Exercise Round-Up: HIIT Prevents Angina; Stretching Reduces IGF-1 & Strength Gains; Cardio + Weights Lower TNF-Alpha; Protein Doesn't Works W/ Glucose Depletion; Polarization More Effective Than Threshold Training

That's (hopefully) not the way you want to "kick off" your year 2013, is it? So keep the booze at bay and party away, tonight ;-)

There are three things of which I would hope that they are on the top ranks in the things you are planning to do in 2013. And aside from proposing to your girlfriend, becoming a parent, graduating from whatever you are currently studying and keeping or, in the unfortunate case you don't have one, getting a job no other goals should be ranked in this must to in 2013 category: Work out, eat health and sleep deep and sufficiently. Against that background today's exercise round-up, which comprises all the few newsworthy papers that have been published during or shortly before the holiday season can actually be regarded as a means of orientation as far as practical realization of your best intentions for 2013 are concerned.

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• HIIT in the evening will keeps the heart attack away (Morikowa. 2012) -- Having a mild angina (coronary spasm was documented and no severe organic lesions were found) is not just no excuse for not working out, the 26 patients in a recent study that was conducted by a team of researchers from Kashiwara City, Japan, clearly shows that the number of spasms (=perceived heart attacks) was reduced from 2 to ZERO (average numbers) per 5 days in the men and women who performed an aerobic interval exercise training in the afternoon.
  
  

  

  Figure 1: Selected significantly improved health markers before and after the 3x workout short-term intervention involving 19 male and 7 suffering from angina (Morikawa. 2012)

  The protocol was performed on three consecutive days. After warming up thoroughly (10min), all subjects performed four sets of 3 min intervals at 75-85% of their heart rate reserve. The work to rest ratio was 1:1. In other words each of the intervals was followed by a phase of 3 minutes of active recovery. The whole session was concluded by a 5-10 minutes cool down.
  
  In conjunction with the initially mentioned benefits in terms of the recurrence of angina attacks the data in figure 1 should actually suffice to motivate you and lazy relatives to invest this small amount of time into the length and quality of your life- don't you think so?

• 

  Figure 2: The group of recreational trained young men (~29 years) that did no stretching at all had slightly, but significantly elevated IGF-1 levels (µg/L) after the workout (Borges. 2012).

  Stretching blunts acute IGF-1 response and 10 week strength gains (8RM test) (Borges. 2012) -- Now, hormonal responses to exercise are certainly not everything, the fact that the non-stretchers (OST) did yet also gain significantly more strength on the bench (19% vs. 7% and 5% in the static stretching during warm-up (SBST) and the stretching before each set (SDST) groups, respectively), the leg press, leg extensions and leg curls should yet call your attention, Mr. and Mrs. "I am so freaking professional that I stretch in between every set" maniacs - after 10 weeks of training the guy next to you who sticks to a handful of warm-up sets for injury prevention is going to outperform you.
  
  Remember this is not about not warming up and making sure that you don't hurt yourself, it's just even more more evidence that the die-hard belief that static stretches are beneficial (which was btw. also the research hypothesis of the Portuguese and Brazilian scientists) is dated text book knowledge.

• Again: Not strength or, but strength and aerobics is the way to go (Ho. 2012) -- While the medical establishment is still reluctant to accept the notion that strength and aerobic training must go hand in hand and many muscle heads still plead, they would lose muscle or hamper their gains, when they hopped onto a treadmill from time to time. The evidence is clear: The advantages are simply non-negligible - for the gymbro trying to look muscular (which requires a low body fat percentage if you don't want to look simply ludicrous), and the average Australian (pre-)obese in a recently published study by Ho, Dhaliwal, Hills, and Pal who found that ...
  

  "Twelve weeks of moderate-intensity aerobic, resistance, but mainly combination exercise training decreased TNF-α in overweight and obese individuals compared to no exercise. Therefore, combination exercise training may be physiologically relevant in decreasing the risk of developing chronic diseases." (Ho. 2012)

  The exercise interventions were either 30 min of aerobic exercise on a treadmill (60 % heart rate reserve; HRR estimated using the Karvonen equation: 220 - age - resting heart rate), 30 min of resistance exercise (four sets of 8–12 repetitions at 10-RMlevel of leg press, leg curl, leg extension, bench press, and rear deltoid row, with each set completed in approximately 30 s with 1-min rest) or a combination of 15 min of aerobic exercise and 15 min of resistance exercise (two sets of the above exercises).
  

  

  Figure 3: The combined training did not only result in a maximal suppression of TNF-alpha, the latter was also highly correlated with the reduction in body fat (esp. in the belly area; cf. Ho. 2012)

  "Starting workload levels for each piece of equipment were tested by participants and if more than 10 repetitions were achieved, the weight was increased and after a short rest participants tried again. Likewise, if less than eight repetitions were achieved, the weight was decreased and after a short rest participants tried again. Participants reported to the Curtin Fitness Centre 3 days a week to complete the required exercise and either exercised at home the other 2 days or at the fitness center.
  
  If exercises were completed at home, dumbbells (adjustable weight 1.5–10.5 kg) were provided for resistance exercises (three sets of 10 repetitions for biceps curls, lunges, dumbbell raise, calf lift, and triceps extension for resistance group while the combination group did two sets of biceps curls and lunges and one set for dumbbell raise, calf lift, and triceps extension; back extension, push ups, and sit ups exercises were also included). Treadmills were equipped with heart rate sensors and participants were instructed to increase weight loads by 2.5-kg increments when they could complete more than 12 repetitions." (Ho. 2012)

  Maybe not the perfect program for you, but I bet you know someone who "wants" to make room for 30 min of exercise in 2013, don't you? Ah,... don't tell them that 67-74% compliance was enough to elicit a 30%+ decrease in TNF-alpha and finally allow the participants to drop body fat, though ;-)

• You can have your peri-workout protein even if you want to exploit the AMPK & PGC-1 bonus of training glycogen depleted (Taylor. 2012) -- Actually I have discussed that in the Intermittent Thoughts more than a year ago, but since the debate just goes on forever, I thought it may be worth posting the results of a recent study pertaining to the issue of peri-workout protein ingestion and its purported (yet non-existent!) negative side effects on the beneficial AMPK response to glycogen depleting exercises (note: that's not the AMPK that's increased in your brain, when you starve yourself for longer time periods, the "bad" one that will make you ravenously hungry, induce overeating and shut down your metabolism).
  

  

  As long as you remain glycogen depleted protein has no effect on the beneficial part of the exercise induced AMPK expression (read more)

  "After performing a glycogen-depleting protocol the evening before, the subsequent morning ten active men performed 45 min steady-state cycling at 50 % of peak power output (PPO) followed by an exercise capacity test (1-min intervals at 80 % PPO interspersed with 1-min periods at 40 % PPO).
  
  In a repeated measures design, subjects consumed 20 g of a casein hydrolysate solution (PRO) 45 min before exercise, 10 g during and a further 20 g immediately post-exercise, or an equivalent volume of a non-calorie taste matched placebo (PLA)." (Taylor. 2012)

  In view of the fact that the post-exercise muscle glycogen was not different between the protein supplementation and the "on empty" trial, it is not exactly surprising that the p-AMPK levels increased threefold and the PGC-1mRNA increased sixfold in the 3h after the workout. And even the blunted increase in eEF2 activation is probably only a sign that the muscle started taking up protein right away and thus did not have ask for more after the workout - That said,Taylor et al. are right to point out that
  

  "athletes who deliberately incorporate training phases with reduced muscle glycogen into their training programmes may consume protein before, during and after exercise without negating signalling through the AMPK cascade." (Taylor. 2012)

  Ah, don't overlook the words "training phases" - remember what I wrote about training glycogen depleted in the context of the PGC-1 a-4 post and doing cardio before a workout? It's an intensity technique and not a necessity for everyone on every training day in 2013. Plus, glycogen depletion does require repletion! Running around 24/7/365 is not an option for 2013.

• 

  Aside "polarization" your cycling performance can also benefit from baking soda & beta alanine (read more)

  Polarize your training and optimize your gains (Neall. 2012) -- What makes HIIT so effective? The cyclicity of high and low intensity, right! It's the same cycle of ups and downs you find everywhere in nature. Against that background it should actually not surprise you that Neal et al. have now found male cyclist record greater training improvements on a polarised model exercise regimen (6.4/hrs per week; 80%, 0%, 20% of training time in low, moderate and high intensity zones) than on a threshold model (7.5hrs per week; 57%, 43%, 0% training intensity distribution).
  
  According to the researchers from the University of Stirling, both groups recorded performance improvements, yet those in the group that followed the polarized regimen saw 5% greater increases in peak power output, 7% greater increases in lactate threshold, and 48% greater increases in high-intensity exercise capacity.

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Thats it for today and in fact for the year 2012. The last one of 365 new posts here at the SuppVersity and probably twice or thrice as many on the SuppVersity Facebook Wall (it would be ~5-6x more on Facebook, if I had started posting short news on Facebook in January already)... Apropos, if you want some additional news before the turn of the year you should make sure to visit www.facebook.com/SuppVersity, today, to read and learn more about.

• A brief history of anti-hangover cures: The ancient Assyrians swore by Ground birds' beaks and myrrh. Raw eel and bitter almonds is a recipe from Europe that was popular during the Middle Ages. The Mongolians were more into  sheep's eyes, while the Chinese must have listened to Thursday's installment of On Short Notice and went with green tea. Us Germans like it traditional (not me though) and eat "Tom's breakfast" (Katerfrühstück), a postbinge breakfast with Bismark Herring, pickles, rollmops and/or sauerkraut (this stuff does work, by the way, 'cause it helps replenish the lost electrolytes).
  Harvard Health Letters headline: "The new medicine: muscle strength. It's not just for bodybuilders. Strength training is critical for all of us." (read more)
• Creatine reduces total antioxidant defenses? Scientists confirm for the 1012532x that creatine works and to make sure somebody even reads their study they overemphasis an increase in uric acid and decreases in TAS in the creatine supplementation group - a reason for concern? (read more)
• Case report: Type I diabetes remission without insulin therapy on gluten-free diet in a 6-year old boy with type 1 diabetes mellitus. (read more)
• Got Acne? Insulin resistance makes men break out. You better don't rely on fasted values, but get an OGGT ASAP(!) cause it turned out to be the most accurate independent predictor of acne at multivariate analysis. (read more)

I guess the one thing that remains to be said now is:  

HAPPY NEW YEAR everyone! 

Don't party too wild, and if you do, drink your green tea before the binge - this is (contrary to the historical advice in the box above) indicated by the latest science you should remember from Thursday's Science Round Up on Super Human Radio ;-)

References:

• Borges Bastos CL, Miranda H, Gomes de Souza Vale R, de Nazaré Dias Portal M, Gomes TM, da Silva Novaes J, Winchester JB. Chronic Effect Of Static Stretching On Strength Performance And Basal Serum Igf-1 Levels. J Strength Cond Res. 2012 Dec 18.
• Ho SS, Dhaliwal SS, Hills AP, Pal S. Effects of Chronic Exercise Training on Inflammatory Markers in Australian Overweight and Obese Individuals in a Randomized Controlled Trial. Inflammation. 2012 Dec 19.
• Morikawa Y, Mizuno Y, Harada E, Katoh D, Kashiwagi Y, Morita S, Yoshimura M, Uemura S, Saito Y, Yasue H. Aerobic interval exercise training in the afternoon reduces attacks of coronary spastic angina in conjunction with improvement in endothelial function, oxidative stress, and inflammation. Coron Artery Dis. 2012 Dec 14.
• Neal CM, Hunter AM, Brennan L, O'Sullivan A, Hamilton DL, De Vito G, Galloway SD. Six Weeks Of A Polarised Training Intensity Distribution Leads To Greater Physiological And Performance Adaptations Than A Threshold Model In Trained Cyclists. J Appl Physiol. 2012 Dec 20.
• Taylor C, Bartlett JD, van de Graaf CS, Louhelainen J, Coyne V, Iqbal Z, Maclaren DP, Gregson W, Close GL, Morton JP. Protein ingestion does not impair exercise-induced AMPK signalling when in a glycogen-depleted state: implications for train-low compete-high. Eur J Appl Physiol. 2012 Dec 23.

Yohimbine & Berberine Protect From Death Due to LPS Intoxication; BCAAs Inhibit Serotonin Metabolism & Cause Anxiety, Tryptophan but not SSRIs Help; Sweet Tea Leaves Are PPAR-G Antagonists & Battle High Lipid + Leptin Levels

Skip the fireworks invest the money in some quality ingredients for a fondue or whatever you like and invest the (often non-negligible) rest of the money in a gym membership for the next year.

Actually my figure of the week is 115,000,000 EUR (~152,000,000 US Dollar), which is the sum my fellow country men and women are about to waste on pyrotechnics this year. And a scientifically unconfirmed addition based on my personal observation: 90% of the worst offenders as far as spending money for fireworks goes are at least overweight. Would be interesting to see, if the use of pyrotechnics on New Years Eve is directly associated with fat mass...

I mean, it could be that they spent so much money on their fireworks that they feel they can only afford the junkfood of which everybody and his/her mama still tend to believe that it would be cheaper than buying fresh products and preparing your own food from those.

Ah, I am ranting. That's usually Carl Lanore's task, so I will better go on with the items I have compiled for the today's last installment of On Short Notice in the year 2012:
 

• Berberine + yohimbine - a synergistic duo to prevent LPS toxicity (Li. 2012) -- With all the recent hoopla about the gut microbiome, I suppose that I don't have to tell you what the acronym LPS stands for, right? Hmm... just to make sure it stands for lipopolysaccharide endotoxins which are produced by gram negative bacteria in your gut and are so "toxic" (in fact they cause profound inflammation) that they can be lethal at higher doses.
  
  

  

  Figure 1: Survival rates (%) after ALB/c mice LPS injection (Li. 2012)

  A group of Chinese scientists have now found that aside from berberine the anti-inflammatory effects of which have been known for quite some time now, yohimbine administered in a daily dose of 2mg/kg (human equivalent 0.16mg/kg) does add to the survival rate of berberine treated rodents (human equivalent 4mg/kg) that were injected intragastrically (so not directly into the blood) with a potentially lethal dosage of 20mg/kg LPS. What's more, taken on its own yohimbine is even more potent than the alkaloid that's found in such plants as Berberis aquifolium, Oregon grape, Berberis vulgaris, Berberis aristata, Hydrastis canadensis (goldenseal), Phellodendron amurense, Coptis chinensis and Tinospora cordifolia.
  
  The mechanism is mediated by the prevention of liver injury, an upregulating of IL-10 production (an anti-inflammatory cytokine), and related anti-inflammatory effects resulting from the suppression of phosphorylation of IkBa, JNK, ERK and IRF3 in macrophages.

• Chronic 9-week high BCAA diet impairs brain tryptophan levels and causes anxiety (Coppola. 2012) -- Scientists from the Duke University took another look at the BCAA-tryptophan depression connection, you may have read about in the context of my "Sugar Addicted or Just Stressed Out?" post from January 3, 2012.
  
  According to the results Anna Coppola and her colleagues are about to publish in the American Journal of Physiology  - Endocrinololgy and Metabolism the provision of a BCAA-enriched diet for 9 weeks leads to both reductions in brain tryptophan levels and an increased turnover of serotonin (5-HT) in rodent brains:
  

  

  Figure 2: Composition of low fat  (LF) and high fat (HF) diets with or without added BCAAs (left); effects on the ratio of tryptophan  to the molar sum of large neutral amino acids with and without supplemental  tryptophan in the drinking water and 5HT turnover in the brain (no supplemental trp, right; Coppola. 2012)

  Both groups (BCAA and non-BCAA) consumed about identical amounts of food as the rodents in the complementary (LF or HF) groups, which confirms that the BCAA content did not modify the taste of the chow or rendered it unpalatable (cannot have been cheap bulk powder then ;-). The reduction in both the availability of tryptophan as well as the increase in serotonin (5-HT) turnover in the brain must in fact have been a consequence of the added BCAAs and are most likely the root of the disrupted transport of tryptophan across the BBB in rats, leading to reduced exploratory behavior of rats in EPM testing, a sign of increased anxiety.

  "Recent studies demonstrating a strong  association between BCAA levels, obesity, and obesity-related metabolic disorders, when linked to the findings reported here, may help to explain the strong association between obesity and behavioral abnormalities, including depression and anxiety." (Coppola. 2012)

  

  As the slight differences between the high an low carb diets show, other nutrients can influence serotonin as well (read more)

  In this regard it is important to point out that these negative side effects were mostly reversible by the provision of 15 mg/100 ml tryptophan in the drinking water of the rodents, but were not alleviated by  the administration of the common serotonine reuptake inhibitor fluoxetine (at 10 mg/kg/day for four weeks).
  
  Bottom line: Isolation is not what you want if what your body has been build for is complex food. And while the single serving of BCAAs you may gulp down during or right before a workout, on the other hand, probably isn't going to harm you. The "I need BCAAs every 30min" approach to gaining muscle mass, may well turn you into a psychotic wrack if you follow it day in and day out for months or years - at least without chronically adding some l-tryptophan to the equation.

• Sweet tea leaves protect against obesity: Once more via PPAR-gamma blockade (Zhou. 2012) -- Actually this is probably not news to anyone out there with a degree in Traditional Chinese medicine. After all, Lithocarpus polystachyus Rehd.(Sweet Tea) is Chinese folkloric medicine that has always been used to treat obesity, diabetes, and hypertension in South China:
  

  "Previous experiments revealed that it contains plentiful bioactive flavonoids and polyphenolic compounds, e.g. phlorizin, trilobatin, 3-hydroxy-phlorizin, etc. These components have extensive pharmacological activities, such as anti-diabetes, memory improvement, anti-aging, inhibition of lipid peroxidation and the growth of human colon cancer cells, and so on." (Zhang. 2012)

  From a "scientific" perspective, however, the efficacy of this herbal medicine as an obesity treatment had still to be elucidated.

  

  Figure 4: Effects of oral gavage of 75 mg, 150 mg and 300 mg/kg of body weight/day of sweet tea extract or placebo (DIO) in conjunction with the 8 weeks on a obesogenic diet (Zhang. 2012)

  In this context it is yet worth mentioning that this study demonstrated for the first time that the aqueous dry leaves extract of Lithocarpus polystachyus Rehd. can potently reduce the worst metabolic side effects of obesity, such as the hypolipidemia, hypoleptinaemia and the degree of insulin resistance (FINS, HOMA-IR, cf. figure 3) what it does not answer, however, is whether the decline in PPAR-gamma is tissue specific, what exactly is behind the profound decline in leptin levels and whether or not lean rodents, let alone humans, who don't consume an obesogenic diet will see anywhere similar benefits.
  
  In other words, this is research in progress, but I suppose something you are going to hear more about at the Supppversity in 2013.

* * * * * *

Apropos hearing or rather reading more, I guess you will realize that you have reached the end of today's installment of On Short Notice which means that you will have to progress to the SuppVersity Facebook Wall if you want a second serving of news on...

• The history of vitamin A as a light sensor and beyond - actually a free full-text I guess those of you who like to "think paleo" may enjoy (read more)
• A paper on "good" and "bad" inflammation, where the author points out that soothing inflammation too much can lead to a reduction in energy expenditure and may therefore not be the king's road to getting rid of the last blubber (read more)
• The food-hitlist of young Americans - Featuring sugar, sugary drinks, sugary bakery, sugary ... as their main energy and carbohydrate sources... (read more)
• Problems with synthroid and generics that have surfaced in a recent study on their efficacy in the treatment of congenital hypothyrodism (read more)

as well as a handful of other news, which are already there or are going to be posted within the next hours. Have a great weekend, everyone! 

References

• Coppola A, Wenner BR, Ilkayeva O, Stevens RD, Maggioni M, Slotkin TA, Levin ED, Newgard CB. Branched-chain amino acids alter neurobehavioral function in rats. Am J Physiol Endocrinol Metab. 2012 Dec 18.
• Li H, Wang Y, Zhang H, Jia B, Wang D, et al. Yohimbine Enhances Protection of Berberine against LPS-Induced Mouse Lethality through Multiple Mechanisms. PLoS ONE. 2012; 7(12): e52863. 
• Zhou CJ, Huang S, Liu JQ, Qiu SQ, Xie FY, Song HP, Li YS, Hou SZ, Lai XP. Sweet tea leaves extract improves leptin resistance in diet-induced obese rats. J Ethnopharmacol. 2013 Jan 9;145(1):386-92.

Appetite Short News: Pavlovian Conditioning at Work in the Obese | Polydextrose as a Satiety Promoter | Parents, Just Like Their Kids, Fall for All the Tricks of the Food Industry

Too lean for Pavlovian Conditioning.

In today's "appetizing" installment of the short news, I have picked three of the latest publications from the scientific journal Appetite, of which I thought that they were newsworthy. In that, I cover the Pavlovian Conditioning of overweight individuals, the benefits of polydextrose on appetite control and the way product labels fool parents and children into buying unhealthy foods.

I have to admit: It's not all practically applicable, but who knows maybe you can use it to smart-ass during the holidays. Or maybe you bake some polydextrose enhanced super-satiating cookies for your family, ha?

More facts for your smart-ass sessions on the holidays ;-)

Bugs Dictate What You Crave

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

The Macrobiotic MaPi2.0 Diet

• Hedonic food cue conditioning in the obese: You know the story about Pavlov's dog starting to salivate, when the bell rang that would usually accompany his next feeding?
  
  Well, a recent study confirms that something very similar is at work in obese, but not lean subjects. While the former remain calm and cool to a visual cue that had previously been given alongside some tasty chocolate milk, the latter began to swallow, a reliable sign of increased salivation. As the scientists from the Allaint International University in San Diego say, these "
  

  are the first results to show differential acquisition of Pavlovian conditioned responding in overweight individuals compared to lean individuals" (Meyer. 2014)

  The fact that the conditioning worked was yet not the only significant finding, Meyer et al. made. They also observed that hedonic food stimuli were significantly more effective 'conditioners' in the obese than neutral stimuli.
  
  Practically speaking the observations the researchers from the Allaint International University in San Diego made, may partly explain the difficulties obese individuals who may have been conditioned / conditioned themselves to hedonic food stimuli for their whole lives have when it comes to controlling their energy intake.
• Polydextrose as a satiety promoter: In their meta-analysis of the current literature on the effects of polydextrose on energy intake, researchers from the US and Finland found that...
  
  • polydextrose consumed with a mid-morning snack reduces energy intake (EI) at lunch time.
  • this reduction in EI at lunch time occurs in a dose-dependent manner.
  • but the energy intake during the rest of the day did not show any difference
  Now this probably wouldn't be newsworthy, then, if a a regression model had not been able to confirm a dose-dependent effect on the reduction of daily energy intake.

Added polydextrose reduces the insulin response to milk (Lummela. 2009)

What exactly is polydextrose? Polydextrose is a glucose polymer that is completely soluble in water. As a food additive it offers the texture of sucrose but provides only 25% of the equivalent energy, or 4 kJ/g. It has been approved for use in foods in over 60 nations and is recognized as a dietary fiber in more than 20 countries (FAO/WHO, 2009). Next to the reduced energy content it has another benefits of the fibrous substance is that its addition to foods like milk can reduce the insulinogenic response to this meals significantly - even in healthy individuals (Lummela. 2009).

• More specifically, the meta-analysis was able to show that the dose of polydextrose consumed correlated significantly with the reduction of nergy intake at lunch (−0.67 Polydextrose (g/day) | 80% correlation; P < 0.01), due to which the energy intake was reduced by 1% per 2.86g of polydextrose per day.
  
  As Ibarra et al. point out, the sex-specific results are consistent with results for the whole group - the effect is thus similarly pronounced in both men and women. Accordingly, the meta-analysis "supports the notion that the consumption of polydextrose reduces voluntary energy intake at a subsequent meal" and that "this reduction in energy intake occurs in a dose-dependent manner" (Ibarra. 2014).
• Parents of preschool children make (non-)sense of front-of-package visuals and claims on food - A recent study from the Colorado State University and the University of Illinois at Urbana-Champaign investigated what parents make of the colorful packaging of foods their kids like to buy and found that most of them tend to "accept misleading front-of-package claims when making quick food decisions" (Abrams. 2014).
  
  

  

  Parents fall for unwarranted claims, and misleading images children for cartoons.

  While playful visuals appeal to children, parents associate them with junk food. That does yet not mean that they would not fall for health claims, realistic graphics, and natural claims which make them classify the junkfoods that were investigated in the study at hand as healthier.
  
  Fruit graphics in particular were misunderstood to indicate that the respective foods actually contained fruit, when they were simply meant to communicate flavors, instead. Against that background it's not surprising that the unsettling result of this study in 28 women and 2 men revealed that "[parents may make unhealthy food choices as a result of front-of-package information" (Abrams. 2014).

Intensity is key to reduce the exercise induced increase in appetite | more

Bottom line: I understand very well that for most of you only news item #2 is of practical value. Item #1, on the other hand, is rather a description of the misery than a solution and #3 is something that you as a SuppVersity reader probably knew, already... that being said, simply adding more polydextrose to the foods dumb parents buy for their kids because there are fruits on the packaging is not going to help their kids becoming overweight adults who begin to salivate, whenever they see the right food cues. A long-term solution to the problem would thus have to start with the production of healthier foods by the food industry and the education of the public who would then no longer fall for the unwarranted health claims on the packaging of children and adult food products | Comment on Facebook!

References:

• Abrams, Katie M., Caitlin Evans, and Brittany RL Duff. "Ignorance is bliss: how parents of preschool children make sense of front-of-package visuals and claims on food." Appetite (2014).
• Ibarra, Alvin, et al. "Effects of polydextrose on different levels of energy intake: a systematic review and meta-analysis." Appetite (2014).
• Lummela, Netta, et al. "Effects of a fibre-enriched milk drink on insulin and glucose levels in healthy subjects." Nutrition journal 8.1 (2009): 45.
• Meyer, Monica D., et al. "Pavlovian conditioning to hedonic food cues in overweight and lean individuals." Appetite (2014).

Pistachio Phenols 90% Bioavailable. Phe, Leu, Glu & Trp - Four Satiating Aminos. Artificial Sweeteners Act as Anti- Convulsants. Dendrobium for Glucose, Lipids & Kidneys

Since I am a little pressed in time, I won't beat around the bush, but rather get to the meat of the matter of this Nutrition Quickie, right away... well, actually today's nutrition quickie has no item on meats, but is has one Dendrobium, which is actually rather a supplement - be that as it may, here you go:

• 

  Since you (hopefully ;-) haven't swallowed a bomb colorimeter, it's actually no wonder that your body can only access 75% and 95% of the energy this little oven can squeeze out of almonds and pistachios. If you went with the Atwood factor (which says fat = 9kcal/g) and simply added fats, proteins and carbs the discrepancy for almonds would even increase to ~35% (Nowotny. 2012)

  Almonds deliver 25% less calories that the nutritional label will tell you (Gebauer. 2012) -- At the FASEB meeting in April 2012, already, scientists from nowhere else than the mighty USDA, respectively the Beltsville Human Nutrition Research Center of the USDA presented the results of a human study that clearly shows that our tummies cannot squeeze out more than 75% of the nutrients a bomb calorimeter does. Nutrition Quickie: 25% Less Kcal in Almonds Than Label Says.
  
  The caloric value on both food labels and respective nutrient tables is thus off 25% too high. And the corrected energy content per 100g of almonds is 456kcal/100g not 575kcal/100g (nutritiondata.com), or even higher values you will find when you google  "almonds kcal" - I am curious if at least the nutrition labes will ever be updated.
  
  A similar but less pronounced mismatch has been found for pistachios by the same researchers earlier this year, already. According to a paper published in the January edition of the British Journal of Nutrition (Bear. 2012), the actual energy content of these heart healthy nuts 565kcal/100g, which is ~5% less than the currently established value. 

• Bioavailability of pistachio polyphenols, xanthophylls, and tocopherols is very high - until you put them into a muffin (Mandalari. 2013) -- Bioavailability, i.e. the ratio of the total amount of a certain molecule that's in the food we eat in intact or at least active form in our bloodstream, can be a real issue for many of the good things the spectral analyzer of brainy scientists detects in our foodstuff.
  
  

  

  Table 1: Phenol, lutein and tocopherol content of the raw, roasted and salted pistacchios and regular and pistaccio (17g/100g) muffins (Madalari. 2012)

  In the upcoming January issue of Nutrition a group of researchers from the UK and Italy report the results of an investigation into the bioavailability of polyphenols, xanthophylls (lutein), and tocopherols (among them the rare gamma-variety) from raw pistachios, roasted salted pistachios, and muffins made with raw pistachios. You can see the original polyphenol, xanthophyll and tocopherol (mind the 90% gamma-tocopherol content, which has better chemoprotective effects than alpha-tocopherol; see "Vitamin(S!) E" post from 2011) content in table 1.
  
  Interestingly enough the availability of the tocopherols was almost identical for all three tested forms (raw, roasted, in muffins) and even the muffin reduced only the bioaccessability of protocatechuic acid (78%) and luteolin (36%), the rest of the phenols achieved the same ~90% Madalari et al. observed for the raw and roasted + salted pistachios in their million dollar model of the human digestive tract (click here for an article about this "artificial gut")

• When the gut "tastes" phenylalanine (PHE), leucine (LEU), glutamate (GLUT) and tryptophane (TRP), satiety ensues (Daly. 2012) -- In their most recent paper Christin Daly et al. report on the cholecystokinin (CCK) release in the gut. According to the scientists from the University of Liverpool (UK) and the Kyushu University (Japan), the effect is mediated by interactions with the gastrointestinal bitter taste receptors. Since CCK inhibits food intake and reduces appetite, this provides another mechanistic explanation for the satiety promoting effects of high protein intakes. The effects was observed only for the L- and not the D-amino acids.
  
  Interestingly, the beneficial effects of  PHE, LEU and GLUT on CCK (but not the TRP-stimulated CCK secretion) were blunted in the presence of gurmarin. "Gurmarin?" Yeah, that's the rodent specific  sweet taste inhibitor in Gymnema sylvestre (note gurmarin does not work in humans; cf. Sigoillot. 2012), which is sold as an anti-diabetes supplement. Inosine, on the other hand increased the CCK release n response to all of the amino acids.
  
  How significant that is specifically for those who have a problem keeping their ravenous appetite in check is however questionable. After all the satiety response to CCK has been shown to be disturbed (at least in rodents; cf. Balaskó. 2012)

• 

  Table 2: Number of mice protected by the administered drug in the MES test (Talevi. 2012)

  Acesulfame potassium, cyclamate and saccharin are potential anti-convulsants (Talevi. 2012) -- It may sound counter-intuitive in view of all the bad stuff you have probably heard about artificial sweeteners, but it is their particular molecular structure and similarities between the T1R3 sweet taste receptor they are supposed to bind to ant several metabotropic glutamate receptors from different species that is probably behind the anticonvulsant effects a group of researchers from the Department of Biological Sciences at the Faculty of Exact Sciences of the National University of La Plata (UNLP) in Buenos Aires, Argentina.
  
  The overall effect size the scientists observed in their rodent model (see table 2) is yet far from earth shattering and generally more pronounced if the sweeteners had been ingested 4h instead of just 20 min before a Maximal Electroshock Seizure (MES) test. Whether this makes them worth "supplementing" is however more than questionable.
  
  Suggested additional reads:
• Stevia - More Than Super Sweet: More Scientific Evidence, More Potential Implications for Weight Loss & -Maintenance, Anti-Diabetic & -Autoimmune and Even Pro-Anabolic Effects
• Fructose Epimer D-Psicose First Sweetener to Actively Promote Weight Loss? Reduced Weight Gain and Direct Inhibitory Effect on Adipocyte Maturation in Rodent + Reduced Postprandial Glucose & Insulin in Human Trial
• The Unsatiating Truth About Aspartame, Acesulfam K, Sucralose & Co: They Don't Induce Glucose or Insulin Spikes, But Do They Make You Hungry?
• other posts with the tag "artificial sweetener"

• Putting things into perspective: While the DPPH radical scavenging activity is not a really good measure of the in-vivo anti-oxidant potency of a given molecule it may yet still be worth mentioning that the one of Dendrobium (IC₅₀ = 29.6 μg/mL) is more than 80% lower than that Areca catechuvar. Cinnamon cassia, Paeonia suffruticosa and Alpinia officinarum extracts which share IC₅₀ values <6µg/mL (Lee. 2003). In other words, you need 80% more Dendrobium than cinnamon, for example, to neutralize the same amount H2O2 radicals.
  Dendrobium extract ameliorates renal fat accumulation, hyperglycemia and hyperlipidemia in rodents on "high fat" diet (Lee. 20012) -- While I cannot say if this is the same Dendrobium extract that's used in a pre-workout supplement that's "all the craze", these days, I can tell you that a group of researchers just published a paper on the renoprotective, hypoglycemic and hypolipidemic effects of an extract from Dendrobium moniliforme (a cursory search revealed that even within this genus of orchids there are at least 90 sub-types ranging from Aochidori to Yuten).
  
  Lee et al. administered the methanolic extract at dosages of 200mg/kg (HED ~16mg/kg) for nine weeks and reduced the elevated serum glucose, total cholesterol concentration and renal lipid accumulation in the HFD-fed mice. It also ameliorated renal dysfunction biomarkers including serum creatinine and renal collagen IV deposition. So that the scientists conclude that methanolic extracts from Dendrobium moniliforme exhibit pleiotropic effects on obesity induced parameters and exert renoprotective effect in HFD-fed mice.

---

That's it for today, unless you are are interested in one of the following facebook news:

• Crape ginger (Costus speciosus Koen) has significant anti-arthritic properties - at least in a rodent model (read more)
• Ayurvedic polyherbal Unani formulation shows promising results in Acne vulgaris patients - 45 days, 45 subjects, significant improvements on Cook's acne scale (read more)
• Endocannabinoids increase, leptin decreases a "sweet tooth" - And you can take this almost literally, since they do actually modulate sweet taste receptor sensitivity (read more)

There are actually a couple more and they will "proliferate" *rofl* even before the next official SuppVersity  post will be published. Reason enough to check by from time to time, or simply "like" the SuppVersity on Facebook in order to keep up with the news.


References:

• Baer DJ, Gebauer SK, Novotny JA. Measured energy value of pistachios in the human diet. Br J Nutr. 2012 Jan;107(1):120-5.
• Balaskó M, Soós S, Párniczky A, Koncsecskó-Gáspár M, Székely M, Pétervári E. Anorexic effect of peripheral cholecystokinin (CCK) varies with age and body composition (short communication). Acta Physiol Hung. 2012 Jun;99(2):166-72.
• Gebauer SK, Novotny JA, Baer DJ. Macronutrient absorption from almonds: the measured energy value of almonds in the human diet. FASEB Journal. 2012;26:820.25.
• Lee SE, Hwang HJ, Ha JS, Jeong HS, Kim JH. Screening of medicinal plant extracts for antioxidant activity. Life Sci. 2003 May 30;73(2):167-79.
• Lee W, Eom DW, Jung Y, Yamabe N, Lee S, Jeon Y, Hwang YR, Lee JH, Kim YK, Kang KS, Kim SN. Dendrobium moniliforme Attenuates High-Fat Diet-Induced Renal Damage in Mice through the Regulation of Lipid-Induced Oxidative Stress. Am J Chin Med. 2012;40(6):1217-28.
• Mandalari G, Bisignano C, Filocamo A, Chessa S, Sarò M, Torre G, Faulks RM, Dugo P. Bioaccessibility of pistachio polyphenols, xanthophylls, and tocopherols during simulated human digestion. Nutrition. 2013 Jan;29(1):338-44.
• Novotny JA, Gebauer SK, Baer DJ. Discrepancy between the Atwater factor predicted and empirically measured energy values of almonds in human diets. Am J Clin Nutr. 2012 Aug;96(2):296-301. 
• Sigoillot M, Brockhoff A, Meyerhof W, Briand L. Sweet-taste-suppressing compounds: current knowledge and perspectives of application. Appl Microbiol Biotechnol. 2012 Nov;96(3):619-30.
• Talevi A, Enrique AV, Bruno-Blanch LE. Anticonvulsant activity of artificial sweeteners: a structural link between sweet-taste receptor T1R3 and brain glutamate receptors. Bioorg Med Chem Lett. 2012 Jun 15;22(12):4072-4.

Is Hypoglycemia Obesogenic? Is the GI Totally Worthless? Is Mild, But Chronic Stress Behind the Diabesity Pandemic? Is Leptin Obesogenic? And How Do You Calculate the Energy Requirements of Diabetics?

One of the mistakes researchers and dieters make time and again, using the scale as their only guide

Since I had a couple of interesting, but not earth-shatteringly exciting studies on obesity, body weight gain, the GI, leptin and a couple of other things lying around, I thought I'd compile a brief potpourri for you to get you on par with the helplessness with which researchers are still facing the diabesity pandemic. So don't expect any of the one-size-fits-it-all solutions the scientists still appear to be looking for from any of the following items. What you may find, however, is some inspiration when you read between the lines or follow up on the suggested reads, I mention. And if that's not the case, you can still browse previous articles on fat loss or simply go to the gym and try the fat loss example routine from the SuppVersity "Step By Step Guide for Your Own Workout Routine" or simply go to be early to preserve your circadian rhythm.

• Going "Hypo" time and again will make you fat (McNay. 2012) -- Usually you think of hyogylcemia as a sign of a lack of energy, yet despite the fact that this may well be the case this very lack in energy has recently been shown to exert obesogenic effects in a rodent model.
  
  

  

  Often a picture says more than 1000 words: Normal (left) and repeatedly hypoglycemic rodents after 8 months of weekly insulin injections (McNay. 2012)

  The weekly injections Ewan C McNay and his colleagues administered to their rodents and the subsequent episodes of hypoglycemia lead to profound weight gain in the absence of diabetes, hyperphagia, changes in hypothalamic NPY or POMC mRNA expression and  the other usual suspects that could explain this phenomenon. The one thing that's left is therefore what the researchers call a "multi-faceted deficit in metabolic regulation" (McNay. 2012) - interestingly enough the 69.5% higher body weight at 12 months went hand in hand with the usual laziness (-25% activity) of people whose brains are starving in abundance (e.g. type II diabetics).
  
  What remains to be seen, though, is whether similar effects would occur in response to "regular" non-insulin induced hypoglycemia. In view of the easy with which crash dieters and people with roller-coaster blood glucose levels gain weight, it is yet not unlikely that it is actually the avoidance of (reactive) hypoglycemia and not so so much the prevention of hyperglycemia that makes low GI diets successful for weight maintenance (for weight loss the picture is more complicated, since this will require a energy deficit and that's a game changer).

• Dietary glycemic index and load are not associated with type II diabetes risk in 12,403 Europeans (Sluijs. 2012) -- Apropos GI, scientists from the University Medical Center in Utrecht did not find statistical significant correlations dietary glycemic index and/or glycemic load and the risk to develop type II diabetes in in a subcohort of the European Prospective Investigation into Cancer and Nutrition Study (n = 12,403 participants).
  
  Even when they compared participants in the highest and lowest quantiles, the increase in risk was only 5% and 7% for GI and GL respectively. Since this is by no means the first study that suggests that the still propagated concept of the beneficial health effects "low GI diets" is faulty, I would suggest you rather watch the actual food items, than their respective glycemic indexes if you intend to ward off obesity and diabetes. Potatoes for example may have a high GI (including sweet potatoes, by the way), but their high potassium and overall mineral content, as well as the mere fact that you can hardly eat the same amount of total carbohydrates you can easily annihilate, when you are eating pasta still makes them one of the best sources of starchy carbs you have (learn more in the Potato Manifesto, Part I & II).

• 

  Figure 1: There were no statistically significant difference in terms of weight gain or loss, but the 2-week re-feed had a greater impact on blood glucose and insulin levels in the high GI group (Lagerpusch. 2012)

  There is use for the GI on a bulk or after a diet, but only if you are concerned about insulin sensitivity (Lagerpusch. 2012) -- While the general value of the GI as a means to distinguish good from bad carbohydrate sources is certainly questionable, the recently published results from a study that was conducted at the Institute of Human Nutrition and Food Science, of the -Albrechts University in Kiel, Germany, does suggest that monitoring the GI of your diet and adding additional fiber to reduce the insulin response to your meals can come quite handy, in phases, where you are particularly prone to store body fat. On a bulk, for example, or even more so when you have been dieting and are trying to return to a normal caloric intake.
  
  According to the results Lagerpusch et al. present in the November issue of the British Journal of Nutrition even healthy young men who were subjected to a 3-week diet phase (-50% in caloric intake) and subsequent overfeeding (+50% in caloric intake) the subjects in the high GI study arm had a 135% higher increase in fasting insulin levels during the refeed than those in the low GI group. In view of the fact that the glucose clearance (measured in an oral glucose tolerance test) was identical, it is not only no wonder that the weight gain did not differ either (see figure 1), but also unlikely that we would see significant differences as far as the fat gains are concerned (the latter were unfortunately not measured in the study at hand). At the same time, longer hyper-caloric high GI diets are certainly a risk factor for both insulin resistance and obesity, so that you are probably still at lower risk with 65g instead of 27g of fibre per day and a mean GI of 40 vs. 74.
  
  If you are interested in the influence of different diets on weight gain and health during overfeeding, I suggest you check out the following two SuppVersity posts: "194 Bananas in Three Weeks" and "A Tale of Macro- and Micronutrient Modifications".

• 

  Figure 2: Chronic mild stress leads to an overactivation of the HTPA and subsequen metabolic dysregulations (Takahashi. 2012)

  Further evidence that chronic mild stress is to blame for the obesity pandemic (Takahashi. 2012) -- As researchers from the Tohoku University Graduate School of Medicine in Japan report in the latest issue of the  American Journal of Physiology - Endocrinology & Metabolism, the localized re-setting of the clock genes in the liver, yet not the hypothalamic suprachiasmatic nuculeus (SCN), of BALB/c mice in response to chronic mild stress exposure elevated and phase-shifted serum corticosterone levels (see figure 2).
  
  Takahashi et al. argue that the observed changes are indicative of an overactivation of the HPA axis, which induced disturbances in the rhythmic expressions of core clock genes, e.g. Clock, Npas2, Bmal1, Per1 and Cry1 in the liver and subsequently circadian patterns of glucose and lipid metabolism-related genes such as the proliferator activated receptor (PPAR) family which favor the storage and hamper the oxidation of fatty acids.
  
  If you want to learn more about clock genes and how you can modify them, (re-)read the SuppVersity Circadian Rhythm Series!

• Scientists develop improved formula to calculate the resting energy expenditure of diabetics (Ikeda. 2012) -- While I would hope that you don't belong to the group who would have to use the new and improved formula scientists from the Department of Diabetes and Clinical Nutrition at the Kyoto University in Japan have now proposed, you may have clients or relatives who could benefit from its high predictive validity (78% +/- 103kcal vs. 50% for Harris-Benedict; 38% for Oxford, 42% for Liuand 63% for Ganpule):
  
  
  What you should keep in mind though, is that this equation was tested on Japanese individuals. Since we know from other studies that there are certain metabolic differences between people with different ethnic backgrounds I would remain a "healthy skeptic" as far as the outcomes of this equation are concerned - the same obviously goes for any other equation, e.g. the ones for athletes I provided in part III of the Female Athlete Triad series.

• 

  If you are interested in ways to modulate your leptin levels that may facilitate weight gain, I suggest you take a look at my second "Carbs Past 6PM Won't Make You Fat" post.

  Leptin induced weight gain? 13% more body fat in 2 weeks, when it hits the wrong part of the brain (Harris. 2012) -- With the mixed results from intervention trials, the enthusiasm around leptin has abated over the past months, the general consensus is yet still that leptin and leptin resistance loom large in the metabolic dysregulation that's at the heart of the diabesity pandemic. Against that background, the results Ruth B.S: Harris presents in her latest paper in the American Journal of Physiology - Endocrinology & Metabolism are unquestionably surprising.
  
  When Harris injected twice the amount of leptin (0.6 µg leptin/day) that had previously been shown to decreased 24 food intake, body fat and lean tissue, when it was injected into the third ventricle of the hindbrain, into the fourth ventricle of her lab rats, the rodents gained an almost incredible amount of 13% body fat within only 2 weeks! And that in the absence of statistically significant change in daily food intake, suggests an "increase in efficiency of energy utilization" (Harris. 2012). Fortunately, further experiments showed that the pro-obesogenic effects of leptin in the 4th ventricle was antagonized when both the 3rd and the 4th ventricle were exposed to leptin. In this scenario the leptin exposure of the 4th ventricle did even protect the lean mass of the rodents from the negative effects the exclusive exposure of the 3rd ventricle had. Overall, the study is yet somewhat chaotic and a clearcut message aside from "look people things are even more complex than we already thought", is probably not going to contribute to a solution of the obesity dilemma in the near future. 

There are, as usual more news on Facebook, some of them, such as the relation between hypothyroidism during pregnancy and the diabetes risk of the offspring later in life, are even related to the topic at hand. And if that's nothing you are interested, you may want to read about ...

• the non-existent effects of coffee consumption before bed on the sleep quality of habitual coffee drinkers (read more),
• the problem with inaccurate vitamin D tests and the absence of a reliable and scientifically sound definition of "vitamin D deficiency" (read more), or
• the strength promoting in-vitro effects of sodium bicarbonate, or in other words, a rather alkaline milieu on muscular force production (read more)

... and if neither of those can satisfy your thirst for more information from the realms of exercise and nutrition sciences, you can still wait for the next serving of facebook news or tomorrow's SuppVersity article :-)


References:

• Harris RB. Leptin-induced increase in body fat content of rats. Am J Physiol Endocrinol Metab. 2012 Dec 4.
• Ikeda K, et al. A new equation to estimate basal energy expenditure of patients with diabetes. Clinical Nutrition. 2012 [article in press] 
• Lagerpusch M, Enderle J, Later W, Eggeling B, Pape D, Müller MJ, Bosy-Westphal A. Impact of glycaemic index and dietary fibre on insulin sensitivity during the refeeding phase of a weight cycle in young healthy men. Br J Nutr. 2012 Nov 28:1-11.
• McNay EC, Teske JA, Kotz CM, Dunn-Meynell A, Levin BE, McCrimmon RJ, Sherwin RS. Long-term, intermittent, insulin-induced hypoglycemia produces obesity without hyperphagia or insulin resistance: a model for weight gain with insulin therapy. Am J Physiol Endocrinol Metab. 2012 Nov 20.
• Sluijs I, Beulens JW, van der Schouw YT, van der A DL, Buckland G, Kuijsten A, Schulze MB, Amiano P, Ardanaz E, Balkau B, Boeing H, Gavrila D, Grote VA, Key TJ, Li K, Nilsson P, Overvad K, Palli D, Panico S, Quirós JR, Rolandsson O, Roswall N, Sacerdote C, Sánchez MJ, Sieri S, Slimani N, Spijkerman AM, Tjønneland A, Tumino R, Sharp SJ, Langenberg C, Feskens EJ, Forouhi NG, Riboli E, Wareham NJ; on behalf of the InterAct consortium. Dietary Glycemic Index, Glycemic Load, and Digestible Carbohydrate Intake Are Not Associated with Risk of Type 2 Diabetes in Eight European Countries. J Nutr. 2012 Nov 28.
• Takahashi K, Yamada T, Tsukita S, Kaneko K, Shirai Y, Munakata Y, Ishigaki Y, Imai J, Uno K, Hasegawa Y, Sawada S, Oka Y, Katagiri H. Chronic mild stress alters circadian expressions of molecular clock genes in the liver. Am J Physiol Endocrinol Metab. 2012 Dec 4.

The Latest Gut Microbiome Modulators: Beneficial Effects of Cacao, Negative Effects of Acidic Water and Preliminary Evidence of the Negative Impact of Gluten & Whole Grains

Pancakes al cacao & your gut: Bad grains and good cacao?

There is an increasing amount of interesting scientific publications on the role of the gut microbiome in health and disease. Unfortunately, the evidence on what exactly influences the number and types of bacteria in our gut in a beneficial way and even what exactly a "beneficial way" actually is, is yet largely unknown.

In today's installment of the SuppVersity Short News, I am going to take a closer look at a selection of recent studies that may shed at least some light at the previously mentioned questions.

You can learn more about the gut & your health at the SuppVersity

Bugs Dictate What You Crave

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

The Macrobiotic MaPi2.0 Diet

• Cacao as a gut microbiome modulator - The first study we're going to look at deals with cacao. Cacao and its effect on the gut microbiome. In said study, 3-week-old Wistar and Brown Norway rats were fed, for 4 weeks, either a standard diet or the following three isoenergetic diets containing increasing proportions of cocoa flavonoids from different sources: one with 0·2 % polyphenols (from conventional defatted cocoa), and two others with 0·4 and 0·8 % polyphenols (from non-fermented cocoa, very rich in polyphenols).
  
  

  

  Only the regular theobromine containing cacao did also reduce the weight gain in the three-week study (Massot-Cladera. 2014).

  What the scientist found, when they analyzed the serum Ig concentrations, faecal IgA levels, microbiota composition and IgA-coating bacterial proportion at the end of the study and compared them to those at the beginning was a significant beneficial effect on the mucosal IgA levels and microbiota composition from all supplements. The 0.2 % cacao diet which contained a higher proportion of theobromine and fibre, however, had a more profound impact on the aforementioned parameters - in spite of the fact that there was less cacao in the diet. Obviously, the caffeine-like bitter alkaloid from cacao is contributes to the beneficial effects of cacao in a similar way as the polyphenols.
  
  As the body weight data in Figure 1 shows, the theobromine containing conventional cacao was also the only one that was able to reduce the diet induced weight gain in the rats. This could, but does not necessarily have to be related to the higher levels of Bacteroides, Bifidobacterium and Lactobacillus bacteria in the gut of the rodents that received the "cheap" conventional cacao.
• Acidic water triggers type I diabetes - probably by modulating the gut microbiome - No, I am not trying to advertise bicarbonate, here. I am just reporting the results of a recent study from the Medical University of South Carolina which found that a stain of mice that's particularly susceptible to type I diabetes developed insulitis and hyperglycemia rapidly, only when the mice were maintained on acidic pH water (AW).
  
  

  

  Suggested Article: "High Dietary Acid Load Doubles Risk of Type II Diabetes in Lean Individuals! Causative or Corollary? Plus: Are Grains, not Meats the Main Offenders in Our Diet?" | read more.

  The scientists also observed that this effect could be countered by fecal transplants and was obviously triggered by changes in the diversity of the gut flora that occurred, when the pH of drinking water was in the acidic range and were probably related to the proinflammatory cytokine response in the intestinal mucosa.
  
  As you as a SuppVersity reader know previous studies in humans have already shown that a "High Dietary Acid Load Doubles Risk of Type II Diabetes in Lean Individuals!" (read more) - Who knows, this could also be related to the effect on the gut microbiome!?
• Gluten and whole grains as modulators of the gut microbome - In two recent randomized cross-over trials, researchers from the University of Copenhagen determined the impact of dietary gluten or whole grains on the gut microbiome and host metabolic health.
  
  What the researchers found was what the recent backlash against gluten and "healthy" whole grains on the internet would suggest the already overweight "[p]articipants had slightly elevated fasting glucose levels and increased waist circumference" (Ibrügger. 2014).
  

  

  Table 1: Overview of the products used in the randomized controlled cross-over trials (Ibrügger. 2014)

  Whether that's related to the effects on the gut microbome is unfortunately something I can't tell you, yet. Why? Well, the currently available paper refers to a future publication that would outline the detailed results. All I can tell you now is that the study used the products listed in Table 1 and, more importantly, that it is its high statistical power, which, due to the large sample size and the crossover design, "allows detecting even small diffrences in the outcome variables" (Ibrügger. 2014).

Suppversity Suggested: "Stevia Kills Good Gut Bacteria - One Study Enough to Stop Using the Natural Sweetener? Probably Not in View of its Anti-Diabetes, Anti-LDL, Anti-Viral & Anti-Cancer Effects" | more

Bottom line: It's a pity that we still can't tell for sure what the "optimal" gut microbiome looks like. Moreover, the currently available scientific evidence suggests that what is considered "optimal" may well depend on your type of diet and / or your metabolic health.

Against that background the previously presented results offer nothing but a brief glimpse at what may become one of the hottest topics in obesity and diabetes prevention in the future. At the moment, though, all the results and any recommendations that are based on these results have to be considered preliminary. And this is also true for the gluten + whole grain study of which you will certainly read again, here at the SuppVersity | Comment on Facebook!

References:

• Ibrügger, S., et al. "Two Randomized Cross-Over Trials Assessing the Impact of Dietary Gluten or Wholegrain on the Gut Microbiome and Host Metabolic Health." J Clin Trials 4.178 (2014): 2167-0870.
• Massot-Cladera, Malen, et al. "Impact of cocoa polyphenol extracts on the immune system and microbiota in two strains of young rats." British Journal of Nutrition 112.12 (2014): 1944-1954.
• Sofi, M. Hanief, et al. "pH of drinking water influences the composition of gut microbiome and type 1 diabetes incidence." Diabetes 63.2 (2014): 632-644.

Fit Kids = Smart Kids, Creatine & Muscle Repair, Epigenetic Transfer From one Leg to Another. Plus: Fat Effects of Anti-Psychotics, Larger Muscle = Greater CNS Impact, Rhodiola a Natural Opiate, Hawthorn for More & Thicker Hair

It's never too early for your first push-up ;-)

"10" is this week's SuppVersity figure of the week. Ten as in "ten push-ups" which is the mean number of push-ups the 12 year-old boys and girls from the Coe study you can read about in one of the items of today's news mash-up aka "On Short Notice". I am honestly not yet sure what to make of it, it's not as bad as what I had expected based on a couple of observations I have made as of late, but it still goes to show you that you cannot take the most fundamental feats of physical fitness for granted, when it comes to pre-/peri-pubertal kids in today's sedentary society.

Now, while I am still trying to make up my mind I would suggest we take a look at the actual outcomes of the study. The 10 push-ups were after all only part of the subject characteristics and not the reason Coe et al. actually conducted their study.

Fit Kids are smart kids - Strength and cardio both matter!

You can hardly start your career as a physical culturist too early, there are simply way too many benefits from giving your body the nutrients and the exercise it needs and therefore it is actually not surprising that conclusion of a recently published paper in the Journal of Sports Medicine and Physical Fitness reads:

"Students with the highest fitness level performed better on standardized tests and students with the lowest fitness level performed lower in class grades" (Coe. 2012)

Interestingly enough, this effect was associated with both cardiorespiratory fitness and strength, which brings us back to yesterday's news about the PGC-1 alpha isoforms (read the comments as well) and the detailed follow up I just decided to post on the whole matter, tomorrow.

Figure 1: Spearman rank correlations and achievements cores in terms of grades (0:min, 80:max), test scores (% of max) and combined (% of mean of all kids; data based on Coe. 2012)

Since this is the first study of its kind to investigate all five established parameters of health-related fitness (HFR), it should also be mentioned that body composition, flexibility and muscular endurance did not show the same statistically significant correlations the scientists observed for cardiorespiratory endurance and muscle strength in the kids (52% boy, 48% girls; all from the same age group ~12 years). Now, it would be nice if the people who design the curricula would keep that in mind, when they add junk after junk to the syllabus and regard sports and being active as an unnecessary diversion from the constant intellectual drills.

Creatine can do much, but it can't accelerate skeletal muscle repair after a workout 

The results of a recent study from the Department of Kinesiology and Physical Education at the Wilfrid Laurier University in Canada (McKinnon. 2012) , in the course of which  a total of 27 male (n = 15) and female (n = 12) participants between the ages of 18-24 completed an experimental training protocol with either

• 2x creatine monohydrate (20g) and a carbohydrate supplement (20g) in order to blend consistency and taste (CREA),
• 2x 40 g of maltodextrin only in 500mL of water (MALTO), or
• no supplementation at all (control)  

The supplement was consumed over a 5-day period (check out the "Pharmacokinetics of Creatine" posts and you will learn that this dosage regimen is an unnecessary overkill - even if you insist on "loading") after which the participants participated in a baseline strength test that was followed by a muscle-damaging protocol that consisted of maximal force eccentric contractions:

Suggested read: "Creatine a Proven Non-Anabolic Agent: It's the Increase in Training Intensity that Will Give You the Hypertrophic Edge (read full story)

"Subjects performed 60 maximal eccentric contractions that were divided into 6 sets of 10 repetitions, with a 45 second rest period between repetitions.  The velocity of eccentric contractions was varied between sets (2 at 75°/sec, 2 at 90°/sec, and 2 at 120°/sec). This protocol has been used in previous studies and has been shown to be an effective means of inducing skeletal muscle damage (Cooke et al., 2009). The researchers also provided verbal encouragement to the subjects to help maintain maximal effort throughout the protocol." (McKinnon. 2012)

After adequate rest, the first of 5 post-tests was conducted. The results (figure 2) clearly show that despite the overall greater force recovery in the creatine group, the relative rebound after an allegedly higher drop was seen in the MALTO group while it was minimal in the no-supplement group.

Figure 2: Force recovery and muscle soreness at 0h, 24h, 48h, 72h, 96h in the control, maltodextrin and creatine groups subsequent to a 5-day suppelemtation regimen (nothing,  2x 20g crea + 2x20g malto, or 2x40g malto (McKinnon. 2012)

Overall the scientists are yet still right, when they say that "creatine supplementation failed to significantly influence indices elbow flexor muscle damage or rate of muscle recovery following eccentric muscle contractions." After all, there were no statistically significant differences between either the muscle force loss and rate of recovery or muscle soreness (small figure in figure 2) between the groups - and it is unlikely that this would change after the initial 96h of recovery.

Additional suggested reads:

• DHEA Blunts Muscle Damage During 5 Days of Combined Endurance, Strength and HIIT Training in Young Men (read more)
• Speed Up Your Regeneration and Propel Your Gains by Taking a HOT Bath Bath 2-Days Before Arduous Workouts (read more)
• Overtraining, Inflammation, Insufficient Repair: Scientists Shed Some More Light on the Counterproductive Triad of Ups & Downs in Testosterone, IL-6, IL-10, COX II & Co (read more)

Ah, I almost forget to mention, you see that the mean isometric peak torque is not even back up to 100% after 96h, right? Remember that whenever you decide that it would be a good idea to do "yet another set of forced reps". It is possible that the seasoned strength training veteran you are, you recover faster than the subjects in the study at hand who had not trained for at least 4 months, but it stands out of question that eccentric forced reps will increase the time you need to regenerate, let alone to see what we are all striving for, i.e. super-compensation effects (see suggested links on the right for more on "doing too much" and faster recuperation after workouts).

Working out one leg changes genes in the other leg as well 

The progress research in the area of epigenetics, i.e. the changes of gene methylation and thus activity in response to nutrition, exercise and other variables you can easily control is actually amazing. With the recent publication of a study into what you may call epi-genetic cross-reactivity further contributing to our insights into the relations of the local and system epigenetic effects of exercise and their respective metabolic downstream effect (Catoire. 2012).

Figure 3: Graphical summary of the study design and selected results (Catoire. 2012)

As you can see in my graphical mini-summary of the study design (top) and outcomes (middle + bottom) in figure 3 there was a whole lot going on... and that despite the fact that I did already spare you a complete page with font 10 lists of genes that changed (you do have the numbers, I guess that shall suffice) and paired them in groups. What's funny is that, when it's all said and done, this does yet again tie in to yesterday's news on PGC-1 alpha 4 - how? Well, let's hear (or read), what the scientists have to say in the discussion of their results:

"Many of the observed exercise-induced changes in gene expression are likely part of an acute stress response related to disturbances in homeostasis elicited by exercise. The most highly induced genes in the exercising leg were all members of the NR4A family, a subgroup of orphan receptors within the nuclear receptor superfamily. NR4A1 and NR4A3 have been reported to be upregulated shortly after acute exercise and during recovery in rat, pig, and human [24], and this upregulation likely occurs locally by contractile stimuli. This finding was confirmed by our study in which we observed an upregulation of NR4As in the exercising, but not in the non-exercising leg. NR4A transcription factors are also known to be induced by adrenaline and noradrenaline. Circulating adrenalin and noradrenalin levels were increased in our study but must exert only a minor effect as NR4As were exclusively induced in the exercising leg,. [...] NR4A1 and 3 are thought to play a key role in regulating energy metabolism and early adaptation. [...] The results may imply that NR4A family might play an important role in the regulation of metabolic responses after exercise." (Catoire. 2012)

The study at hand does thus add yet another puzzle piece to the image of the crossroads of the endocrine (from one tissue to the other) and intracrine (in this case in the exercised muscle) effects of energy and metabolic changes on the one hand and muscular contraction and local stress, on the other hand. As closely interwoven as they are, we are now - thanks to the novel gene essays - able to see through the complex network, understand what exercise does to our physiology and can then, in the next step, come up with ways to modulate these effects for our own benefit.

It is clear that this is not going to be easy and the presence of two "mutants" among the 12 relatively old  study participants (52 year; "old" only for studies like this, of course!) suggests that any cookie cuter solutions are probably about to fail. I mean, if you have got two guys out of twelve where the overall magnitude of gene expression changes in the exercising and non-exercising leg were very similar, it is more than likely that you would see these and other anomalies very frequently; and each of them would have to be considered if you wanted to design he optimal workout (nutrition and supplementation) regimen for an individual (good news for personal trainers, if you know what you are doing, no sciency compendium is ever going to replace you ;-)

In rehab, doctors and therapists use the neurological stimulation a stiff leg receives, when you move the other while looking into a mirror that fools you into believing that the stiff leg would be moving as well.

In that it does not even really matter, whether the observed anomalies were actually due to genetic differences or, as the scientists suspect simply the result of unconsciously performed isometric contractions in of the non-exercising leg. The ensuing neuronal activation could have brought about similar effects as they are observed (and intended) during mirror therapy (see image on the right), where an involuntary neural stimulation of the muscles in a stiff leg occurs, when the mirror fools you into believing that you actually just moved your stiff leg, or other body part, when it was in fact only the counter-lateral limb that moved (note: one of the latest reviews of the literature says about its efficacy in stroke rehab would facilitate the recovery of "motor function, activities of daily living and pain" and could be recommended "at least as an adjunct to normal rehabilitation for patients after stroke"; cf. Thieme. 2012).

With the effects of neural stimulation, which has already been shown to induce gene expression changes via increased calcium concentrations in the skeletal muscle as well as via other mechanisms (Long. 2007; Kanzleiter. 2009; Chin. 2010, we do thus have a third player in the epigenetic / protein regulatory exercise orchestrate that does now consist of a metabolic, a contractile / stress mediated and a neuronal component. As far as skeletal muscle hypertrophy is concerned, the local expression does still appear to be the major determinant of adaptation and thus growth - to train your left leg only expecting that the other will grow due to "bystander effects" is therefore almost as hilarious as skipping leg day with the lame excuse that your legs would grow from training your biceps ;-)

On ultra short notice

With that I'll call it a day as far as the detailed posts are concerned and invite you to come back tomorrow, when I am going to pick up on this discussion in a detailed post on the Roa study on PGC-1 alpha 4, muscle growth, myofiber composition, strength development, workouts and the whole megillah. For the time being here is a bunch of unsorted other things I considered newsworthy:

• Anti-psychotics increase lipid synthesis by depressing it!? What sounds totally counterintuitive, is actually the main message of an editorial to the latest issue of the Journal of Lipid Research, in which Skreede, Steen & Ferno argue that a paper by Canfrán-Duque et al. clearly suggests that the obesity and hypercholesterolemic effects of 2nd generation anti-psychotics such as clozapine, risperidone, and ziprasidone are brought about by the counter-regulatory upregulation of cellular lipogenesis in response to their suppressive effect on cholesterol synthesis. (Skreede. 2012)
• The greater the muscle group you work, the larger the impact on the central nervous system will be (Rossmann. 2012) -- In the end everybody will know that intuitive, back and leg days are the hardest and most taxing to the whole system. Based on a trial involving eight young men who performed exhaustive large (cycling – BIKE) and small (knee extensor – KE) muscle mass dynamic exercises at 85% of the modality-specific maximal workload, scientists from Salt Lake City did now provide further experimental evidence that supports the notion that the CNS tolerates a greater magnitude of peripheral fatigue and likely a greater intramuscular metabolic disturbance when the pertinent afferent signaling comes from small vs. large muscle groups . 
• Rhodiola Rosea turns out to be an opiate (Lee. 2012).-- In a recent study scientists from the Chi-Mei Medical Center in Yong Kang, Tainan City, Taiwan were able to show that the popular but questionable (as far as the significance of its effects are concerned) adaptogen rhodiala decreased the systolic blood pressure of spontaneously hypertensive rats. Intriguingly the effect was blunted by the administration of the selective opioid μ-receptor antagonist, cyprodime, but not by naloxonazine, an antagonist specific to opioid μ1-receptor, which suggests that a direct effect on the opiate receptor. Moreover, the level of mood enhancing and relaxing beta-endorphins rose in both wild type and hypertensive rodents (with the effect being more pronounced in the latter)
• Chinese hawthorn for the hair, not the heart (Shin. 2012) -- I guess if you hear hawthorn or Crataegus you will probably think of its purported beneficial effects on heart health. Now if the results from a recent rodent study are applicable to humans, as well, you will soon have to establish a novel neuronal connection between (Chinese) hawthorn and your scalp, or rather the hair on your scalp . With its beneficial effects on the initiation of the anagen phase in mice in teloge and the ensuing increase in skin color, thickness of the hair shafts, and density (number and size) of the hair. Oral C. pinnatifida extract (at a human equivalent dose of ~320mg/day) could soon be all the rage among men and women who fear for their superb head of hair.

I think this is enough for today. There is a life beyond the SuppVersity not for you, of course, but for me - so while you head over to the SuppVersity facebook page for even more news, I am going to enjoy Saturday night ;-)

References:

• Canfrán-Duque, A., M. Casado, Ó. Pastor, J. Sánchez-Wandelmer, G. Peña, M. Lerma, P. Mariscal, P. Bracher, M. Lasunción, and R. Busto. Atypical antipsychotics alter cholesterol and fatty acid metabolism in vitro. J Lipid Res. 2012 [in press]
• Catoire M, Mensink M, Boekschoten MV, Hangelbroek R, Müller M, et al.  Pronounced Effects of Acute Endurance Exercise on Gene Expression in Resting and Exercising Human Skeletal Muscle. PLoS ONE 7. 2012; 11: e51066.
• Chin ER. Intracellular Ca2+ signaling in skeletal muscle: decoding a complex message. Exerc Sport Sci Rev. 2010 Apr;38(2):76-85. 
• Coe DP, Pivarnik JM, Womack CJ, Reeves MJ, Malina RM. Health-related fitness and academic achievement in middle school students. J Sports Med Phys Fitness. 2012 Dec;52(6):654-60. 
• Kanzleiter T, Wilks D, Preston E, Ye J, Frangioudakis G, Cooney GJ. Regulation of the nuclear hormone receptor nur77 in muscle: influence of exercise-activated pathways in vitro and obesity in vivo. Biochim Biophys Acta. 2009 Aug;1792(8):777-82. 
• Lee WJ, Chung HH, Cheng YZ, Lin HJ, Cheng JT. Rhodiola-Water Extract Induces β-endorphin Secretion to Lower Blood Pressure in Spontaneously Hypertensive Rats. Phytother Res. 2012 Nov 28.
• Long YC, Glund S, Garcia-Roves PM, Zierath JR. Calcineurin regulates skeletal muscle metabolism via coordinated changes in gene expression. J Biol Chem. 2007 Jan 19;282(3):1607-14.
• Rossman MJ, Venturelli M, McDaniel J, Amann M, Richardson RS. Muscle mass and peripheral fatigue: a potential role for afferent feedback? Acta Physiol (Oxf). 2012 Dec;206(4):242-50. 
• Shin HS, Lee JM, Park SY, Yang JE, Kim JH, Yi TH. Hair Growth Activity of Crataegus pinnatifida on C57BL/6 Mouse Model. Phytother Res. 2012 Nov 12.
• Skrede J, Steen VM, Ferno J. Antipsychotic-induced increase in lipid biosynthesis: activation through inhibition? Journal of Lipid Research. December 7, 2012 [Epub ahead of print] 
• Thieme H, Mehrholz J, Pohl M, Behrens J, Dohle C. Mirror therapy for improving motor function after stroke. Cochrane Database Syst Rev. 2012 Mar 14;3:CD008449.