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Phototherapy Doubles Fat Loss (11 vs. 6%) & Improvements in Insulin Sensitivity (40 vs. 22%) and Helps Conserve Lean Mass in Recent 20 Weeks 'Exercise for Weight Loss Trial'

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LLLT has also been shown to improve the appearance of cellulite (Jackson. 2013) | Learn more about what really helps against cellulite in this SV Classic
You know that I am not a fan of isolated "exercise / supplement for weight loss trials", but there's one thing I like about them. When the diet is not controlled for and the subjects still lose weight, it is very likely that the intervention is going to work in the real-world, as well. And if the exercise protocol is both manageable and useful, as it was the case in a recent study from the University of Sao Paulo (Sene-Fiorese. 2015), this makes me even more inclined to actually write about the study, even though it may be - from a mere scientific perspective - not provide "bulletproof" evidence of what's the exact cause of the effects, the exercise or supplement, it's effect on energy intake or both.
Learn more about the nuances of dieting and fat loss here, at the SuppVersity

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But let's return to the study at hand: Manageable and useful, in this case, meant three exercise sessions per week with 30 minutes of aerobic training and 30 minutes of resistance training per session.
"During the intervention period, the voluntaries [sic!] followed a combined exercise training therapy. The protocol was performed three times per week and included 30 minutes of aerobic training and 30 minutes of resistance training per session. The aerobic training consisted of running on a motor-driven treadmill (Movement®) between 70 and 85% of maximal heart frequency, which was determined previously by treadmill submaximal test. The resistance exercise training was composed using exercises for the main muscular groups: bench press, leg press, sit-ups, lat pull-down, hamstring curls, calf raises, Straight-Bar Cable Curl (biceps), triceps pushdown, adductor and abductor chairs [see Table 1]. Training loads were successively adjusted, with volume and intensity being inversely modified and the number of repetitions being decreased to between 6 and 20 repetitions for three sets. The training loads were adjusted in each training session and evaluated according to the increase in participants’ strength. Thus, the training was conducted with maximal repetitions (RM)" (Sene-Fiorese. 2015).
For the study, the scientists recruited a total of 64 adult obese women via classic newspapers and magazines as well as electronic media, TV and radio. The inclusion criteria were (i) primary obesity, body mass index (BMI) between 30 and 40 kg/m², (ii) age between 20 and 40 years old. Exclusion criteria were (i) the use of cortisone, anti-epileptic drugs; (ii) history of renal disease; (iii) alcohol intake; (iv) smoking; and (v) secondary obesity due to endocrine disorders. The inclusion and exclusion criteria were assessed by clinical evaluation by physician (endocrinologist).
Table 1: The scientists a resistance training protocol that had previously been used in Foschini (2010)
While the treatment consisted of physical exercise intervention and the individual application of phototherapy immediately after the end of the exercise training session for all volunteers. The scientists randomly assigned the subjects to an active ET-PHOTO and a "SHAM" control group ET-SHAM.
This is a placebo controlled study! I think it's worth highlighting the fact that both groups believed they'd received the treatment, because all subjects had to go to the phototherapy sessions, but the device was actually turned on only for those in the ET-PHOTO, not for those in the ET-SHAM group.
In the ET-SHAM group the device which emits light at a wavelength that's too long for the human eye to actually see it was turned off. Thus the subjects in the SHAM = control group received a simulated phototherapy application ... and yes, that's basically the same thing as the "placebo group" in your average supplement study..
Figure 1: Photo of the Device, Illustration of the Area of Application; Device Information, Irradiation and Treatment Parameters (Sene-Fiorese. 2015).
"The phototherapy equipment was developed by Laboratory Technology Support-LAT, Center for Research in Optics and Photonics Institute of Physics in São Carlos city at University of São Paulo-USP. The device is a prototype equipment that was submitted for registration as a new patent. The device is composed of four plates made of rubberized material measuring 20 by 20 centimeters (cm) each. Each two plates are connected to an electronic control box. The emitters of Ga-Al-As diode Lasers are distributed in the plate every 2.5 cm, totaling 16 emitters per plate and 64 emitters in total. The prototype is illustrated and irradiation parameters are [mentioned in Figure 1]" (Sene-Fiorese. 2015).
As I already hinted at in the previous paragraph, 805 nm is a pretty high wavelength. It's classified as near-infrared (near as in "near, but not in the visible spectrum"), which is too "long" to be seen by human beings... what it was not too long for, though, was to augment the beneficial effects the 48 workouts the subjects performed over the whole study period had on the women's body composition and metabolic health.
Figure 1: Overview of the changes in body comp and glucose metabolism in both groups (Sene-Fiorese. 2015).
What is (imho) pretty astonishing is yet not the fact that benefits occurred, but rather that these benefits were not just statistically significant, but also practically relevant. I mean you will certailny agree, that it makes a difference if you lose 11% or 6% body fat and improve your insulin sensitivity by 40% vs. 22% - right?

If we also take into account that the the scientists observed similarly profound differences when they analyzed the subjects adiponectin levels, which decreased by 7% in the SHAM group (bad) and increased by a whopping 20% (good!) in the PHOTO group, it's really hard to argue that the benefits wouldn't be worth the hassle, even though one may question the accuracy of the body fat / lean mass data which was measured with a body impedance, instead of a DEXA device. Since the overall results do support significant additive effects, there's simply no reason to assume that the BIA data would be incorrect. In addition, BIA is actually relatively useful if you measure relative changes in body composition. If you want a correct one-time reading of your body fat, though, I wouldn't rely blindly on what a BIA device says.
Bottom line: As the authors point out, their latest study "demonstrated for the first time that phototherapy enhances the physical exercise effects in obese women undergoing weight loss treatment promoting significant changes in inflexibility metabolic profile" (Sene-Fiorese. 2015). While I would probably have replaced the grammatically questionable and nondescript phrase"inflexibility metabolic profile" with something more tangible like "insulin sensitivity" or "glucose control," Sene-Fiorese's conclusion is generally right.

The same LLLT therapy has also been shown to almost double the muscle gains in a study with an 8-week eccentric training program | more
Furthermore their findings may be somewhat surprising, but they are by no means unrealistic in view of the existing evidence that demonstrates that phototherapy (or low-level-laser-therapy | LLLT) is effective as an adjuvant tool in non-invasive body countering. It has been shown to help w/ the reduction of cellulite, fatigue, pain, blood circulation, wound healing, lipid metabolism and recovery after exercise (Neira. 2002; Ferraresi. 2010; Aquino. 2013; Paolillo. 2013; Houreld. 2014), as well as to increase  the mitochondrial activity in irradiated cells by up-regulating genes involved in the mitochondrial complexes (Masha. 2013).

Unfortunately, our understanding of the underlying mechanisms that make LLLT so effective is still in its infancy. It is yet most likely that they are mediated on a cellular level by increases in PGC-alpha (the mitochondria builder) and sirtuins like SIRT-1. These proteins are all important regulators of mitochondrial function; and as you may remember from previous SuppVersity articles, they are also activated by resveratrol and a bunch of other supplements that have been shown to increase the health of the cells' mitochondria. How exactly the previously reported increases in muscle gains or the profoundly accelerated fat loss in the study at hand are brought about, will have to be elucidated in future studies, though | Comment on Facebook!
References:
  • Aquino Jr, Antonio E., et al. "Low-level laser therapy (LLLT) combined with swimming training improved the lipid profile in rats fed with high-fat diet." Lasers in medical science 28.5 (2013): 1271-1280.
  • Ferraresi, Cleber, et al. "Effects of low level laser therapy (808 nm) on physical strength training in humans." Lasers in medical science 26.3 (2011): 349-358.
  • Foschini, Denis, et al. "Treatment of obese adolescents: the influence of periodization models and ACE genotype." Obesity 18.4 (2010): 766-772. 
  • Houreld, Nicolette N. "Shedding light on a new treatment for diabetic wound healing: a review on phototherapy." The Scientific World Journal 2014 (2014).
  • Masha, Roland T., Nicolette N. Houreld, and Heidi Abrahamse. "Low-intensity laser irradiation at 660 nm stimulates transcription of genes involved in the electron transport chain." Photomedicine and laser surgery 31.2 (2013): 47-53.
  • Neira, Rodrigo, et al. "Fat liquefaction: effect of low-level laser energy on adipose tissue." Plastic and reconstructive surgery 110.3 (2002): 912-922.
  • Paolillo, Fernanda Rossi, et al. "Infrared LED irradiation applied during high-intensity treadmill training improves maximal exercise tolerance in postmenopausal women: a 6-month longitudinal study." Lasers in medical science 28.2 (2013): 415-422.
  • Sene‐Fiorese, Marcela, et al. "The potential of phototherapy to reduce body fat, insulin resistance and “metabolic inflexibility” related to obesity in women undergoing weight loss treatment." Lasers in Surgery and Medicine (2015).

Nucleotides the 'Next Big Thing' in Ergogenic Supplements? Faster Force-Recovery & Cortisol + CK Modulation in New, Increased Endurance & Immune Effects in Previous Studies

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Nucleotides are building blocks of our DNA and RNA and - as preliminary evi- dence suggests - ergogenic supplements for athletes on intense workout routines. In that, "intense" is the key word, 'cause normally our bodies can produce enough nucleotides on their own.
Nucleotides? Yeah, this are the small subunits, of nucleic acids like DNA and RNA. They are essential to nearly all biological processes including DNA and RNA synthesis, coenzyme synthesis, energy metabolism, cellular signaling and protein homeostasis and can be produced by our bodies "on demand" via de novo synthesis. Just like some of the non-essential amino acids which may become essential under certain circumstances, though, our bodies' own nucleotide production facility are often incapable of meeting the needs of rapidly proliferating tissues.

As Sterczala et al. (2015) point out in the introduction to their latest paper in the Journal of Strength and Conditioning Research, a salvage pathway is therefore required to synthesize nucleotides from exogenous sources (Gil. 2002).
If you are overtraining even the best ergogenic won't help you recover!

Never Train Just "To Burn Calories", Folks!

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As such, dietary nucleotides are necessary to maintain immune function, tissue growth and cellular repair. Sounds familiar? Yeah, all of those functions are affected by exercise, which can (at least temporarily) significantly increase one's nucleotide demands to levels that cannot be supplied by endogenous (=the body's own) synthesis, alone. A recent study which shows that the blunted hypertrophic response in aged skeletal muscle is associated with decreased ribosome biogenesis even suggest that this may be one of the reasons old muscle won't grow (Kirby. 2015). Consequently, there has been a growing interest in the potentiaL implications of exogenous nucleotide supplementation on exercise-induced immune
responses.
"Aside from increases in salivary immunoglobulins, McNaughton et al. (2006 & 2007) have observed a decreased cortisol response to exercise, which would partially explain the reduced immunosuppression. Animal models have observed similarly attenuated cortisol responses to stressful stimuli (Palermo. 2013, Tahmasebi-Kohyani. 2012). Given the roles of cortisol in gluconeogenesis and glycogenolysis, a reduced cortisol response may indicate a reduction in the metabolic stress of the exercise bout as a result of nucleotide supplementation. In the days following stressful exercise, [chronically (!) | see red box to learn why this is important] elevated cortisol levels could impair recovery, as cortisol can increase protein degradation and inhibit protein synthesis (Hickson. 1993; Kraemer. 2005)" (Sterczala. 2015). 
So, while we don't want to block the cortisol response to exercise altogether (here's why), Sterczala et al. are right: Attenuating or controlling it may quite beneficial. Especially if this attenuation occurs in the daysafter the exercise-stressor, when you want your cortisol levels to return to normal. Unfortunately, Ostojic et al. (2012 & 2013) and McNaughton et al. (2006 & 2007) who have already demonstrated the beneficial effects of nucleotide supplementation following acute exercise, did not control for the immune and cortisol response during the recovery period after the exercise stimulus. In addition, their studies involved cycling and running exercises which are, as Sterczala et al. rightly point out, "quite different in terms of muscle recruitment and metabolic demands when compared to heavy resistance exercise" (Sterczala. 2015). Therefore, the effects of nucleotide supplementation on the response patterns to resistance exercise are currently unknown and thus the perfect research object for a new study - Sterczala et al.'s new study.
Only the cortisol, not the GH, IGF-1 or testosterone response to exercise correlate w/ increased lean mass gains  in response to 12w of resistance training (West. 2012).
The acute cortisol response to exercise is not your enemy! In fact, the seminal study by West et al. (2012) which investigated the associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort of young men after weight training shows: Neither the increases in testosterone, nor the growth hormone or IGF-1 excursions right after the workout is associated with lean mass gains in response to a standardized 12-week resistance training regimen. The cortisol excursions right after the workout, on the other hand, are statistically significantly associated with increases in lean mass. So, make no mistake: We don't want to blunt cortisol altogether. If anything, we want to control it - especially on the daysafter an intense workout.
Said study used a double blinded, cross-over, within subject design, with ten young men and ten women participating in the acute heavy resistance exercise protocol (AHREP) following a loading period with either a nucleotide supplement or placebo supplementation phase.
Do you remember that protease supple- mentation (e.g. 1,000mg Bromelain) has recently been shown to have ergogenic effects in athletes, too? 
"The nuBound® (Nu Science Laboratories, Inc., Boston, MA [the sponsor of the study]) supplement contains dietary nucleotides, which are extracted from yeast (saccharomyces cerevisiae). During the supplement treatment cycle, subjects took two capsules of nuBound® daily, one upon waking, and one following exercise. The two capsules (1000mg) contained 278mg of dietary nucleotides, 375mg amino acids (l-glutamine, l-methionine, l-lysine), riboflavin (4.5mg), folate (400mcg), biotin (188mg) and pantothenic acid (12mcg). Other ingredients included fructo-oligosaccharides (chicory root), inositol and sodium citrate.

During the placebo cycle, subjects followed a dosing schedule identical to the supplement cycle. The placebo capsules were identical in size, shape and color to the nucleotide supplement but contained only lactose and magnesium stearate. During the first treatment cycle, subjects recorded their daily dietary intake on a diet log. The log was then used to help subjects replicate their diet during the second treatment cycle. Subjects also replicated their activity protocol during the study for each cycle" (Sterczala. 2015)."
Each cycle (placebo - PL; nucleiotides - NT) began with a two week loading phase in which subjects took the supplement while maintaining their normal exercise routines. At the beginning of the third week, an acute heavy resistance exercise protocol (AHREP) was completed. To assess the effects on recovery, subjects reported to the laboratory 24, 48 and 72 hrs following the AHREP for additional blood draws and performance testing. Before and after the the acute heavy resistance exercise protocol (AHREP), and at 24, 48, and 72 hrs thereafter, blood samples were analyzed for cortisol, myeloperoxidase, and absolute neutrophil, lymphocyte and monocyte counts. Creatine kinase was analyzed pre-AHREP and at 24, 48, and 72 hrs post-AHREP. Performance measures, including peak back squat isometric force and peak countermovement jump power were also analyzed.
Figure 1: Effects of nucleotide (NT) and placebo supplement (PL) preload for two weeks on cortisol (~stress) and creatine kinase (~muscle damage) response to exercise (Sterczala. 2015).
As you can see in Figure 1 the nucleotide supplementation resulted in significant (P ≤ 0.05) decreases in observed cortisol and MPO acutely following the AHREP, as well as significantly lower CK values at 24 hrs post. The AHREP significantly affected leukocyte counts, however, no treatment effects were observed (which is in contrast to previous studies, but in view of the disconnect between this markers and practically relevant immune outcomes, like the susceptibility to infection, irrelevant).
Figure 2: While the improved cortisol and CK are nice to see, only the accelerated force recovery in the isometric back-squat test may actually be practically relevant for athletes (Sterczala. 2015).
What is significantly more important than any of these markers of muscle stress, muscle damage or immune function is the fact that the the nucleotide supplement increased the peak force in the back squat isometric force test (albeit not the power during counter-movement jumps) immediately post AHREP and at 24 hrs and 48 hrs (see Figure 2). After all, changes like these, and not improvements in markers of whatever are what really matters for athletes.
With Ostojic's 2013 study we do have initial evidence that nucleotide supplements will also have practically relevant ergogenic effects - in this case increases in maximal (to exhaustion) running endurance.
Bottom line: One question you may rightly be asking now is whether the changes Sterczala, et al. observed are actually practically relevant. To answer this question we'd need additional (longer-term) independent (non-sponsored) studies to investigate strength and size gains, directly. Still, the accelerated recovery of maximal isometric force, in the study at hand, and the increased time to exhaustion in Ostojic's 2013 study, in which the researchers investigated the effects of sublingual nucleotides on running in young, physically active men, we cannot negate, that there is evidence to support the notion that nucleotide supplements may be more than another supplemental non-starter that affects the response to exercise without increasing meaningful outcomes like endurance or recovery (proven), strength or hypertrophy (evidence is still lacking).

Personally, I would still wait before I spend money on nucleotide supplements. And this is why: (A) The aforementioned long-term studies with really relevant study outcomes, like increases in VO2max or time trial performance in endurance and increases in muscle size and strength in strength athletes have not yet been conducted. And (B) even though I am not suggesting that the study results were doctored, I would be more inclined to buy and / or recommend nucleotide supplements if the existing studies had not all been sponsored by Nu Science Labs, the makers of the nuBound nucleotide supplement | Comment on Facebook!
References:
  • Gil, A. "Modulation of the immune response mediated by dietary nucleotides." European Journal of Clinical Nutrition 56 (2002): S1-4.
  • Hickson, et al. "Exercise and inhibition of glucocorticoid-induced muscle atrophy." Exercise and sport sciences reviews 21.1 (1993): 135-168.
  • Kraemer, William J., and Nicholas A. Ratamess. "Hormonal responses and adaptations to resistance exercise and training." Sports Medicine 35.4 (2005): 339-361.
  • Kirby, et al. "Blunted hypertrophic response in aged skeletal muscle is associated with decreased ribosome biogenesis." Journal of Applied Physiology 119.4 (2015).
  • Mc Naughton, L., D. J. Bentley, and P. Koeppel. "The effects of a nucleotide supplement on salivary IgA and cortisol after moderate endurance exercise." Journal of sports medicine and physical fitness 46.1 (2006): 84.
  • Mc Naughton, Lars, David Bentley, and Peter Koeppel. "The effects of a nucleotide supplement on the immune and metabolic response to short term, high intensity exercise performance in trained male subjects." Journal of sports medicine and physical fitness 47.1 (2007): 112.
  • Ostojic, Sergej M., and Milos Obrenovic. "Sublingual nucleotides and immune response to exercise." J. Int. Soc. Sports Nutr 9 (2012): 31.
  • Ostojic, Sergej M., Kemal Idrizovic, and Marko D. Stojanovic. "Sublingual Nucleotides Prolong Run Time to Exhaustion in Young Physically Active Men." Nutrients 5.11 (2013): 4776-4785.
  • Palermo, Francesco Alessandro, et al. "Effects of dietary nucleotides on acute stress response and cannabinoid receptor 1 mRNAs in sole, Solea solea." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 164.3 (2013): 477-482.
  • Sterczala, et al. " The Physiological Effects of Nucleotide Supplementation on Resistance Exercise Stress in Men and Women." Journal of Strength and Conditioning Research (2015): Publish Ahead of Print.
  • West, Daniel WD, and Stuart M. Phillips. "Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training." European journal of applied physiology 112.7 (2012): 2693-2702.

Your MUFA + PUFA Intakes Determine Your True Vitamin E Requirements - N-3s are the Worst Offenders + Even MUFAs Need Buffering | Tool to Calculate Your Individual Needs

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Nature knows best: Oils and other high PUFA foods come with a naturally high amount of vitamin E (see Fig 1).
As a SuppVersity reader you shouldn't be surprised to hear that there's a link between the amount of highly oxidizeable polyunsaturated fatty acids (omega-3 and omega-6) you consume and the amount of vitamin E you "need" to protect them from being oxidized by free radicals.

The reason we usually speak about vitamin E in this context is that vitamin E (mostly alpha-tocopherol) is recognized as a if not the key essential lipophilic antioxidant in humans. It protects lipoproteins (cholesterol), PUFA, cellular and intra-cellular membranes from damage.
Learn more about hormesis and potential neg. effects of antioxidants at the SuppVersity

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Antiox. & Health Benefits Don't Correlate
For a recent review, scientists from DSM Nutraceuticals in Brussels and the Human Development and Health Academic Unit at the Faculty of Medicine of the University of Southampton partnered up in order to "evaluate the relevant published data about vitamin E requirements in relation to dietary PUFA intake" (Raederstorff. 2015).
Table 1: Overview of the currently recommended daily intakes for vitamin E (Monsen. 2000).
For their 10-page review, which does not take into account the interactions between tocopherols, the 'classic' vitamin E, and tocotrienols (this is not really negligent, because only the tocopherols are essential and the interactions between the different forms of vitamin E are not fully elucidated, yet), the scientists considered both evidence from animal and human studies; evidence that indicates that our basal requirement of vitamin E, namely 4–5 mg/d of RRR-α-tocopherol when the diet is very low in PUFA, are way below the RDA of 15mg/day. Now obviously, most Westerners do not fall into the category of people with a "minimal intake of PUFA". Accordingly, their vitamin E requirements are higher, and thus probably in the range of the recommended daily allowance.
You don't even have to consume exuberant amounts of anti-oxidants like vitamin E to ruin your gains. A recent study shows: Icebaths will do the same. By soothing the inflammatory response to exercise, they will also shut down the adaptational processes | learn more
I am healthy, I don't have to care! If you really believe that, you may be healthy but stupid. Even the healthiest person on earth will produce free radical specimen. In fact, ROS are essential for the adaptational processes that occur in response to exercise and involved in normal glucose regulation. On the other hand, very recent scientific evidence highlights that adequate cellular vitamin E levels are necesssary for muscle membrane repair and the rescue of myocytes from necrosis (Howard. 2011; Labazi. 2015). Scientists believe that these benefits are the result of an increased speed and efficacy of membrane repair mechanisms like membrane fusion events. It should thus be obvious that managing, not worshipping or annihilating ROS with adequate amounts of vitamin E and other anti-oxidants should be your primary goal (one you can achieve w/out supps).
Still, the fact that our basal vitamin E requirements, i.e. the amount of vitamin E we would need if we didn't stuff ourselves with tons of PUFAs, amounts to only ~30% of today's RDA (see Table 1) for adult men and women should make us reconsider the necessity and usefulness of vitamin E supplements. I mean, who of you is actually consuming 30g of MUFA, and 22g of PUFA from sources that do not come with adequate amounts of vitamin E?
Figure 1: All suggested oils from the "Quest for the Optimal Cooking Oil"-Article from December 2014 contain way more vitamin E than they'd need to buffer their own PUFA / MUFA content (learn more about the best cooking oils).
If you look at the data in Figure 1, which is a comparison of the actual content of vitamin E in mg and the amount of vitamin E that would be necessary to buffer the "unstable" fats in the three oils you will remember from the "Quest for the Optimal Cooking Oil", the answer to the previously raised question is probably going to be "very few". After all, most of the largely unprocessed we consume contain way more than 100% of the amount of vitamin E they would have to provide to protect the inherent MUFAs and PUFAs from oxidation.

Each unsaturated fatty acid has its specific effect on your vitamin E requirements

Against that background it is no wonder that vitamin E deficiency is a more of less unheard of thing in the Western world. No one here consumes less than the absolute minimum of 4-5mg/day (Harris. 1963; Valk. 2000) for months or longer. The only way to still develop relative vitamin E deficiency is thus to consume processed foods or supplements that do not contain enough vitamin E to satisfy the increase in vitamin E demands due to the specific unsaturation of their fat content.
Table 2: Vitamin E requirements - in mg of vitamin E per gram intake of the respective fatty acid - for different unsaturated fatty acids found in human diets (Raederstorff. 2015)
Since the latter increases almost linearly with the degree of unsaturation of the PUFA in the relative ratios of 0·3, 2, 3, 4, 5 and 6 for mono-, di-, tri-, tetra-, penta- and hexaenoic fatty acids, respectively, Harris'& Norris' (1963), as well as Horwitt's (1986) equations, which do not take into account that omega-3 fatty acids, for example, have a much more pronounced impact on your vitamin E requirements than omega-6s or MUFAs, are now obsolete.
Equation 1: Use this equation or the SV Calculator to determine your personal requirements based on your intakes of  different forms of mono- (M1 and polyunsaturated (M2-6) fatty acids (Equ. from Raederstorff. 2015).
Today, Equation 1 has taken their place. In Equ. 1 Mn is the amount of dietary MUFA/PUFA with n double bonds in grams (see Table 2). If you know how much of the individual unsaturated fats you consume you can thus easily calculate your personal vitamin E requirements - requirement, of which I bet that you will cover them with the vitamin E from cooking and salad oils, alone (compare Figure 1).
Chicken legs, old man? Must have been too much antioxidants - Learn how too much vitamin C + E can blunt the increases in total lean body mass, and leg mass in elderly men after 12 weeks of highly standardized, intense strength training: No wonder, the vitamins virtually suffocated the necessary stressors | read more.
Bottom line: I guess you are already waiting for the link to the calculator I promised, right? Let's just briefly put the result that even the average westerner needs "only" 12-20 mg of natural vitamin E per day into perspective. On the one hand, that's more than you'd find in a few really trashy foods people like to eat. On the other hand, that's only 17-30IU/day and thus 13-24x the amount of vitamin E you will find in many multi-vitamin, and vitamin E pills (many contain 400IU or 269mg), which appaers hilarious considering the fact that whole foods that are high in unsaturated fats will always come with the required amount of vitamin E.

If that does not sooth your mind and you want to know exactly how much your need, here's the spreadsheet I promised. I am sure it's significantly less than the >120mg/day that impaired the size gains of the elderly subjects in the recently discussed study by Bjornsson. It's much less, right? Comment on Facebook!
References:
  • Monsen, Elaine R. "Dietary reference intakes for the antioxidant nutrients: vitamin C, vitamin E, selenium, and carotenoids." Journal of the American Dietetic Association 100.6 (2000): 637-640.
  • Harris, Philip L., and Norris D. Embree. "Quantitative consideration of the effect of polyunsaturated fatty acid content of the diet upon the requirements for vitamin E." The American journal of clinical nutrition 13.6 (1963): 385-392.
  • Howard, Amber C., Anna K. McNeil, and Paul L. McNeil. "Promotion of plasma membrane repair by vitamin E." Nature communications 2 (2011): 597.
  • Horwitt, M. K. "Interpretations of requirements for thiamin, riboflavin, niacin-tryptophan, and vitamin E plus comments on balance studies and vitamin B-6." The American journal of clinical nutrition 44.6 (1986): 973-985.
  • Labazi, Mohamed, et al. "The antioxidant requirement for plasma membrane repair in skeletal muscle." Free Radical Biology and Medicine 84 (2015): 246-253.
  • Raederstorff, Daniel, et al. "Vitamin E function and requirements in relation to PUFA." British Journal of Nutrition (2015): 1-10.
  • Valk, and Gerard Hornstra. "Relationship between vitamin E requirement and polyunsaturated fatty acid intake in man: a review." International Journal for Vitamin and Nutrition Research 70.2 (2000): 31-42.

Training to Failure and Modifying Rest Times: Two Ways to Maximize Muscle Activity? Two Studies, Similar Implications

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This is what science looks like... Well, at least in the Hiscock study, where the subjects, 10 young men with at leas 12 months of training experience did regular and hammer dumbbell curls on the preacher bench - (photo | Hiscock. 2015).
In today's SuppVersity feature article, I am going to address not one, but two potentially highly relevant articles from the Journal of Strength and Conditioning Research (Looney. 2015) and the European Journal of Sport Science (Hiscock. 2015). What makes these papers interesting is the fact that both investigated the effect of commonly prescribed remedies to "bust a plateau" by providing novel growth triggers: (a) Training to failure and (b) modifying rep schemes and whether you fail or don't fail on every set.

If you believe in what you can read in many articles on strength training, both, training to failure and decreasing rest times / drop sets should significantly increase the muscle activity and thus - this is the most important thing - the number of motor units that are recruited during the exercises.
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But is this actually true? I mean, is there a link between EMG activity, the number of motor units that are firing and the way you train? I guess, it would be wise to take a brief look at the pertinent research before we get to design and results of the individual studies. So, what do we have? As Looney et al. point out, motor unit activity can be measured through electromyography (EMG) which is commonly considered to reflect the neural drive to the muscle. Since the electrical impulse should be proportional to the number of motor units that are firing and in view of the fact that the latter determines the acute force output, it should be obvious that increasing force demands result in higher EMG amplitude due to the greater recruitment of motor units and faster firing rates necessary to increase the contractile force.
Figure 1: Previous studies show that the motor unit recruited (or at least it's indicator, the mean EMG values) increases over the duration of sustained or repeated muscle actions at a constant force level (Masuda. 1999 - l; Mottram. 2005 - r)
Unfortunately, more does not necessarily help more. If you take a closer look at the existing research you have to realize you cannot stretch this proven increase of the EMG amplitude (Carpentier. 2001; Fuglevand. 1993; Lind. 1979; Masuda. 1999; Mottram. 2005; Petrofsky. 1982) infinitely. Over prolonged exercise / contraction times, the initially increasing firing rates will eventually decrease. That this is the case is interpreted by many scientists as evidence of the the fact that the initial rise in EMG amplitude is just a compensatory mechanism for sustaining contractile force as fatigue accumulates (when the individual fibers fatigue, more are recruited to sustain the same force). This hypothesis appears to be confirmed by numerous investigations that have demonstrated that EMG amplitude increases during dynamic exercise as the extent of the effort, or number of repetitions performed, increases (Hasani. 2006; Spreuwenberg. 2006; etc.).
Why is it even important that all muscle fibers contract? The reason should be obvious, but I am happy to explain it once more. It is the contraction that's responsible for the exercise induced increase in GLUT-4 receptor expression and mTOR phosphorylation. In view of the fact that the latter determine the increase in glucose uptake and protein synthesis after a workout, you obviously want as many muscle fibers to contract as possible. Or, to put it differently: If you don't use it you won't grow it, bro... well, at least not to the same / optimal extent.
This is where the "train to failure to maximize motor unit recruitment"-theory comes from. After all, this observation indicates that usually inactive motor units are going to fire only during prolonged training at high intensities (best to failure). As usual, though, there are problems with this theory:
"While the increase in EMG amplitude observed during repeated muscle actions has been explained by increased central drive necessary to sustain force as fatigue accumulates, it is inconclusive whether fatigue derived from earlier performed exercise induces greater EMG amplitude during subsequent exercise. Previous studies have shown EMG amplitude diminishes after strenuous resistance exercise protocols. In contrast, Smilios et al. demonstrated progressive increases in EMG amplitude over a series of 20-repetition sets with gradually decreasing resistance interspaced with 2-minute rest periods. Further uncertainly exists pertaining to consecutive maximal effort sets with progressively lighter resistance performed without allotted rest periods. This frequently incorporated training technique, commonly known as a “drop set”, has remained relatively uninvestigated" (Looney. 2015).
Needless to say that we all expect that lighter weights can stimulate greater motor unit recruitment, if you use them in dropsets, but as Looney et al. say, the science that would conclusively confirm that is simply not there (yet). The goals of Looney's study were thus as follows:
  • Firstly, confirm / refute the assumption that EMG amplitude would be significantly greater in light resistance exercise (50% 1RM) performed in rested conditions to a maximal number of repetitions than to a submaximal number of repetitions. 
  • Secondly, assess whether the EMG amplitude would be significantly lower in maximal repetition sets performed in rested conditions with 50% 1RM resistance than with heavy resistance (90% 1RM). 
  • Thirdly, test whether the EMG amplitude would be greater in maximal repetition 50% 1RM resistance sets performed in pre-fatigued conditions (no prior rest period) than in rested conditions. 
As the authors rightly point out, the "findings of this investigation would provide critical information on understanding the changes in neuromuscular physiology during dynamic exercise related to variable levels of target repetitions, resistance, and fatigue" (Looney. 2015) and may thus be of great value to scientists (initially, because the would have to still check the practical consequences of any increases in motor recruitment) and coaches + athletes (later). What the Hiscock study in which the researchers evaluated the rate of perceived exertion (RPE) and its correlation with muscle activation and lactate levels can add to the table is information on the effect of another parameter: Different rest times.
If you don't do them as an intensity add-on / finisher don't do partial reps at all - "Full Rom, Full Gains" | more
Don't forget that form, time under tension and the range of motion matter, as well. In 2013, for example, I discussed the results of a study by McMahon et al. that leaves little doubt that the increased mechanical stress and workload (remember work is the product of force x time) from doing exercises over the full range of motion will trigger greater morphological and architectural adaptations in response to resistance training than doing the same exercises over only a partial range of motion. Unfortunately, the evidence in favor of the significance of optimal form (beyond going over the full range) and the time under tension for optimal gains is less convincing and in parts contradictory.
In order to avoid any confusion, though, let's initially look at the Looney study in isolation. In said study ten resistance trained men (age, 23±3 yr; height, 187±7 cm; body mass, 91.5±6.9 kg; squat 1RM, 141±28 kg) had EMG electrodes attached to their vastus lateralis and vastus medialis muscles on two occasions:
  • A drop set day, on which he subjects performed three consecutive maximal repetition sets at 90%, 70%, and 50% 1RM to failure with no rest periods in between. 
  • A single set day, on which the subjects performed a maximal repetition set at 50% 1RM to failure (no "dropping" involved). 
The analysis of the EMG data yielded overall unambiguous results: The maximal repetition sets to failure at 50% and 70% 1RM resulted in higher peak EMG amplitude than during submaximal repetition sets with the same resistance. In view of the fact that the peak EMG amplitude was significantly (P ≤ 0.05) greater in the maximal 90% 1RM set than on any of the other sets the subjects performed, the classic drop set with 90%, 70% and 50% 1RM should thus still have an edge over any regular "low intensity + high rep to failure" single set training. The question remains, however, whether it will also have the edge over conventional training?
Figure 2: Very general summary of the research interests and designs of the two studies discussed in today's SuppVersity article by Looney et al. (2015) and Hiscock et al. (2015)
We will get back to that question in the bottom line. In the mean time, let's briefly take a look at another, quite surprising result, one that will also lead us to the results of the previously mentioned study by Hiscock et al. (2015): The lack of association between the ratings of perceived exertion (CR-10). In contrast to what most of you certainly expected, the fatigue levels did not differ over the intensity range of loads and did not reflect the degree motor unit recruitment in any way (see Figure 3). You as an individual without the necessary technical equipment are thus probably unable to tell hor many motor units you've actually recruitment in a workout; and - even more importantly - the mere fact that you have to crawl instead of walk out of the gym is not a sign of a productive workout.
Figure 4: Mean number of repetitions (left, top), rate of perceived exertion (RPE | left, bottom), and peak EMG amplitude as a measure of motor recruitment (Looney. 2015).
You don't want to believe that? Well, bad luck for you: This result appears to be confirmed by Hiscock's study, in which 10 recreationally trained (>12 months of previous resistance training) did DB Curls and DB Hammer Curls on the preacher bench for three sets with their preferred arm at a constant load of 70% of their individual 1-RM over 4 trials:
  1. 3 sets × 8 repetitions × 120 s recovery between sets; 
  2. 3 sets × 8 repetitions × 240 s recovery; 
  3. 3 sets × maximum number of repetitions (MNR) × 120 s recovery; 
  4. 3 sets × MNR × 240 s recovery.
After each of the exercises the participants rated their overall and active arm muscle rate of perceived exertion (RPE-O and RPE-AM) and the data was correlated with the biceps brachii and brachioradialis muscle EMG activity during each set for each trial.
Figure 5: Despite sign. higher volumes (see boxes) and a 100% increase in rate of perceived local muscular exertion there was no significant increase in muscle activity with lifting 70% of the 1RM for 8 vs. to failure (Hiscock. 2015).
Just like in the Looney study, the measured rates of perceived exertion in the Hiscock study had did not correlate with with either the muscle activation or the lactate accumulation in the biceps. Rather than that, it appears as if the subjects' bicepses didn't even care about rep schemes and failure. While the RPE increased significantly, when the subjects trained to failure, the mean and peak EMG activity levels in Figure 5 are more or less identical for all rep x intensity (+/- failure) schemes.
So what's the significance of the results, then? If you put some faith into Looney's conclusion, it is that the results of his (and I may add Hiscock's study, too) confirm "previous recommendations for the use of heavier loads during resistance training programs to stimulate the maximal development of strength and hypertrophy" (Looney. 2015).

SuppVersity Suggested Topical Article: "Failure, a Necessary Prerequisite for Max. Muscle Growth & Strength Gains? Another Study Says 'No Need to Fail, Bro!'" | read more
Reducing the load and training to failure (Looney's "single set" day) or reducing the rest times and or switching from a set rep number to training to failure (Hiscock's groups A-D), on the other hand, has no effect on motor recruitment and could, in view of potentially increased recovery times due to higher rates of perceived exertion w/ training to failure, rather hinder than facilitate rapid strength and size gains. Whether the same is the case for the drop-set, though, is not 100% clear. With the peak muscle activity occurring in the first set, you cannot argue that the stimulus was weakened. On the other hand, there's a proven reduction in total volume (reps x weight | Melibeu Bentes. 2012) of which long-term studies would have to investigate whether the can impair your strength and size gains.

Overall, there is still little doubt that the results of the two studies I discussed today support the notion that "going heavy" is still the way to activate a maximal number of muscle fibers. Whether this does also mean that it is necessarily the best way to make those fibers grow and or increase their glucose uptake, however, is still not fully proven. The same goes for the usefulness of training to failure, of which some studies suggest that failure does not matter, while others appear to indicate that "failing" is almost necessary to maximize your gains - as usual, I've written about both of them and will continue to do so in the future, so stay tuned if you want to be among the first to learn what works best for strength and hypertrophy training ;-) | Comment on Facebook!
References:
  • Carpentier, Alain, Jacques Duchateau, and Karl Hainaut. "Motor unit behaviour and contractile changes during fatigue in the human first dorsal interosseus." The Journal of physiology 534.3 (2001): 903-912.
  • Fuglevand, A. J., et al. "Impairment of neuromuscular propagation during human fatiguing contractions at submaximal forces." The Journal of physiology 460.1 (1993): 549-572.
  • Gibson, A. St Clair, E. J. Schabort, and T. D. Noakes. "Reduced neuromuscular activity and force generation during prolonged cycling." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281.1 (2001): R187-R196.
  • Hassani, A., et al. "Agonist and antagonist muscle activation during maximal and submaximal isokinetic fatigue tests of the knee extensors." Journal of Electromyography and Kinesiology 16.6 (2006): 661-668.
  • Hiscock, Daniel J., et al. "Muscle activation, blood lactate, and perceived exertion responses to changing resistance training programming variables." European Journal of Sport Science ahead-of-print (2015): 1-9.
  • Lind, Alexander R., and Jerrold S. Petrofsky. "Amplitude of the surface electromyogram during fatiguing isometric contractions." Muscle & nerve 2.4 (1979): 257-264.
  • Looney, David P., et al. "Electromyographical and Perceptual Responses to Different Resistance Intensities in a Squat Protocol: Does Performing Sets to Failure With Light Loads Recruit More Motor Units?." The Journal of Strength & Conditioning Research (2015).
  • Masuda, Kazumi, et al. "Changes in surface EMG parameters during static and dynamic fatiguing contractions." Journal of Electromyography and Kinesiology 9.1 (1999): 39-46.
  • McMahon, Gerard E., et al. "Impact of range of motion during ecologically valid resistance training protocols on muscle size, subcutaneous fat, and strength." The Journal of Strength & Conditioning Research 28.1 (2014): 245-255.
  • Mottram, Carol J., et al. "Motor-unit activity differs with load type during a fatiguing contraction." Journal of neurophysiology 93.3 (2005): 1381-1392.
  • Petrofsky, Jerrold Scott, et al. "Evaluation of the amplitude and frequency components of the surface EMG as an index of muscle fatigue." Ergonomics 25.3 (1982): 213-223.
  • Smilios, Ilias, Keijo Häkkinen, and Savvas P. Tokmakidis. "Power output and electromyographic activity during and after a moderate load muscular endurance session." The Journal of Strength & Conditioning Research 24.8 (2010): 2122-2131.
  • Spreuwenberg, Luuk PB, et al. "Influence of exercise order in a resistance-training exercise session." The Journal of Strength & Conditioning Research 20.1 (2006): 141-144.

Kids' Low GL Breakfast Boosts Cognitive Performance 24h Later | Maternal Low Protein Diet Programs High Myostatin, Low Muscularity | Beef Beats Pickled, Not Baked Herring

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We all know this is not a healthy breakfast. What we don't or rather didn't know, though, is that you have to test on two consecutive days to find out how unhealthy it actually is for your kids' brains. With Young's study we learned that.
In what? That's probably what you are asking yourself now that you've read that beef beats pickled, but not baked herring, right? Well the answer to this question can be found in my brief summary of the results of Svelander's recent meal-response study. It's, as you may have guessed, the insulin response that sucks for pickled herring. What sucks even more, though, are mothers who are afraid of protein. After all, Liu's latest study shows that they may be setting their kids up to a life as skinny fatness.

When I come to think about it, this may yet be better than giving your kids a high glycemic load breakfast to take to school. After all, Young's latest study shows quite impressively what previous studies may have missed. The ill effects of high GL breakfasts on cognition are neither immediate, nor restricted to the late AM. No, they rather last for 24h+ and maybe even longer.
Learn more about fasting and eating / skipping breakfast at the SuppVersity

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Breaking the Breakfast Habit

Fasting, Cardio & the Brain

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review
  • Maternal low-protein diet affects myostatin signaling and protein synthesis in offspring's skeletal muscle - Ok, we are talking about swine, but (a) many human beings behave much worse than swine and (b) swine are actually a much better model of human metabolism than rodents and many primates (the real reason they are not the standard model is that they are too large and too long-lived, which means they need too much space, the studies last too long and get much too expensive).

    It is thus more than likely that a very similar effect on myostatin and protein synthesis as it was observed by Liu et al. in their latest study in the European Journal of Nutrition where the swine who were fed a protein-deficient diet with only 6% of the energy from protein gave birth to piglets with (a) significantly reduced body weight, (b) significantly reduced muscle weight, (c) extremely reduced relative muscle weight (to body weight) and (d) small muscle with miniscule intramuscular domains.
    Figure 1: Body weight, muscle weight (LD), myofiber cross sectional are and rel. muscle weight (LD/BW) of piglets born to sows on protein sufficient (12% | SP) and deficient (6% | LP) diets (Liu. 2015).
    While you can see all of that in Figure 1, the reasons for the lack of muscularity can be seen in Figure 2 which tells you that the piglets that were born to mothers on the low protein (LP) diet had significantly increased myostatin (remember myostatin blocks protein synthesis) and accordingly reduced S6K levels.

    With the former being the controller and the latter being the executor of protein synthesis, the results of Liu's study leave little room for speculation: A diet that contains only 6% protein - for humans ~20-30g (depending on your baseline intake) - may increase your offspring's risk of becoming under-muscled and skinny fat... what? No, I didn't say "beware vegans" - that was you!
  • Herring (pickled & baked) vs. beef, round one - fight! When it comes to the postprandial lipid and insulin responses among healthy, overweight men, the baked herring is said to be the #1 "health choice" - and here's why.

    In the corresponding study, scientists from the Chalmers University of Technology, and the Gothenburg University had seventeen healthy, overweight men (mean age 58 years, BMI 26.4–29.5 kg/m2) consume standardized lunches together with 150g of baked herring, pickled herring or baked, minced beef on three occasions in a crossover design. Blood samples were taken just before and up to 7 h after the meal. The postprandial response was measured as serum concentrations of triglycerides (TG), total cholesterol and lipoproteins (LDL, HDL and VLDL), insulin, 25-OH vitamin D (which did not change, by the way) and plasma fatty acid composition.
    Figure 2: Insulin response of eventeen healthy, overweight men (mean age 58 years, BMI 26.4–29.5 kg/m2) to std. lunches w/ baked or pickled herring, or baked, minced beef (Svelander. 2015). 
    In contrast to the pickled version, where the added sugar messed with the insulin and insulin response (the latter is not shown in Figure 2), both, the baked herring and the baked, minced meat did quite well. Differences in the cholesterol response as you'd expect them did not exist. There was however a small, albeit allegedly statistically significant advantage for the fish(es) in terms of the triglyceride response, which was lower than in the minced beef trial.

    Whether that's actually due to the extra omega-3s and whether it is even half as health-relevant as the scientists conclusions that their result "supports previous studies on the beneficial effects of herring on cardiovascular health" (Svelander. 2015) is yet highly questionable, if you asked me.
  • Isomaltulose effectively reduced the GL of kids breakfasts and has beneficial effect on their cognitive performance in the late AM and on a 2nd day! If you are following the SuppVersity news on Facebook, you will know that although previous research has associated the glycaemic load (GL) of a meal with cognitive functioning, typically the macro-nutrient composition of the meals has differed, raising a question as to whether the response was to GL or to the energy, nutrients or particular foods consumed.

    With the latest study from the University of Wales Swansea, this different. The study that was conducted by Hayley Young, and David Benton contrasted two breakfasts that offered identical levels of energy and macro-nutrients, although they differed in GL, i.e. the insulinogenic effect of the (otherwise identical) carbohydrate content
    "Using a repeated-measures, double-blind design, 75 children aged 5–11 years, from socially deprived backgrounds, attended a school breakfast club and on two occasions, at least a week apart, they consumed a meal sweetened with either isomaltulose (Palatinose™) (GL 31.6) or glucose (GL 59.8). Immediate and delayed verbal memory, spatial memory, sustained attention, reaction times, speed of information processing and mood were assessed 1 and 3 h after eating" (Young. 2015).
    Now, what is interesting and quite revealing with respect to the mixed results of previous investigations is that the nature of the meals did not influence any measure of cognition or mood after an hour; however, after 3 h, children’s memory and mood improved after the lower-GL breakfast.
    Figure 3: Kids who consumed the low GL meal with isomaltulose vs. glucose on day one had sign. improved information processing (left) and spatial memory (right) on day two (Young. 2015).
    What is even more striking, though, is the second-day effect on the speed at which the kids processed information faster and their spatial memory, which improved significantly when on the day after the kids had consumed the low GL meal. This observation is total news and it clearly suggest that the benefits of low GL meals on cognition are not necessarily acute, but may rather be accumulating.

    Overall, the kids were thus able to process information faster and had better spatial memory later in the morning, when they had the low glycemic load (GL) breakfast that was prepared with isomaltulose vs. glucose. The reason why you need any form of "sugar" (isomaltulose is still a sugar) in your kids' breakfast is still beyond me, though.
Is myostatin relevant for mass monsters only, or for normal trainees, as well? You can find the answer to this smart and justifiable question in this SV Classic Article: "More Evidence That Myostatin is an Important Inhibitor of Diet and Exercise Induced Muscle Gains in You & Me" | read more
Bottom line: If I had to pick only one study, I'd pick the Young study as my highlight of this brief nutrition science review and I'd say that it should be obvious why. I mean, come on: Who would have expected that eating a low glycemic load breakfast would yield significant cognitive benefits on the day after you consumed it even if your "day two"-breakfast does not have a low glycemic load?

For me, this is even more exciting than the sad revelation that low protein diets trigger epigenetic changes that are associated with significant increases in myostatin, subsequent decreases in protein synthesis and a significantly reduced muscle weight ... I can thus only hope that no pregnant woman actually believes that eating less than 10% protein would be good for her own health or the health of her unborn child | Comment on Facebook!
References:
  • Liu, Xiujuan, et al. "Maternal low-protein diet affects myostatin signaling and protein synthesis in skeletal muscle of offspring piglets at weaning stage." European journal of nutrition (2014): 1-9.
  • Svelander, Cecilia, et al. "Postprandial lipid and insulin responses among healthy, overweight men to mixed meals served with baked herring, pickled herring or baked, minced beef." European journal of nutrition (2014): 1-14.
  • Young, Hayley, and David Benton. "The effect of using isomaltulose (Palatinose™) to modulate the glycaemic properties of breakfast on the cognitive performance of children." European journal of nutrition (2014): 1-8.

Gluten Research Update: Cesarean Section, Breast Feeding, Noocebo Effects and the ‘Right’ &‘Wrong’ Bacterial ‘Poop’

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As read on the SV Facebook: Baking makes gluten resilient to digestion, the presence of protein does the opposite. The food matrix makes the difference.
In view of the fact that "gluten" is or isn't (literally) in everyone's mouth or tummy, I thought that it may make sense to keep you up-to-date on the latest interesting research in the area of non-celiac gluten sensitivity and celiac disease.

Don't worry I am not going to bother you with the typical Internet bogus about how cancer, obesity and everything else we are or are not suffering from (yet) is triggered by gluten. What I will do, though, is to summarize and discuss the results of two recent studies and one review on the connection between our microbiome and our very individual susceptibility to gluten-related health problems
You can learn more about the gut & your health at the SuppVersity

Fiber for Female Fat Loss

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

Is Gluten Intolerance Real?
  • Celiac disease and non-celiac gluten sensitivity may be all about the microbiome and begin at the very moment you're born via cesarean section and worsen when you're not breastfed - In a soon-to-be-published review in Nutrients Cenit et al. try to elucidate whether gluten intolerance and celiac disease are consequences or triggers of significant imbalances in the bacterial composition of the human microbiome and how one or the other may eventually come about..

    As the authors point out, there are in fact studies which suggest that the early colonization of the infant’s gut in conjunction with environmental factors (e.g., breast-feeding, antibiotics, etc.) could influence the development of our kids' oral tolerance to gluten.
    Figure 1: Proposed model for celiac disease (CD) pathogenesis. Specific host genetic makeup and environmental factors could promote the colonization of pathobionts and reduce symbionts, thus leading to dysbiosis. Dysbiosis may contribute to disrupting the immune homeostasis and gut integrity, thereby favoring CD onset and aggravating the pathogenesis (Cenit. 2015).
    In that, the early colonization of the intestinal tract is of particular importance, because it programs a normal or abnormal immune reaction to gluten (and other potential allergens). It is thus no wonder that celiac disease and a whole host of other autoimmune diseases have been linked to a lack of, or an improper early colonization of the intestinal tract and the consequential misprogramming of the immune cells. In that, it has been suggested that the resulting dysbiosis may affect autoimmunity by altering the balance between tolerogenic and inflammatory members of the microbiota and, therefore, the host immune response.

    Needless to say that the increased risk of autoimmune diseases is a standalone problem. It is after all not a mere reaction to the bacteria, but a bacterially induced phenomenon that involves the epigentic reprogramming of a whole host of genes. This process is however (unfortunately) so complex that we haven't yet fully understood the individual bacteria-gene and gene-gene interactions. Everyone, who tells you otherwise is lying - probably to sell his snake oil or snake oilish lifestyle advise.
    Figure 2: While there's one outlier, 3/4 studies on the effects of breastfeeding when the first gluten containing foods are introduced show significantly reduced risks of developing celiac disease (Akobeng. 2006).
    Among the few things we do know, though, is that breastfeeding and the way it promotes the early colonization of the gut with Bifidobacterium spp. is associated with a reduced risk of gluten intolerance. This is particularly true, if gluten containing foods are introduced while the kids are still breastfed (-52% according to a meta-analysis by Akobeng et al. 2006).
Breast milk contains a gliadin specific anti-body - What does that mean?Özkan et al. were the first to describe the presence of gliadin-specific IgA antibodies in breast milk (Özkan. 2000). The presence of significant amounts of this anti-body in the breast-milk (and even more in the colostrum) of 105 healthy mothers (aged 17 – 36 years) is generally understood to be one of the potential pathways by which breast milk and colostrum can protect children from celiac disease by educating the immature immune system of newborn children.
  • The fact that these benefits do not apply for every breastfed child may be explained by (epi-)genetic polymorphisms of the mother, such as the altered concentration of several immune markers that have been observed by several researchers in the breast milk of mothers with celiac disease (Olivares. 2014). If that's in fact the case, it's hardly astonishing that the number of celiac patients began to rise when the use of formula peaked and is exploding now that more and more women with celiac disease (or non-celiac gluten sensitivity) are feeding their children with "non-protective" breast milk. We must be careful, though, not to jump to conclusions. There are, after all, as Cenit et al. point out "no robust prospective studies revealing how differences in breast milk composition and intestinal microbiota acquisition and evolution early in life might ultimately protect or contribute to CD onset" (Cenit. 2015).

    A similar healthy skepticism is necessary with respect to the link of cesarean sections and an increased susceptibility to gluten sensitivity (Dominguez-Bello. 2010). While it would appear logical to assume that the lack of exposure to the vaginal microbiome may contribute to the previously mentioned misprogramming of the immune system, it would be overtly simplistic to assume that gluten wouldn't be a problem if we were all breastfed and born the natural way.
    Figure 3: Increases in risk of full-blown celiac, intestinal inflamation and the presence of markers of celiac disease in the blood in subjects with previous exposure to antibiotics; in all fairness it must be said that the risk increase decreased when individuals who were exposed within the last 24m were excluded - even then the reduced 30% increase was statistically significant and practically relevant, though (Mårild. 2013)
    In conjunction with the indisputable link between the (early) use of antibiotics (Mårild. 2013 | see Figure 3) and the first successful efforts to ameliorate the chronic inflammation in celiac guts with prebiotics, there is yet little doubt that the "right" microbial make-up may be what distinguishes celiacs from patients with non-celiac gluten insensitivity and the still large number of people who don't appear to react to gluten at all.
  • Study in healthy subjects, celiacs and their relatives suggests that the way your bacteria metabolize gluten may make you sick - From the first study, or rather review, I've analyzed in this feature article we've already learned that the inability to digest or handle gluten may be transmitted via certain immune factors in the breast milk from mother to child. It is thus particularly interesting that scientists from the Universidad de Léon in Spain who compared the stool of sixteen healthy volunteers on normal diet, eleven healthy volunteers on gluten-free diet (GFD), seventy-one relatives of CD patients on normal diet and sixty-nine relatives on GFD for several proteolytic activities, cultivable bacteria involved in gluten metabolism, SCFA and the amount of gluten found that significant differences in how celiac disease patients metabolized gluten.
Good news for celiacs: With the increasing awareness of celiac disease and gluten intolerance and the ever-increasing market shares of gluten-free products, it has become relatively easy to eat gluten-free, these days. Against that background it is all the more important that a recent study shows remission rates of 37% and general improvements in more than 50% of the patients in a recent study investigating the efficacy of gluten-free diets in celiacs over a four-year period (Newnham. 2015). The only potentially "bad" news is that all subjects gained significant amounts of body fat - specifically in the first year. The lean body mass indices, which did also improve, on the other hand, improved only very slowly and irrespective of status at diagnosis.
  • Table 1: Cultivable bacteria involved in gluten metabolism isolated from faeces of healthy subjects, active coeliac disease patients and firstdegree relatives (Caminaro. 2015).
    In contrast to healthy volunteers, their feces showed a significantly higher glutenasic activity (FGA), tryptic activity (FTA), SCFA, but lower levels of faecal gluten. That's interesting, yet counter-intuitive. After all, we've previously thought that one of the main problems of celiac disease and non-celiac gluten sensitivity is that the proteins are not broken down. Rather than that the results of the study at hand suggest that celiacs harbour bacteria that generate immunogenic peptides or pro-inflammatory metabolites which are the actual triggers of the problem (otherwise they'd have to poo out at least as much gluten as the other subjects on the gluten-free diets).

    Needless to say that this result does, once more, point toward fecal transplants or prebiotics as potential future treatment options celiac disease and non-celiac gluten sensitivity... with the only problem being: We don't know yet which bacteria we want to support and which to annihilate to solve the problem. If you look at the data in Table 1, though, killing the Clostridium and promoting the Lactobacillus population could be a first step to reinstalling a less celiac-prone gut microbiome.
  • More 60% of non-celiac gluten patients don't react to gluten in randomized clinical study - That's certainly an impressive number Zanini et al. report in their latest paper in Alimentary Pharmacology and Therapeutics (Zanani. 2015).

    Let's hope aspergillus niger does not produce the wrong proteins when breaking down gluten otherwise it would make NCGS worse not better. Thus, further studies are needed. 
    In the corresponding study the researchers studied 35 non-CD subjects (31 females) that were on a gluten-free diet (GFD), in a double-blind challenge study. Participants were randomised to receive either gluten-containing flour or gluten-free flour for 10 days, followed by a 2-week washout period and were then crossed over. The main outcome measure was their ability to identify which flour contained gluten. Secondary outcome measures of the study from the University and Spedali Civili of Brescia in Italy were based upon Gastrointestinal Symptoms Rating Scale (GSRS) scores (criteria & results see Figure 4).

    In contrast to what the Internet experts are trying to make you believe, only 12 and thus hardly more than 34% of the allegedly highly gluten-intolerant patients were able to tell when they were fed gluten-containing flour based on increases in pain, reflux, indigestion, diarrhoea, and constipation.
    Figure 4: Increased severity of symptoms according to whether subjects were able to distinguish whether they were fed a gluten-containing or gluten-free diet (Zanani. 2015).
    Seventeen participants (49%), on the other hand, swore black and blue that they had been fed the gluten-containing flour when they were on the gluten-free diet (and if you look at the data in Figure 4, they even felt worse than those who were actually sensitive ;-).

    Now, what's most intriguing about this is that the study proves that there's a non-negligible noocebo effect involved, when it comes to non-celiac gluten sensitivity. One that's powerful enough to have people experience real increases in pain, reflux, indigestion, diarrhoea, and constipation... that tells you something about how infections reading too much bogus on the internet is, right?
Is Noneliac Gluten Sensitivity Legit? A Recently Published Review of the Latest Scientific Evidence on NCGS by Alex Leaf (Guestpost) May Help You Decide Whether you Even Want to Do the Painstaking Test | more
Bottom line: By including yet another study that puts a huge question mark behind the allegedly ever-increasing prevalence of non-celiac gluten intolerance into this write-up I am not trying to suggest that this pathogenesis does not exist. I am just trying to remind you that there is good evidence that it can also be triggered by the mere assumption that you have NCGS.

With that being said, the actual topic of this feature article is not the noocebo effect of the aggressive gluten-free propaganda, but rather the evidence of the existence of a physiological link between "dysbiosis" (in the broadest sense), the subsequent mal-metabolism of gluten by the "wrong" bacteria in your gut and the occurence of gluten sensitivity and full-blown celiac disease.

As bad as this may sound, the potential existence of this link between the gut microbiome and gluten sensitivity is actually good news: If the influence of your current gut bugs is in fact as huge as some of the scientists speculate, it should be possible to ameliorate, if not annihilate, the symptoms by reinstalling a "corrected" gut microbiome that helps celiacs and individuals with non-celiac gluten sensitivity metabolize gluten "correctly". This in turn could eventually even reverse the epigenetic changes that are causally involved in the inflammatory immune response to gluten and thus alleviate at least the nasty problems that occur if celiacs consume really small amounts of gluten incidentally. Whether it will fully reverse celiac disease, though, appears more than just questionable to me | Comment on Facebook!
References:
  • Akobeng, Anthony K., et al. "Effect of breast feeding on risk of coeliac disease: a systematic review and meta-analysis of observational studies." Archives of disease in childhood 91.1 (2006): 39-43.
  • Caminero, et al. "Differences in gluten metabolism among healthy volunteers, coeliac disease patients and first-degree relatives." British Journal of Nutrition (2015): Ahead of print.
  • Dominguez-Bello, Maria G., et al. "Delivery mode shapes the acquisition and structure of the initial microbiota across multiple body habitats in newborns." Proceedings of the National Academy of Sciences 107.26 (2010): 11971-11975.
  • Mårild, Karl, et al. "Antibiotic exposure and the development of coeliac disease: a nationwide case–control study." BMC gastroenterology 13.1 (2013): 109.
  • Newnham, Evan D., et al. "Adherence to the gluten‐free diet can achieve the therapeutic goals in almost all patients with coeliac disease: A five‐year longitudinal study from diagnosis." Journal of gastroenterology and hepatology (2015).
  • Olivares, Marta, et al. "Human milk composition differs in healthy mothers and mothers with celiac disease." European journal of nutrition 54.1 (2014): 119-128.
  • Özkan, T., T. Özeke, and A. Meral. "Gliadin-specific IgA antibodies in breast milk." Journal of international medical research 28.5 (2000): 234-240.
  • Zanetti, et al. "Randomised clinical study: gluten challenge induces symptom recurrence in only a minority of patients who meet clinical criteria for non-coeliac gluten sensitivity." Alimentary Pharmacology and Therapeutics (2015): Ahead of print.

Strength & Conditioning Update - Sep '15: Reduced Rest, 200kcal Extra-EE (+30%) | Dehydration Turns Sprint to Jog | Knee Wraps More Power, Lower ROM & Vastus Activity

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No, this is not the first time you read about "battling the rope" and how it could be an excellent form of fat burning and conditioning HIIT training. In my previous article "Want to Get Ripped & Strong? 'Battling the Rope' Could be THE Exercise to Do!" I've already discussed the proven long-term benefits of this intense conditioning exercise | learn more.
Usually, I handpick the three best studies for overviews like this, but with the Journal of Strength and Conditioning research, this is not always easy. With the September issue, only some studies are interesting, and there are no real "blockbuster" that would deserve an article on their own. Don't get me wrong. There's still interesting information, there but I guess what's most interesting is significantly more open to debate than usually.

Accordingly, today's research update contains my very personal favorites from September 2015 issue of this journal. Well, my favorites minus one study by Soares et al. (2015) about which I've written in my April 2015 article "Single- vs. Multi-Joint, Rookie vs. Gymrat - How Much Rest is Required in Trained Athletes if Noobs Need 72h or More?" (read it!), when the study was published initially as an online exclusive "ahead of print" print article five months ago.
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  • Rest intervals and their effects on metabolism and velocity loss during battling the rope and ballistic bench press exercises - With the studies by Ratames, et al. (2015) and Garcia-Ramos et al. the latest issue of the JSC contains not one but two studies that deal with the effects of reducing the inter-set (rope) and inter-rep (ballistic bench press = "bench throws") times.
    Figure 1: Aerobic and anaerobic energy expenditure with 2 and 1 minute rest between 30s bouts of battling the rope in the welve men and 10 women (age = 20.8 6 1.3 years) who participanted in Ratamess study (ibid. 2015).
    While Ratames' study shows the expected increase in energy expenditure and fatty oxidation, as well as the lactate levels and heart rates of the female subjects, when the rest-time between the 8 sets of 30-second intervals (15 seconds of single-arm waves and 15 seconds of double-arm waves) of battling the rope were reduced from two to one minute, the results of the study by Garcia-Ramos (2015) require a correlation analysis to confirm that increasing the inter-set rest during "bench throws" (=ballistic bench presses) with 30%RM, 40%RM, or 50%RM from 6 to 12 seconds ameliorated the otherwise linear decrease in the maximal number of reps significantly.

    Want to Design a Killer Workout? Reduce the Rest Times and Burn 37% More Energy During Your Workout!
    In view of the effect that both outcomes where expected, it may be most intriguing that the 33% and 32% increases in total energy expenditure in the men and women (respectively) in Ratamess study were significantly more pronounced than what one may have expected from a mere reduction in rest times. Based on Ratamess previously discussed study that involved a full body resistance training workout and increases in energy expenditure of up to 37%, SuppVersity veterans should not be too surprised by the efficacy increase due to the reduction of the rest times. One thing you should keep in mind, however, is that any decrease in rest times will also lead to an increase in fatigue. In the Ratamess study, the increased in the rate of perceived exertion was 14% in the female and 21% in the male subjects.
  • No, hydration doesn't matter for marathoners, only - While we usually think of endurance athletes when we talk about the effects of (de-)hydration on exercise performance, the reality is that everyone can experience the ergolytic (=performance decreasing) effects of dehydration. Against that background, it's sad that the number of studies that quantify these effects is very limited. With Davies et al.'s (2015) latest contribution we do now have the first detailed study on the effects of dehydration on repeated sprint performance which is highly relevant for almost every teamsport and may also give us insights into the effects of dehydration on high(er) rep strength training.

    In their study, the researchers from several universities had eight male collegiate baseball players complete intermittent sprints either dehydrated (DEHY) by 3% body mass or euhydrated (EU). To induce the state of dehydration the men were subjected to heat with controlled fluid restriction occurring 1 day before the trial. During the actual trial, which was repeated with appropriate time for recovery, the participants completed twenty-four 30-m sprints divided into 3 bouts of 8 sprints with 45 seconds of rest between each sprint and 3 minutes between each bout.
    SuppVersity Suggested: Learn why sodium restriction in athletes is a stupid idea (learn more)
    The study outcomes, perceived recovery status (PRS), heart rate (HR), ratings of perceived exertion (RPE) (0–10 OMNI scale), and perceived readiness (PR) scale, as well as the session RPE (SRPE), were recorded after every sprint, and 20 minutes after completing the entire session, respectively.
    Figure 2: Sprint times and rates of perceived exertion after each bout of exercise (Davies. 2015).
    The authors' 2 (condition) × 3 (bout of sprints) repeated-measures ANOVA revealed a significant main effect of condition on mean sprint time (p = 0.03), HR (p < 0.01), RPE (p = 0.01), and PR (p = 0.02).

    In addition, the scientists' post hoc tests showed significantly faster mean sprint times for EU vs. DEHY during the second (4.87 ± 0.29 vs. 5.03 ± 0.33 seconds; p = 0.01) and third bouts of sprints (4.91 ± 0.29 vs. 5.12 ± 0.44 seconds; p = 0.02). Heart rate was also significantly lower (p ≤ 0.05) for EU during the second and third bouts. Post hoc measures also showed significantly impaired (p ≤ 0.05) feelings of recovery (PRS) before exercise and increased (p ≤ 0.05) perceptual strain before each bout (PR) during the second and third bouts of repeated sprint work (i.e., RPE and PR) and after the total session (SRPE) in the DEHY condition.

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    It is thus hard to argue with Davis' conclusion that all three observed effects, i.e. the impaired sprint performance, the negatively altered perception of recovery status before exercise, and the increased RPE and HR response are reasonable arguments to make sure you're always staying well hydrated. Plus: If you think of the recently discussed study on the way hydration can help you avoid type II diabetes (read it again), this advise is just as relevant for non-athletes.
  • Expected but often disclaimed reduction in vastus lateralis activity when squatting with knee wraps - Ok, ok... there's one thing that's missing here: The reduction occurs if the weight that's used with and without the knee wraps is identical. If, however, you are able to squat 10% more, which is very likely, since studies indicate increases of >20% in maximal isometric force during the squat exercise, independent of the level of stiffness of the knee wrap (Gomes. 2014), the results of Gomes' latest study (2015) are no real reason to worry about your gains.
    Figure 3: Changes in vastus lateralis (A), gluteus maximimus (B) EMG activity and knee and hip angles (C) when doing back squats with (KW) or without (NW) knee wraps (Gomes. 2015).
    Eventually it would just have been a reduction in vastus lateralis activity, anyway. For the gluteus the activity doesn't change, anyways; and that in spite of the fact that the range of motion (the knee angle | Figure 3, right, black bars) is reduced when you're squatting with knee wraps (KW) vs. without wraps (NW).
Bottom line? You don't really need one, do you? So, instead of giving you another summary of the already dicussed implications of the (in part unsurprising) results of the previously discussed studies, I am inclined to give you a second serving in form of an extra-study.

Figure 4: Hooper and his colleagues from the Ohio State University believe that the increased fast ball, and driving / approach shot accuracy in high-level baseball pitchers and golfers they observed when the athletes wore upper body compression garments is mediated by improved proprioceptive cues during upper-body movements (Hooper. 2015).
The study was conducted at the Ohio State and dealt with the effects of upper-body (!) compression garment on athletic performances. Now, while we do have ample evidence of often subtle, but significant benefits of lower body compression garments, the study at hand is the first one I have read that reports significant performance improvements in eleven Division I collegiate pitchers (age: 21.0 ± 2.9 years; height: 181.0 ± 4.6 cm; weight: 89.0 ± 13.0 kg; body fat: 12.0 ± 4.1%) and 10 Division I collegiate golfers (age: 20.0 ± 1.3 years; height: 178.1 ± 3.9 cm; weight: 76.4 ± 8.3 kg; body fat: 11.8 ± 2.6%) in terms of fastball accuracy (30% improvement) and driving (21%) as well as accuracy (17%), respectively. That's quite a significant benefit for high-level athletes - an effect of which the authors, Hooper et al. (2015), believe that it was "most likely mediated by improved proprioceptive cues during upper-body movements" (Hooper. 2015) | Comment on FB!
References:
  • Davis, J.-K, Laurent, CM, Allen, KE, Green, JM, Stolworthy, NI, Welch, TR, and Nevett, ME. Influence of dehydration on intermittent sprint performance. J Strength Cond Res 29(9): 2586–2593, 2015
  • García-Ramos, A, Padial, P, Haff, GG, Argüelles-Cienfuegos, J, García-Ramos, M, Conde-Pipó, J, and Feriche, B. Effect of different interrepetition rest periods on barbell velocity loss during the ballistic bench press exercise. J Strength Cond Res XX(X): 000–000, 2015 
  • Gomes, Willy Andrade, et al. "Acute effects on maximal isometric force with and without knee wrap during squat exercise." Int J Sports Sci 4.2 (2014): 47-49.
  • Hooper, DR, Dulkis, LL, Secola, PJ, Holtzum, G, Harper, SP, Kalkowski, RJ, Comstock, BA, Szivak, TK, Flanagan, SD, Looney, DP, DuPont, WH, Maresh, CM, Volek, JS, Culley, KP, and Kraemer, WJ. Roles of an upper-body compression garment on athletic performances. J Strength Cond Res 29(9): 2655-2660, 2015
  • Ratamess, NA, Smith, CR, Beller, NA, Kang, J, Faigenbaum, AD, and Bush, JA. Effects of rest interval length on acute battling rope exercise metabolism. J Strength Cond Res 29(9): 2375–2387, 201
  • Soares, S, Ferreira-Junior, JB, Pereira, MC, Cleto, VA, Castanheira, RP, Cadore, EL, Brown, LE, Gentil, P, Bemben, MG, and Bottaro, M. Dissociated time course of muscle damage recovery between single- and multi-joint exercises in highly resistance-trained men. J Strength Cond Res 29(9): 2594–2599, 2015.

Water Before Meals Doubles Weight Loss Success - Study Said to Confirm Diet Myth Gets Falsely Overgeneralized

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Could this large glass of water really be the "diet game changer" some mainstream media make it look like? Or, are we - once again - dealing with the abuse of science to attract readers by propagating dubious dieting myths?
The advice to "drink a glass of water before every meal" is about as old as human efforts to lose weight. Yet despite the fact that an increase in daily water consumption is widely advocated as a useful tool to aid weight loss and even included in popular weight loss programs like Weight Watchers, there is, according to the latest systematic review of the association between water consumption and body weight,  little evidence to support this practice outside of energetically restricted interventions (Muckelbauer. 2013).

In other words: While we do have evidence that replacing caloric beverages with water/diet beverages works (Tate. 2012), we have little evidence that simply drinking more will accelerate weight loss and almost no evidence of the potential benefits water preloading before meals, in particular.
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Quite surprising, isn't it. I mean, it should be obvious that drinking a glass or two of water before a meal would be a highly promising strategy to reduce meal energy intake by modifying an individuals’ perception of fullness prior to eating by, as Parretti et al. (2015) put it, "consuming a 'preload' of water". Nevertheless, Daniels' 2010 systematic review identified only two small laboratory studies that specifically investigated whether water preloading reduced energy intake. As Parretti et al. point out in the introduction to their own study,
"[b]oth studies compared participants given a water preload of 500 ml for 30 min before an ad libitum meal with those not given a preload and found that energy intake at the meal was lower for the preload group compared with the no-preload group" (Parretti. 2015). 
Thus, evidence to suggest that water preloading may improve the effectiveness of weight loss programs is there. Experimental evidence to confirm that is yet ultra-scarce. In fact, the only RCT (Dennis. 2015) to directly examine the effects of water preloading before meals on weight loss was published five years ago. In said study, 48 adults with overweight or obesity were allocated to a hypocaloric diet plus 500 ml of water before meals every day (water preload group) or a hypocaloric diet alone intervention (nonwater group) over 12 weeks.
Figure 1: Dennis et al. were the first to show that drinking 500 ml of water before meals everyday can boost the weight loss success of overweight and obese individuals participating a 12-week diet intervention (Dennis. 2010).
As you can see in Figure 1, the subjects in the water group lost ~2kg more weight than their peers and showed a 44% greater decline in weight over the 12 weeks than the nonwater group. That's interesting because the energy intake during test meals was suppressed by the additional water load only at baseline, yet not after 12 weeks on the preloading protocol (see Figure 2).
Figure 1: In a previous study the beneficial effect of the water preload on food energy intake wore off. The subjects in Dennis' study still lost more weight with the preload, but with respect to the long-term efficacy of drinking 500ml of water before every main meal this is an important result we should not forget (Dennis. 2010).
One of the things we will have to look for when analyzing Paretti's more recent study is thus whether she made sure to check if the appetite reducing effects persist. After all, their study was very similar to the one by Dennis, with an important difference in the study population which was not predominantly middle aged or older white men and women in Paretti's study. Otherwise there are only very few surprises with regard to the study design. Here's what we're talking about:
  • a two-group randomized controlled trial with eighty-four adults with obesity 
  • all participants were given a face-to-face weight management consultation at baseline (30 min) and a follow-up telephone consultation at 2 weeks (10 min)
  • participants were randomized to either drinking 500 ml of water 30 min before their main meals or an attention control group where participants were asked to imagine their stomach was full before meals (*)
  • primary outcome was weight change at 12-week follow-up
In that, the "(*)" denotes something you might consider weird... and what should I say? It is weird to imagine that your stomach is full before a meal, but that's Parretti's way of turning a regular RCT into an attention controlled RCT, where the dummy procedure disguised the true intent of the study and provided a nonspecific intervention that in some ways matched preloading.
Table 1: Self-reported adherence for both groups - (I) intervention group, (C) control group (Parretti. 2015).
It is thus not really surprising that the subjects in the control group (C) hardly managed to follow the scientists advise once a week, while the majority of the subjects in the intervention group (I) consumed their water preload on at least two of three meals per day. The data in Table 1 does yet still leave no doubt that the adherence declined significantly over the 12-week period. Whether the Parretti study is able to answer the previously raised question, if the chronic use of water preloads may reduce their efficacy, is thus highly questionable. I mean, after 12 weeks, almost half of the subjects didn't use the preload anymore.
Table 2: Self-reported fullness and satiety scores for both groups - (I) intervention group, (C) control group; fullness and satiety scores can range from 1 to 10 (Paretti. 2015)
Against that background, I would not interpret the stable satiety and fullness levels from week 2-9 as evidence that there is no such habituation effect. And in view of the lack of data on the actual food intake, the satiety and fullness data is pretty much irrelevant, anyways (just as there's a disconnect between mTOR and actual muscle gains, there are also disconnects between appetite, fullness and food / energy intake - if you don't measure the relevant outcome you're groping in the dark).
Figure 2: Weight loss (in kg) over the 12-week study period (unadjusted values | Parretti. 2015)
What is relevant and hard to reject, though ,is the fact that the water preloading group lost 1.3 kg more than the subjects in the control group (see Figure 2) - with a statistically significant difference of 1.2 kg still remaining when the data was adjusted for ethnicity, deprivation, age, and gender, the lack of which had been an issue in the previously referenced study by Dennis et al. (2010).
The reason I am still not thrilled is simple: Parretti's study was celebrated in the laypress as the breakthrough research that demonstrates that you can easily lose weight by simply drinking 500ml of water before each and every of your meals. Unfortunately, this is not just a broad overgeneralization of the results it is simply a completely false interpretation of the study. What Parretti's study does suggest (not prove) is that drinking 500ml will accelerate the weight loss on energy reduced diet.

"Chewing gums will help you lose weight" - That's another commonly heard dieting myth. One that may actually be true, though... albeit only if the gum is a nicotine gum, which could in fact promote fat loss | more
Trigger vs. support - That's an important difference! The most significant result of the initially referenced meta-analysis by Muckelbauer et al. was after all the disparity between studies of individuals dieting for weight loss and those who were on ad libitum diets. A disparity which suggest a weight-reducing effect of increased water consumption occurs only if you are on an energetically reduced diet (just like the subjects in the study at hand). In studies in general mixed-weight populations like you and me, however, such an effect has - as of yet - not been observed. It is thus more than questionable, whether pre-diluting each and every of your meals with 500ml water is going to help you stay lean. What it may do - and that's in fact something the Peretti study suggests - is to help you stick to a calorically restricted diet and thus lose weight faster and more effectively | Comment on Facebook!
References:
  • Daniels, Melissa C., and Barry M. Popkin. "Impact of water intake on energy intake and weight status: a systematic review." Nutrition reviews 68.9 (2010): 505-521.
  • Dennis, Elizabeth A., et al. "Water Consumption Increases Weight Loss During a Hypocaloric Diet Intervention in Middle‐aged and Older Adults." Obesity 18.2 (2010): 300-307.
  • Muckelbauer, Rebecca, et al. "Association between water consumption and body weight outcomes in children and adolescents: A systematic review." Obesity 22.12 (2014): 2462-2475.
  • Parretti, Helen M., et al. "Efficacy of water preloading before main meals as a strategy for weight loss in primary care patients with obesity: RCT." Obesity (2015).
  • Tate, Deborah F., et al. "Replacing caloric beverages with water or diet beverages for weight loss in adults: main results of the Choose Healthy Options Consciously Everyday (CHOICE) randomized clinical trial." The American journal of clinical nutrition 95.3 (2012): 555-563.

Four Ways to Turn Your AM Push-Up Routine into a Full-Body Workout: Wobble Board, Stability Disc, Fitness Dome, and TRX Suspension Trainer Under Scientific Scrutiny

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Based only on the study at hand, the TRX system does not seem to be significantly superior to the three other systems. In conjunction w/ previous research, discussed in the light-blue info box and the bottom line, though, it appears to be the best, certainly most versatile device.
Ok, the push up is already a full body movement, but as a recent unsponsored study from the University of Valencia shows, the muscle activation during push-ups performed under stable and unstable conditions varies significantly. So significantly, in fact, that certain muscle groups, such as the serratus aneterior, may be hammered twice as heavy when you use the "right" instability devices... and the best thing: None of the devices Borreani et al. tested will overrun the budget of a well-equipped homegym.

With that being said, let's take an initial look at the contestants. There's the classic push-up (not shown in Figure 1, because it requires no extra-device, but the floor), the (A) wobble board, the (B) stability disc, the (C) fitness dome, and the (D) TRX Suspension Trainer.
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The study participants were young fit male university students (n = 30; age: 23 ± 1.13 years; height: 178.87 ± 8.21 cm; body mass: 78.01 ± 8.5 kg; body fat percentage: 11.48 ± 3.18%; and biacromial (shoulder) width: 42.22 ± 12.81 cm) who voluntarily participated in this study. With a minimum of 1 year of resistance training experience, performing at least two sessions/wk at moderate to vigorous intensity, none of them was a rookie - an advantage of that makes the results of the study more relevant to the average gymrat.
Figure 1:  The unstable devices used in the present study: (A) wobble board, (B) stability disc, (C) fitness dome,
and (D) TRX Suspension Trainer which will obviously hang from the ceiling  (Borreani. 2015).
Each participant took part in two types of sessions: (1) familiarization and (2) experimental sessions, both at the same time in the morning. The first session occurred 48-72 hours before the data collection in the experimental session. Several restrictions were imposed on the volunteers: no food, drinks, or stimulants (e.g., caffeine) to be consumed 3-4 hours before the sessions and no physical activity more intense than daily activities 12 hours before the exercises. They were instructed to sleep >8 hours the night before data collection.
  • The familiarization session familiarized the participants with the push-up exercise, unstable devices, movement amplitude, body positioning, and the cadence of movement that would later be used during data collection. Participants practiced the exercises one to three times each.
  • The actual protocol started with the application of the EMG electrodes on the subjects' anterior deltoid (DELT), serratus anterior (SERRA), rectus femoris (FEM), and lumbar multifidus (LUMB), on the dominant side of the body.

    After the subjects were all wired up (in the literal sense), they started the push-ups in an extended arm (up) position with forearms and wrists pronated and feet at the biacromial (shoulder) width. In the down position, the forearm and wrists were kept pronated, whereas the elbow was flexed at ~90 and the shoulder was abducted at ~45 . The hip and spine were maintained neutral during all repetitions; this was verified using a laser device during the execution of the repetitions (Black & Decker, series LZR6TP9). Furthermore, each participant used a standardized grip at biacromial width (based on the distance in centimeters between the tips of the right and left third digits).

    Each participant performed five consecutive repetitions under all conditions. A 2-second rate for descent and ascent of an individual push-up cycle was maintained by a 30-Hz metronome (Ableton Live 6, Ableton AG, Berlin, Germany) to standardize the speed of movement. Visual feedback was given to the participants in order to maintain the range of movement and hand distance during the data collection.
If you've read  the summary carefully you will be astonished that the "pecs", i.e. the pectoralis major wasn't attached to an electrode, as well. From a practical perspective, that's unquestionably a downside of the study at hand. From a mere science perspective, though, it is only logical, because the scientists were interested in the co-activators, not the primary mover (see box below for the answer to the question that you may be asking yourselves, now ;-).
Science knows better than bros: The narrow push up activates both, triceps and pecs best (Cogley. 2005).
What about the pecs than? As previously explained, the pectoralis was not the main research interest of Borreani et al. From previous studies, we know however that doing narrow(er) push-ups will increase the activity of both triceps and biceps (Cogley. 2005 | see Figure on the left). Based on the lack of effect of the instability devices on "front delt" activity and the proven lack of influence of creating an instability by doing push ups on / with a Swiss Ball in various forms (Lehman. 2006) on pectoralis activity, it would be prudent to assume similar i.e. no effects on pecs activity with any of the instability devices in this study.

At least for the TRX system which is by any means the device that makes the most significant difference in how you perform the exercise, though, the muscle activity of the pectoralis major has been shown to increase. In the corresponding 2013 study by Snarr, the increase varies largely from one participant to the other, but reaches a stat. sign. plus 16% on average (Snarr. 2013a).
With that being said let's take a look at the results, of which I'd hope that you'd still agree that they're really interesting:
Figure 2: Muscle activity during regular floor pushup and push-up using the instability devices; all data expressed relative to respective values in the floor push-up trial; non-sign. effects were observed only for the delts (Borreani. 2015).
As you can see, there were no significant differences for the DELT muscle between the regular push-up an the device assisted push-up conditions. However, statistically significant differences were found among the different conditions for ...
Figure 3: Some orientation for those of you that don't know the muscle names: (1) anterior deltoids, (2) serratus anterior, (3) rectus femoris (4) lumbar multifidus
  • the serratus anterior, where all exercises being at least 2.9x more effective than the regular push-up
  • the rectus femoris, where the TRX Suspension System really excels, while the Stability Disc and Fitness Dome offer only minor advantages
  • the lumbar multifidus, where the all devices triggered an increase in muscle activation, yet only the difference for the TRX Suspension System reached statistical significance
If we go by the statistical standards, Borreani et al. are thus right to say that "not all unstable devices enhance muscle activation compared to traditional push-ups" (ibid. 2015). If we take a look at the relative mean activation patterns, though. All devices have some advantages.
Push ups in a TRX Suspension System are at least as effective as the classic crunch for the rectus abdomins aka the "abs" (Snarr. 2013b). In a previous study, Snarr et al. have also observed increased EMG activity in the pectoralis major (chest / pecs). Evidence I already discussed in the previous light blue box.
So what's the best device, then? I guess that's difficult to say, because "best" relative, in this case: While you and your trainer will have to decide which muscles are worth getting some extra attention, I personally would probably use the TRX System. It is the only device that leads to statistical significant increases in muscle activity in all, but the most common synergist of the pectoralis, the front delts, and makes the classic push up an even better core stability exercise. In fact, a previous study by Snarr et al. (2013b) shows that it is more than on par with the crunch when it comes to rectus abdominis (abs) activity. In conjunction w/ the previously discussed evidence that it increases pecs activity by 16% (see blue box), that's quite convincing for me, although it takes some time until you master the TRX system.

And what about the other devices? Well if you look at the data, the only good reason to use Wobble Board and Fitness Dome excel is the increased serratus activity, for which I'd rather do the good old dumbbell pullovers across a bench (you can also use a water crate in the home gym ;-). Pullovers may not "widen the chest", as some bodybuilders say, but they will create the illusion of doing just that by making the serratus grow (see muscle position in figure 3). Ah,... and the word "illusion" brings me to the last message of the bottom line: The mere fact that the EMG activity increases by X% does not mean that the muscle size and strength gains will increase by the same amount - it just increases the chance that both will increase  | Comment on Facebook!
References
  • Borreani, Sebastien, et al. "Muscle activation during push-ups performed under stable and unstable conditions." Journal of Exercise Science & Fitness (2015).
  • Cogley, Robert M., et al. "Comparison of muscle activation using various hand positions during the push-up exercise." The Journal of Strength & Conditioning Research 19.3 (2005): 628-633.
  • Lehman, Gregory J., et al. "Shoulder muscle EMG activity during push up variations on and off a Swiss ball." Dynamic Medicine 5.1 (2006): 7.
  • Snarr, Ronald L., and Michael R. Esco. "Electromyographic comparison of traditional and suspension push-ups." Journal of human kinetics 39.1 (2013a): 75-83.
  • Snarr, Ronald L., et al. "Electromyographic activity of rectus abdominis during a suspension push-up compared to traditional exercises." Age (yrs) 25.3.91 (2013b): 22-33.

Milk Fat Globule Membranes Power Up Strength Gains by Improving the Wiring of Subjects' Muscles | Plus: Its Proven Health, EPO & Immune-Boosting Effects Won't Hurt Either

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At the moment it is by no means clear which type of athlete / gymrat would benefit from milk fat globule membrane supplementation and which wouldn't. It's after all well possible that the effects Soga et al. observed in rookies wouldn't occur in adv. trainees or professional athletes.
After the study on nucleotide supplements the Satako Soga's latest paper on the dietary supplementation with milk fat globule membrane is #2 on the list of studies with promising new ergogenics in less than a month. In view of the fact that the last year has been devoid of any true innovations, this is a welcome diversion from writing about whey (or other protein powders), creatine, beta alanine and baking soda, as well as the occasional study on HMB for me.

In spite of the fact that this is a follow up on previous rodent studies from the same researchers, I must warn you not to to expect too much of MFGMs, yet. More data and studies with more realistic resistance training + supplementation protocols from independent labs are warranted before MFGMs may eventually appear next to the previously mentioned top dogs on a list of "SuppVersity Recommended Supplements".
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But hey, let's keep the skepticism for the bottom line and take a look at what the scientists from the Kao Corporation did with their fourteen Japanese subjects. The men, who were aged 31–48 years and did not participate in regular strength training before the study, took 1 g of the  structural membranes of milk which are usually covering the triglyceride globules that are dispersed as emulsified bodies in milk or 1g of an identically looking whole milk powder as a placebo in tablet form for 4-weeks (composition see Table 1).
Table 1: Composition of MFGM and whole milk powder (Soga. 2015)
"On the exercise training enforcement days [i.e. the days on which the subjects were required to train], the subjects were instructed to take the tablet within 1 h before training. On the other days, the subjects were instructed to consume the tablet at the time of their choice during their daily routines.
The MFGM was prepared from buttermilk by filtering and centrifugation. The MFGM and whole milk powder compositions were analyzed at Japan Food Research Laboratories (Tokyo, Japan)" (Soga. 2015).
The exercise routine the subjects from both groups had to follow consisted of two workouts per week. The workouts had to be performed on nonconsecutive days for 4 weeks using StrengthErgo 240 stationary cycling exercise machines (Mitsubishi Electric Corporation, Tokyo, Japan). On these machines, the subjects completed 3 sets of 15 % maximal voluntary contraction (MVC) cycle exercises for 60 s and 7 sets of 20 % MVC cycle exercises for 40 s at 50 rpm.
Preliminary rodent studies show that sign. increases in swimming time to exhaustion occur with as little as the equivalent of 1g/day of MFMG (Haramizu. 2014a) - The dose-dependency of the effects suggest that it may be worth taking more than 1g/day for humans, too.
What's the optimal dosage? It is way too early to answer this question with confidence, but the dosage in Soga's study was selected based on the results of previous rodent studies, where the equivalent of the 1 g the subjects consumed in the study at hand turned out to be the minimal effective dosage. In view of the fact that you will find the same amount of MFGM in just 600 ml of full fat milk, I am yet inclined to believe that it may be worth checking if dose-escalations would not yield even better and still side-effect free increases in strength gains and/or increases in endurance performance and fatty acid oxidation as they were observed in previous rodent studies (Haramizu. 2014a). Furthermore, preliminary data from a 4-week safety evaluation by Hari et al. (2015) shows that even 6.5 g/day are without side-effects in healthy humans.
Physical function tests and surface electromyography (EMG) were conducted at baseline and at the end of the study period. In addition, some hemotological parameters were tested of which - surprise - the data in Figure 1 tells you that MFGMs have a small, but statistically significant "EPO-effect" and are thus capable of raising both the red blood cell and hemoglobin content - an effect that has been observed in rodents too (Haramizu. 2014b) and may be ascribed to the incorporation of MFGM phospholipids into red blood cells which would in turn be less vulnerable to exercise-related or other stressors. Whatever the reason for these changes may be, they are certainly in line with the previously mentioned (see red box) increase in fatty acid oxidation during endurance exercise that may be facilitated by an RBC and hemoglogin related increase in oxygen transport.
Figure 1: The significant increase in red blood cell and hemoglogin content could explain the previously observed increases in endurance performance and fatty acid oxidation in Haramizu et al. (2014a). The buffered decrease in white blood cell may not be statistically significant, but may still indicate beneficial effects on the immune system (Soga. 2015).
Both the increase in RBC and hemoglobin, as well as the buffering of the albeit non-significant decline in white blood cells in the placebo group, which may be a response to the exercise-induced stress and evidence of an immune-boosting effect of MFGM supplementation during any potentially exercise induced immune suppression, do yet need further investigation before they can be explained mechanistically.

No further research is needed, though, to state that all other blood markers. These included AST + ALT (liver health), glucose and triglycerides + cholesterol, neither of which was affected by the supplement. The latter cannot be said of the increase in leg extension strength before and after the intervention and the EMG activity which showed highly significant inter-group differences.
Do I even have to supplement? I mean, I can just drink 600ml of full fat milk, right? I don't doubt that you can do just that. The problem is that the milk you can drink will probably be pasturized - a process of which Cano-Ruiz et al. (1997) have shown that it will induce significant and potentially functionally relevant differences in the composition of the milk fat globule membrane. Whether the supplement that was used at the study at hand was made during the production of buttermilk before or after pasteurization is not clear. If we assume it was made after pasteurization, though, you could in fact hope for similar results from pasteurized whole milk. Otherwise, the milk would have to be raw (even if it is, though it cannot be guaranteed that the same amount of MFGMs from milk will have identical effects).
In fact, the differences in Figure 2 are pronounced enough to ask the question: Were they induced by the supplementation alone or did the pathetic training regimen have an effect here, as well? As I am going to point out in the bottom line one paragraph below, we will need studies with more realistic training programs to answer this question in a way that's relevant for trainees like you and me. In the mean time, however, there is no debating "that the daily intake of 1 g MFGM combined with regular, twice weekly exercise improved skeletal muscle strength (leg extension) in middle-aged adults, despite a lack of change in muscle mass" (Soga. 2015).
Figure 2: The MFGM supplementation lead to significant increases in leg extension strength, of which the increase in EMG activity (likewise sign.) suggests that they were mediated by neuronal changes (Soga. 2015).
The same goes for the increase in RMS of surface EMG, which indicates that the dietary provision of MFGM increased the average (RMS = root mean square) motor unit activity during muscle contraction and may thus mechanistically explain why the subjects got stronger even though they didn't make substantial gains in muscle mass: The supplement helped them to "make the most" of the muscle they had. This hypothesis is in line with results from rodent studies which
"[...] revealed that dietary MFGM combined with regular exercise improved muscle strength in adult mice primarily by stimulating the pathway involving “nervous system development” in the skeletal muscle (Haramizu. 2014b). This pathway includes functional annotations such as formation of synapses, growth of neurites, or development of NMJ. Dietary MFGM combined with exercise increased skeletal muscle expression of docking protein-7 (Dok-7) and muscle-specific receptor tyrosine kinase in mice, both of which play a critical role in NMJ [neuromuscular junction] formation. Defects in NMJ function causes muscle weakness in neuromuscular disorders, and Dok-7 gene therapy improves NMJ formation and rescues the motor activity" (Soga. 2015).
And still, even at the risk that I may sound like a broken record, I have to repeat that without future research it is impossible to tell (a) whether the assumptions we've made about the increase in red blood cell count are accurate and, maybe even more importantly, (b) who, i.e. which type of athlete, will benefit most from using MFGM supplements.
MFGMs can do much more! It's not like this was the first study on MFGMs. It's just the first study on exercise performance in humans. In rodents performance incre- ments (see red box), as well as increases in RBC and EMG have long been established. In older women MFGMs have been shown to improve or fully reverse frailty (Kim. 2015). As hinted at in the conclusion, the addition of MFGMs to infant formulas will also narrow the gap in cognitive development and lipid composition (+future VCD risk) between breastfed and formula-fed infants (Timby. 2014a,b).

Other purported benefits include anti-cancer effects (Lemonnier. 2003) stress protection, the potential to reduce the risk of Alzheimer's (Spitsberg. 2005) and increase gastrointestinal intergrity (Snow. 2010), and beneficial effects on blood lipids (Noh. 2004) and cardio-vascular health where some researchers expect beneficial, while others fear detrimental effects (Riccio. 2004; Spitsberg. 2005; Singh. 2006). Since most of these effects have been observed in vitro or in rodent studies, it is yet by no means clear which of them would occur in response to MFGM supplementation.
Bottom line: As I already pointed out in the introduction, it is way too early to celebrate MFGMs as "the next big thing" or the supplemental reincarnation of the "a gallon of milk per day" protocol which would have provided its followers a highly significant 6g+ dose of MFGM on a daily basis.

The reason(s) we need further research are simple. Firstly, we need independent validation of the results that were generated by scientists who work for a company that produces milk fat globule membranes. Secondly, studies in trained individuals in whom the purportedly mechanistically involved improvements in the neuronal wiring of the muscle may be significantly less pronounced, as well as studies involving more realistic resistance training and endurance training protocols to confirm the beneficial effects that were observed in this study and the rodent study by Haramizu et al. which found significant increases in maximal endurence (see red box) are required to be able to tell for whom MFGM supplements will be beneficial. And third- and lastly, experiments with different dosing protocols (timing and amount) are necessary to determine the optimal dosing schemes - preferably for different types of exercises.

With that being said, MFGMs are still one of the more promising newcomers, lately. Their effects are after all not restricted to performance enhancing in the narrow(er) sense, but extend into the realms of general health and fitness (see box on the right hand side of this bottom line). In conjunction with their potential use as additives to baby formula, where they have already been shown to improve risk markers of future cardiometabolic disease and the babies' cognitive development to an extent that marginalizes the benefits of breast-feeding in these areas, make them one of the hottest candidates on my personal "still insufficient evidence, but promising"-list of supplement to keep an eye on | Comment on Facebook!
References:
  • Cano-Ruiz, M. E., and R. L. Richter. "Effect of homogenization pressure on the milk fat globule membrane proteins." Journal of Dairy Science 80.11 (1997): 2732-2739.
  • Haramizu, Satoshi, et al. "Dietary milk fat globule membrane improves endurance capacity in mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307.8 (2014): R1009-R1017.
  • Haramizu, Satoshi, et al. "Habitual exercise plus dietary supplementation with milk fat globule membrane improves muscle function deficits via neuromuscular development in senescence-accelerated mice." SpringerPlus 3 (2014): 339.
  • Kim, Hunkyung, et al. "Effects of Exercise and Milk Fat Globule Membrane (MFGM) Supplementation on Body Composition, Physical Function, and Hematological Parameters in Community-Dwelling Frail Japanese Women: A Randomized Double Blind, Placebo-Controlled, Follow-Up Trial." PloS one 6.10.2 (2015): e0116256.
  • Lemonnier, Lori A., et al. "Sphingomyelin in the suppression of colon tumors: prevention versus intervention." Archives of Biochemistry and Biophysics 419.2 (2003): 129-138.
  • Riccio, Paolo. "The proteins of the milk fat globule membrane in the balance." Trends in food science & technology 15.9 (2004): 458-461.
  • Singh, Harjinder. "The milk fat globule membrane—A biophysical system for food applications." Current Opinion in Colloid & Interface Science 11.2 (2006): 154-163.
  • Snow, D. R., et al. "Membrane-rich milk fat diet provides protection against gastrointestinal leakiness in mice treated with lipopolysaccharide." Journal of dairy science 94.5 (2011): 2201-2212.
  • Soga, Satoko, Noriyasu Ota, and Akira Shimotoyodome. "Dietary milk fat globule membrane supplementation combined with regular exercise improves skeletal muscle strength in healthy adults: a randomized double-blind, placebo-controlled, crossover trial." Nutrition Journal 14.1 (2015): 85.
  • Spitsberg, V. L. "Invited review: Bovine milk fat globule membrane as a potential nutraceutical." Journal of dairy science 88.7 (2005): 2289-2294.
  • Timby, Niklas, et al. "Neurodevelopment, nutrition, and growth until 12 mo of age in infants fed a low-energy, low-protein formula supplemented with bovine milk fat globule membranes: a randomized controlled trial." The American journal of clinical nutrition 99.4 (2014a): 860-868.
  • Timby, Niklas, et al. "Cardiovascular risk markers until 12 mo of age in infants fed a formula supplemented with bovine milk fat globule membranes." Pediatric research 76.4 (2014b): 394-400.

Whey vs. Casein - Casein-Exclusive Increase in GLUT-4 Expression Beats Whey's Insulinogenic Effect // Creatine Builds Legs of Young & Old, Rookie & Pro, BB & Cyclist

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If you drink "old school" protein shakes with milk and eggs, you don't have to worry if casein or whey is better on hypercaloric diets ;-)
Creatine, whey and - at least optionally - casein are on the list of "must have" supplements for anyone who has been following a solid workout routine a decent high(er) protein diet for a year or longer. And even though this makes any news study on one of the three potentially interesting for a huge part of the SuppVersity readers, the results are often so unsurprising that they are hardly worth an individual SuppVersity article...

I mean, let's be honest: You wouldn't be excited if I wrote about study #1023 showing a practically irrelevant acute increase in protein synthesis, let alone totally meaningless increases in mTOR in response to the ingestion of whey protein, would you?

For today's installment of the short news, I will picked two studies that are at least not as simplistic (and useless) as the previously mentioned 1023rd whey protein study.
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Study #1 sheds some light onto the intricate differences between the way(s) whey and casein may differently affect our energy balance, gut hormones, glucose metabolism, and taste preference (Pezeshki. 2015), while study #2 is actually a meta-analysis that makes a first attempt to actually quantify the average effect of creatine on leg strength (Lanhers. 2015).
  • Whey or casein? The answer to this question probably depends on your goals - That's at least what the complex results of a similarly complex series of experiments from the Snyder Institute for Chronic Diseases at the University of Calgary appears to suggest (Pezeshki. 2015). In the corresponding study, the researchers determined the effects of dietary whey, casein, and a combination of the 2 on energy balance, hormones, glucose metabolism, and taste preference in rats.

    Yes, this does mean that we must not uncritically transfer the results to humans. It does not mean, however, that we cannot use the results of Pezeshki's study, at all. Much of what we know and have later proven in human studies about our metabolism has initially been observed in rodents. Doing the same experiments with humans would not just have been significantly more expensive, it would also have been thwarted by misreported energy intakes and a lack of dietary control. So, if you belong to the "it's a rodent study, so I ignore it, if the results don't fit my world-view" faction, you are free to fast forward to the Lanhers study. If not, here's the elevator pitch on the two experiments the scientists conducted:
    • The hormone / energy expenditure experiment: Obesity Prone CD (OP-CD) rats were fed a high-fat control diet (33% fat energy) for 8 wk, and then randomly assigned to 4 isocaloric dietary treatments (n = 12/group): the control treatment (CO; 14% protein energy from egg white), the whey treatment (WH; 26% whey + 14% egg white), the casein treatment (CA; 26% casein + 14% egg white), or the whey plus casein treatment (WHCA; 13% whey + 13% casein + 14% egg white) for 28 d. Measurements included food intake, energy expenditure, body composition, metabolic hormones, glucose tolerance and key tissue markers of glucose and energy metabolism.
    • The food intake / preference experiment: Naive Obesity Prone CD (OP-CD) rats (not the same rats as in experiment 1) were randomly assigned to 3 groups (n = 8/group). During an 8 d conditioning period, each group received on alternate days either the CO or WH, CO or CA, or CO or WHCA. Subsequently, preferences for the test diets were assessed on 2 consecutive days with food intake measurements at regular intervals.
    If you take a look at my compilation of the most relevant data in Figure 1, you will see significant improvements in glucose management in all groups (Figure 1 | G). You should yet also be able to see that the most significant increase in GLUT-4 expression and thus the muscles ability to take up glucose occurred in the casein and mixed protein groups. In the whey group, on the other hand, where the insulin levels were the highest the increase in GLUT4 receptor expression was negligible and the 60 minutes post value for glucose after the glucose tolerance est was higher, but not significantly higher than in either the mixed protein or casein group.
    Figure 1: 0-60 minute hormone, glucose, cytokine and gene response to glucose tolerance test in diet-induced obese rodents fed diets containing either low amounts of protein or high amounts from whey, casein or a combination of whey + casein (Pezeshki. 2015).
    Since you will usually hear that whey is the #1 glucose repartitioner this may seem odd. In view of the fact that insulin can only drive glucose into the cells if they actually "stretch out their glucose "suckers", i.e. the GLUT-4 receptors, it is yet only logical - and that despite the fact that we cannot (yet) explain the differential GLUT-4 response. 
Whey or casein hydrolysate - or rather no protein - what to use in your intra-workout beverage for endurance? Find out in this SV Classic
What types of casein and whey were used? In spite of the fact that it may be highly relevant to know if we are talking about fast digesting and extremely insulingogenic whey hydrolysate (I assume we are) or regular whey concentrate or isolate (I assume we are not), the scientists don't provide any information on the exact nature of the supplemental whey and casein protein in the diet. And even though this may be less relevant for casein, I would like to point out that most rodent studies use cheap calcium or sodium caseinates which are digested much more rapidly that micellar casein, the casein you may be thinking of when you hear "casein" (I am pretty sure it was not casein hydrolysate, though). If you want to be skeptical about the interpretation of the results, don't focus on the fact that it's a rodent study. A lack of specificity like the one in regard to the exact nature of the protein supplement is at least as good a reason to be careful with the interpretation of the results of this study as the species of the subjects ;-)
  • What remains to be seen, though, is whether this measurable, but not in all details statistically significant difference actually matters. If you look at the food intake and preference data in Figure 3. It would seem as if it didn't. I mean, if we apply "Taubes'ian" logic, here, the high(er insulin levels in the whey group should have made the rats overeat...
    Figure 2: Daily food intake during conditioning trials. Rats were fed, on alternate days, a control diet or whey (A), casein (B), or a combination of whey and casein (C). Mean hourly food intakes on 2 consecutive days of preference testing, with access to both control and one of the high protein diets (D, E, F | Pzeshki. 2015). 
    ... a brief glimpse at the data in Figure 2, however, tells you that this was clearly not the case. It is thus not surprising that the final lean and fat mass percentages in Figure 3 did not differ significantly between the groups, even though some of you will notice a non-significant lean vs. fat mass advantage for the casein group. 
  • Eventually, it would still appear unwarranted to use the study at hand to argue in favor of casein instead of whey protein as your protein supplement of choice. If you are yet already following my suggestion to mix the two (read even more), the results of the study at hand would be another reason to stick to that practice.

    Overall, we do yet have to remember that significant treatment effects in response to the increase in protein were observed in all groups. In that, it may be true that the casein group had the highest reduction in food intake (30-43% reduction) and appears to have ended up with a slightly better body composition, but hey, we are talking about non-significant differences in a study that was not just done on rodents, but on obese rodents ... and you know that the weight status obese vs. lean / athletic can make more of a difference in the way people / lab animals react to supplements than the difference between man and mouse.
  • Creatine and lower limb strength - what to expect? You are probably asking yourself now: "Why on earth is Adel so interested in this meta-analysis?" Well, the answer is as simple as it is personal: The only body part of mine that appears to to have ever really benefited from creatine supplementation, strength-wise, are my legs. Accordingly, I was attracted to the Lanhers' meta-analysis, because I hoped to find some clues on why this may be the case.

    Now, I guess I don't give away too much, when I say that the paper didn't provide me with new insights in this respect. What the scientists' compilation and meta-analysis of the data did do, however, was to confirmation that I am not the only one whose "wheels" respond extremely favorably to creatine supplementation: One of the main results of Lanhers' meta-analysis of 60 (!) studies is after all that the effect of creatine supplementation on leg strength is not just statistically significant in almost every study they reviewed, it is also and maybe even more importantly and astonishingly independent of population characteristics, training protocols, and supplementary doses and duration (reread this - you don't have to superdose it!).

    In that, I find it particularly striking that even training for mostly aerobic team sports, like handball, for example, can trigger significant increases in squat performance if the players are consuming 3-5g of creatine before or after their training sessions (Note: In the corresponding study by Izquierdo, the handball players also saw significant increases in bench press performance - It's thus by no means as if creatine was a "leg strength booster", only!).
    Figure 4: Meta-analysis on maximal weight lifted (kg) in squat. CI confidence interval, M male, SD standard deviation, T0 baseline, T1 following supplementation (Lanhers. 2015).
    For the total workout volume (not shown in Figure 4), Lanhers et al. report almost identical effect sizes as the researchers determined them based on the absolute increase in squat performance in kg (see Figure 4); and just like the relative strength gains, the relative volume increases did not depend on the training status or age (subjects were 21-69 years old) of the subjects.

    In view of these results, there's really no good reason to doubt the scientists' conclusions that (a) "[c]reatine supplementation is effective in lower limb strength performance" and (b) works "for exercise with a duration of less than 3 min". If you also take into account that the average effect size for weight and volume are in the range of ~30% irrespective of the population characteristic, training protocols, and supplementary doses and duration, I hope that you can agree that there's also no reason to doubt my repeatedly voiced recommendation to "take your creatine bros" ... ah, and take it with sodium bicarbonate, obviously ;-)
Bottom line: In view of the fact that both items of today's short news already have their own bottom lines, I am not sure if you even need an extra summary, but here you go: With the Pezeshki study we have initial evidence to question the longstanding, but hardly researched assumption that whey is the protein of choice for weight loss and glucose management. In spite of the fact that the results show only trends towards better body composition and improved glycemia with casein vs. whey and need confirmation in non-obese, even better athletic human beings, I will keep an eye on potential follow-up or related studies.

Suggested SuppVersity Classic: "10+ Things You Probably Didn't Know Whey & Peptides That Form During its Digestion Can Do" - When you've read this article, I promise you will (re-)appreciate the benefits of whey and forget the Pezeshki study until a follow-up / related study is published | more
In that, I don't believe we will see an earth-shattering difference between the two protein sources in any potential follow-up, but what I really would like to know is the reason and mechanism behind the unexpected and unexplaind casein-induced increase in GLUT-4 receptor expression on the cell surface Pezeshki et al. observed in the study at hand (other studies often measure only total GLUT4!).

In contrast to the Whey vs. Casein study, Lanhers' meta-analysis of the effects of creatine on leg muscle strength and maximal training volume is so simple to interpret that you can summarize its implications in one sentence: "If you know that creatine will make you stronger, irrespective of how old you are, how you train and whether you take only 3g of much more, you either want to be weak or must be an idiot if you don't take it" | Comment on Facebook!
References
  • Izquierdo, M. I. K. E. L., et al. "Effects of creatine supplementation on muscle power, endurance, and sprint performance." Medicine and Science in Sports and Exercise 34.2 (2002): 332-343.
  • Lanhers, Charlotte, et al. "Creatine Supplementation and Lower Limb Strength Performance: A Systematic Review and Meta-Analyses." Sports Medicine (2015): 1-10.
  • Pezeshki, et al. "Dietary Whey and Casein Differentially Affect Energy Balance, Gut Hormones, Glucose Metabolism, and Taste Preference in Diet-Induced Obese Rats." The Journal of Nutrition. First published ahead of print August 26, 2015.

Food Matrices: Protein & Fat Ameliorate Glucose Spikes After Standardized Glucose Load | Plus: Timing Matters if You Want to Turn Regular into Resistant Starch

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This is what it's all about. Real food does not come in form of "macros". It comes in form of complex food matrices that determine its effect on one's health - including one's glycemic health.
You will probably remember that I have touched on a specific aspect of the effects of and interactions between different macronutrients in what scientists often refer to as "food matrices" on the glycemic response to standardized glucose loads in previous articles like the famous "True or False?" article that dealt with the question: "Will Adding Fat to A Carby Meal Lower the Insulin Response?" (read it).

You don't remember this or any of the other articles? Well, in that case, I probably have to tell you again that the mere fact that the postprandial glucose are lower does not mean that a certain food or combination of certain macronutrients would increase your insulin sensitivity (adding fat to a high carbohydrate meal certainly doesn't do that, believe me).
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While this is possible for certain supplements like berberine and other AMPK activators, it is mandatory that we differentiate the following three cases:
  1. Reduced postprandial blood glucose levels in response to an increase in insulin sensitivity as it is triggered by exercise or AMPK activators,
  2. Reduced postprandial blood glucose levels in response to increased insulin levels as they occur with the co-ingestion with whey protein and
  3. Reduced postprandial blood glucose levels in response to increased insulin levels and a decreased rate of absorption of glucose as it is the case if you add fat to carbohydrates.
That was too fast? Too complicated? Or both? Never mind. The discussion of two recent articles from the Lund University and the Yong Loo Lin School of Medicine (see blue box) will hopefully help you understand the difference - I promise ;-)

Let's take a look at study design, results and implications

In their study, Wathik Alsalim and his colleagues from the Lund University in Sweden and the Consiglio Nazionale delle Ricerche in Italy investigated the integrative impact of macronutrients on postprandial glycemia, β-cell function, glucagon and incretin hormones in man. The subjects were male and female Caucasian subjects, aged 30-70 years and BMI 20-35 kg/m², without diabetes (normal fasting glucose and normal HbA1c) or with T2D without any pharmacological glucose-lowering therapy and HbA1c <60 mmol/mol (<7.8%).
"Exclusion criteria were liver disease, diabetic nephropathy, proliferative diabetic retinopathy, pregnancy or breast feeding, treatment with oral antidiabetic or insulin, previous myocardial infarction, coronary heart disease or angina pectoris, previous surgery on the gastrointestinal tract, larger surgical intervention the last 12 weeks or treatment with oral steroids or thiazide diuretics" (Alsalim. 2015).
Participants were studied at the Lund University's Clinical Research Center on four occasions in a randomized cross-over design, separated by at least four and maximally eight weeks. After overnight-fast (no food after 10pm), subjects were provided with antecubital vein catheter. After two baseline samples at 5, and 2 mins, they ingested in randomized order either one of the macronutrients alone
  • glucose - 330kcal = 83g; Skåne University Hospital Pharmacy, Lund, Sweden,
  • protein mixture - 110kcal = 30g; ISO WHEY protein consisting of milk and egg protein
  • fat emulsion - 110kcal = 24ml; 50% long-chain triglycerides and 50% water;
The response to the individual macros was then compared to the ingestion of a 550kcal meal containing 330kcal (60%) from glucose, 110kcal (20%) from protein and 110kcal (20%) fat - a proportion of which the scientists say that it "was selected to represent a common meal with 60% carbohydrate, 20% protein and 20% fat" (Alsalim. 2015).
Figure 1: To allow for maximal control, the "meal" (macro composition on the right) was a shake (Alsalim. 2015).
Water was ingested at the same time of each load to standardize the ingested volume to 400ml; all ingestions were consumed within 5 min. Blood samples were taken throughout a 300min period after each challenge test.
Both vegetable oils and ghee had identical (beneficial) effects on the starch composition, but they have to be added  during boiling or before frying and boiling (Kaur. 2015).
Modifying the glycemic potential and starch content of foods with fats - In the initially cited article, Collier & O'Dea restricted their study to potatoes, only. In a more recent study, Kaur et al. investigated the effects of adding fat to white bread and rice, as well and what's even more important they did so during, not after the cooking process. In other words, instead of "buttering" potatoes, as Collier et al. did it, Karr et al. conducted a study in which they assessed the starch digestibility of white and red rice prepared with 2 oil types: vegetable oil (unsaturated fat) and ghee (clarified butter, saturated fat) added at 3 different time points during the cooking process (“before”: frying raw rice in oil before boiling, “during”: adding oil during boiling, and “after”: stir-frying cooked rice in oil | details).

Unfortunately, the results are less "unique" than the design of the study. (A) Red rice produced a slower digestion rate than white rice. (B) The digestibility of white rice was not affected by oil type, but was affected by addition time of oil, in general. (C) Adding oil “after” (stir-frying) to white or red rice resulted in higher slowly digestible starch. In that, (D) adding the fat before or during cooking and frying respectively had the most significant effect on the subject's postprandial glycemic response and the resistant starch content of the food.
Now, guess what? Yes, yes, and no ... the glucose meal was not the most insulinogenic one. Accordingly, we have to be careful not to mistake the scientists' conclusion that "[a]dding protein and fat macronutrients to glucose in a mixed meal diminishes glucose" (Alsalim. 2015) as evidence that fat and protein will reduce the potential obesogenic effect of carbohydrates. After all, the data in Figure 2 leaves no doubt that we are not talking about effect (a) from our list at the beginning of the article, i.e. a reduction in glucose excursions in response to "an increase in insulin sensitivity as it is triggered by exercise" (see introduction).
Figure 2: Glucose and insulin response as well as corresponding insulinogenic index and insulin clearance of the individual macros and the mixed meal - all data expressed relative to the values of 110kcal of glucose (Alsalim. 2015).
Rather than that, the reduced glucose AUC was a result of (c), i.e. an increase in insulin levels due to increased insulin production, as well as a decreased clearance of insulin and a decreased rate of absorption of glucose (-16%, -52%, -59% and -70% reduced glucose influx through the portal vein at 30, 45, 60 and 90 min after the meal) - and with the increased insulin levels you will also run an increased "risk" of fat storage (whether you gain weight will still depend on your overall energy intake not your insulin levels, though).

Figure 3: Insulin is not always the bad guy. A 2004 study by Hallschmid, et al. shows that it's centrally mediated effects in the brain can actually help men (but not women) lose weight effortlessly, when they administer it cyclically (only chronically elevated insulin levels are truly problematic) intranasally.
At this point, it may be necessary to point out that the increase in insulin in response to the co-ingestion of protein and fat does not imply that guzzling glucose on its own would be healthier than eating a mixed meal. In conjunction with the increases in the important (fat burning) satiety hormone GLP1, which were observed only in the diabetic subjects, though, these changes are yet far more beneficial for the average type II diabetic than they are for the lean athlete, who doesn't need the extra-insulin to maintain normal blood glucose levels and may even consider them an obstacle on his / her way to single-digit body fat levels.
So what? Just as the previously discussed study on butter + potatoes, the study at hand does not confirm that you just have to add fat (and protein) to a meal to stay lean and healthy forever. The GLP-1 increase, which occured only in the diabetics, and the significant increase in insulin production, which occurred in both diabetic and healthy subjects, fully explain the reduced glucose spikes and can be considered "beneficial" only for type II diabetics, who can thus compensate their insulin resistance w/ even more insulin. For lean / healthy individuals who get the questionable benefit of increased GIP and insulin levels, but don't benefit from the increase in GLP-1, the benefits - if there are any - are less obvious.

Are You Afraid that the Fructose Boogieman Clogs Up Your Liver? Citrulline or Alanine, Glycine, Proline, Histidine and Aspartate Mix Will Protect You + Maybe Lean You Out
If there's an advantage of adding protein and fat to carbs in order to reduce the postprandial glucose excursions in lean individuals, that's probably not the often heard of "stay lean" effect, but rather a long(er) term health advantage. Elevated postprandial glucose levels have after all been linked to type II (as a consequence of the ill effects of elevated glucose on your pancreas | Robertson. 2003) and type III diabetes (type III = all sorts of downstream effects of constantly elevated glucose levels like Alzheimer's | Steen. 2005), increased inflammation and cardiovascular disease risk and a lot of other ailments you certainly want to avoid even more urgently than being pot-bellied or "chubby" | Comment on Facebook!
References:
  • Alsalim et al. "Mixed meal diminishes glucose excursion compared to glucose by several adaptive mechanisms in man." Diabetes, Obesity and Metabolism (2015): Accepted article.
  • Collier G, O'Dea K. The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. Am J Clin Nutr. 1983 Jun;37(6):941-4.
  • Hallschmid, Manfred, et al. "Intranasal insulin reduces body fat in men but not in women." Diabetes 53.11 (2004): 3024-3029.
  • Kaur B, Ranawana V, Teh AL, Henry CJ. "The Glycemic Potential of White and Red Rice Affected by Oil Type and Time of Addition." J Food Sci. (2015).
  • Robertson, R. Paul, et al. "Glucose toxicity in β-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection." Diabetes 52.3 (2003): 581-587.
  • Steen, Eric, et al. "Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease-is this type 3 diabetes?." Journal of Alzheimer's disease 7.1 (2005): 63-80.

Trying to Lose Fat & Get "Toned" W/Out Training or Diet? Taking 1-3 mg Melatonin Helps Women Lose 7% Body Fat, Gain 3.5% Lean Mass in Recent 12 Months-Long RCT

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Since the natural melatonin production decreases as we age, it is (unfortunately) possible that younger women wouldn't see the same benefits as the >56 year-old subjects of the study at hand.
No, I am not recommending laziness here, and I doubt that you will arrive at a cover model physique with nothing but a handful of melatonin pills, but the results of a recent study from the Aarhus University Hospital in Denmark are too intriguing not to devote a whole SuppVersity article to them.

In said study, Anne Kristine Amstrup and colleagues tested whether there's anything to the rumors that have it that "melatonin [has] a positive effect on body weight and energy metabolism" (Amstrup. 2015). As the researchers rightly point out, previous "evidence for this relies mainly on animal models" (ibid). It was thus about time for someone to "determine the effects of melatonin on body composition, lipid and glucose metabolism in humans" (ibid).
Want to learn more about melatonin? The SuppVersity is the place to be.

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M. Anti-Alzheimer + Anti-Body Fat Agent
In this case, said human beings were 81 post-menopausal Caucasian women (aged 56-73 years) diagnosed with osteopenia (T-score between -1 and -2.5 in the hip or spine). The Danish scientists randomized the women to receive
  • either melatonin, at a dosage of 1 or 3 mg per day, or
  • an identically looking placebo nightly (timing matters!)
for a total time-period of 12 months. There were no dietary or exercise interventions, but all study subjects received a daily supplementation of 800mg calcium and 20ug vitamin D3 (which obviously wouldn't affect the results, also because all of the participants had taken Ca + D3 for at least 3 months before the study began). With DXA, ...
"To assess body composition, we used a whole body scan by dual X-ray absorptiometry (DXA, Hologic Inc., Waltham, MA, USA). We performed scans at baseline and after one year of treatment. Assessments included total and subtotal body mass (g), lean mass (g), fat mass (g) and percentages of body fat. We calculated body mass index (BMI) as body weight (kg) divided by height² (in metres)" (Amstrup. 2015).
... and a detailed analysis of the blood of their subjects, the body composition and biochemical analyses were similarly thorough as the randomization protocol which was performed by an external pharmacy (Skanderborg Pharmacy).
Beware! If you take melatonin anytime but 1-2h before bed (fasted), it may backfire! If you don't remember why and how timing matters, I suggest you re-read my 2014 article about how taking melatonin at the wrong time of the day may actually make you fat and insulin resistant.
Each block consisted of eight individuals. In the blocks, the women were randomly allocated to treatment, i.e. four received placebo, while two received 1mg of melatonin and two received 3mg melatonin.
Figure 1: Changes in body composition (left) and adiponectin (right) in response to 1-3mg of melatonin taken at night over a 12-months period without further exercise or diet intervention (Amstrup. 2015).
This is also why I have little doubt that we can rely on the data in Figure 1 which shows an astonishingly pronounced reduction in fat mass and a borderline-significant increase in lean mass in the melatonin groups, when the subjects on the placebo supplements gained total (and %) body fat and lost lean mass in the same 12-months period.
Melatonin As Potent as Letrozole in Inhibiting Aromatization | more
You are an athlete who does not care about losing weight? Data from a Spanish study leaves no doubt that you can still benefit from taking melatonin. In their soon-to-be-published study, researchers from the Universidad de Granada a high dose of melatonin restored the normal circadian rhythm of melatonin production, reduced the nocturnal activity and the activity and position during lunch/nap time - "[t]ogether, these data reflect the beneficial effect of melatonin to modulate the circadian components of the sleep-wake cycle, improving sleep efficiency," the authors say (Leonardo-Mendonça. 2015).
The one thing I would still like to repeat is what I already mentioned in the caption of the thumbnail to this article: Since the natural melatonin production decreases as we age and menopaus (Okatani. 2000), it is (unfortunately) possible that younger women wouldn't see the same benefits as the >56 year-old subjects of the study at hand.
Figure 2: Rodent studies also show that melatonin supplementation prolongs the lifespan of the average mouse (Pierpaoli. 1994) and rat (see data in graph) significantly (Oaknin-Bendahan. 1995).
In a similar vein, it cannot be said with any certainty, whether men will benefit to the same extent as the post-menopausal women in the study at hand. While studies in rodents clearly suggest that melatonin works its weight reducing, life pro-longing (see Figure 2) in both male and female middle-aged rodents (Rasmussen. 1999; Wolden-Hanson. 2000), as well as rats who are fed an obesogenic diet like the standard American diet (Prunet-Marcassus. 2003), men are no little mice... but I guess you know that ;-)
So what? Well, melatonin is a hormone, not one with that builds muscle, but as the study at hand proves one with non-debatable "beneficial effects on body composition in terms of reduced fat mass and borderline significantly increased lean mass in post-menopausal women".  What's particularly interesting is that this effect can be achieved with relatively small doses of melatonin (1 and 3mg/d) and without any of the unwanted effects on blood lipids, glucose metabolism or markers of kidney and liver health you would see with other hormonal substances with proven body-recompositioning effects.

Will Melatonin Reduce Your Testoste- rone Levels? A Review of the Existing Evidence Experimental Human Data Says: Unlike in rodents, the longterm administrationf melatonin to men appears to rather increase vs. decrease their T levels.
In this context it is also worth mentioning that the authors believe that their "findings may be explained by a melatonin-driven increase in osteogenesis resulting in decreased adipogenesis". Bone instead of fat cells? Well, as SuppVersity reader and follower of the SuppVersity Facebook News-Channel you will have read about the cellular underpinnings of this transformation before. Against that background it is not unreasonable of Amstrup et al. to conclude that "[o]n the basis of [their] study, melatonin maybe an interesting therapeutic agent for future treatment strategies against [...] age-related changes in body composition" (Amstrup. 2105). Whether it is a must have supplement for younger (more athletic) individuals, though, will have to be determined in future human trials, of which I doubt that they will be publicly funded  | Comment on FB!
References:
  • Amstrup, et al. "Reduced fat mass and increased lean mass in response to one year of melatonin treatment in postmenopausal women: A randomized placebo controlled trial." Clinical Endocrinology (2015): Accepted article.
  • Leonardo-Mendonça RC,  et al. "The benefits of four weeks of melatonin treatment on circadian patterns in resistance-trained athletes." Chronobiol Int. 11 (2015): 1-10. 
  • Oaknin-Bendahan, Sol, et al. "Effects of long-term administration of melatonin and a putative antagonist on the ageing rat." Neuroreport 6.5 (1995): 785-788.
  • Okatani, Yuji, Nobuyuki Morioka, and Akihiko Wakatsuki. "Changes in nocturnal melatonin secretion in perimenopausal women: correlation with endogenous estrogen concentrations." Journal of pineal research 28.2 (2000): 111-118.
  • Prunet-Marcassus, Benedicte, et al. "Melatonin reduces body weight gain in Sprague Dawley rats with diet-induced obesity." Endocrinology 144.12 (2003): 5347-5352.
  • Rasmussen, Dennis D., et al. "Daily melatonin administration at middle age suppresses male rate visceral fat, plasma leptin, and plasma insulin to youthful levels." Endocrinology 140.2 (1999): 1009-1012.
  • Wolden-Hanson, T., et al. "Daily Melatonin Administration to Middle-Aged Male Rats Suppresses Body Weight, Intraabdominal Adiposity, and Plasma Leptin and Insulin Independent of Food Intake and Total Body Fat 1." Endocrinology 141.2 (2000): 487-497.

Massage Therapy Speeds Recovery in Bodybuilders After Eccentric Workouts - DOMS + CK ↓ / Performance ↑

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While many athletes use it and trainers all around the world are convinced that it works, the evidence on what exactly massage therapy does or doesn't do to an exhausted athlete's muscle and lymphatic system is scarce. Even the assumption that it helps reduce DOMS may be based on a placebo effect. After all, it's impossible to conduct a truly double-blinded massage study.
If they can afford it, athletes often employ their own massage therapist. It is commonly believed that sport massage after intensive exercise might improve power and perceptual recovery in sportsmen and -women. As Mehdi Kargarfard et al. (2015) point out in their latest paper, "few studies have been done in this area" to confirm what everyone appears to believe to be a scientific fact" (Kargarfard. 2015).

Accordingly, the researchers' latest study aimed to examine the effect of massage on the performance of bodybuilders - a group of athletes of which only few will be able to afford their own massage therapist, although they may in fact be among those athletes who could benefit most from massage therapy of which scientists believe that it reduces DOMS and speeds up recovery by removing accumulated extracellular fluid from the muscles, thus reducing swelling and pain via increased blood and lymph circulation - and at least the net outcome, i.e. a subjective reduction in DOMS (learn more) has been confirmed consistently (Bąkowski. 2008; Ali. 2012; Andersen. 2013; Visconti. 2014; Urakawa. 2015).
Learn more about supplements of which people say they help w/ recovery the SuppVersity

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GLU as Intra-Workout BV?

BCAAs deplete neurotransmitters
If we assume that the mechanism has been correctly identified, massage therapy appears to work very differently from ice-baths of which a recent study has shown that it may actually impair the training-induced adaptation process by soothing the fire that's fueling the corresponding processes (learn more in "Using Ice / Cold Water Immersion After Workouts Will Impair Muscle and Strength Gains, as well as Vascular Adaptations").
Table 1: Descriptive statistics of the participants (Kargafard. 2015).
What makes the study particularly interesting is that the N=30 subjects were all healthy young men (28.77 ± 3.54 years) who were free of any supplement and steroid use, but had at least 2 years experience in bodybuilding (Table 1). The participants were randomly assigned using the permuted block randomisation method to either a massage (n = 15) or a control (n = 15) group. Participants were excluded if they had any relative or absolute contraindications to exercise or exercise testing.
  • Tests were performed 1 week prior to the commencement of the treatment protocols and conducted during an 8-week preseason training period to limit the training effect. 
  • Both groups performed five repetition sets at 75–77% of 1RM of knee extensor and flexor muscle groups. The massage group then received a 30-min massage after the exercise protocol while the control group maintained their normal passive recovery. More specifically, ...
    "... the participants were asked to perform squats to 90º knee flexion for five sets at 75% 1RM until exhaustion (but not less than 10 repetitions); then they had to perform leg press to 90º knee flexion for five sets at 75–77% 1RM until exhaustion (but not less than 10 repetitions). One-minute rest intervals were given between sets. If a participant could not complete 10 repetitions without assistance from the spotters, the initial intensity was reduced until at least 10 repetitions could be achieved. This was followed by a 5-min rest and an isometric protocol to induce DOMS in the right quadriceps muscle" (Kargarfard. 2015).
  • Participants’ diets and medications were recorded and remained constant throughout the experimental period, which excludes a distortion of the results.
Criteria under investigation included: plasma creatine kinase (CK) level, agility test, vertical jump test, isometric torque test, and perception of soreness.
So why are you confident that massage therapy is not going to backfire? Well, as I pointed out previously in this article, there is no evidence of direct anti-inflammatory effects as they have been ascribed to ice-baths or vitamin supplements that could blunt the necessary hormetic response to exercise. Rather than that, data from a recently published study by Andrzejewksi et al. suggest that repeated massage may contribute to processes of creation of new and development of already existing vascular networks in the skeletal muscle tissue during increased exercise", which is the exact opposite of the proven detrimental effects of ice-baths (Andrzejewski. 2015). It does thus appear very unlikely that the overall long-term effects of massage therapy are going to be detrimental. A long-term study with bodybuilding specific outcomes, like strength and hypertrophy is still necessary, because a low risk of negative effects does not imply that there are going to be increased gains in strength or size.
All variables were measured over 6 time periods: baseline, immediately after the DOMS inducing protocol, right after the massage, and 24, 48, and 72 h after the massage, the scientists describe as follows:
"30-min standardised supine massage was performed by a licensed massage therapist with 3 years of experience on the exercised/right thigh of participants in the massage group after 2 h following the muscle soreness inducing exercise protocol. To maintain consistency and reproducibility for the entire massage procedure, tape-recorded messages were announced to remind the therapist when to change the massage strokes being performed. Western massage techniques of effleurage, petrissage, and vibration were used.

While there are rumors that massage therapy may also help you shed bod weight, this has been shown only for different techniques: "Electro-Cut" Your Body Fat - Study Shows 5.6 cm and 4.9% Reduction in Waist & Body Fat in Young Women in 6 Weeks
Each massage began with 4 min of effleurage consisting of 2 min of light stroking with the palm around the knee, and 2 min of light stroking over the medial thigh. Effleurage was followed by petrissage, which consisted of 2 min of twohanded palm kneading of the anterior thigh muscles, 2 min of two-handed thumb kneading over the medial thigh, 2 min of circular two-handed lifting of the anterior thigh, 1 min of pressing and spreading the tissues perpendicular to the long axis of the thigh, and 1 min of rolling the fingertips over the anterior thigh muscles. Two minutes of vibration was added between the petrissage techniques of circular lifting of the anterior thigh muscles and pressing and spreading the tissues.

The massage was then concluded with 3 min of effleurage over the anterior and medial thigh. While massages were performed on the experimental group, participants of the control group were asked to remain seated and to maintain their normal passive recovery regime as well as to refrain from performing any additional exercises or stretches"
(Kargarfard. 2015).
What the scientists found when they analyzed their results was (a) the obvious, i.e. significant (P < .001) decreases in jumping, agility performance, and isometric torque, but significant (P < .001) increases in CK and muscle soreness levels in all subjects.
Will foam rolling do the same? Whether it will do the same would require future studies with direct comparisons. What I can tell you, though, is that studies by MacDonald et al (2014) and Pearcey et al. (2015) consistently showed similar results, i.e. decreased DOMS and accelerated recovery / preserved muscle function with foam rolling after intense workouts.
There was yet also (b) a significant difference between the control and the massage group who demonstrated a better recovery rate as evidenced by:
  • faster recovery of vertical jump performance and maximal muscle torque (measured when subjects were fixed w/ 90º of hip and knee flexion on an isokinetic dynamometer) from 24-72h in response to the  massage therapy,
  • reduced increases in creatine kinase (CK) levels, a relatively unspecific marker of muscle damage, after the massage therapy.
What was not observed was a meaningful difference in the agility test, where the pre-test difference was similar before and after the test and treatment.
Figure 1: Creatine kinase (CK | top, left), jump height / distance (bottom, left), agility test times (top, right) and visual analog scale rating for DOMS (bottom, right) for the two study groups (Kargarfard. 2015).
In view of the fact that the study wasn't blinded (for obvious reasons), it is also not clear how much of the subjective reduction in DOMs may just have happened in the subject's head. In conjunction with the previously mentioned faster recovery of performance markers and CK, though, it appears to be very reasonable to follow Kargarfard's conclusion that "As such, a post-exercise massage session can improve the exercise performance and recovery rate in male bodybuilders after intensive exercise" (Kargarfard. 2015).
Since the purported mechanism is very different, it's unlikely that there will be similarly negative long-term consequences as they've been observed w/ ice baths.
Bottom line: In spite of the lack of being double-blinded, the consistency of objective and subjective performance and DOMS markers can be considered sufficient evidence for the existnece of sign. short-term benefits of massage therapy on athletes' recovery.

If we assume my previously mentioned hypothesis that the accelerated manual removal of "debris" after workouts was much different from the anti-inflammatory effects of ice-baths / and cold water immersion therapy is correct, there is also no reason to believe that massage therapy would have a similarly detrimental long-term effect on the training-induced adaptation to exercise as we've recently seen them in response to ice-baths | Comment on Facebook!
References:

  • Ali, Rasooli S., et al. "Influence of massage, active and passive recovery on swimming performance and blood lactate." The Journal of sports medicine and physical fitness 52.2 (2012): 122-127.
  • Andersen, Lars L., et al. "Acute effects of massage or active exercise in relieving muscle soreness: Randomized controlled trial." The Journal of Strength & Conditioning Research 27.12 (2013): 3352-3359.
  • Andrzejewski, Waldemar, et al. "Increased skeletal muscle expression of VEGF induced by massage and exercise." Folia Histochemica et Cytobiologica 53.2 (2015): 145-151.
  • Bąkowski, Paweł, et al. "Effects of massage on delayed-onset muscle soreness." Polish Orthopedics and Traumatology 73.4 (2008): 261-265.
  • Kargarfard, M, et al. "Efficacy of massage on muscle soreness, perceived recovery, physiological restoration and physical performance in male bodybuilders." Journal of Sports Sciences (2015): Ahead of print.
  • MacDonald, Graham Z., et al. "An acute bout of self-myofascial release increases range of motion without a subsequent decrease in muscle activation or force." The Journal of Strength & Conditioning Research 27.3 (2013): 812-821.
  • MacDonald, Graham Z., et al. "Foam rolling as a recovery tool after an intense bout of physical activity." Med Sci Sports Exerc 46.1 (2014): 131-142.
  • Pearcey, Gregory EP, et al. "Foam rolling for delayed-onset muscle soreness and recovery of dynamic performance measures." Journal of athletic training 50.1 (2015): 5-13.
  • Urakawa, Susumu, et al. "Manual therapy ameliorates delayed‐onset muscle soreness and alters muscle metabolites in rats." Physiological reports 3.2 (2015): e12279.
  • Visconti, Lorenzo, et al. "Effect of massage on DOMS in ultramarathon runners: A pilot study." Journal of Bodywork and Movement Therapies (2014).

Intermittent Fasting Works, But is It Better Than "Regular" Dieting? What Do the Latest Reviews / Meta-Analyses Say?

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Don't eat unless this brunette,... ah, I mean her clock tells you to eat. That's intermittent fasting (IF) - well, at least one out of at least three versions of eating by the clock people call "intermittent fasting". Needless to say that this doesn't make it much easier to decide if IF works or not.
It has been some time since I wrote about "Intermittent Fasting" ("lean gains"-style, i.e. eat in a 6h-8h window everyday), "Fasting" (don't eat at all) and "Alternate Day Fasting" (eat very little / usually ~800kcal one day / and normal the next one, repeat). Against that background it is worth devoting a whole SuppVersity Research Update to the latest studies and reviews of IF and ADF.

In the corresponding papers, Tinsley and La Bounty review the "effects of intermittent fasting on body composition and clinical health markers in humans", Varady et al. discuss "the determinants of weight loss success with alternate day fasting" and Seimon et al. address the question whether "intermittent diets provide physiological benefits over continuous diets for weight loss?", as part of a short report in form of a systematic review of clinical trials.

So, where do I start? I guess it would be best to build the article around the most extensive and for many of you probably most interesting analysis by Seimon et al. that's about to be published in one of the next issues of Molecular and Cellular Endocrinology: "Do intermittent diets provide physiological benefits over continuous diets for weight loss? A systematic review of clinical trials" (Seimon. 2015)
Do you have to worry about muscle loss and metabolic damage, when you're fasting?

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Habits Determine Effects of Fasting

Breaking the Fast & the Brain

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review
Usually I don't do this, but in view of the tons of articles I have already written about Intermittent Fasting, I feel like it is possible to start with the conclusion which says that "[i]ntermittent fasting thus represents a valid – albeit apparently not superior – option to continuous energy restriction for weight loss." Accordingly, the question I still owe you an answer to is "WHY?", i.e.: "What makes intermittent fasting 'a valid' weight loss strategy?", and "Why is it 'valid - albeit nor superior'?" Well, the answers to these questions are neither straight forward nor can they be answered objectively. As every review and/or meta-analysis, Seimon's paper ends with the researchers' subjective interpretation of selected, objective data. Data from a total of 40 publications involving humans of any age or body mass index that had undergone a diet involving intermittent energy restriction, 12 with direct comparison to continuous energy restriction. What all of these studies have in common is that they measured one or more of the following variables: Body weight, body mass index, or body composition before and at the end of energy restriction.

Table 1: The Aguin study is one out of many that shows that both intermittent and chronic energy restriction work and produce statistically (see p-values) identical changes in body composition, size and relevant markers of lipid and glucose metabolism (Arguin. 2012)
What they did not share, though, was the type of "Intermittent Fasting". Practically speaking, this means that 31 of the 40 publications "involved ‘intermittent fasting’ of 1-7-day periods of severe energy restriction" - were thus rather "fasting" or "alternate day fasting" than classic "intermittent fasting" studies. More specifically: Seimon et al. also included studies like Arguin et al. (2012) in which the subjects were either dieting for 15 weeks at a moderate energy restriction or for 3 cycles of 5 week at higher energy deficits were interspersed by 3 cycles of 5 weeks on a calorically sufficient diet and the results were compared after each intervention, as well as one year thereafter. These obviously more important parameters are summarized in Table 1, and they don't show any inter-group differences.
How much weight / fat loss and health improvements can you expect? While the Seimon study is excellent for detail, Tinsley's and La Bounty's short review features the more concise overview of the figures - albeit with the same general message, i.e. "intermittent fasting (in the broadest sense) works, but whether it's more effective than continuous energy reductions must be determined on an individual level". This does not negate that (a) alternate-day fasting trials of 3 to 12 weeks in duration appear to be effective at reducing body weight ( 3%–7%), body fat ( 3–5.5 kg), total cholesterol ( 10%–21%), and triglycerides ( 14%–42%) in normal-weight, overweight, and obese humans, and (b) that whole-day fasting trials lasting 12 to 24 weeks also reduce body weight ( 3%–9%) and body fat, and favorably improve blood lipids ( 5%–20% reduction in total cholesterol and 17%–50% reduction in triglycerides). Research on time-restricted feeding aka "lean gains"-style intermittent fasting, on the other hand, is still "too limited" (ibid.) to draw clear conclusions.
Now, while the Arguin study is not correctly summarized in the tabular overview of all studies they reviewed, the most important information, i.e. the fact that the cyclic diet does not provide any significant advantages or disadvatages over continuous dieting is true. Based on the meta-analysis by Seimon et al., the following take-home messages can be stated:
  • The drop out rates were comparable for interventions involving intermittent energy restrictions (IER) and continuous energy restrictions (CER).
  • Significant reductions in body weight, size (waist, hip, etc.) and adiposity can be achieved with both intermittent energy restrictions (IER) and continuous energy restrictions (CER).
  • If we go by weight loss which happens to be the most frequently measured study outcome in Seimon's selection of studies, the results are comparable for IER and CER.
  • Study suggests: Your goals may determine whether a low or high fat diet is the better basis for your alternate day fasting fat loss diet | more
    A reduced drive to eat, on the other hand, appears to be a unique advantage of intermittent energy restrictions, where eating very little for a fixed time period appeared to be easier to handle for the subjects then the grazing that's part of many CER interventions.

    This is an important results, after all, one of the mainstream arguments against intermittent or alternate day fasting is that they will trigger an overcompensation on the (re-)feeding day - a phenomenon that was not observed.

    On the contrary, "participants only consuming an average of 95% of their calculated energy needs on feed days" (Seimon. 2015). This is particularly noteworthy because "this apparent suppression of the drive to eat occurred despite decreased circulating levels of the appetite-reducing hormone, leptin, following IER" (Seimon. 2015). Whether this is related to an increase in ketone bodies in the IER studies that was non-existent or less pronounced in the CER trials will still have to be elucidated, though.
  • A trend towards mood disturbance, tension, anger and confusion was observed in only one study. A study by Hussin et al. (2013) that was done in aging normal-weight men and the results of which stand in contrast to what Johnson et al. found in overweight subjects in 2007.
    Figure 1: Intermittent energy restrictions (IER) appear to be better suited for the obese, whose mood improves during th fast, while the mood of lean subjects decreases sign. (Hussin, 2013 & Johnson. 2007).
    In conjunction with the increased drop-out rates in Hussin's study, we may argue that a lack of triglyceride and FFA releasing adipose tissue may make IER interventions harder to adhere to - probably, because of a simple lack of available energy during the fast.
  • So, "Intermittent Fasting Does Now Make You Fat"? Do the Facebook Posts Lie? Not Necessarily, but Many People Forget that IF Works Only if it Reduces Your Energy Intake | more
    In view of the sign. reductions in leptin in IER interventions it is hardly surprising that Seimon et al. didn't find convincing evidence that IER would ameliorate the reduction in resting metabolic rate that's an inevitable (temporary) side effect of any dieting regimen.

    One (de Groot. 1989) out of three studies that made a direct comparison between the two even found a further reduction in resting metabolic rate (RER) in the IER group, the others found no difference (Hill. 1989; Harvie. 2011; Arguin. 2012). Overall, it would yet appear as if any potentially existing difference was negligible.

    Other metabolic adaptations such as a reduced IGF1 production were observed only in trials where the subjects fasted with liquid meals (Kroeger. 2012).
  • No difference and on average comparable improvements in glucose homeostasis were observed in the 20 studies that tested respective parameters in detail. While there are individual studies that suggest advantages for one or another method, the overall picture that emerges is that there are no systematic differences - a conclusion that would also explain the - in parts - contradictory results from pertinent studies.
  • Lastly, it must not go unmentioned that the addition of exercise to IER will make it - just as it is the case for CER, by the way - more effective and will thus shed more fat (and maintain more lean mass) than IER alone.
    Figure 2: The combination of alternate day fasting and exercise reduces uncontrolled and emotional eating in 64 obese subjects over the course of a 12-week study (Bhutani. 2013).
    Somewhat surprising, but in view of the overall anti-appetite effect of fasting not impossible is that the combination of exercise with IER also reduced the subjects' craving for uncontrolled and emotional overeating (Bhutani. 2013).
In view of the fact that only 12 of the 40 publications included in Seimon's review directly compared IER with CER, it is yet important to remember that we are far from being able to tell who will benefit most and who least from "intermittent fasting" (in the broadest sense). If you review the above summary of the results, you will yet have to agree that it would appear as if men and women who still have a ton of weight to lose could fare better with intermittent or alternate day fasting, while lean individuals may, but don't necessarily have to struggle with the lack of readily available energy during the fast.
Figure 3: While race matters and Caucasians appear to do much better on alternate day fasting regimen, the baseline body weight (and BMI | not shown) doesn't make a difference in the 4 ADF trials Varady et al. reviewed (2015).
At least in the 8-week ADF studies Varady et al. reviewed in their previously mentioned short report in Obesity Research and Clinical Practice, however, the initial body weight was not a good predictor of weight loss success. Rather than that, "[s]ubjects aged 50—59 y achieved greater (P = 0.01) weight loss than other age groups" and "Caucasian subjects achieved greater (P = 0.03) weight loss than other races" (Varady. 2015) with the alternate day (ADF) version of "intermittent fasting".

With only 5 out of the 40 studies in Seimon's review having a follow-up and no follow-up in any of the ADF studies in the previously cited short report by Varady et al. (2015), the long-term benefits or detriments must be considered largely under-researched, at the moment, too.
Evidence From the Metabolic Ward: 1.6-2.4g/kg Protein Turn Short Term Weight Loss Intervention into a Fat Loss Diet. 1.6g/kg not 2.4g/kg Offers Optimal Muscle Protection | learn more!
So what's the verdict then? Well, firstly: Intermittent fasting works. It's not exactly well-researched, though. Accordingly, it is difficult to say (a) who would benefit most  / lest, (b) which form of intermittent fasting ("lean gains" 6-8h window everyday vs. alternate day vs. total fasting) works best and (c) how (a) and (b) interact with with each other: It is for example well possible that the discrepancy between the effect on appetite in lean vs. obese individuals I highlighted in the main body body of this article occurs only with simple (as in Hussin. 2013), yet not with more complex methods of fasting as ADF or the 6-8h fasting window at a freely chosen point in time.

Overall, the best advise I can give you is thus to try if and which type of intermittent fasting works for you. What I cannot recommend is any form of extended fasting, where you are consuming very low amounts of energy (like 400-600kcal) for more than just one day. In addition, you want to make sure to lift weight and consume enough (~1.5g/kg) protein even on fasting days to conserve lean muscle mass | Comment on Facebook!
References:
  • Arguin, Hélene, et al. "Short-and long-term effects of continuous versus intermittent restrictive diet approaches on body composition and the metabolic profile in overweight and obese postmenopausal women: a pilot study." Menopause 19.8 (2012): 870-876.
  • Bhutani, Surabhi, et al. "Effect of exercising while fasting on eating behaviors and food intake." J Int Soc Sports Nutr 10.1 (2013): 50.
  • de Groot, Lisette CPGM, et al. "Adaptation of energy metabolism of overweight women to alternating and continuous low energy intake." The American journal of clinical nutrition 50.6 (1989): 1314-1323.
  • Harvie, Michelle N., et al. "The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women." International journal of obesity 35.5 (2011): 714-727.
  • Hill, James O., et al. "Evaluation of an alternating-calorie diet with and without exercise in the treatment of obesity." The American journal of clinical nutrition 50.2 (1989): 248-254.
  • Hussin, N. M., et al. "Efficacy of fasting and calorie restriction (FCR) on mood and depression among ageing men." The journal of nutrition, health & aging 17.8 (2013): 674-680.
  • Johnson, James B., et al. "Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma." Free Radical Biology and Medicine 42.5 (2007): 665-674.
  • Seimon, Radhika V., et al. "Do intermittent diets provide physiological benefits over continuous diets for weight loss? A systematic review of clinical trials." Molecular and Cellular Endocrinology (2015).
  • Varady, Krista A., et al. "Determinants of weight loss success with alternate day fasting." Obesity Research & Clinical Practice (2015).

The Way You Train Shapes Your Muscle Size and Function - Study in Powerlifters, Bodybuilders & Controls Suggests Effects Go Beyond Hypertrophy & MHC Fiber Composition

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Don't worry, this exercise is not going to reverse all the effects of your training. Still, in view of the intriguing results of the study at hand, it would be interesting if the fiber-type unspecific effects in powerlifters are reversed when you stop powerlifting / exercise altogether and/or start lifting with higher volumes and lower intensities (bodybuilding style volume training).
There are visible and invisible differences between bodybuilders, powerlifters and normal men. The former ones are so obvious that it wouldn't be very interesting to address them in a study. The latter, on the other hand, are, other than you'd expect, hardly researched, but - as the results of a recent study from the Manchester Metropolitan University, and a bunch of other European Universities and research centers shows - more pronounced and significantly more fundamental than some of you may have thought.

As Meijer et al. point out in the introduction to their soon-to-be-published paper in the peer-reviewed scientific journal Experimental Physiology, the performance of a power athlete is largely determined by two traits: the maximal force and power generating capacity of the recruited muscles, and the ability to maintain force and power for a prolonged period of high intensity efforts.
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Needless to say that the peak muscle power and force will to some extent dependent on muscle volume and physiological cross-sectional area of the muscle, respectively. In accordance with the above definition of what one's power will depend on, though, the mitochondrial density in the recruited muscle fibres does yet figure as well. I mean, you don't want to run out of steam on your 3rd rep of squats, do you? That's what I thought. Thus, Meijer et al. are right to point out that "[i]deally, an  athlete seeks to maximize both muscle power and endurance" (Meijer. 2015).

Myostatin Limits Muscle Hypertrophy in Everyone! Even Normal Gymrats May Benefit from Blockers, if any of them Actually Worked  Learn more!
The problem with this maxim, however, is that you cannot maximize both, the fibre cross-sectional area (FCSA) and its mitochondrial density. In fact, studies suggest that the FCSA at a given mitochondrial density is limited by the maximal extracellular oxygen tension (Van der Laarse et al., 1997; Wessel et al., 2010) or the myonuclear domain sizes (learn more).

It is thus only logical that studies on myostatin negative animals show that limit the amount of hypertrophy beyond which it becomes disadvantageous for sustainable power (learn more). Weak big, vs. small(er), yet strong muscles. That sounds like powerlifting vs. bodybuilding, right?
Although the fiber composition of bodybuilders, gymrats, endurance rowers and sedentary control differs, it is not - according to the results of the study at hand - the only and maybe not even an important determinant of maximal power (data based on Jürimäe. 1997)
Hold on, why's that even newsworthy? As the authors themselves highlight, their study is the first to show that "long-term resistance exercise, represented here by power athletes and body builders, increases the force generating capacity of muscle fibres" (Meijer. 2015). Now, this alone is not really exciting, what is intriguing, though, is that "this increase in force was only in power athletes associated with a significant increase in the power generating capacity of single muscle fibres" (ibid.) - and thus largely independent of the fiber type composition of the muscles (learn more).

Accordingly, on single fiber basis, the power generating capacity of a body builder (BB) is not only lower than that of a powerlifter, it's actually not even higher than that of an untrained individual (C) - and that despite the fact that the individual muscle fibers are significantly larger. As the authors further explain, "[t]his unexpected observation was explicable by a lower fiber specific tension in BB compared to C fibres". In this context it is important to point out that the C and PA group in the study at hand performed a comparable, albeit relatively low amount of aerobic exercise, it is thus "likely that the effects shown in PA can be attributed to the high-intensity low-volume resistance training," (ibid.), alone.
Well, that's obviously what Meijer et al. thought, as well, when they phrased the following hypotheses about the way the muscle fiber specific tension (F0) of 12 male bodybuilders (BB | BB: 29.8 ± 4.8y; 177.8 ± 4.1 cm; 91.7 ± 13.4 kg), 6 male powerlifters / power athlete (PA | 23.4 ± 3.9 y; 185.0 ± 4.3 cm; 103.0 ± 7.3 kg) and 14 non-competitive / weight lifting controls (C | 24.0 ± 3.5 y; 180.9 ± 5.3 cm; 77.9 ± 6.3 kg) differ in the introduction to their latest paper:
"PAs is characterized by high-intensity low-volume resistance training with supplemental aerobic exercise. Since BBs train for bulk and PAs for function we hypothesize that fibres from PAs will have a higher specific power and F0 than those from BBs. We expect an increase in specific power and F0 in PAs and BBs (for BBs especially in type II fibres) compared to C." (Meijer. 2015). 
To test whether this hypothesis is correct, the researchers compared muscle fibre contractile properties of biopsies taken from m. vastus lateralis of 12 bodybuilders (BB; low- to moderate-intensity high-volume resistance training), 6 power athletes (PA; high-intensity low-volume combined with aerobic training) and 14 controls (C). To do that you have to take samples from the muscle and test the maximal isotonic contractions on a single muscle fibre in vitro.
Figure 1: Typical examples of three IIA muscle fibres. Circles represent the measured force-velocity data. The continuous line shows the fitted force-velocity curve and the dashed line shows force-power curve (top). Specific tension of skinned m. vastus lateralis fibres is inversely related to muscle fibre cross-sectional area (bottom) - For both rows of data: Non-resistance trained controls (left), bodybuilders (middle), power athletes (right | Meijer. 2015).
As the data in Figure 1 shows, the scientists' analysis of their subjects' muscle fibers produced unsurprising and surprising results:
  • BBS have larger muscle fibers (unsurprising) - The fibre cross-sectional area (FCSA) was 67% and 88% (P<0.01) larger in BB than in PA and C, respectively.
  • There's no difference in fiber size between C and PA (surprising?) - Unlike the difference between bodybuilders, power athletes and control, the existing difference in fiber size between PA and C did not reach statistical significance. 
  • BB and PA fibres are stronger (unsurprsing) - BB and PA fibers developed a higher maximal isometric tensions (32%, 50%, P < 0.01) than those of C. 
  • BB & C fibers are significantly weaker than PA fibers (unsurprising) - The specific tension (F0) of BB fibres was 62% and 41% lower than that of PA and C fibres (P < 0.05), respectively. 
  • The increased peak power of PA fibres was not related to fibre type (surprising) - Irrespective of fibre type, peak power (P) of PA fibres was 58% higher than that of BB fibres (P < 0.05), while BB fibres –despite considerable hypertrophy- had similar PP as C fibres. 
With the latter result standing in contrast to the long-held believe that training induced changes in fiber composition like an increase in the proportion of power-specific MHC IIa,b fibers in power athletes and an increase in "enduring" type II fibers (MHC IIx) in bodybuilders were responsible for the strength and power differences, the study at hand provides initial evidence that that the effects of the way you train go way beyond selective type IIa,b vs. type IIx hypertrophy.
Sedentary Individuals, Endurance & Strength Athletes: Their Fitness, Training & Hormones and How They Effect the Ratio of Fast- to Slow-Twitch Fibers | learn more.
Bottom line: The study at hand provides the first reliable evidence that high-intensity low-volume resistance training as it is performed by power lifters triggers significantly different adaptational processes than the low- to moderate-intensity high-volume resistance of bodybuilders - adaptational processes that go beyond the fiber-specific hypertrophy effects that are responsible for the alleged muscle fiber composition changes in trainees.

Since the former is a completely novel result, we can only speculate about the underlying mechanism. Meijer et al. "postulate that the decrease in specific tension is caused by differences in myofibrillar density and/or post-translational modifications of contractile proteins" (Meijer. 2015).

That's obviously a very unspecific hypothesis that warrants further investigation and elaboration in future studies; not just to confirm it, but also to elucidate (a) the time it takes for these changes to take place and (b) whether they are reversible by (1) changing the way you train (2) staying away from the gym, altogether | Comment on Facebook!
References:
  • Jürimäe, Jaak, et al. "Differences in muscle contractile characteristics among bodybuilders, endurance trainers and control subjects." European journal of applied physiology and occupational physiology 75.4 (1997): 357-362.
  • Meijer et al. "Single muscle fibre contractile properties differ between bodybuilders, power athletes and controls." Experimental Physiology (2015): Accepted article.
  • Van Der Laarse, W. J., et al. "Size principle of striated muscle cells." Netherlands journal of zoology 48.3 (1997): 213-223.
  • Van Wessel, T., et al. "The muscle fiber type–fiber size paradox: hypertrophy or oxidative metabolism?." European journal of applied physiology 110.4 (2010): 665-694.

Blood Flow Restriction in Athletes: Did We Get it All Wrong? Must BFR-Cuffs be Worn After, not During Each Set?

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If that's you. It's well possible that you've done it all wrong. Wearing the cuffs after the set may be the way to go!
You may have followed up on my recent suggested read in the SuppVersity Facebook News and read up on the recent scientific debate on the (non-)usefulness of training with cuffs (BFR-style). Well, after reading the full text of a recent study by Conor W. Taylor et al. (2015), I have to say: Maybe we have only done it wrong.

In their study, the researchers from the Loughborough University in Leicestershire had their subjects, 28 healthy trained males who were cycling 120 ± 66 km per week, all cuffed up after each set of a standardized sprint training. That's very dufferent from trying to sprint with cuffs on your legs (and usually reduced intensity) and appears to be - that's at least what the study results suggest - a potential game-changer.
You can learn more about BFR and Hypoxia Training at the SuppVersity

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Now, the good news is: The study involved both an acute and chronic exercise + BFR study of the effects of post-spring-training blood flow restriction.
  • In Study 1, a between groups design determined whether 4 weeks (2 d/wk) of SIT (repeated 30 s maximal sprint cycling) combined with post-exercise blood flow restriction (BFR) enhanced maximal oxygen uptake (VO2max) and 15km cycling time trial performance (15km-TT) compared to SIT alone (CON) in trained individuals.
  • In Study 2, using a repeated measures design, participants performed an acute bout of either BFR or CON. Muscle biopsies were taken before and after exercise to examine the activation of signalling pathways regulating angiogenesis and mitochondrial biogenesis.
As a science expert you'll know that study 2 probably wouldn't have been done if the results of Study 1 had not been encouraging.
Figure 1: Pre- to post-changes in VO2max (absolute, top-right), relative (top-left), MAP (bottom-left), 15k time trial (bottom-right) | I marked the individuals who saw positive and negative effects for you, the # on the buttons indicate the number of subjects who benefited (green) or saw no / detrimental effects (orange | original data from Taylor. 2015).
"Encouraging", in this case, means that the scientists observed a highly significant VO2max with post-workout BFR by 4.5% (P = 0.01) but was unchanged after CON.
So, does the increase in VO2 have anything to do with my gainz? Directly? No. But if there's an effect on hypertrophy it would - just as the effect on VO2 found in the study at hand - depend on increases in the stress response. Now, the more recent studies have shown that the necessary reduction in weight lifted when you do it with cuffs makes it practically useless for athletes. So, in conjunction with the study at hand, it's only logical to ASSUME that using the hypoxic stress after a set COULD provide an ADDITIVE stimulus (normal BFR training takes away from the regular stimulus, because it will.force athletes to refuce the weights and cannot fully compensate for that | see the results of this study.
The small advantage in the 15k time trial, on the other hand, did not reach statistical significance. That's "bad news", but the trend indicates that this might change with long(er) term studies.
Figure 2: Changes (%) in physiological and performance variables before and after CON and BFR training interventions (Taylor. 2015).
Whether that may change with a longer-term study will still have to be elucidated. What appears to be certain, though, is that the existing difference is not mediated by changes in PGC-1α, VEGF and VEGFR-2 mRNA expression between protocols. In fact, of all parameters the scientists tested to identify the underlying mechanism only the  mRNA levels of HIF-1α, the hypoxia-inducible factor 1-alpha, of which a recent paper by Lindholm and Rundquist (2015) highlights that it would be otherwise attenuated with long-term endurance exercise and thus lead to a blunted response to long-term exercise training (that's why rookies see fast results and pros only marginal results), differed significantly between groups (P = 0.04) 3 h after the cuffs were applied to the subject's legs.
Bottom line: While it is possible that the differences the scientists observed were triggered by BFR induced extra-stress (namely hypoxia, thus increases in Hypoxia-inducible factor 1-alpha), we will need additional (longer-term) studies to prove practically relevant improvements in time-trial performance and identify a definitive mechanism.

The benefits of blood flow restriction in healthy athletes may be less pronounced than the advocates would have it. If reversing the order of exercise and applying the cuff can solve that, this would be awesome!
With that being said, the results - although not fully convincing, yet - are quite exciting. After all, they really suggest that instead of training with cuffs, athletes who want to benefit from the additional low oxygen stress would have to copy the protocol of the study at hand and thus apply lower limb blood flow restriction within 15s of each sprint... or after each set of leg curls or squats? Well, that's a question we cannot answer based on the study at hand, but it would certainly be interesting to test what would happen if you applied the cuffs right after a set of biceps curls. Well, as you can see, there's still a lot of research to be done and as you know, the SuppVersity is going to be where you can learn about the results first ;-) | Comment on Facebook!
References:
  • Lindholm & Rundqist, et al. "Skeletal muscle HIF-1 and exercise." Experimental Physiology (2015): Accepted Article.
  • Taylor, et al. "Acute and chronic effect of sprint interval training combined with post-exercise blood flow restriction in trained individuals." Experimental Physiology (2015): Accepted Article.

Testosterone Gel Augments Increases in Lean Mass Gains (+3.9kg in 6 Months) in Older Intensely Training Men, but Testim Blocks Decrease in Marker of Heart Disease Risk

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Building muscle becomes increasingly harder, the older you get. While there's no evidence that any of the overpriced natty T-boosters can solve this problem, Testim(R) can. That's at least what a recent Danish study shows.
If you believe in what you read in the ads for testosterone boosters, all you'd have to do to get jacked was to increase your testosterone levels by a few percentages.

In view of the fact that it took transdermal testosterone gels and a 100% increase in bioavailable testosterone (most T-boosters boast of boosting total testosterone by 20-40%) in a recent study from the Odense University Hospital and the University of Southern Denmark (Glintborg. 2015) to trigger - albeit significantly - muscle gains of +3.5 kg in older subjects on a high intensity resistance training regimen, it is highly questionable how capable the average "natural muscle builder" really is ... but let's not rant and rather take a look at what really works (for the elderly, at least).
If you want to build muscle forget T-booster and optimize your protein intake 

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So, the study at hand was actually not designed to elucidate the effects of testosterone on lean mass gains or fat loss, but rather to investigate testosterone's ability to augment or block the exercise-induced reductions in soluble CD36 a protein. CD36??? Well, I have to admit this is not exactly the best known inflammatory protein, but in view of the fact that it has been associated with the obesity induced increase in atherosclerosis risk (Handberg. 2006), it is an important one.

To quantify said effects, a group of Danish scientists measured the changes in soluble CD36 (sCD36) and body composition in response to a testosterone treatment (TT) and/or strength training (ST) in men with low-normal testosterone levels (Glintborg. 2015).
Table 1: Baseline characteristics of the subjects | TT, testosterone treatment; (ST) strength training. Data presented as median (interquartile range); No significant differences, Mann-Whitney test between groups. Bio T, Bioavailable testosterone; LEFM, lower extremity fat mass; SAT, subc. adipose tissue; VAT, visc. adipose tissue (Glintborg. 2015).
All in all, the researchers recruited 54 men aged 60–78 years with testosterone levels below 7.3 nmol/L (that's the usual cut-off for hypogonadism differential diagnosis) and waist circumferences above 94 cm for a randomized double-blinded, placebo-controlled study in which the subjects were assigned to four different groups:
  • the testosterone aka TT group in which the subjects were treated with 50–100 mg/day of testosterone from Testim per day (n= 20),
  • the placebo aka PLA group in which the subjects were treated in which the subjects received an identically looking placebo supplement (n= 18),
  • the strength training aka ST group in which the subjects followed a standardized progressive heavy strength training program (n= 16), and
  • the combined groups with ST + TT or ST + PLA
To determine the success of the interventions, the scientists used both, the levels of soluble CD36 (sCD36) and determined the total and regional fat mass by Dual X-ray absorptiometry (DEXA) and magnetic resonance imaging (MRI) after three (half-way) and six months (end of the intervention).
Figure 1: Changes in body composition (left) and bioavailable testosterone levels (right | Glintborg. 2015).
As you can see in Figure 1, the testosterone treatment augmented the increases in lean mass in response to the standardized high intensity resistance training protocol that involved 3 supervised resistance training workouts per week (minimum two workouts) consisting of 5-min bicycling for warm-up (approximately 100 W) plus a standardized full body workouts (6-10 reps at the respective RMs, weights were increased progressively) with leg presses, knee extensions, leg curls, chest presses, latissimus pull downs, back extensions, and crunches.

And the effect was not just statistically, but also practically significant: Instead of the meager 0.6 kg without testosterone treatment, the subjects on T-gel gained a whopping 4.5 kg (that's +650%). That's truly impressive.
Dose response relationship of muscle gain (in kg) per mg of testosterone enanthate from previous SV article; the white line indicates a dose that would probably have produce testosterone levels identical to baseline (calculated based on Bhasin. 2001 | learn more!)
Beware of jumping to conclusions! In view of the age and the low baseline testosterone levels of the subjects it is unwarranted to assume that you or anyone else in the prime of his year (and testosterone production ;-) will see the same, or even similar increases in size gains as the 60y+ agers in the study at hand. Addition due to user question: It is also not necessarily certain that the same results will be seen with any other form of administering T. If you achieve stable high-normal T levels with injectables, though, it is pretty sure that people with initially low T-levels will benefit. I highly suggest you read my article"Quantifying the Big T" if you want to know more about the dose-response ratio (also in young men) | read it!
What was less impressive were the changes in body fat: While both TT and ST had beneficial effects on the total amount of body fat (-1.4kg in the TT group vs. +1.2 kg, -0.8kg and -0.7kg in the PLA, ST and ST + TT groups, respectively), there were no significant decreases in waist circumference a primary marker of metabolic disease risk and indicative of the amount of "bad" visceral fat you're carrying around - a result of which we are going to see that it is in line with the lack of effect on the previously mentioned artherosclerosis risk marker CD36.
Figure 2: In spite of the fact that the atherosclerosis risk factor sCD36 usually correlates with obesity, its reduction by exercise was blunted by the provision of exogenous testosterone even though the fat loss in the ST + TT group did not differ significantly from that in the ST + PLA (testosterone-free) training group (Glintborg. 2015).
While the latter, i.e. CD36 and thus the putative artherosclerosis risk, improved significantly in the resistance training group (without T-gel), the addition of 50-100mg of transdermal testosterone appears to reverse or impair the exercise-induced improvements in artherosclerosis risk and entail the risk of an unwanted increase in this allegedly important CVD risk marker. The obvious question is thus: How significant is the increase in sCD36 in the testosterone treated "best+ agers"?
Figure 3: Scientists believe that the association between CD36, atherosclerosis, diabetes and CVD is mediated by its effects on macrophage foam cell formation (Febbraio. 2001).
So, is TRT dangerous? Well, atherosclerosis is only one out of several diseases in which sCD36 is elevated. Increased CD36 has also been associated with the development of metabolic diseases such as type 2 diabetes, and overall cardiovascular disease (Febbraio. 2001). In view of the fact that this correlation appears to have a mechanistic background that relates to the way CD36 stimulates macrophage foam cell formation, it is hard to discount the ill effects of testosterone on CD36 as irrelevant. Against that background, we would yet have to expect that studies investigating the long-term effects of testosterone treatment on atherosclerosis and CVD risk show distinct risk increases. This, however, is not the case - at least not consistently.

Rather than being associated with a distinct increase in CVD risk, the available data on the effects of testosterone treatment on heart health shows both positive, as well as negative effects (Haddad. 2007). Along with the publication of several very recent studies, an updated meta-analysis by Morgentaler et al. (2015) even suggests that the tides, which have long been "anti-TRT" are now turning so that the "[c]urrently available evidence weakly supports the inference that testosterone use in men is not associated with important cardiovascular effects" (Morgentaler. 2015).

Eventually, we or rather patients and clinicians will yet need more and larger randomized trials of TRT being used in men at risk for cardiovascular disease to better inform the safety of long-term testosterone use. Studies that measure only the short-term response of alleged markers of CVD risk, such as CD36 in the study at hand, are eventually of little use, when it comes to finding a definitive answers to the question whether TRT increases CVD risk. What they can tell us, though, is that TRT is a powerful tool to alleviate and reverse the age-related decline in muscle mass - in isolation and, even more so, in conjunction with high intensity resistance training | Comment!
References:
  • Bhasin, Shalender, et al. "Testosterone dose-response relationships in healthy young men." American Journal of Physiology-Endocrinology And Metabolism 281.6 (2001): E1172-E1181.
  • Febbraio, Maria, David P. Hajjar, and Roy L. Silverstein. "CD36: a class B scavenger receptor involved in angiogenesis, atherosclerosis, inflammation, and lipid metabolism." Journal of Clinical Investigation 108.6 (2001): 785.
  • Glintborg, Dorte, et al. "Differential effects of strength training and testosterone treatment on soluble CD36 in aging men: Possible relation to changes in body composition." Scandinavian journal of clinical and laboratory investigation ahead-of-print (2015): 1-8.
  • Haddad, Rudy M., et al. "Testosterone and cardiovascular risk in men: a systematic review and meta-analysis of randomized placebo-controlled trials." Mayo Clinic Proceedings. Vol. 82. No. 1. Elsevier, 2007.
  • Handberg, Aase, et al. "Identification of the Oxidized Low-Density Lipoprotein Scavenger Receptor CD36 in Plasma A Novel Marker of Insulin Resistance." Circulation 114.11 (2006): 1169-1176.
  • Kvorning, Thue, et al. "Mechanical Muscle Function and Lean Body Mass During Supervised Strength Training and Testosterone Therapy in Aging Men with Low‐Normal Testosterone Levels." Journal of the American Geriatrics Society 61.6 (2013): 957-962.
  • Morgentaler, Abraham, et al. "Testosterone therapy and cardiovascular risk: advances and controversies." Mayo Clinic Proceedings. Vol. 90. No. 2. Elsevier, 2015.

Vitargo™, Red Bull™ + Co. Research - Are They Worth It? Beef Can Keep Up W/ Whey For Gains! "Creatine Loading" = Too Much of a Good Thing - ISSN Research Review '15 #1

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When you're running on a treadmill it obviously takes more than one serving of Red Bull or other commercial energy drinks to kickstart your workout performance | learn more below.
Initially I wanted to cherry pick only the most interesting study results that were presented in form of of poster presentations at the Twelfth International Society of Sports Nutrition (ISSN) Conference and Expo in 2015. After looking at the research that is - as of now - only available in form of (albeit often detailed) abstracts, I decided that there are way too many interesting studies to cover only three of them in depth or all of them only cursory. Accordingly, I decided to start a SuppVersity Mini Special with this being the first out of 3-4 issues in which I will briefly discuss the most significant results of those of the roughly two dozen studies, I (a) believe are of greatest interest to you and (b) feel comfortable talking about without having all the details in form of the still to be published full texts.
Read more about ISSN and other studies at the SuppVersity

Vitargo, Red Bull, Creatine & More | ISSN15 #1

Pump Supps & Synephrine & More | ISSN15 #2

High Protein, Body Comp & More | ISSN15 #3

Pre-Exhaustion Exhausts Your Growth Potential

Full ROM ➯ Full Gains - Form Counts!

Body Pump, Cardio & Exercise Expenditure
  • The latest research on Vitargo(TM) -- The mere fact that the latest study on Vitargo(TM) was presented in "three servings", on the latest ISSN meeting, i.e. (1) on the glucose and insulin response (Almada. 2015), (2) on the incretin response (Anzalone. 2015) and (3) on the power output during a subsequent bout of resistance exercise (Van Eck. 2015), could raise some concerns about the objectivity of the results, but is as Patrick Jacobs kindly reminded me common scientific practice.. So, let's put the skepticism aside and take a look at the study design and results.

    Post-Workout Glycogen Repletion | Read the my overview article.
    Sixteen resistance trained men participated in a double-blind, placebo-controlled, randomized crossover study, which consisted of three testing sessions, each separated by one week. In sessions 1-3, subjects completed a glycogen depleting cycling bout of 60 minutes at 70% VO2 max, followed by six, one-minute sprints at 120% VO2 max.

    Immediately post-exercise subjects ingested a placebo (PLA), or a low molecular (LMW) or high molecular weight (HMW) CHO (=Vitargo(TM)) solution (10%) providing 1.2g/kg body weight CHO; assigned randomly. Blood samples were taken prior to ingestion and every ten minutes for 2h.

    For the "first" and "second" serving of the study this was enough. These mini-presentations dealt with the insulin, glucose and incretin response to the two supplements, only. For the "third serving", however, the scientists included performance data from a subsequent bout of exercise, during which the participants did 5 sets of 10 repetitions of back squats (75% 1RM) "as explosively as possible" (if subjects paused for more than 2 seconds or were unable to complete a rep, resistance was lowered by 13.6 kg | Van Eck. 2015).
    Figure 1: Overview of the most relevant results (LMW = low molecular weight CHO vs. HMW = Vitargo (TM) high molecular weight CHO) from Almada (2015), Anzalone (2015) and Van Eck (2015).
    As you can see in my overview of the most relevant results, the scientists did not find practically meaningful differences in study I-II. In study III, which compared the effects of low to high molecular weight carbohydrates (LMW vs. HMW) on squat performance 2h after the glycogen-depleting workout, this was slightly different:
    "HMW conferred a likely beneficial effect in Sets 4 and 5 (92.5% and 88.7% likelihood, respectively), compared to PLA; while ingestion of LMW conferred only a possibly beneficial effect (68.7%) and likely beneficial effect (83.9%) in Sets 4 and 5, respectively" (Van Eck. 2015).
    And still, if you read the conclusion, "the ingestion of a HMW CHO solution providing 1.2 g/kg CHO may allow athletes to sustain power output in a subsequent resistance training session when time between training sessions is limited" (Van Eck. 2015), carefully, you will notice the words "likely" and "possibly" which signify the putative nature of the effect. What may be even more relevant than that, is yet that few of you will do glycogen-depleting exercises at 4:00 pm and hit the gym again for an intense leg workout at 6:00 pm. Accordingly, the practical relevance of the "sustained power output" Van Eck et al. observed is probably restricted to a small group of professional athletes. For people who fall into this category or strength athletes training twice a day, though, using Vitargo (TM) may in fact offer significant benefits.
  • Beef and whey support lean mass gains similarly effectively -- If you are asking yourself if beef isolate protein is a good or at least decent replacement for whey, the post-workout protein supplementation "gold standard" some people can't use due to its (albeit low) lactose content, a recent study from the University of Tampa (Sharp. 2015) has the answer you are looking for.
    Figure 2: Relative improvements in muscle size (hypertrophy) and body fat (fat loss) in response to beef isolate or whey protein supplementation; expressed relative to maltodextrin placebo (Sharp. 2015).
    As the data in Figure 2 tells you, it will make a good replacement! If we go by the average increase in lean mass and loss of fat mass, the beef isolate that was consumed in amounts of 2x20g per day either immediately after each of the 5 weekly workouts (3 resistance training, 2 cardio; 8 weeks total, daily undulating periodization) or at a similar time in the day, you may even argue that the beef protein had the overhand over its "milky" competitor. If we take the individual variations into account, though, the 1% lean mass and almost 3% fat loss advantage (DXA values) of the beef protein turns out to be statistically non-singifican.

    The same goes for differences in strength gains, of which the researchers found that they were identical not just in the two supplement, but also in the supplement and control groups. The lack of additional power during the bench press test may, as the researchers point out, be ascribed to both increases in neural and morphological adaptations" (Sharp. 2015) which would "negate" (ibid.), or as I would phrase it, 'override' potential additive effects of any of the protein supplements (whey and beef, alike).
  • Energy drinks a waste of money on the treadmill? At first sight, the results of the latest study by Sanders et al. (2015) do in fact suggest that energy drinks were a total waste of money for those of you who are consuming them before a regular cardio workout on the treadmill. After all, none of the tested drinks lead to statistically significant improvements in either perceived treadmill exercise performance or running economy assessed via oxygen consumption at 70% treadmill exercise.
In contrast to treadmill running, the performance during a cycling time-trial can be improved by the consumption of an energy drink - a potential explanation for the difference may be that the subjects in the Ivy study consumed 2x  more Red Bull than the subjects in Sanders' study.
Energy drinks don't work? Well, the overall research shows a more diverse picture. While a previous study by Astorino et al. (2012) and a similar study by Candow et al. (2009) that tested the effects of Red Bull on repeated sprint performance and its effects on time to exhaustion, respectively, yielded similarly disappointing results, Ivy et al. (2009) and Forbes et al. (2007) found benefits. More specifically, the researchers observed significant increases in upper body muscle endurance (yet no effect on anaerobic peak or average power during repeated Wingate cycling tests in young healthy adults | Forbes. 2007) and improved cycling time-trial performance (without concomitant increase in perceived exertion | Ivy. 2009) - albeit with 2x more Red Bull than in the study at hand (500ml vs. 250ml).
  • Now, some of you may argue that all you care about when you buy an energy drink is that it makes it easier for you to hit your target time on the treadmill. Well, I can understand that, but in view of the fact that neither of the caffeine laden 8.4 oz. Red Bull®, 16 oz. Monster Energy ®, 2 oz. 5-hour ENERGY® drinks affected the subjects subjective rates of perceived exertion, it does appear questionable that these drinks can actually help you.

    It does thus stand to reason that Sanders et al. conclude that the "results [of their latest study] do not support manufacturers' claims regarding their product's ability to boost performance" (Sanders. 2015). The scientists are yet also right that it would be necessary to find out whether time trial or time to exhaustion sprint and endurance performance benefit, as respective studies may be better suited to reliably "assess if these energy drinks can, in fact, improve exercise performance" (ibid.) - and in view of the fact that previous studies with corresponding outcomes yielded conflicting results (see blue box above), I can fully subscribe to that: We need more (non-sponsored) quality studies ;-)
  • More evidence that creatine loading is not the way to go -- In Gann et al.'s latest study, fourteen (Cr = 7, Pl = 7) non-resistance-trained (i.e. < thrice weekly, 1 year prior) men between the ages of 18-30 were randomly assigned by age and body weight to orally ingest a powdered dextrose placebo or creatine monohydrate (Gann. 2015).

    After baseline strength and body composition testing procedures, participants ingested creatine or placebo at a dose of 0.3g/kg lean body mass/day (≈ 20-25g/day) for a 5 day loading phase immediately followed by a 42-day maintenance phase at a dose of 0.075g/kg lean body mass/day (≈ 5-7g/day). The participants followed a periodized 4 day per week resistance-training program split into two upper body and two lower body workouts per week, for a total of 7 weeks. Blood and muscle samples were obtained at Day 0, 6, 27, and 48. Statistical analyses were performed utilizing separate two-way ANOVA for each criterion variable employing a probability level of ≤ 0.05.
    Figure 3: Don't be fooled by shiny ads! While there is evidence that some forms of creatine will be faster absorbed than creatine monohydrate, only the addition of dextrose (and ALA or baking soda) have actually been shown to increase the muscular retention of creatine in experiments (Jäger. 2011) 
    As you'd expect, the addition of creatine lead to significant increments in total body mass (p = 0.03) and lean body mass (p = 0.01). What creatine did not do, though, was to affect the amount of body fat the subjects were carrying around. The latter decreased to a similar extent in both groups in response to resistance training, alone (p = 0.001) - without any effect of creatine supplementation. Much to my personal surprise, the same was the case for the subjects' muscle strength, which was - likewise - increased to the same extent in both groups.

    So what? Well, in contrast to the uncommon lack of effect on muscle strength, the lack of effect on body fat is sad, but had to be expected. Both findings are yet not why this study made the SuppVersity Cut. That is or rather was Gann's observation that the loading phase lead to significant increases in of urinary creatine (p = 0.036), and urinary creatinine (p = 0.01) in the creatine group compared to placebo. This "excess amounts of serum and urinary creatine and urinary creatinine content" (Gann. 2015) provides further evidence that the (still common) practice of creatine loading is useless and 100% safe certainly only in the short term. In the long term, however, I'd highly suggest that you avoid super-dosing on creatine - I mean, why would you want to use 20g per day, when 3-5 g per day is enough (Wilder. 2001) and more than will "lose" once the creatine levels of your muscles are saturated (the exact washout time is unknown, but studies indicate it may be >40 days of consuming no creatine at all | Deldicque. 2008)?
Intra-workout BCAA supplements are marketed specifically to resistance trainees. If they do have anti-catabolic effects, though, those are - just like potential fatigue reducing effects - significantly more likely to occur in endurance trainees | learn more
What else? In the bottom line of this mini-series I will briefly reference those studies that did not make the SuppVersity Cut for various reasons. Studies like those on the benefits of BCAAs, for example (Kephart. 2015 or Mumford. 2015). For this kind of study I would need the full-text, not just the abstract to tell you how relevant conclusions like the "BCAA supplement did not appear to enhance recovery benefits compared to a CHO control", "a few areas of performance were bolstered to a point of practical importance"(Kephart. 2015) or "BCAA supplementation [...] may benefit immune function during a prolonged cycling season" (Mumford. 2015), actually are. As soon as the corresponding full papers you have published I will obviously make good for any performance-relevant information I may be missing by ignoring the abstracts, today | Comment on Facebook!
References:
  • Almada, Anthony L., et al. "Effect of post-exercise ingestion of different molecular weight carbohydrate solutions. Part 1: The glucose and insulin response." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P30.
  • Astorino, Todd A., et al. "Effects of red bull energy drink on repeated sprint performance in women athletes." Amino acids 42.5 (2012): 1803-1808.
  • Anzalone, Anthony J., et al. "Effect of post-exercise ingestion of different molecular weight carbohydrate solutions. Part II: The incretin response." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P31.
  • Candow, Darren G., et al. "Effect of sugar-free Red Bull energy drink on high-intensity run time-to-exhaustion in young adults." The Journal of Strength & Conditioning Research 23.4 (2009): 1271-1275.
  • Deldicque, Louise, et al. "Kinetics of creatine ingested as a food ingredient." European journal of applied physiology 102.2 (2008): 133-143.
  • Forbes, Scott C., et al. "Effect of Red Bull energy drink on repeated Wingate cycle performance and bench-press muscle endurance." International journal of sport nutrition and exercise metabolism 17.5 (2007): 433.
  • Gann, Joshua J., et al. "Effects of a traditionally-dosed creatine supplementation protocol and resistance training on the skeletal muscle uptake and whole-body metabolism and retention of creatine in males." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P2.
  • Ivy, John L., et al. "Improved cycling time-trial performance after ingestion of a caffeine energy drink." International journal of sport nutrition 19.1 (2009): 61.
  • Jäger, Ralf, et al. "Analysis of the efficacy, safety, and regulatory status of novel forms of creatine." Amino Acids 40.5 (2011): 1369-1383.
  • Kephart, Wesley C., et al. "Ten weeks of branched chain amino acid supplementation improves select performance and immunological variables in trained cyclists." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P20.
  • Mumford, Petey, et al. "Effects of sub-chronic branched chain amino acid supplementation on markers of muscle damage and performance variables following 1 week of rigorous weight training." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P29.
  • Sanders, Gabriel J., et al. "The effect of three different energy drinks on oxygen consumption and perceived exertion during treadmill exercise." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P1.
  • Sharp, Matthew, et al. "The effects of beef protein isolate and whey protein isolate supplementation on lean mass and strength in resistance trained individuals-a double blind, placebo controlled study." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P11.
  • Van Eck, Leighsa E., et al. "Effect of post-exercise ingestion of different molecular weight carbohydrate solutions. Part III: Power output during a subsequent resistance training bout." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P32.
  • Wilder, Nathan, et al. "The effects of low-dose creatine supplementation versus creatine loading in collegiate football players." Journal of athletic training 36.2 (2001): 124.

Synephrine More Ergogenic, Than Thermogenic? Pump Supps Revisited - L-Arginine, L-Citrulline and Respective Whey-Peptides & -Nitrates | ISSN Research Review '15 #2

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Synephrine, arginine, citrulline - Which pre-workout ensures that you're "on fire"?
As I pointed out previously, my initial idea to cherry pick only the most interesting study results that were presented in form of of poster presentations at the Twelfth International Society of Sports Nutrition (ISSN) Conference and Expo in 2015 didn't work out. The number of interesting studies is is simply too much for a single SuppVersity article to discuss them all.

Accordingly, I am now posting the 2nd serving of what is going to be a multi-part series of articles with brief discussions of the most significant results of the >20 studies and short references to those that didn't make the SuppVersity cut in this, previous and future installments of this series for one reason or another.
Read more about ISSN and other studies at the SuppVersity

Vitargo, Red Bull, Creatine & More | ISSN'15 #1

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

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

Keto Diet Re- search Update | ISSN'15 #4

The Misquantified Self & More | ISSN'15 #5

BCAA, Cholos-trum, Probiotics & Co | ISSN'15 #6
  • Synephrine More Ergogenic Than Thermogenic? There was not just one, but two poster presentations and a full paper that has been published only days ago on synephrine containing supplements at the ISSN meeting and on the ISSN website, respectively. Synephrine? Yes, that's the supplemental non-starter, ah... I mean allegedly powerful fat burner from orange peels. The one with promising fat loss results in rodents, but discouraging results in practice.

    Luckily, the studies that were presented in form of posters by scientists from the Texas A&M University (Jung. 2015 & Dalton. 2015) at the ISSN meeting did not deal with synephrine as fat burner. Rather than that, Jung et al. and Dalton et al. took a look at the short- and long-term safety of synephrine as a pre-workout. A pre-workout that contained either 3g beta alanine, 2g creatine nitrate, 2g arginine AKG, 300mg N-acetyl tyrosine, 270mg caffeine, and 15mg Mucuna pruriens, alone (PLA) or the same baseline ingredients and synephrine.
    Figure 1: Number of reps on sets 1-3 & 4-6 in the control and treatment conditions (Ratamess. 2015)
    Now, the fact that some synephrine in your preworkout won't kill you is not really exciting. I have to admit that. What is exciting... at least sort of, though is the fact that the questionable thermogenic turned out to be an effective ergogenic in the already published and thematically related study by Ratamess and colleagues (Ratamess. 2015). A study that shows that p-synephrine of which previous studies indicate that it is a potent, but highly selective β-3 adrenoreceptor may nor be the best fat burner (the good old ephedrine was a pan-receptor activator and clenbuterol& co target the β-3 receptor, maybe that's also why the fat loss results are rather disappointing) , but at least an underestimated ergogenic.
Is p-synephrine different from synephrine? That's a good question without a clear question. Most supplements that list synephrine on the label actually contain P-hydroxy-α-{methylaminomethyl}-benzylalcohol aka p-synephrine, a protoalkaloid compound that differs from m-synephrine and o-synephrine structurally and comes in form of to stereoisomers in most supplements - the l-enantiomer and the d-enantiomer as the racemate d,l-synephrine. While the latter have been shown to be present in bitter orange, other forms, like the m,s-isomer may are suspected to be adulterations from synthetic phenylephrine supplement producers use to "spike" (Allison. 2005) their products (I assume this was not the case with the samples the researchers in the study at hand used, but the chaos wrt to the types of synephrine puts a huge "?" behind the assumption that you'll see the same effects from any given synephrine or synephrine + caffeine supplement. 
  • As the data in Figure 1 goes to show you, the p-synephrine supplement, which was administered to twelve healthy, college-aged men at a dosage of 100mg either alone (S) or in conjunction with 100 mg caffeine (SCF) for three days. On the day on which the subjects participated in a standardized resistance exercise protocol consisting of 6 sets of squats for up to 10 repetitions per set using 80 % of their one repetition-maximum (1RM) with 2 min of rest in between sets, the supplement was ingested 45 minutes before the workout. In comparison to the placebo treatment synephrine alone triggered a significant increase in total repetitions and volume load. When synephrine was combined with 200 mg of caffeine, it also increased the mean power and velocity of squat performance. What did not change in response to either synephrine alone or caffeine and synephrine, though, were the blood lactate levels or the rate of perceived (RPE) exertion the subjects reported on the usual visual analogue scales.

    For me personally, that's a surprising result. For the scientists it "indicate[s that] supplementation with S and SCF can enhance local muscle endurance during resistance exercise" (Ratamess. 2015); and I have to admit: They are right. One thing you should keep in mind, though, is that unlike caffeine, where you often see reductions in RPE and thus an effect you will feel, synephrine will - even if it works - do its purported "magic" more subtly.
  • The Latest on "Pump Supplements" - Creatine, Arginine, Citrulline, Nitrates -- To make sure that this series is not turning into a 12-part article, I will address the results of Moon's, Suzuki's and Vogel's results in one item (since Moon's paper basically summarizes the results of studies by Falcone and Joy, I won't discuss those separately) .

    Figure 2: Increases in blood flow volume (BFV) 33 minutes after the ingestion of 1.87g of RC, 3.67g of CP (citrulline content 1.87g), 1.87g of RA, or 3.07g of AP (arginine content 1.87g) before 3 sets of 15 arm curls (Moon. 2015).
    Moon et al.'s comparison of citrulline's and arginine's ability to increase the exercise-induced vasodilation and blood flow yielded unsurprising results that confirm that citrulline-based ingredients are more effective than arginine-based ingredients for modulating vasodilation and blood flow. Now that alone wouldn't be news-worthy if the scientists had not tested the effects of both, rawe L-citrulline (RC) and raw L-arginine (RA) and, citrulline and arginine bound to a whey peptide (CP and AP, respectively).

    I guess I am not going to surprise you, when I tell you that regular arginine was the worst vasodilator in this quartet. What is more surprising, though, is the extent to which the peptide bonding increased the vasodilating effects of regular citrulline and even arginine. With the the former producing 2x higher increases in vessel diameter and 9% higher increases in blood glow volume than regular citrulline (let's not even mention regular arginine | see Figure 2) the effects are pronounced enough to be potentially "feelable" and "visible" during a workout.

    Citrulline & Glutathione - GSH Amplifies & Prolongs CIT's NO Boosting Effects During + After Biceps Workout | learn more.
    Against that background I would be curious to see, whether the likewise recently reported performance enhancing effects of citrulline Suzuki et al.'s observed in twenty two well-trained young men who consumed 2.4 g / day of L-citrulline or placebo for 7 days and they took 2.4 g of L-citrulline or placebo 1 hour before 4 km cycling time trial on day 8 would be enhanced by bonding citrulline to whey peptides.

    I mean, if citrulline-whey-peptides appear to offer the same effects citrulline does, but at a higher efficacy, their beneficial effect on cycling time trial performance of which the Suzuki et al. argue that it was mediated by an up-regulation of plasma NO availability should be superior to that of raw citrulline, as well, right?

    And now that we are already talking about what really matters, i.e. performance enhancements, not increases in blood flow, it would also be interesting to see a follow up on the last "pump supplement" study to be mentioned in this installment of the ISSN Research Review: A study by Vogel et al.'s on the vasolidating effects of an arginine-nitrate based pre-workout supplements that shows significant increases in brachial artery diameter. Increases that are quantitatively similar to those Moon et al. observed for citrulline-whey-peptides in the previously discussed study. That does not mean, though that they are equally effective, though. To be able to say that we would need a study in which both agents are compared head-to-head. Unless this study is done and a follow up on Vogel's study proves that the increases in blood flow will actually produce significant performance gains, the only thing I can say about arginine nitrate is: It's interesting, but with respect to its ergogenic effects more studies have to be done.
You don't believe citrulline can do anything for you? Check this out: 8g/day Citrulline Increase Leg Workout Performance - More Reps on Leg Press, Hack Squat & Leg Ext. in Exp. Gymrats (more)! It is thus by no means useful for "cosmetic pumps", only 
Studies that didn't make the cut in this issue are Brooke Bouza et al.'s study on the exercise and calorie information on menus (Bouza. 2015) as well as O'Conner et al.'s tart-cherry study (O'Connor. 2015). That's not because there were methodological issues or something. It's much simpler: The notion that "exercise and calorie information on menus is not enough to improve food choices in Hispanic adults" (Bouza. 2015) is about as unsurprising as the word "potentially" (O'Connor. 2015) in the conclusion of O'Connor's study is daunting. And by the way, now that you know that tart cherry "potentially increases running performance and attenuates post-race markers of inflammation" you actually know the most relevant finding of O'Connor's study, right? | Comment on Facebook!
References:
  • Allison, D. B., et al. "Exactly which synephrine alkaloids does Citrus aurantium (bitter orange) contain?." International journal of obesity 29.4 (2005): 443-446.
  • Bouza, Brooke, et al. "Exercise and calorie information on menus is not enough to improve food choices in Hispanic adults." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P3.
  • Dalton, R., et al. "Safety and efficacy of a pre-wrkout dietary supplement with and without synephrine." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P5.
  • Falcone, Paul H., et al. "Acute hemodynamic effects of L-arginine, arginine nitrate, and arginine peptide on exercise-induced vasodilation and blood flow in healthy men." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P10.
  • Joy, Jordan M., et al. "A comparison of raw citrulline and citrulline peptide for increasing exercise-induced vasodilation and blood flow." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P18.
  • Jung, Y. P., et al. "Effects of 8 weeks pre-workout dietary supplement ingestion with and without synephrine on blood chemistry panel." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P4.
  • Moon, Jordan R., et al. "A comparison of citrulline and arginine for increasing exercise-induced vasolidation and blood flow." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P6.
  • O'Connor, A., et al. "Short-term powdered tart cherry supplementation encircling an acute endurance challenge potentially increases running performance and attenuates post-race markers of inflammation." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P7.
  • Suzuki, Takashi, et al. "Oral L-citrulline supplementation enhances cycling time trial performance in healthy well-trained males." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P52.
  • Vogel, Roxanne M., et al. "Acute hemodynamic effects of a multi-ingredient performance supplement on brachial artery vasodilation and blood flow volume following elbow flexion exercise in healthy young men." Journal of the International Society of Sports Nutrition 12.Suppl 1 (2015): P28.
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