical function and safety of rebaudioside A, a naturally occurring steviol glycoside, for use in food and beverages. Food Chem Toxicol. 2008 Jul;46 Suppl 7:S1-S10.
• Geuns JM. Stevioside. Phytochemistry. 2003 Nov;64(5):913-21. Review.
• Matsui M, Matsui K, Kawasaki Y, Oda Y, Noguchi T, Kitagawa Y, Sawada M, Hayashi M, Nohmi T, Yoshihira K, Ishidate M Jr, Sofuni T. Evaluation of the genotoxicity of stevioside and steviol using six in vitro and one in vivo mutagenicity assays. Mutagenesis. 1996 Nov;11(6):573-9.
• Melis MS. Effects of chronic administration of Stevia rebaudiana on fertility in rats. J Ethnopharmacol. 1999; 167:157–161 
• Miyamoto N, Wakahara T, Ema R, Kawakami Y. Further Potentiation of Dynamic Muscle Strength after Resistance Training.  Medicine & Science in Sports & Exercise. Publish Ahead of Print
• Mori N, Sakanoue M, Takcuchi M, Shimpo K, Tanabe T. Effect of Stevioside on fertility in rats. J Food Hyg Soc Jpn. 1981; 22:409–414.
• Nakayama K, Kasahara D, Yamamoto F. Absorption, Distribution, Metabolism and Excretion of Stevioside in Rats. Shokuhim Eiseigaku Zasshi. 1986; 27(l):l-8.
• Oliveira-Filho RM, Uehara OA, Minett CASA, Valle LBS. Chronic administration of aqueous extract of Stevia rebaudiana (Bert.) Bertoni in rats: endocrine effects Gen. Pharmac. 1989; 20:187–191. 
• Planas GM, Kuæ J. Contraceptive properties of Stevia rebaudiana Science. 1968;162:1007.
• Shiotso S. Fertility study of Stevia decoction in rats. Tech J Food Chem Chemicals. 1996; 4:108–113.
• Sinchomi D, Marcorities P. Etude de l'activité anti-androgénique d'un extrait de Stevia rebaudiana Bertoni. Plantes médicinales et phytothérapie. 1989; 23:282–287.
• Toyoda K, Matsui H, Shoda T, Uneyama C, Takada K, Takahashi M. Assessment of the carcinogenicity of stevioside in F344 rats. Food Chem Toxicol. 1997 Jun;35(6):597-603.
• Ueda SY, Miyamoto T,  Nakahara H, Shishido T, Usui T, Katsura Y,  Yoshikawa T, Fujimoto S: Effects of exercise training on gut hormone levels after a single bout of exercise in middle-aged Japanese women. SpringerPlus. 20132:83.
• Urban JD, Carakostas MC, Brusick DJ. Steviol glycoside safety: is the genotoxicity database sufficient? Food Chem Toxicol. 2013 Jan;51:386-90.
• Wingard RE Jr, Brown JP, Enderlin FE, Dale JA, Hale RL, Seitz CT. Intestinal degradation and absorption of the glycosidic sweeteners stevioside and rebaudioside A. Experientia. 1980 May 15;36(5):519-20.
• Yamada A, Ohgaki S, Noda T, Shimizu M. Chronic toxicity of dietary Stevia Extracts. J Food Hyg Soc Jpn. 1985; 26:169–183.
• Yodyingyuad V, Bunyawong S. Effect of stevioside on growth and reproduction. Human Reproduction. 1991; 6: 158–165.
• Xili L, Chengjiany B, Eryi X, Reiming S, Yuengming W, Haodong S, Zhiyian H. Chronic oral toxicity and carcinogenicity study of stevioside in rats. Food Chem Toxicol. 1992 Nov;30(11):957-65.

Optimal Carnosine Loading: Taking Beta Alanine With Food Renders the Cheap Bulk Stuff more Potent Than Fancy Time-Released Preparations. Preview: Science Round-Up: Daylight Saving, Stevia Toxicity, Protein Excess & More

Since it's Thursday my voice is back and I am already looking forward to today's SuppVersity Science Round-Up in which Carl Lenore an I are going to "attack" the following topics (tune in live at 1PM EST),

That pills can rarely compete with whole foods is something you've heard on SHR and read on the SuppVersity often, but that pills - in this case beta alanine pills - are better, when the content is mixed into the food instead of being prepared in form of time-released or whatever else caps may be news to some of you.

• Summer time and the jet-lag is there... the effects and idiocy of daylight saving.
• Stevia an anti-fertility sweetener, carcinogen and yet another welcome root of all evil?
• Dairy & weight loss revisited, when even the abstract contradicts the conclusion.
• Does too much protein make you fat? Yes it does - at least that's what the latest epidemiological data says.
• Fish oil makes women hungry, exercise satisfies their cravings and improves gut hormone signalling.
• High dietary restraint makes women lose their nocturnal progesterone surge

I decided to pick a fast, put practically relevant topic as the SuppVersity news of the day: Beta Alanine Supplementation; or, to be even more precise: "Optimal" beta alanine supplementation.

The less tingles the better!?

What type of food did the subjects eat? In the acute test the data in figure 1 (left + right) is based on, the subjects consumed a standardized breakfast consisting of 4 slices of white bread with chocolate-hazelnut paste, 200ml semi-skimmed milk, 1 banana and 125gr fruit yogurt, and a second meal with 150gr baguette topped w/ 40gr young cheese, 30gr mayonaise and vegetables with a 33cl orange juice (data not shown in figure 1). In the chronic ingestion study (figure 1, middle) participants in the w/ meal groups had 1x800mg cap with their three regular main meals and the fourth with a snack.

As a diligent student of the SuppVersity you will know that a major problem with beta alanine  in scientific studies is that even the "time-released" tabs, the scientists usually use can produce this tingling sensation in all sorts of the body (I can tell you about that, from my more is more days back in the day; you really won't believe in which places you can "tingle" ;-) After my initial excitement and putting some thought into the hitherto still not 100% understood origin of the tingles, I did yet realize that they are not just unnecessary for the BA to work but could in fact be a negative (also physiologically negative) side effect of too much of the potentially toxic substance floating around in your blood stream (cf. Beta Alanine Suffocates Cardiomyocytes; other previous posts on BA).

Don't worry, it is totally unlikely that you will ever achieve serum concentrations that could do any harm, but one thing you should remember is that what you are striving for is not a high amount of beta alanine (BA) in your body. Your goal is to ramp up the intramuscular carnosine stores and that works only if the BA does recombine with the essential amino acid histidine and is subsequently stored within the skeletal muscle.

Food as an "advanced delivery formula"

The recombination / incorporation process is likely to be rate limited, so that it is only logical that any "overshoot" of beta alanine (again nothing your body likes to  have floating around in the system) is going to be cleared before it can do its carnosine loading job. A job that is therefore facilitated by "packaging" the BA molecules with fillers & co in tabs, or - much cheaper and obviously way more natural - by simply ingesting it with food.

Figure 1: Selected time-frame of 8h blood profile of plasma insulin and beta-alanine (BA) after ingestion of 800mg of BA after meal in between meals or with meal (left and right). Effect of chronic ingestion of 4x800mg/day BA for five weeks with or w/out food in regular and sustained released form  ( Stegen. 2013)

As the data in figure 1 that's based on the results of a soon-to-be-published study by Stegen et al. goes to show you, the "food advantage" is (as usual ;-) the 34 male and female subjects (age 19.4y; weight 66kg, daily BA intake at baseline ~230mg/day) derived from ingesting the BA with meals may not be earth shattering.

Still, the subjects who took the BA with a meal did not just have higher muscular carnosine levels than those who took the pure powder, at least in the slow-twitch fibers of the soleus, which are actually not that beta alanine affine as their counterparts in the gastrocnemius, the cheap and ingeniously simple "take it with food" solution to BA supplementation also outperformed the obviously pricier pre-prepared slow-release formula.

Where does the beta alanine go to, if not into the carnosine stores? 

The scientists did yet also make another interesting observation, while only 1.6% of the beta alanine was excreted in the urine (slow release formula) the muscular uptake and the incorporation efficiency of exogenous BA into carnosine is actually so low that "the vast majority (~160g or 95-96%) of the ingested BA is neither going into muscle carnosine nor into the urine" (Stegen. 2013).

While respective scientific studies would still have to be conducted, the most likely hypothesis to explain the "disappearance" of beta alanine are:

• Oxidation and use for energy production: While the contribution of alpha-amino acids to energy delivery in muscle and other tissues is usually quite low, as compared to carbohydrates and fat, their usage increases (up to 10% of total energy usage) with increasing amounts of the AA in the bloodstream. Evidence suggests that this is also the case for beta-amino acids, where and "excess" would obviously be achieved with dosages as they were used in most of the previous research on beta alanine supplementation (Harris. 2006, Hill. 2007; Baguet. 2009).
  
  This hypothesis is also supported by the recent revelation that GABA transaminase activity, the enzyme that's required to initiate the oxidation of beta alanine increases upon  BA supplementation (Everaert.2013)

• Alternative pathways including uptake and incorporation into carnosine in other tissues: While it is not impossible that other organs (e.g. the kidney, liver or brain) avail themselves of small quantities of BA to up their own carnosine levels it is, as the scientists point out " unlikely that the conversion of BA into carnosine in other (non-muscle) tissues is of any quantitative significance, because presence of carnosine and carnosine synthase in non-muscle tissues is several orders of magnitude lower than in muscle" (Stegen. 2013)

Now that we have gotten that straight, the one question that remains is actually pretty simple, unlike the answer unfortuntately....

How does the meal improve the the bioavailability of BA

Personally I still feel that the main effect is the prolonged elevation of beta alanine, the scientists themselves however propose another (at least confounding) factor, which would also explain why simply taking the slow release formula won't work even if it is released just as slow as regular BA with food:

While BA still is often named in the same breath with creatine, the effect size and the likelihood that athletes will see any benefits at all is much smaller than in the case of the supplemental top dog (learn more in  "Beta-Alanine Does not Make it From Bench to Pool Side: Are the Effects Too Short-Lived? Is Swimming the Wrong Sport? Or Was the Dosage of 3.2g/day Simply Too Low?")

"Clausen et al.showed that Na+/K+ pumps in skeletal muscle are stimulated by insulin over a range of concentrations down to low physiological levels (Clausen. 2003). Therefore, it is possible that meal-induced elevations in serum insulin are capable of triggering the sodium-dependent transporter TauT. In our study, a meal-induced effect could only be confirmed in soleus muscle. Considering the fact that this is a more insulin-sensitive muscle, it is not unlikely that the soleus responds better on insulin induced BA uptake. In addition Lavoie et al. demonstrated that insulin-induced translocation of Na+/K+ ATPase subunits to the plasma membrane (Lavoie. 1996), one of the two possibilities to increase Na+/K+ ATPase activity, is restricted to oxidative fiber-type skeletal muscles which are predominantly present in soleus."

Sounds more than logical and can also explain the differential effect on the oxidative = slow twitch fibers of the soleus (cf. figure 1, middle). With the insulin enhanced "pump activity" you have a mechanistic increase in BA uptake, no wonder that this improves the bioavailability, right?

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Bottom line: From now on you buy your beta alanine in bulk and spoon-feed yourself with your 4x800mg of BA (the dosage used in the study at hand) after your preferably carb-containing meals and snacks. Don't worry BA is one of the few amino acid supplements that don't have a disgusting taste to them. You can actually add it directly to the food, but I would refrain from doing that before you prepare your meal. As simple as the BA molecule may be, we still don't know what kind of chemical reaction it may be exposed to if you actually cook it or do whatever other "nasty" things to it ;-)

References:

• Baguet A, Reyngoudt H, Pottier A, Everaert I, Callens S, Achten E, and Derave W. Carnosine loading and washout in human skeletal muscles. J.Appl.Physiol. 2009; 106:837-42.
• Clausen T. Na+-K+ pump regulation and skeletal muscle contractility. Physiol Rev. 2003; 83:1269-324.
• Everaert I, De Naeyer H, Taes Y, Derave W. Gene expression of carnosine-related enzymes and transporters in skeletal muscle. Eur J Appl Physiol. 2013 Nov 4.
• Harris RC, Tallon MJ, Dunnett M, Boobis L, Coakley J, Kim HJ, Fallowfield JL, Hill CA, Sale C, and Wise JA. The absorption of orally supplied beta-alanine and its effect on muscle carnosine synthesis in human vastus lateralis. Amino.Acids. 2006; 30:279-89.
• Hill CA, Harris RC, Kim HJ, Harris BD, Sale C, Boobis LH, Kim CK, and Wise JA. Influence of beta-alanine supplementation on skeletal muscle carnosine concentrations and high intensity cycling capacity. Amino.Acids. 2007; 32:225-33. 
• Lavoie L, Roy D, Ramlal T, Dombrowski L, Martin-Vasallo P, Marette A, Carpentier JL, and Klip A. Insulin-induced translocation of Na+-K+-ATPase subunits to the plasma membrane is muscle fiber type specific. Am.J.Physiol. 1996; 270:C1421-C1429.
• Stegen S, Blancquaert L, Everaert I, Bex T, Taes Y, Calders P, Achten E, Derave W. Meal and Beta-Alanine Coingestion Enhances Muscle Carnosine Loading. Med Sci Sports Exerc. 2013 Mar 5.

Tongkat Ali - Malaysian Viagra W/ Anti-Belly Effect: More Than 30% Reduced Omental Fat Pad Size + Corresponding Increases in Testosterone W/ Human Equiv. of 4g+/Day

It's efficacy in situations like this has more scientific back-up than any of the muscle building of fat burning promises some Tongkat Ali supps come with.

By now, most of you should have read the article on the testosterone "boozing" effects of alcohol and realized that the post workout Margarita probably comes off second best, when we compare it to whey and may - at least until we don't know otherwise - actually be pathological (=the result of a disturbance of the normal hormone metabolism in the liver). That being said, we better go back the "tried(!) and proven(?)" stuff. I mean a herb that goes by the name "Long Jack" does already sound way more promising than a "Blood Mary" doesn't it?

"Long Jack? ;Malaysian viagra? Ok, I am in!"

As the popular name already implies, the root of Eurycoma longifolia Jack, an evergreen plant that belongs to the family Simaroubaceae has a long (all puns intended) tradition in folk medicine. For which purposes? Well, in Malaysia, where people obviously like it a little more explicit, it's called "Tongkat Ali" (TA) and means (literally translated) "Ali's walking stick"... if that ain't explicit enough for you, just call it the "bushman's viagra", or whatever you like.

What's interesting and important to know though is that medicinal value highly of the root extract depends on the soil the plant was grown on. Tongkat Ali from the Malaysian Peninsular, for example, has higher concentrations of phytochemical compounds, such as eurycomaride, tannins, high molecular weight polysaccharides, glycoproteins, mucopolysaccharides and alkaloids of the quassinoid group, than TA from Thailand, Vietnam or Indonesia (Jiwajinda. 2001; Miyake. 2009). This is an important fact to keep in mind, when you buy your TA and a potential reason why you (a) may require way higher dosages than science would suggest to see any effect or (b) may not experience any of the benefits you may have hoped for (e.g. raging libido, increased testosterone and, as you are about to learn in today's article, loss of belly fat).

"Did I hear fat loss?" Yeah, you did!

I have to concede, the hitherto unrecognized fat loss effects Solomon et al. report in their latest paper that's about to be publishe in the peer reviewed journal andrologia were actually the main reason the 14-day rodent experiment the South African researchers conducted eventually made it into the SuppVersity news. The meager testosterone increase of +30% alone doesn't give me a kick, at all. I mean there are way more potent natural testosterone boosters out there that don't exert any beneficial downstream effects on your physique. So why should we bother?

Figure 1: Relative (in % of pre values) body weight, testes weight, prostate weight, weight of the epididymal and omental fat pads, the gastrocnemius muscle and the testosterone levels of the rodents after 14 days on the high or low dose of the extract (

And in fact, the 5.7% reduction in body weight the rodents in both the low (200mg/kg) and high dose (800mg/kg) arm of the study experienced would be quite the opposite of what you'd usually expect as a downstream effect of increased testosterone levels in otherwise healthy rodents. With a statistically significant increase in sperm vitality in the low dose and a less pronounced statistically non-significant increase in sperm vitality in the high dose group, as well as the highly significant increases in sperm count in both groups, it is yet very unlikely that the already small amount of body weight the rodents lost in the course of the 14-day experiment was a sign of toxicity or whatever.

What's more likely is that the overall weight loss effect is simply the result of the highly significant -31.9% reduction in omental and probably other not explicitly measured body fat (not the epididymal fat, i.e. the fat around the reproductive organs, though).

"How much of this stuff do I need?"

Don't be fooled: The testosterone and libido boosting effects we see in the study at hand is something dozens of other herbs can do as well, thin of the study on Nigella Sativa from one of the past installments of "On Short Notice", for example.

Provided you can get your hands on a correspondingly potent extract, it probably would not be necessary, and certainly a waste of valuable ressources to take more than the low dose regimen (HED 4g/day) , which is, compared to what we have hitherto seen in human trials, still hilariously much.

For the fertility part of the equation, way smaller doses of as little as 300mg of a freeze dried water extract from TA (brandname Physta(R)) have shown quite astonishing results in a group of 30-55 year old male subjects who achieved a 44.4% higher sperm motility, 18.2% higher semen volume and subjectively improved erectile performance after 12-weeks on this commercially available product (Ismail. 2013).What you should at least keep in mind though is the fact that financing of the study was provided by Biotropics Malaysia Berhad, the producer of Physta.

Similar fertility related results were also reported by Tambi et al. in 2010 (another "proprietary extract" ;-) and a handful of older and in some cases non-peer reviewed studies. As far as more physical culture related effects are concerned, a recent review by Chen et al. concludes that

"Eurycoma longifolia Jack, or 'tongkat ali', has not appeared to elicit any ergogenic effect on endurance performance in a limited number of studies of these herbs. However, future studies of this herb are definitely warranted because there might be a dose-dependent response and the supplementation duration of the previous studies might have been too short." (Chen. 2013)

It would therefore appear as if TA was more of "classic" libido & testosterone booster than an ergogenic. Something like tribulus and maca and just as those two probably of very dubious usefulness for young athletic men in the prime of their reproductive years.

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Bottom line: That being said, Long Jack could be worth a try for everyone with already (or temporarily ;-) reduced testosterone levels, at least if we trust the judgement of Tami et al. who conclude their 2013 study into the effects of 1 month on 200g of a water-soluble TA extract with the words: "The standardised water-soluble extract of Tongkat ali proved to be a suitable herbal supplement in overcoming symptoms of LOH [late onset hypogonadism]." (Tambi. 2013)

The veterans among the SuppVerity readers may remember that I also covered the 2013 study by Tambi et al. on the usefulness of TA for men hypogonadal men (learn more)

If you still insist to try it, you should keep an eye on the eurycomanone and 13α(21)-dihydroeurycomaone content of whatever product you are buying, because these are the two fractions which will increase LH and FSH production and are thus probably responsible for jacking up your testosterone and sperm production (Low. 2013).

What? You cannot find a product that's standardized for those? Not even a supplement producer losing a word about their existence? Well, that's how this business works. Cite the studies and discard all the nasty details you don't like...


References:.

• Chen CK, Muhamad AS, Ooi FK. Herbs in exercise and sports. J Physiol Anthropol. 2013 Mar 8;31:4. doi: 10.1186/1880-6805-31-4. Review.
• Ismail SB, Wan Mohammad WM, George A, Nik Hussain NH, Musthapa Kamal ZM, Liske E. Randomized Clinical Trial on the Use of PHYSTA Freeze-Dried Water Extract of Eurycoma longifolia for the Improvement of Quality of Life and Sexual Well-Being in Men. Evid Based Complement Alternat Med. 2013;2013:429268.
• Jiwajinda S, Santisopasri V, Murakami A, Hirai N, Ohigashi H. Quassinoids from Eurycoma longifoliaas plant growth inhibitors.Phytochemistry. 2001; 58:959–962
• Low BS, Das PK, Chan KL. Standardized quassinoid-rich Eurycoma longifolia extract improved spermatogenesis and fertility in male rats via the hypothalamic-pituitary-gonadal axis. J Ethnopharmacol. 2013 Feb 13;145(3):706-14.
• Miyake K, Tezuka Y, Awale S, Li F, Kadota S.Quassinoids fromEurycoma longifolia. J Nat Prod. 2009; 72:2135–2140. 
• Solomon MC, Erasmus N, Henkel RR. In vivo effects of Eurycoma longifolia Jack (Tongkat Ali) extract on reproductive functions in the rat. Andrologia. 2013 Mar 6.
• Tambi MI, Imran MK. Eurycoma longifolia Jack in managing idiopathic male infertility. Asian J Androl. 2010 May;12(3):376-80. doi: 10.1038/aja.2010.7. Epub 2010 Mar 29.
• Tambi MI, Imran MK, Henkel RR. Standardised water-soluble extract of Eurycoma longifolia, Tongkat ali, as testosterone booster for managing men with late-onset hypogonadism? Andrologia. 2013 May;44 Suppl 1:226-30.

Understanding Muscle Hypertrophy - Study Sheds More Light on Process of Satellite Cell Recruitement: SRF, IL-6, STAT3, COX2, IL4 + More Funky Acronyms With Important Roles in the Structural Component of Muscle Growth.

No pain inflammation, no gain? In the long(er) run this could in fact be true.

All of you who followed my advice to "like" the SuppVersity Facebook page and are thus keeping up with the numerous additional news I am posting there, should actually have seen the news item on the non-significance of the exercise-induced interleukin-6 (IL6) response for the exercise induced improvements in glucose metabolism (read more). The mere fact that the glucose metabolism of IL6(-) mice, which are mice who simply cannot express IL6, is still improved by "working out" does yet by no means preclude that the demonized cytokine does play a fundamental role in the exercise-induced systemic and local benefits. In fact, an even more recent rodent study would suggest that a certain degree of inflammation and the respective increase in IL6 immediately after a workout is even essential for persistent skeletal muscle hypertrophy.

As you may remember from the Intermittent Thoughts on Building Muscle Series there is more to skeletal muscle hypertrophy than the simple messages such as "increases protein synthesis by X%" that are printed in shiny letters on the boxes of hundreds of the currently available "natural muscle builders" on the real and digital shelves of the supplement vendors. One of these "mores" is the recruitement of satellite cells, muscle stem cells that are incorporated into the musculature to replace damaged myonuclei or increase the myonuclear density to allow for greater protein accretion (learn more).

Decreasing domain sizes = better function + higher growth propensity

"Hold on those are rodents and rodent studies are not relevant!" While it is a good thing to critically assess whether the results of a certain study can be species specific. The contemporary practice to question all rodent studies which are not part of your own cherry picked arsenal is getting onto my nerves. So, please check out the pretty analogues (short term unfortunately) human study by McCay from 2009 (McCay. 2009), before you stop reading after spotting the word "rat" in this article.

It is this process of satellite cell activation and incorporation of which Gwenaelle Begue and her colleagues from the University of Montpelier have now confirmed that it depends on the activation of the IL-6/STAT1/STAT3 signaling pathway in a prolonged 10 weeks resistance training scenario. In the course of the latter,  36 male Wistar rats were randomly assigned to one out of the following six groups:

• CTL2, CTL4, CTL10 (CTL = non-training controls, n = 6 in each group) and 
• TR2, TR4 and TR10, which were rats trained for 2, 4 and 10 weeks. 

The rodents in the TR-X groups were supposed to climb an apparatus with initially 50% later up to 210% of their body weight strapped to their back, five times a week. The load was increased every two days, if the rodents still managed to do "10 reps" = climb 10 steps and reached quite impressive levels of 120% of the body weight after two, 150% of the body weight after four and 210% after ten weeks of training.

Where is the rodent squat machine?

No rodent squat in the study at hand, but the "stair climbing" is a better full-body workout, anyways.

Now, this may not be as "realistic" a program as the rodent squat Aguiar et al. used in their 2013 study, but is is - and this is interesting - very similar to a test that has been done by many researchers with myostatin negative mice. As you will remember from the Intermittent Thoughts on Building Muscle Series (click here to read the pertinent part) those heavily muscled mice are unable to lift their own bodyweight, mainly because of the fact that the myonuclear domains within their muscle grew beyond a threshold where they absence of an adequate number of myonuclei per volume unit enders the muscle useless.

"Healthy" muscle growth does therefore require both, protein synthesis (increase in volume), as well as structural adaptations, so that the domain size does remain constant - at least!

"10 weeks of resistance training did not affect the myonuclear domain"

Against that background the last subheading, which is in fact a direct citation from the full text of the Begue paper is - contrary to what a non-SuppVersity reader could believe - good news. Very good news, to be precise:

Figure 1: Changes in fiber type ratios (left), cross sectional diameter according to fiber type (middle) and  fiber area per myonucleus (right; Begue. 2013)

As you can see in figure 1 (right hand side), there was even a small, yet statistically non-significant decrease in the fiber area each myonucleus had to control and that despite quite impressive increases of 77%, 92% and 100% in the cross-section of the type-I, type-IIa and type-IIx fibers of the animals (figure 1, middle).

Satellite cell recruitment, necessary of optional if you want to get big?

In this context, Begue et al. speficially point out that the "recruitment of additional nuclei derived from SC incorporated into muscle fibers" occurs parallel to the better known "resistance training induced enhancement of protein synthesis" that occurs "after the training session and last[s] up to 24–48 h in humans" (Bengue.2013). 

"Indeed, several works in humans have evidenced an increase in the number of myonuclei per fiber when fiber size increases approximately more than 25% (Kadi. 2004; Petrella. 2008). Thus, the myonuclear domain (i.e. the theoretical amount of cytoplasm supported by a single myonucleus in a muscle fiber) remained constant although a large increase in fiber CSA via the addition of SC-derived nuclei occurs." (Begue. 2013)

Since estrogen plays an important role in the regeneration of the satellite cell pool, it's pretty likely that you can literally "SERM your growth potential away" (learn more)

Notwithstanding the heavily quoted results of the 2011 study by McCarthy et al. in which the reasearchers were able to demonstrate that rodent muscle can grow even when it is satellite cell depleted, my personal conviction is that the latter process, i.e. the incorporation of new (not just even the replacement of damaged myonuclei is an obligatory prerequisite for persistent gains.

With +40% increased domain sizes, after only two weeks, it would have been interested to see how things would have developed in the subsequent weeks. I bet(!), the normal mice would have kept growing while their satellite cell depleted peers would have hit a plateau, where their own body woul have pulled the emergency brake aka myostatin (in this context, it's also interesting to remark that myostatin stops the proliferation of satellite cells and does thus indirectly divert the existing ones towards differentiation and incorporation into the muscle, cf. figure 2)

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Bottom line: The study at hand delivers further evidence for the intimate connection between "inflammation" or rather the expression of the still demonized inflammatory cytokine interleukin-6 and the incorporation of "fresh" satellite cells into the muscle. With the latter being a necessary prerequisite to keep the domain sizes within functionally optimal limits while the cross section of the fibers is expanding (the muscle is growing), it is likely an (I want to emphasis that!) not yet disproven that continuous muscle growth requires satellite cell recruitment.

Basically you can think of it like the Army. While it is (or at least has historically been) relatively easy to find any recruits (=increase protein synthesis), people who are qualified to become officers and coordinate the actions of the rank and file are hard to find and without an adequate number of them you will end up with a chaotic mess instead of a powerful army. That's actually pretty much what happens to the myostatin negative mice, who may be able to recruit officers,... ah, I mean to recruit satellite cells, but simply outgrow the maximal pace of satellite cell incorporation.

Figure 2: IL-6 is the first myokine you should remember, it "wakes" the quiescent satellite cells up, he COX-2 activated IL-4 is myokine #2 and initiates the differentiation / incorporation process which will eventually result in the formation of a new nucleus. .

What, oh yes, of course! I had almost forgotten the unfortunately quite complicated connection to IL-6. If you take a parting look at the figure on the right, you will realize that a diagram explains things much better than I could. In fact, the "motor" of the whole growth business is the contraction induced expression of serum responsive factor, of which Guerci et al. have found in 2013 that it is the previously missing link between muscular contractions on the one hand and the expression of myokines, who happen to be the same molecules we know as "inflammatory cytokines" in other contexts. Il-6 and the COX-2 activated IL-4 are then getting things rolling (Guerci. 2013)... what? No, I cannot tell you whether taking antioxidants will block that, but I can promise you that you will learn more about this tie-in within the next 7 days, so stay tuned ;-)

What I can tell you in advance, though, is that strength and size gains of IL-6(-) mice are compromised (Serrano. 2008). So even if I would have to qualify my previous statement that satellite cells are necessary for continuous growth - one thing is sure: Their activation by IL-6 is necessary for optimal growth.

References:

• Begue G, Douillard A, Galbes O, Rossano B, Vernus B, Candau R, Py G. Early Activation of Rat Skeletal Muscle IL-6/STAT1/STAT3 Dependent Gene Expression in Resistance Exercise Linked to Hypertrophy. PLoS One. 2013;8(2):e57141. 
• Guerci A, Lahoute C, Hébrard S, Collard L, Graindorge D, Favier M, Cagnard N, Batonnet-Pichon S, Précigout G, Garcia L, Tuil D, Daegelen D, Sotiropoulos A. Srf-dependent paracrine signals produced by myofibers control satellite cell-mediated skeletal muscle hypertrophy. Cell Metab. 2013 Jan 4;15(1):25-37.
• Kadi F, Schjerling P, Andersen LL, Charifi N, Madsen JL. The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. J Physiol. 2004; 558: 1005–1012.
• McCarthy JJ, Mula J, Miyazaki M, Erfani R, Garrison K. Effective fiber hypertrophy in satellite cell-depleted skeletal muscle. Development. 2011; 138: 3657–3666
• McKay BR, De Lisio M, Johnston AP, O'Reilly CE, Phillips SM, Tarnopolsky MA, Parise G. Association of interleukin-6 signalling with the muscle stem cell response following muscle-lengthening contractions in humans. PLoS One. 2009 Jun 24;4(6):e6027. doi: 10.1371/journal.pone.0006027.
• Petrella JK, Kim JS, Mayhew DL, Cross JM, Bamman MM. Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: a cluster analysis. J Appl Physiol. 2008. 104: 1736–1742
• Serrano AL, Baeza-Raja B, Perdiguero E, Jardí M, Muñoz-Cánoves P. Interleukin-6 is an essential regulator of satellite cell-mediated skeletal muscle hypertrophy. Cell Metab. 2008 Jan;7(1):33-44.

Ultimate Post-Workout Testosterone Booze: Hard Liquor Increases Late PWO Testosterone Levels by Almost 100%

"No pain no gain?" No, that ain't the blood dropping from you wound hands.Those are the remnants of your next goto PWO drink. A Bloody Mary!

While I have been covering all sorts of testosterone-related stuff within the past couple of weeks, one thing has still been missing: The classic herb from the darkest jungle that'll increase the testosterone levels of one out of the two testers the respective company claims to have beta-tested their product on by whatever incredible percentage. Ok, I must admit, I don't have such an herb at hand at the moment, but what about Bloody Mary? No, not for the tomato juice, although that would be an awesome addition (learn more about "TomatoRade(R)") to the alcohol!

Alcohol? You're kiddin' me... right!?

At least at first glance it certainly looks as if you could hardly find better news for all the partying muscle heads out there, than the soon-to-be-published paper by Jakob L. Vingren, David W. Hill, Harsh Buddhadev, and Anthony Duplanty from the Department of Kinesiology, Health Promotion and Recreation at the University of North Texas (Vingren. 2013). After all, the four Texans discovered that the ingestion of booze instead (and probably also along with) your protein shake after your workout will prolong and amplify the "anabolic state" you're in once you leave the gym fo a couple of hours. Bullshit? No, it's not April the first, yet.

The participants were 8 healthy previouly resistant trained men (21-34 years; 87.7kg, 177 cm, 15.1 % body fat) who performed 6 sets of 10 repetitions of Smith machine squats starting at 80% of 1RM and 2 min of rest between sets (assisted forced reps, when necessary) after an appropriate warm-up:

Figure 1: Relative changes in free and total testosterone, SHBG, the testosterone to cortisol ratio and estradiol levels; data expressed relative to values at rest (Vingren. 2013)

You see? No changes in SHBG, cortisol and only a statistically non-significant increase in estradiol, but a persistent elevation of free and total testosterone. How that works? Well, you just pick a drink of your choice (the scientists obviously simply dilluted ethanol in water so that the mixture would have 19%) and drink as much of it as would be necessary to cover your "post workout ethanol requirements" of 1.09g/kg of lean body mass.

Want to know more about the net gains / fat loss testosterone produces? Or are you interested in the negative consequences of really low testosterone levels? Click here to learn more.

Did you know that a very recent study from the University of Chile shows that testosterone works its muscle building magic via the very same PI3K/Akt and mTOR pathways you are targeting with your hitherto non-alcoholic post-workout nutrition (Basualto-Alacon. 2013)? Since testosterone does yet also act on the androgen receptor, it can't be excluded that the effects are (a) additive / synergistic or (b) a certain degree of T-induced androgen receptor activation is necessary for the PI3K/Akt pathway to work. If you want to learn more about post workout browse through previous article on the matter, here.

A guy with a lean body mass of 65kg, for example would need ~71g of pure alcohol. That's about 668ml of regular red wine or drink enough Bloody Mary's to his TBA (testosterone boozing allowance) of ~165ml of vodka (100% proof). If we further assume he gets his Bloody Mary mixed according the standards of the International Bartenders Association, he would have to make room for 4x Bloody Marys in his gymbag ;-)

Sound easy right? But does it help at all?

You probably did not start boozing already, right? Otherwise you would not pose smart questions like the one in the above subheading. Obviously, the researchers asked themselves a very similar question: Can this poison really be ergogenic? Unfortunately, their answer does not really go beyond serving us the same old paradigm of the "anabolic milieu", the validity of which is more than questionable (suggested read: "Does the "PWO Elevation of Testosterone Influence Muscle Growth?"):

Strength, cardio or both for the optimal T:C ratio? (learn the answer)

"Although the T:C [ratio between testosterone and cortisol] is a crude measure, it response shows that the elevated in testosterone in the latter stages of recovery following ethanol ingestion is not associated with a corresponding elevation in cortisol, a hormone with catabolic and anti-anabolic physiological effects. The results for the T:C ratio suggest that a more  anabolic milieu exists during the latter stages of recovery from resistance exercise following ethanol ingestion." (Vingren. 2013)

In the researchers defense, it does yet have to be said that they do not simply ignore the fact that the significance of workout induced changes in the "anabolic milieu" in terms of immediate skeletal muscle growth may have been overrated.

Now, while we do not have any studies on the "the effect of post-exercise ethanol ingestion on protein accretion" (Vingren, 2013), we do have studies showing that the ingestion of alcohol in general appears to hamper the recovery from resistance training (Barnes 2010; Barnes 2013) and increases the suppressive effect of exhausting endurance exercise on testosterone production (Heikkonen. 1996). The logical conclusion, Vingren et al. draw is thus that it "remains unclear" how the ethanol induced maintenance of high free and total testosterone levels in the hours after a workout would affect the muscular adaptation processes and their downstream effects on muscle size and strength in response to resistance exercise.

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Bottom line: Personally I don't believe that 1.5 pints of red wine make the ideal post workout drink, not just because they are lacking protein, but rather in view of the previous research from Barnes and Heikkonen which may not disprove the possibility that 1.06g of ethanol after a workout could potentially exert "anabolic" effects that will eventually manifest in greater gains in muscle size or strength, but should suffice to rate an already highly questionable hypothesis "very unlikely".

Click on the image above to read my previous article series called "Chest Fat, Bitch Tits, Chesticles, Gynecomastia, Lipomastia and Co.: Infinite Ways to Name it, 45 Ways to Prevent It". Plus: Is your gyno in fact just too much body fat? (read more)

We should also take into account that the mechanism by which this increase or, to be precise, the absence of a decrease in total testosterone and the 2nd spike in free testosterone come about, may very well decide whether it's a good or bad thing. When I think of alcohol I usually think of the liver and, when I think of the liver, alcohol and testosterone, I think of the accumulation of estrogen in heavy drinkers with a alcoholic fatty liver, which renders them prone to develop gynecomastia. Why? Simply because their liver cannot get rid of the end-products of the hormonal cascade. So, if the higher testosterone levels are simply the result of a temporarily hampered hormone metabolism in the liver, it stands to reason that the results are unlikely to increase your strength and muscle growth, right?

Overall the study at hand is thus nice for some intellectual masturbation, but should not serve as an excuse for regular alcohol consumption. Physical culture and booze were, are and will always remain incommensurable.

References:

• Barnes MJ, Mundel T, Stannard SR. Acute alcohol consumption aggravates the decline in muscle performance following strenuous eccentric exercise. J Sci Med Sport. 2010; 13(1):189-93.
• Barnes MJ, Mundel T, Stannard SR. The effects of acute alcohol consumption and eccentric muscle damage on neuromuscular function. Appl Physiol Nutr Metab. 2013; 37(1):63-71.
• Basualto-Alarcón C, Jorquera G, Altamirano F, Jaimovich E, Estrada M. Testosterone Signals through mTOR and Androgen Receptor to Induce Muscle Hypertrophy. Med Sci Sports Exerc. 2013 Mar 6.
• Heikkonen E, Ylikahri R, Roine R, Välimäki M, Härkönen M, Salaspuro M. The combined effect of alcohol and physical exercise on serum testosterone, luteinizing hormone, and cortisol in males. Alcohol Clin Exp Res. 1996 Jun;20(4):711-6.
• Vingren JL, Hill DW, Buddhadev H, Duplanty A. Post-Resistance Exercise Ethanol Ingestion and Acute Testosterone Bioavailability. Med Sci Sports Exerc. 2013 Mar 6.

High Intensity Exercise & Decreased Post-Exercise Energy Expenditure? Why the Latest Study Results are No Reason To Stop Working Out or Return to the "Fat Burning Zone"

Is HIT obesity incompatible? One thing appears to be sure - the purported post-workout increase in energy expenditure is reversed in the obese.

You may remember the positive results of the 100 squats a day challenge from the SuppVersity news on Friday, right? If you do, you will probably also remember the red box in which I mentioned the ongoing debate that's revolving around the issue, whether or not regular bouts of vigorous physical activity can protect you from the detrimental effects of sitting around 8h+ per day (see "100 Squats A Day Challenge"). While it may not really help us to answer the question whether "sporadic" activity is enough, a recently published study in the journal of the International Association for the Study of Pediatric Obesity certainly provides an interesting and novel angle on the debate.

What happens after you've burned those extra calories?

In a series of three experiments, a group of French researchers tried to elucidate why most of the studies that investigate the effect of physical activity on the change / loss of body fat report sub-optimal results. Within the last two decades, researchers such as Goran et al. (1992), Morio et al. (1998) or Donelly, et al. (2003), have repeatedly suggested that the primary reason for insufficiency of physical activity alone to modulate body weight was not restricted to the compensatory intake of food, but would - at least partly - be mitigated by a compensatory decrease in total daily energy expenditure (DEE).

As usual the existing evidence in ambigous, but a 1999 study by Kriemler et al. provided evidence that the high intensity exercise early in the morning will result in a decreased energy expenditure during the res of the day and the following day (Kriemler. 1990). Since Kriemler and his colleagues relied exclusively on the heart rate of their subjects to assess the energetic expenditure, Thivel et al. re-investigate the purported metabolic slow down in response to high intensity exercise in a series of three experiments.

• 

  The fitter you are the greater the benefits of working out at high intensities (learn more)

  Study 1 involved only obese adolescents and used a combination of heart rate and accelerometer data to evaluate the energy expenditure

• Study 2 was conducted with lean (17% body fat) and obese (44% body fat) adolescents and evaluated the energy expenditure by the means of a SenseWear Armband

• Study 2 involved only obese adolescents and used the most sophisticated measuring technique, a open-circuit whole-body calorimeter in a metabolic chamber

In study 1 and 2 the subjects had to perform a cycling exercise consisting of 3 x 10 min at 70%VO2max (EX), while study 3 compared a 3 x 11 min at 75% VO2max high intensity (very long) interval protocol to a 3 x 20 min at 40% VO2max low intensity extremely long interval protocol (click here to learn how to design a real high intensity interval workout).

Does HIIT slow down the obese metabolism or does it simply increase laziness?

While the general trend, the scientists observed was pretty meaningless (more on that in the "bottom line"), the differences we see between the studies and between lean and obese subjects are quite telling and do in fact relate back to the initially mentioned question of "working out like crazy" and "sitting around lazy" the rest of the day.

Figure 1: "Energy expenditure" in the exercise and control trials of the three studies (Thivel. 2013)

In order to appropriately interpret the data we  have to remind ourselves of what the scientists actually measured in the different studies. Study 1 used accelerometer and heart rate data and did thus access a mixture of metabolic and physical activity. Study 2 used just the SenseWear Armband with a build-in accelerometer, which - despite being more sophisticated than a simple pedometer, still measures only physical activity. Lastly, in study 3, the metabolic chamber actually measures the "true" energy expenditure irrespective of whether that's due to an increase / decrease in metabolic rate or in response to exercise / sitting around.

• Let's start with the third study, since it's the most sophisticated one. What do we see in the middle of figure 1? Right, we see that conducting a 30min HIIT workout reduces the energy expenditure during the afternoon (-9.2%), but the total daily energy expenditure in a well-controlled scenario and measured with sophisticated equipment is still 8.9% higher than in the non-exercise scenario.
• So what about study two then? There is no debating that the afternoon energy expenditure in the obese groups dropped, but wait... what do we actually measure here? Right. That's not necessarily the amount of energy the obese youths actually expended. It's just a measure of their physical activity. It is thus not sure, if the obese youths did, as the scientists imply, not still end up with a higher daily energy expenditure. After all, the heart rate remains elevated after a workout in unfit vs. fit individuals. Plus, even with the "physical activity only" measure the exercise trial yielded a marginal, but statistically non-significant higher total energy expenditure for the day. In the lean subjects the exercise advantage amounted to 233kcal and was thus clearly significant - irrespective of the (imho) inadequate measuring method.
• The results of study one actually speak for themselves: The energy expenditure, which does, as we have noted before, include both, physical activity (accelerometer data) and metabolic rate (heart rate data), simply does not decline after the morning workout.

I guess, I actually don't have to "summarize" the above even more, but since I understand all of you who have been complaining about missing "summaries" in many of the older SuppVersity posts I still will provide you with the obligatory bottom line.

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Now that you know it's not bad for you, read up on all previous HIIT articles at the SuppVersity.

Bottom line: "High intensity" exercise is not useless and it does not (in the presence of adequate nutrient intakes) shut down your metabolism. It may be true that especially people who are not used to working out and will thus be correspondingly fatigued after a by no means "high" intensity "HIIT" workout at 70% of their VO2max (actually this is more of one of those stupid "fat burning workouts") tend to decrease their activity levels during the rest of the day, but the beauty of high intensity workout is that they increase your conditioning and as you are getting fitter, this behavioral but not metabolic compensatory effect is going to decline.

And best of all, as long as you don't succumb to the "I worked out, so I can have my cream pie today" idiocy, you are going to lose weight even while this adaptation process is still taking place. Why? Well, the two studies that don't rely on physical activity (study 1 & 3) only to determine the energy expenditure are telling me that you spend ~9% more energy if you work out for half an our at a not too intense pace in the morning. Whether this will help you to escape the detrimental health effects of sitting around the rest of the day is yet questionable, because health in not determined by the difference between caloric intake and expenditure... but whom am I telling that? You know that anyway, right?

References:

• Donnelly JE, Kirk EP, Jacobsen DJ, Hill JO, Sullivan DK, Johnson SL. Effects of 16 mo of verified, supervised aerobic exercise on macronutrient intake in overweight men and women: the Midwest Exercise Trial. Am J Clin Nutr 2003; 78: 950–956. 
• Goran MI, Poehlman ET. Endurance training does not enhance total energy expenditure in healthy elderly persons. Am J Physiol 1992; 263: E950–E957.
• Kriemler S, Hebestreit H, Mikami S, Bar-Or T, Ayub BV, Bar-Or O. Impact of a single exercise bout on energy expenditure and spontaneous physical activity of obese boys. Pediatr Res 1999; 46: 40–44
• Morio B, Montaurier C, Pickering G, et al. Effects of 14 weeks of progressive endurance training on energy expenditure in elderly people. Br J Nutr 1998; 80: 511– 519.
• Thivel D, Aucouturier J, Metz L, Morio B, Duché P. Is there spontaneous energy expenditure compensation in response to intensive exercise in obese youth? Pediatr Obes. 2013 Feb 28.

Diabetes: Green Tea on Par With Metformin. 1-Andro: 4.7kg Muscle in 4 Weeks. EPA: Increased Protein Synthesis & Autophagy in Vitro. Phthalates: How Much is in Your Food?

Believe it or not a soon-to-be published study that was sponsored by a the German LBS and presented to the public two days ago found that 1 out of 20 German kids below the age of 14 thinks about having liposuction done (figures based on LBS Kinderbarometer. 2013).

5% that's the SuppVersity Figure of the Week and it's the percentage of German kids below the age of 14 years who are thinking about getting liposuction done. I am not sure, whether I should feel sorry or enraged... not about the kids obviously who probably feel miserably in their own skin, but for the parents, the food industry and the government with their "expert" advisers whispering into their left ear and the junk food industry lobbyists who are holding a megaphone to the politicians right ear and a razor-blade to their throat. I guess, I'll settle for both, feeling sorry for the kids and being mad at the adults.

But enough of this let's get to some recent science news. Let's see... oh yeah, why don't we just start out with something 15% of the German kids (this is the number of already obese kids) are probably going to need sooner or later: diabetes medication.

Metformin not unique, green tea just as effective?!

(Sundaram. 2013) -- I know this sounds almost like a marketing scam from some snake oil... ah, green tea vendor, but according to a soon-to-be-published paper in Phytomedicine does have almost identical effects on the glucose metabolism of diabetic (streptozotocin + high at diet = std. model of type II diabetes), as metformin does.

Figure 1: Glucose and insulin levels in healthy and  streptozotocin induced diabetic rodents receiving different doses of green tea (75, 150, 300mg/kg) or metformin (500mg/kg; Sundaram. 2013)

In fact, a short glimpse on the data in figure 1 should suffice to tell you that green tea is on a mg/mg basis even more potent than metformin. I would still caution any true diabetics out there not to drop their medication for the endproduct you get if you buy1 kg of fresh green tea leaves from the plant C. sinensis from the Nilgiris, India, dry them in the shade for two weeks, pulverize them and finally create a 1:10 ethanol extract, store that in the fridge for one week and then finally filter and evaporate it at a temperature of <50°C.

Did you know that the macronutrient composition (esp. the protein content) can have major impacts on your neurotransmitters and mood? No, then revisit this older SuppVersity article and learn more.

Not diabetic, then you may be interested in this: A non-negligible side note of the study at hand is that the GTE that was so good for the sick rats, did nothing, I repeat, absolutely nothing for the glucose metablism of the healthy rats on the high carb, low fat chow. Still, a recent study from Japan suggests that your psychological well-being (not tested in the rodents ;-) alone would justify the consumption of one, two or even three cups of green tea or coffee per day (Pham. 2013). After all, Pham et al. observed in their most recent study which is going to be published in one of the future installments of the peer-reviewed journal Public Health Nutrition that both, green tea and coffee consumption are inversely related with the odds ratio of depression in the Japanese working population. In this case, the scientists are yet pretty sure that it's none of the fancier components, but simply the caffeine content that is responsible for the >40% reduced risk of depression in tea/coffee aficionados.

You may be asking yourself why I mention the lengthy procedure of preparing that extract, right? Well, different source, different preparation methods, different effects. This and the fact that a human diabetic is not a streptozotocin treated rodent of a high fat diet put a huge question-mark behind and premature conclusions like "green tea is a better anti-diabetic than metformin".

After all those years, 1-Andro still works.

(Granados. 2013) -- It is certainly debatable in how far this qualifies as "news", after all, 1-androsterone is the "mother of all prohormones", but I still guess that one or another of the average muscle heads out there will still be intrigued to hear that researchers from the Human Performance Research Laboratory of the Department of Sports and Exercise Sciences at the West Texas A&M did actually dare to test the effects of 330mg/day 1-AD, which were administered for 4 week with 16 session of a structured RT program, on the physique and  health of 16 males (23±1yrs; 13.1±1.5%BF; 5.3±1.0yrs RT experience; the 1-AD used in the study was probably that of a larger US producer that's still available  online and has a slightly different nomenclature, i.e. 3-hydroxy-5alpha-androst-1-en-17-one).

Figure 2: Relative changes in muscle mass (total change above the bars) and kidney, "liver" and lipoprotein metabolism after four weeks on a 1-AD clone (Granados. 2013)

The results I plotted for you in figure 2 actually speak for themselves: Increases in lean mass and strength on the positive and deteriorations of the kidney (creatine), liver (S-GOT) and lipid metabolism (HLD, LDL, total cholesterol) are exactly what you can expect from a mild prohormone like this.  

EPA triggers protein synthesis and inhibits breakdown... in the petri dish

CLA and fish oil, are they "anabolic" in human trials (learn more)?

(Kamolrat. 2013) -- You will probably remember the SuppVersity article on the potential "anabolic" effects of fish oil and CLA from February, 25, 2013, where not a single of the human studies showed beneficial effects of fish oil supplementation on training induced muscle gains, right? Well, a soon-to-be-published paper from the Biochemical and Biophysical Research Communications does at least confirm that Maculoso et al. were not totally off the track, when they suspected that fish oil could be "anabolic". Contrary to their hormonal understanding, the results of the study at hand do yet suggest that high serum concentrations of EPA may increase the expression of local control factors of protein synthesis in a way that does not necessarily render them anabolic, but would suggest that they may help people with muscle wasting disorders.

If you take a look at the data in figure 3, which holds all the statistically significant effects the scientist observed, the most important advantage of EPA vs. DHA in murine C2C12 myotubes after L-leucine stimulation unquestionably is the EPA-specific decrease in protein breakdown.

Figure 3: Protein breakdown, marker of protein synthesis and apoptosis in EPA or DHA treated C2C12 myotubes in the petri dish (Kamolrat. 2013)

What the scientists don't tell you though is that the effect size may be negligible, that the enhanced anti-protein breakdown (note:protein breakdown does not equal cell death) effects are only present when the cells are incubated with leucine and - most importantly - that FOX3a, which was likewise significantly elevated, "is necessary and sufficient for the induction of autophagy in skeletal muscle in vivo" (Mammucari. 2007), is upregulated in catabolic states of testosterone deficiency (White. 2013), and is suppressed by HSP70 (heat shock protein expressed in response to eustress such as exercise; cf. Senf. 2008). No wonder no human trial was ever able to demonstrate the anabolic effects of fish oil.

Phthalates in your food chain - addendum to last week's short news

Once again, I am not trying to make you panic about the individual serving of whatever is on the following list. The current state of research clearly suggests that the individual contribution of endocrine disrupting plastics from each of these items is way below what can harm an adult (and sexually mature) individual. When I went through the latest data Arnold Schecter et al. present in their latest paper in Environmental Health Perspectives, there were - for my liking - still too many patterns emerging to simply ignore this paper (I cannot simply copy & paste all the data, but the you can download the supplemental data here):

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  Figure 4: The metabolites of all measured phtalates in a 2013 study from the Columbia University were significantly elevated in 56 infertile vs. 56 fertile couples (Tranfo. 2013). I know, correlation is not causation, but I would venture the guess that none of the 1/6 couples who are infertile (McArthur. 2007) will care about the difference...

  Pork, the supposedly unhealthiest meat source has the highest estimated mean phthalate concentration of any food group. 
• The "good apple" juice of which Dennison et al. report that daily intakes equal or greater than 12 fl oz/day are associated with short stature and with obesity in two and five-year old children in New York (Dennison. 2013), is topped in terms of its phthalate content only by diet lemon tea  - another of those "healthy" beverage.
• The "healthy" vegetable oils are the absolute #1 dietary source of BBzP, of which a group of researchers from the Columbia University has only recently been able to show that children who were exposed to BBzP prenatally had a >50% higher risk of developing eczema within the first 2 years of their lives (Just. 2013).

I guess, I could cite a couple of other "happy coincidences", but I don't want to bore you away, before we get to something that should really make us reconsider the convenience of our "Plasti-Nation(s)", specifically the convenience of getting "scientifically formulated baby foods" for your children.

Figure 5: Dietary exposure (in µg/kg body weight; calculated on average intake of the various food items) from beverages, milk, other dairy, fish, fruits/vegetables, grain, beef, pork, poultry, vegetable oils and condiments (Schecter. 2013)

I wonder which science says that the foods babies eat should contain 4.3x more phthalates (on a per kg body weight basis), than the junk adults are eating.

• Several studies have reported an increased risk of allergic disease among children with higher childhood phthalate exposure, as well as increased airway inflammation.
• Some human studies suggest that in-utero phthalate exposure could lead to abnormal genital and behavioral development.
• Based on our current understanding, diet and dust are the predominant sources of DEHP and BBzP, while cosmetics are the major source of DEP.

Ok, this is of course a result of the fact that babies weight less than adults do, but it is also a consequence of the fact that the baby foods are freaking "plasticized" - regardless of whether you buy them in glass or plastic containers. A fruit homogenate sold in glass bottles for example contained 235ng/g DEHP (about as much as paper-packaged butter, by the way) and was topped only by plastic food such as ham (1158ng/g). Again, way below the amount of DEHP that's deemed to be toxic, but is it really coincidence that a group of scientists from the University of Washington and the Havard Medical School only recently published an opinion paper (Braun. 2013), in which they formulate the take home messages I quote in the red box to the right... just food for thought, of course!

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I guess you know what's next!? Correct: "That's it for today! Check out the facebook news, such as

• 

  Wolverine doesn't care about the phthalates in milk, but what about homogenization? (read more)  could be the only face of the "Got Milk" campaign who does not have to care about potential negative health effects of homogenized milk.

  Thyroglobulin levels could be a measure of adequate iodine intake -- Both, too high and too low iodine intakes will result in increased thyroglobolin levels (read more)

• Dairy & blood pressure - revisited & acquitted -- "[....]the preponderance of evidence indicates dairy foods are beneficially associated with blood pressure" (read more)

• Supplement users are a special kind of people -- Specifically health conscious, for example, and this will necessarily distort all epidemiological guesswork like "taking supplement X is associated with Y" (read more)

• Retinoic acid & testosterone: While vitamin A does not figure in the LH induced increase in testosterone production it's presence in the testes appears to be necessary to keep the basal testosterone production up (read more)

if you still can't get enough of the latest on exercise, nutrition and supplementation science and have a nice Saturday evening (+ night)!"

References:

• Braun JM, Sathyanarayana S, Hauser R. Phthalate exposure and children's health. Curr Opin Pediatr. 2013 Feb 16.
• Dennison BA, Rockwell HL, Baker SL. Excess fruit juice consumption by preschool-aged children is associated with short stature and obesity. Pediatrics. 1997 Jan;99(1):15-22.
• Granados J, Gillum T, Hodges C, Kuennen M. 3-hydroxy-5alpha-androst-1-en-17-one Enhances Muscular Gains but Impairs the Cardio-metabolic Health of Resistance Trained Males. International Journal of Exercise Science. TACM 2013.
• Just AC, Whyatt RM, Perzanowski MS, Calafat AM, Perera FP, Goldstein IF, Chen Q, Rundle AG, Miller RL. Prenatal exposure to butylbenzyl phthalate and early eczema in an urban cohort. Environ Health Perspect. 2013 Oct;120(10):1475-80. doi: 10.1289/ehp.1104544. Epub 2013 Jun 13.
• Kamolrat T, Gray SR. The effect of eicosapentaenoic and docosahexaenoic acid on protein synthesis and breakdown in murine C2C12 myotubes. Biochem Biophys Res Commun. 2013 Feb 21.
• Mammucari C, Milan G, Romanello V, Masiero E, Rudolf R, Del Piccolo P, Burden SJ, Di Lisi R, Sandri C, Zhao J, Goldberg AL, Schiaffino S, Sandri M. FoxO3 controls autophagy in skeletal muscle in vivo. Cell Metab. 2007 Dec;6(6):458-71. 
• McArthur SL. Infertility Fact Sheet. ABC Health & Well-Being. 2007 <http://www.abc.net.au/health/library/stories/2007/05/30/1919840.htm> retrieved March, 09, 2013.
• Schecter A, Lorber M, Guo Y, Wu Q, Yun SH, Kannan K, Hommel M, Imran N, Hynan LS, Cheng D, Colacino JA, Birnbaum LS. Phthalate Concentrations and Dietary Exposure from Food Purchased in New York State. Environ Health Perspect. 2013 Mar 6.
• Senf SM, Dodd SL, McClung JM, Judge AR. Hsp70 overexpression inhibits NF-kappaB and Foxo3a transcriptional activities and prevents skeletal muscle atrophy. FASEB J. 2008 Nov;22(11):3836-45.
• Sundaram R, Naresh R, Shanthi P, Sachdanandam P. Modulatory effect of green tea extract on hepatic key enzymes of glucose metabolism in streptozotocin and high fat diet induced diabetic rats. Phytomedicine. 2013 Feb 27.
• Tranfo G, Caporossi L, Paci E, Aragona C, Romanzi D, De Carolis C, De Rosa M, Capanna S, Papaleo B, Pera A. Urinary phthalate monoesters concentration in couples with infertility problems. Toxicol Lett. 2013 Aug 13;213(1):15-20.
• White JP, Gao S, Puppa MJ, Sato S, Welle SL, Carson JA. Testosterone regulation of Akt/mTORC1/FoxO3a signaling in skeletal muscle. Mol Cell Endocrinol. 2013 Jan 30;365(2):174-86.