Yes, that's how real cinnamon look like. It does not grow as powder in plastic boxes on trees as I suspect the members of the generation McBurgerSubway believe ;-)

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Table 1: Content of Coumarin 1, Cinnamyl Alcohol 2, Cinnamaldehyde 3, Cinnamic Acid 4, Eugenol 5, Cinnamyl Acetate 6 in Cinnamomum Species and Commercial Samples (g/kg) | DUL = Detected under limits of quantitation; ND = not detected (Wang. 2013).

Effect of 6g of cinnamon on post-prandial blood glucose in healthy subjects (Hlebowicz. 2007). This hefty dose also slowed down gastric emptying and triggered non-significant increases in satiety in 14 healthy subjects after high CHO meals.

What's the optimal dosage? Even though the overview in Figure 1 suggests that "more helps more", Anand, et al. (2010) observed negative effects on the liver of rodents at dosages that would tantamount to ~40g of cinnamon per day. Ok, I assume you already apprehended that this is madness, but in the world of fitness maniacs and mad bodybuilders I thought it would be worth mentioning that even the coumarin free Ceylon cinnamon appears to have ill side effects when it is consumed in extremely high dosages. It would thus appear to be more reasonable to target an intake of 3-6 g of cinnamon with every major meal (it slows down gastric emptying and reduces postprandial blood glucose, therefore it makes sense to take it with a meal | Hlebowicz. 2007, see Figure to the left).

Figure 1: Relative changes in fasting blood glucose and HbA1c levels of pre-diabetic subjects (Medagama. 2015)

• Figure 2: Molecular mechanisms of Cinnamon by which it exerts hypoglycaemic activity. (Medagama. 2015).

  direct effects on the insulin receptor have been observed for Cinnamtannin B1, a proanthocyanidin isolated from the stem bark of Ceylon cinnamon that activates the phosphorylation of the insulin receptor β-subunit on adipocytes as well as other insulin receptors,
• indirect effects on glucose management that are mediated by increased GLP-1 levels, a satiety hormone that decreases the amount of insulin that is necessary to clear glucose from your blood - as Medagama points out, probably by improving glucose transport,
• direct effects on the GLUT-4 glucose uptake receptor, the expression of which is increased by 42.8 % to 73.1 % in brown adipose tissue and muscle by cinnamon in a dose dependent manner,
• indirect effects on insulin sensitivity that are mediated by the effects of cinnamon on the expression of PPAR (α) and PPAR (γ), the increase of which is linked to increased glucose uptake - unfortunately, also in fat cells,
• direct effects on carbohydrate availability that are mediated by the inhibition of the amylase enzyme that is responsible for breaking down complex carbs into simple sugars,
• indirect effects on the endogenous production of glucose in the liver that is inhibited by cinnamon (glucogenesis, i.e. the storage of sugar in the liver, on the other hand, is promoted), and
• indirect effects that are brought about by the reduced rate of gastric emptying that will naturally slow down the absorption of glucose after a meal.

Glucose Control Beyond Carb Reduction ➲ Amino Acids, Proteins, Peptides | learn more!

So, what's the verdict about cinnamon and pre-diabetes? As Medagama points out in the conclusion to the previously referenced recently published review, "[b]oth true cinnamon and cassia cinnamon has the potential to lower blood glucose in animal models and humans" (Medagama. 2015). The problem is yet that we do not have reliable long-term safety studies for both, the problematic, potentially coumarin-laden regular cinnamon, as well as the expensive 99% coumarin-free Ceylon cinnamon, which has actually never been tested in human studies (rodent studies suggest that it works at least as well, though).

Addendum: As previously hinted at, there is no evidence from human studies that the "healthier", "true cinnamon" aka Ceylon cinnamon even works. Well, I just noticed that there's a single, rarely cited study in healthy individuals from the Lund University in Sweden that says that Ceylon cinammon has no effect whatsoever on glycemia and thus concludes "The Federal Institute for Risk Assessment in Europe has suggested the replacement of C. cassia by C. zeylanicum or the use of aqueous extracts of C. cassia to lower coumarin exposure. However, the positive effects seen with C. cassia in subjects w/ poor glycaemic control would then be lost." (Wickenberg. 2012)

To recommend regular cinnamon as a standard-supplement, you'd take everyday for years, on the other hand cannot really be recommended - not for pre-diabetics and by no means for healthy, active individuals who have no reason to take supplements with non-muscle specific glucose partitioning effects, anyways. If you want to improve your glucose management folks, work out - a glycogen-depleting strength or HIIT workout, that's the only scientifically proven muscle specific glucose repartitioner | Comment on Facebook!

• Akilen, R., et al. "Glycated haemoglobin and blood pressure‐lowering effect of cinnamon in multi‐ethnic Type 2 diabetic patients in the UK: a randomized, placebo‐controlled, double‐blind clinical trial." Diabetic Medicine 27.10 (2010): 1159-1167.
• Anand, Prachi, et al. "Insulinotropic effect of cinnamaldehyde on transcriptional regulation of pyruvate kinase, phosphoenolpyruvate carboxykinase, and GLUT4 translocation in experimental diabetic rats." Chemico-biological interactions 186.1 (2010): 72-81.
• Anderson, Richard A., et al. "Cinnamon extract lowers glucose, insulin and cholesterol in people with elevated serum glucose." Journal of Traditional and Complementary Medicine (2015).
• Blevins, Steve M., et al. "Effect of cinnamon on glucose and lipid levels in Non–insulin-dependent type 2 diabetes." Diabetes care 30.9 (2007): 2236-2237.
• Crawford, Paul. "Effectiveness of cinnamon for lowering hemoglobin A1C in patients with type 2 diabetes: a randomized, controlled trial." The Journal of the American Board of Family Medicine 22.5 (2009): 507-512.
• Hlebowicz, Joanna, et al. "Effect of cinnamon on postprandial blood glucose, gastric emptying, and satiety in healthy subjects." The American journal of clinical nutrition 85.6 (2007): 1552-1556.
• Khan, Alam, et al. "Cinnamon improves glucose and lipids of people with type 2 diabetes." Diabetes care 26.12 (2003): 3215-3218.
• Mang, B., et al. "Effects of a cinnamon extract on plasma glucose, HbA1c, and serum lipids in diabetes mellitus type 2." European journal of clinical investigation 36.5 (2006): 340-344.
• Suppapitiporn, Suchat, and Nuttapol Kanpaksi. "The effect of cinnamon cassia powder in type 2 diabetes mellitus." Journal of the Medical Association of Thailand= Chotmaihet thangphaet 89 (2006): S200-5.
• Vanschoonbeek, Kristof, et al. "Cinnamon supplementation does not improve glycemic control in postmenopausal type 2 diabetes patients." The Journal of nutrition 136.4 (2006): 977-980.
• Wang, Yan-Hong, et al. "Cassia cinnamon as a source of coumarin in cinnamon-flavored food and food supplements in the United States." Journal of agricultural and food chemistry 61.18 (2013): 4470-4476.
• Wickenberg, Jennie, et al. "Ceylon cinnamon does not affect postprandial plasma glucose or insulin in subjects with impaired glucose tolerance." British journal of nutrition 107.12 (2012): 1845-1849.

Not allowing young athletes to lift weights may in fact increase, not decrease, their injury risk and hamper their recovery.

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Figure 1: Mean values ± standard deviation of the muscle volume of volleyball athletes in mid-adolescence and late adolescence; %-ages indicate relative mid-to-late differences (Mersmann. 2015).

"pronounced hypertrophy of the patellar tendon led to a mechanical strengthening of the tendon in relation to the functional and morphological development of the muscle - [...] adaptive processes [that] may compensate the unfavorable relation of muscle strength and tendon loading capacity in mid-adolescence and might have implications on athletic performance and tendon injury risk" (Mersmann. 2015).

Heyna et al. have demonstrated as early as 1982 that young athletes who regularly perform resistance training exercises are not just less likely to be injured, they also recover faster (Hejna. 1982).

"[t]his evidence is based on the beneficial adaptations that occur in bones, ligaments, and tendons following training and is further supported by epidemiologic-based reports. Lehnhard and colleagues were able to significantly reduce injury rates with the addition of a strength training regimen to a male soccer team. [...] Hejna and coworkers reported that young athletes (13-19 years) who included resistance training as part of their exercise regimen demonstrated decreased injuries and recovered from injuries with less time spent in rehabilitation when compared with their teammates" (Myer. 2006).

Figure 2: Mean values ± standard error (bars) of (a) patellar tendon cross-sectional area (CSA) as a function of tendon length (in 10% intervals from proximal to distal; n = 18), (b) tendon force-elongation relationship (obtained from ramp contractions, see 'Methods' section; n = 12), and (c) maximum tendon force and stress (calculated for iMVCs; n = 12) of volleyball athletes in mid-adolescence (white) and late adolescence (black | Mersmann. 2015)

So, what's the verdict, then? The study at hand refutes the general claim that a non-uniform adaptation of muscle and tendon in young athletes may result in increased tendon stress during mid-adolescence. Furthermore the comprehensive overview of the effects of resistance training Myer et al. present in their 2006 review shows that additional "resistance training is not only a relatively safe activity for young athletes but that it may also be useful to reduce injuries during competitive play" (Meyer. 2006). To tell your young athletes to stay away from the gym is thus tantamount to telling them not to care about injury prevention.

As the 2014 International Consensus Statement on Youth Resistance Training in the British Journal of Sports Medicine (Lloyd. 2013) points out, it is yet important that your kids and youthsare following "[a]ppropriately designed resistance training programmes" if you actually want to make sure that they reduce, not increase, sports-related injuries. As such, LLoyd et al. even say that resistance training programs "should be viewed as an essential component of preparatory training programmes for aspiring young athletes" (Llyod. 2013 | my emphasis) | Comment on Facebook!

• Lloyd, Rhodri S., et al. "Position statement on youth resistance training: the 2014 International Consensus." British journal of sports medicine (2013): bjsports-2013.
• Mersmann, F., et al. "Muscle and tendon adaptation in adolescent athletes: A longitudinal study." Scandinavian Journal of Medicine & Science in Sports (2015).
• Myer, Gregory D., and Eric J. Wall. "Resistance training in the young athlete." Operative techniques in sports Medicine 14.3 (2006): 218-230.

About to go for a walk? Have fructose for breakfast to keep the hunger at bay.

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"Three isocaloric meals were used in the present study. [...] Briefly, all meals had similar macronutrients and provided 1.0 g∙kg−1 body weight CHO for each participant. The LGI meal was composed of cooked spaghetti, egg, and full-fat milk. The LGIF meal comprised rice vermicelli, egg, ham, and fructose. The HGI meal involved rice vermicelli, egg, ham, and glucose. In the LGIF and HGI meals, approximately 25% of energy was derived from the fructose or glucose beverage (nearly 25 g for a 60 kg person). The calculated GI values for the LGI, LGIF, and HGI breakfasts were 41, 39, and 72, respectively. All meals were freshly prepared in the morning of each main trial, and the preparation procedure was standardized."

Figure 1: Appetite Sub-Score. b: P < 0.05 vs. LGIF. LGI: Low-GI meal without fructose; LGIF: Low-GI meal including fructose beverage; HGI: High-GI meal (Sun. 2015).

But isn't fructose the appetite increasing, liver clogging devil? While it may be the devil in the books of a couple of researchers who have nothing else to publish, the specific effect of fructose on appetite are far from being proven to be good or bad. (Rodin. 1990 & 1991). While it appears as if the isolated consumption of high amounts of free fructose has negative effects on appetite control (Lowette. 2015); and still, there's  no debating that fructose has the general ability to blunt food intake compared to an isocaloric amount of glucose in healthy individuals, as it has been shown by Rodin in 1991 (see Figure on the left).

Figure 2: Glucose and insulin response to the test meals; significant differences were observed for high GI (HGI) compared to the other meals and initially for the fructose meal, where the glucose levels increased slightly more rapidly than in the low GI (LGI) reference meal -  in spite of identical calculated GI values, by the way (Sun. 2015)

Figure 3: The appetite suppressing effects of fructose preloads in the absence of exercise have been known ever since Rodin's 1990 study on the effects of fructose vs. glucose and water preloads on food intakes (Rodin. 1990).

"[t]he effect of fructose on appetite has been substantially investigated. Earlier studies have indicated that fructose beverages suppressed energy intake more than glucose beverages did (Rodin, 1990 and Rodin, 1991). The underlying mechanism has been attributed to the metabolism of fructose in the liver and the effect of insulin" (Sun. 2015).

Make you choice - cholesterol and regular sugar (left), or fat free and fructose-laden? In the end it all may not even matter. In spite of that, you shouldn't forget that fruit is not the enemy, isolated fructose in drinks is.

So, what's the verdict? I'd like to cite the original conclusion first, before adding my two cents: "It appears that fructose content in, rather than the GI of, a pre-exercise breakfast meals affect subjective appetite score during the recovery period after 1-hr of brisk walking" (Sun. 2015).

There's no doubt that this is right, but there are important qualifications with respect to the real-world significance of the results: Firstly, the absence of a post-recovery test meal, where the actual food intake would have been measured, is a major methodological problem of the study at hand. Even though changes in appetite of a similar magnitude will usually translate in changes in food intake, this is not a necessity. Therefore the actual food intake and the mechanism for the appetite suppression have to be elucidated in future trials.

In the mean time, I'd suggest you do your own test-run. If it works, fine. If not, you don't have to care about the results of follow-up studies, anyway. Why? Well, what works for the virtual average study participant does not necessarily have to work for you | Comment on Facebook!

• Anderson, G. Harvey, and Dianne Woodend. "Effect of glycemic carbohydrates on short-term satiety and food intake." Nutrition Reviews 61.5 (2003): S17.
• Blundell, John E., and Neil A. King. "Physical activity and regulation of food intake: current evidence." Medicine and science in sports and exercise 31 (1999): S573-S583.
• Lowette, Katrien, et al. "Effects of high-fructose diets on central appetite signaling and cognitive function." Frontiers in nutrition 2 (2015).
• Melzer, Katarina, et al. "Effects of physical activity on food intake." Clinical nutrition 24.6 (2005): 885-895.
• Rodin, Judith. "Comparative effects of fructose, aspartame, glucose, and water preloads on calorie and macronutrient intake." The American journal of clinical nutrition 51.3 (1990): 428-435.
• Rodin, Judith. "Effects of pure sugar vs. mixed starch fructose loads on food intake." Appetite 17.3 (1991): 213-219.
• Sun, Feng-Hua, Stephen Heung-Sang Wong, and Zhi-Gang Liu. "Post-exercise appetite was affected by fructose content but not glycemic index of pre-exercise meals." Appetite 96 (2016): 481-486.

If you feel totally wasted after every workout, I have bad news for you. In the two-a-day studies at hand the rest between the first and second workout was only 2h! Not exactly much time to recover, but the idea is to "train low" (on glycogen) on the second workout.

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• Daily training (Daily - aka "High") - In this group the subjects alternated between 100-min steady-state aerobic rides (AT) one day, followed by a high-intensity interval training session (HIT; 8x5 min at maximum self-selected effort) the next day.
• Twice every second day training (Two-A-Day - aka "Low") - Subject who had been randomly assigned to this group performed the AT, first, then 1–2 h later, the HIT. 

Figure 1: Markers of fact glycogen use and fat oxidation during steady state exercise after 3 weeks of training (Yeo. 2008)

Figure 2: During the training sessions the HIIT performance is initally lower, but even then the increased capacity to oxidize fat and thus ability to spare gluocose pays off in slowly increasing performance markers (no sign. difference anymore) after only 7 HIIT sprints - during a race the fat oxidation boost (right) may be even more important (Yeo. 2008)

Figure 3: Relative performance increases from pre- to post-test (left) and glycogen levels before and after exhausting bouts of knee extensor exercises (right) | high = daily training, low = twice a day, but only every other day (Hansen. 2005).

"Just One More Set" (1/2): Metabolic Response to 10,000kg vs. 20,000kg Regimen. EPOC: Do Reps and Loads Both Figure? And What About Elite Athletes Do They Need More? Find answers to these questions, here!

Bottom line: While it should be obvious that (a) further research is necessary and (b) the benefits of two-a-day training will depend on your training goals, the (older) studies presented in this article clearly support what Hansen et al phrase like this: "training twice every second day may be superior to daily training" (Hansen. 2005).

Ok, while the benefits for cyclists are obvious, it will have to be proven that the additional one or two reps or the extra high intensity set you may be able to do due to the improvements in glycogen sparing fatty oxidation will actually increase your muscle gains, but the mere possibility that training twice a day every other day could be better than training everyday, which is something I see people do at the gym regularly, is intriguing, isn't it? Comment!

• Hansen, Anne K., et al. "Skeletal muscle adaptation: training twice every second day vs. training once daily." Journal of Applied Physiology 98.1 (2005): 93-99.
• Yeo, Wee Kian, et al. "Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens." Journal of Applied Physiology 105.5 (2008): 1462-1470.

Tribulus terrestris extracts - While the boxing gloved protect a boxers fists from damage, the TT extracts may protect his muscle. Recent study yields surprising results and insights into the performance enhancing effects of TT and why it may have failed to work in previous studies.

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Table 1: Training protocol of the boxers with high intensity and high volume training (Ma. 2015) | Abbreviations: HR, heart rate; RM, repetition maximum.

"All athletes received similar 3-week high intensity training and 3-week high volume training separated by a 4-week rest. Besides special technical training, the main part of the high intensity training was strength training including maximum strength training (twice a week, on Tuesday and Friday) and speed strength training (twice a week, on Monday and Thurs day). For high volume training [see Table 1], the boxers undertook endurance training (10,000 m race every day and low to moderate intensity rope skipping twice a week, on Tuesday and Friday), and special technical training and speed strength training similar to high intensity training" (Ma. 2015).

Figure 1: Differences in relative changes of IGF-BP3, the ratio of IGF/IGF-BP3, mean power, relative mean power and creatine kinase (CK) - higher values denote significant increases compared to control (E), lower values decreases in (E+TT) vs. (E) (all p < 0.05) | data calculated based on Ma. 2015

Figure 2: Overview of the general role of IGF-1; focus on what is missing when it declines as we age (Berryman. 2013).

Read this highly suggested SuppVersity Classic: Beware of falling victim to the "Brocebo Effect", Bros! Brocebo? Add 10kg to Your Bench in Days with Sugar-Based "Anabolic Steroids". Old Study Shows, Many "Natural Anabolics" Could Work Solely via Placebo Effects | learn more

What's the verdict, then? In view of the large influence the exact ratio and concentration of saponins will probably have on the effect of a given TT extract and its variability according to region, harvest and the part(s) of the plant that was/were used to prepare the extract (see red box) it is not impossible that previous studies by Antonio et al (2000) and Rogerson et al (2007) simply didn't find performance benefits in resistance-trained men and rugby players, because they used the 'wrong' extracts (or the training was not intense enough, some of the benefits in the study at hand were after all blunted performance decreases during intense training).

While it is hard to determine whether or not this hypothesis is true, there's no reason to debate the conclusion Ma et al draw based on their more recent results in trained boxers - a conclusion that reads: "Taking 1,250 mg capsules containing TT [...] alleviated muscle damage and promoted anaerobic performance of trained male boxers, which may be related to the decrease of plasma IGFBP-3 rather than androgen in plasma" (Ma. 2015) | Comment on Facebook!

• Antonio, et al. "The effects of Tribulus terrestris on body composition and exercise performance in resistance-trained males." International Journal of Sport Nutrition and Exercise Metabolism, 10 (2000): 208–215.
• Berryman, Darlene E., et al. "The GH/IGF-1 axis in obesity: pathophysiology and therapeutic considerations." Nature Reviews Endocrinology 9.6 (2013): 346-356.
• Frystyk, Jan. "Exercise and the growth hormone-insulin-like growth factor axis." Medicine and science in sports and exercise 42.1 (2010): 58-66.
• Ma, Yiming, Zhicheng Guo, and Xiaohui Wang. "Tribulus Terrestris extracts alleviate muscle damage and promote anaerobic performance of trained male boxers and its mechanisms: Roles of androgen, IGF-1 and IGF binding protein-3." Journal of Sport and Health Science (2015).
• Milasius, K., R. Dadeliene, and Ju Skernevicius. "The influence of the Tribulus terrestris extract on the parameters of the functional preparedness and athletes’ organism homeostasis." Fiziol Zh 55.5 (2009): 89-96.
• Rogerson, Shane, et al. "The effect of five weeks of Tribulus terrestris supplementation on muscle strength and body composition during preseason training in elite rugby league players." The Journal of Strength & Conditioning Research 21.2 (2007): 348-353.
• Wang et al. "Effects of Tribulus terrestris on exercise ability, endocrine and immune functions of over-trained rats." Journal of Shanghai University of Sport 46 (2010).
• Yin, Liang, et al. "The Effects of Tribulus Terrestris on the Time of Exhaustion in Rats with High Intensity Training and Its Mechanism." Journal of Shanghai University of Sport 5 (2013).
• Zhang, Shuang, et al. "[Effect of gross saponins of Tribulus terrestris on cardiocytes impaired by adriamycin]." Yao xue xue bao= Acta pharmaceutica Sinica 45.1 (2010): 31-36.

Looking for a new routine for your new-years gym resolution? This SuppVersity article offers suggestions that will pay off in form of strength gains.

The method used int he study is an alternative to classic periodization schemes.

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Table 1: Study design: constant and variable loading parameters (Eifler. 2015).

• CL - constant load and constant volume of repetitions over 6 weeks.
• IL - increases in load and decreasing volume of repetitions made every 2 weeks.
• DL - decreases in load and increasing volume of repetitions made every 2 weeks.
• DCL - daily changing load and volume of repetitions.

"Both 10-RM-testing and 1-RM-testing were designed with the following procedure: 5 minute general warm-up with an intensity of 60% of the theoretical maximum heart rate; one warm-up set with 50% of the load in the first test set; performance of 3 at most test sets to quantify RM (trial and error principle) by 3 minutes rest interval between test sets. Pre- and post-testing occurred at the same time of day to eliminate the potential influence circadian rhythm on strength. The documentation of the test results followed standardized test protocols. At each date of testing, all participants were interviewed about their current state of motivation and their form of the day. Moreover, the temporal gap between the last resistance training session and the presence of muscle soreness and muscle stiffness were recorded" (Eifler. 2015).

Figure 1: Effect sizes of the 6-week training intervention with different loading schemes (Eifler. 2015); * denotes significant differences compared to all other groups - in short: only the DCL workout made a significant difference.

Figure 2: Relative strength increases in the four study groups (Eifler. 2015); due to the large inter-individual differences, evidenced by the long error bars, the DCL advantage was not statistically significant.

This is not the first SuppVersity article discussing evidence in favor of "changing up things more frequently". Back in 2012 I already discussed Spinetti's linear vs. undulating periodization studies w/ similar benefits on the subjects' strength gains.

So what's the verdict, then? Just as the author says, while DCL is widely known, the fact that it is rarely practiced may have average and extraordinary gymrats miss out on a "potential for improving resistance training in commercial fitness clubs" (Eifler. 2015). After all, there's little doubt that the data from the study at hand "indicates that resistance training following DCL is more effective for advanced recreational athletes than" (ibid.) more conventional loading patters, i.e. CL, IL, DL.

Whether the benefits are due to a novelty effect that would be lost over long(er) training periods and whether the same or similar benefits could be achieved in untrained subjects will have to be determined in future research, for the time being however, daily changing load (DCL) and volume of repetitions appears to be worth adding to your list of things to try in the gym in 2016 | Comment on Facebook!

• Eifler, Christoph. "Short-term effects of different loading schemes in fitness-related resistance training." The Journal of Strength & Conditioning Research (2015).
• Macefield, Ritch. "Usability studies and the Hawthorne Effect." Journal of Usability Studies 2.3 (2007): 145-154.
• Rhea, Matthew R., et al. "A comparison of linear and daily undulating periodized programs with equated volume and intensity for strength." The Journal of Strength & Conditioning Research 16.2 (2002): 250-255.

Studies in men suggest no effect of the hormonal response on training outcome - What about women? A news study provides insights that may be relevant for both female and male gymrats.

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Figure 1: Sign. associations between PWO hormone levels and lean mass, as well as fiber size increases (West. 2012).

Figure 2: Changes in anabolic and catabolic hormones in response to AM and PM HIIT and RT training (Toon. 2015).

Higher sprint cadence (RPM) during HIIT, higher increase in DHT in the female study participants (Toon. 2015).

DHT another acute phase reactant? Even though the overall results of the study suggest that increased pre- vs. post workout changes in DHT as Toone observed the with higher RPM-numbers during HIIT sprints are not the reason, but rather the consequences of training at higher intensities, it is worth mentioning that this is the first study to observe the existence of an association between DHT and HIIT performance in women and that the results are in line with the results of previous research suggesting that DHT, not its precursor, testosterone, has a direct influence on skeletal muscle force production in vitro. 

"[...] it could be beneficial to perform resistance training in the afternoon preceded by interval exercise in the morning in order to stimulate a hormonal milieu that may be more conducive to stimulating muscle protein turnover" (Toon. 2015). 

"The trial consisted of a 20 min effort at a target power of 80% of the average power obtained during the maximal 20 min TT, followed by a 5 min break, before completion of a bout of repeated sprint interval cycle exercise consisting of 10 x 30 s sprinting, with 90 s recovery. The session was self-paced with real-time numerical feedback provided on elapsed time, cadence and power. Participants were given verbal encouragement at specific time-points throughout the trial. The same protocol was repeated for the second main trial one week later. Participants were permitted to drink water ad libitum throughout the trials. Trials were completed in a group setting as a group of six and a group of eight. A trial timeline schematic is displayed [in Figure 3]" (Toon. 2015).

Figure 3: Design of the last and most important experiment of the study (Toone. 2015).

Figure 4: The hormonal response is rather the consequence than the trigger of acute performance.

What does that mean? Practically speaking this would confirm what I have said about the initially cited West study in several previous SuppVersity articles. In said study, cortisol probably has no mechanistic effect on muscle size. Rather than that, the increase in cortisol could serve as a measure of how much effort the subjects put into their workouts; and this, in turn, determined their muscle gains (more effort = bigger growth stimulus = greater gains).

The meager and transient increase in testosterone after your workouts has none of the muscle building and fat shedding effects of exogenous testosterone. The latter however, can turn back the time and an aging pouch into a true best-ager | learn more.

In the study at hand, the situation appears to be similar. Mood and effort determine performance and hormonal response of the female study participants. Accordingly, there may be associations between exercise performance and certain hormones, but those are of corollary, not causative nature. In the absence of an additional experiment that would investigate the correlations and associations between mood, effort, RPE, hormones and the exercise-induced adaptation in the long run, we can still only speculate that making the workouts more fun and stimulating maximal effort would promote both, the adaptive response and the hormonal response and thus confirm that mood and effort are in fact the most relevant determinants of the outcome of your workouts | Comment!

• Phillips, Stuart M. "Strength and hypertrophy with resistance training: chasing a hormonal ghost." European journal of applied physiology 112.5 (2012): 1981-1983.
• Toone, Rebecca. Assessing the Hormone Response to High Intensity Exercise and Identifying Associations with Performance. Diss. University of Bath, 2015.
• 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 BMI or rather the associated level of inflammation and bodyfatness determines your D3 requirements.

There are many ways to get your vitamin D learn more the SuppVersity

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"model the effect of vitamin D supplementation on the 2.5th percentile, the median and the 97.5% percentile of serum 25(OH)D concentrations [and an] exponential model [and] logistic regression [for the estimates and] to estimate the probability of having serum levels above a lower and below an upper serum 25(OH)D concentration, [respectively]" (Veugelers. 2015). 

Figure 1: Plot of the results of the model calculations (left) and my visualization (right) of the calculated vitamin D requirements in IU/day for normal-weight, overweight and obese individuals (Veugelers. 2015).

So what's the verdict, then? While the study at hand certainly provides the hitherto best estimate of our individual vitamin D3 requirements, I still wouldn't put blind faith into the results of Veugelers' model calculation. To be sure you're not too extra-ordinary to be average, I would suggest you test your 25OHD levels after 6 months on the suggested dosage. If you're "in the zone", everything is fine. If not, adjust appropriately.

Fat loss will trigger decent increases in vitamin D, but vitamin D will not trigger significant fat loss | more

Apropos adjusting, as the authors point out, the previously discussed figures may not even be the most practically relevant result of the study. Rather than that, it is the "large extent of variability in 25(OH)D concentrations" of which the authors rightly say that it "makes a RDA for vitamin D neither desirable nor feasible" (Veugelers. 2015) that's the most relevant results of the study.

And yes, you've read that right. The 400, 600 and 1000 IU/day RDA you will find in different countries all over the world is total bogus, not just because it is too low, but because stating a recommended daily allowance based only on the age, not the weight, or rather inflammatory status of an individual, is absolute bogus | Comment on Facebook!

• Luxwolda, Martine F., et al. "Traditionally living populations in East Africa have a mean serum 25-hydroxyvitamin D concentration of 115 nmol/l." British Journal of Nutrition 108.09 (2012): 1557-1561.
• Veugelers, Paul J., Truong-Minh Pham, and John Paul Ekwaru. "Optimal Vitamin D Supplementation Doses that Minimize the Risk for Both Low and High Serum 25-Hydroxyvitamin D Concentrations in the General Population." Nutrients 7.12 (2015): 10189-10208.
• Waldron, Jenna Louise, et al. "Vitamin D: a negative acute phase reactant." Journal of clinical pathology (2013): jclinpath-2012.

Does this look as if sprinting would impair muscular development of arms or any other muscle? I mean, come on - look at the average sprinter: Many gymrats dream of the arms and overall muscular physique they have; no wonder that the data from the full-text shows a different picture than the abstract would suggest.

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Figure 1: According to the study, you better don't do HIIT sprint training after an intense arm workout if you don't want to ruin the strength and size gains you "primed" with curls and co (photo from Kikuchi. 2015)

• The RT program was designed to induce muscular hypertrophy (3 sets x 10 repetitions (reps) at 80% 1 repetition maximum [1RM] of arm curl exercise), and was performed in an 8-week training schedule carried out 3 times per week on nonconsecutive days. 
• Subjects assigned to the CT group performed identical protocols as strength training (ST) and modified sprint interval training (4 sets of 30-s maximal effort, separated in 4m 30-s rest intervals) on the same day. 

Figure 1: Relative changes in VO2max (conditioning), muscle size (CSA) and strength (1-RM) over 6 wks (Kikuchi. 2015).

If you take a closer look at the individual muscle  size and strength development, you should notice that being afraid that sprints would ruin your arm development is unwarranted and the statistical significance and effect sizes of the changes practically irrelevant.

Beware of bling faith in abstracts! If you look at my plot of the individual data the scientists luckily published with their full-text, it is yet obvious that this study does not prove and if we are honest, not even really suggest that there practically relevant negative effects of doing HIIT in this workout. If you just read the conclusion to the abstract, which reads "our data indicate that con-current lower limb sprint interval training interfere with arm muscle hypertrophy and strength" (Kiku-chi. 2015), you may be inclined to make unne-cessary changes to your workout that are neither necessary or productive. After all, the objective result of the study is that in some individuals it is possible that the addition of HIIT to an arm workout may have a minor impact on their gains.

In view of the facts that there's (a) one person with a roughly ~41% increase in sleeve sizes in each group and that (b) the average increase in sleeve size would be 23% in the CT and only 21% in the RT group if the two outlayers who lost muscle (one in each group) were excluded, though, I would suggest you ignore this possibility unless you realize that you're making no gains at all with concurrent training. This doesn't falsify the scientists' conclusion, which is based on scientific standard procedure, i.e. look for statistical significant results, use those to make your conclusion, but I felt I needed to write this article to put the theoretically correct interpretation of results of an unquestionably under-powered study into perspective | Comment!

• Kikuchi et al. "The effect of high-intensity interval cycling sprints subsequent to arm-carl exercise on muscle strength and hypertrophy in untrained men: A pilot study." Journal of Strength and Conditioning Research Publish (2015): Ahead of Print | DOI: 10.1519/JSC.0000000000001315

Parr et al. suggest that ecdysterone should be added to the WADA list.

If you want to build muscle forget T-booster and optimize your protein intake 

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Figure 1: Myotube diameter in the in vitro study after incubation with DHT, IGF-1 or Ecdysterone (Parr. 2015).

Figure 2: Anabolic effect of ecdysterone (Ecdy) expressed as fiber size of soleus muscle in intact rats (Parr. 2015).

Hormonal Response to Exercise, Revisited: A Consequence, not a Determinant of Your Mood, Effort & Performance | learn more

Bottom line: In spite of the fact that the study provides quite convincing evidence in favor of the unexpected potency of Ecdysterone, there is a problem with dosing. While the scientists say they used 5mg/kg body weight in order "mimic the situation in athletes", the correct rodent equivalent of the aforementioned dosages of up to 1g per day would be roughly 50-75mg/kg per day and thus far more than the meager 5mg/kg the researchers used.

In other words, if they didn't accidentally give us the human equivalen dose instead of the actual rodent dose, those 1g/day some bodybuilders may be taking should be way more than you'd need to see significant increases in muscle gains and that is a problem.

Why? Well, not because I'd believe that dosages as high may have toxic side effects, but rather in view of the fact that you can hardly imagine that a drug as effective as that wouldn't be all over the place in the discussions on pertinent bulletin boards. A 2006 study by Wilborn et al. even fuels the doubts, because it found no performance or hypertrophy effects in the 15 out of 45 subject of their 8-week training study who consumed 30 mg of 20-hydroxyecdysone per day from an allegedly standardized (but not tested) extract from Suma root. An even older study by Simakin et al. (1988), however, appears to confirm the existence of potent anabolic effects of ecdysterone in humans with significant increases in lean (6-7%) and reductions in fat mass (10%) in a 3-week study on 78 highly-trained male and female subjects. In view of the conflicting evidence, I am still very skeptical whether (a) the results translate to human beings, whether (b) the growth promoting effect is maybe restricted to slow twitch fibers and thus of little use to bodybuilders and whether (c) the supplements that are already being sold actually contain ecdysterones | Comment!

• Gorelick-Feldman, Jonathan, et al. "Phytoecdysteroids increase protein synthesis in skeletal muscle cells." Journal of agricultural and food chemistry 56.10 (2008): 3532-3537.
• Gorelick-Feldman, Jonathan, Wendie Cohick, and Ilya Raskin. "Ecdysteroids elicit a rapid Ca 2+ flux leading to Akt activation and increased protein synthesis in skeletal muscle cells." Steroids 75.10 (2010): 632-637.
• Parr, Maria Kristina, et al. "Estrogen receptor beta is involved in skeletal muscle hypertrophy induced by the phytoecdysteroid ecdysterone." Molecular nutrition & food research 58.9 (2014): 1861-1872.
• Parr, M. K., et al. "Ecdysteroids: A novel class of anabolic agents?." Biology of sport 32.2 (2015): 169.
• Simakin, S. Yu. "The Combined Use of Ecdisten and the Product'Bodrost'during Training in Cyclical Types of Sport." Scientific Sports Bulletin 2 (1988).
• Suzuki, S., and T. Yamamuro. "Long-term effects of estrogen on rat skeletal muscle." Experimental neurology 87.2 (1985): 291-299.
• Syrov, V. N. "Comparative experimental investigation of the anabolic activity of phytoecdysteroids and steranabols." Pharmaceutical Chemistry Journal 34.4 (2000): 193-197.
• Wilborn, Colin D., et al. "Effects of methoxyisoflavone, ecdysterone, and sulfo-polysaccharide supplementation on training adaptations in resistance-trained males." Journal of the International Society of Sports Nutrition 3.2 (2006): 19-27.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References:

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

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

Lean more about frying, MUFAs,PUFAs & co at the SuppVersity

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

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

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

The Quest for the Optimal Cooking Oil: Heat Stable, Low PUFA & Cholesterol Free - High MUFA Sunflower / Canola, Olive, Coconut & Avocado Oil Qualify for the TOP5 | Learn more!

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

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

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

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

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

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

Want to "Advance" Your Creatine? Add Bicarbonate | read more

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Learn more about building muscle and strength at www.suppversity.com

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

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

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

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

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

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

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

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

8x Increase in "Mitochondria Building" Protein PGC1-Alpha W/ Medium Inten-sity Exercise in Glycogen Depleted Elite(!) Cyclists | Learn more

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

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

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

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

Combination of 5-aminolevulinic acid (ALA) with sodium ferrous citrate (SFC) works by reviving the mitochondria.

Read more short news on various topics here at the SuppVersity

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"[the subjects'] exercise efficiency had likely reached the steady state and would thus enable us to detect only the effects of ALA intake on their exercise efficiency without accounting for the acute effects of exercise training" (Masuki. 2015b).

Figure 1: Experimental protocol. Ex, graded cycling exercise test; IWT, interval walking training. The study was conducted using a randomized, placebo-controlled, double-blind crossover design. In each supplement intake, subjects ingested 250 mg of either 5-aminolevulinic acid (ALA) + sodium ferrous citrate (SFC) or placebo supplement (250 mg × 2 = 500 mg/day). See Table 2 for details of the supplement compositions (Masuki. 2015b).

ALA + iron supplementation lead to sign. improvements in glycemia in an oral glucose tolarence test in low doses in mildly hyperglycemic and in high doses in all subjects of a 2013 study by Higashikawa.

Seriously, what about iron overload? Yes, you're right to ask. After all, the iron intake per day in the ALA+SFC trial was three times higher than the RDA value. Still, even though subjects showed no symptoms of iron deficiency anemia in the health examination before participating in the study, their [Hb] did not change after ALA+SFC supplementation. Since it is also "unlikely that SFC was independently incorporated into the mitochondrial function in the ALA+SFC trial", the scientists "surmise that the simultaneous ingestion of a mixture of ALA and iron ion is necessary to attain the results" (Masuki. 2015b) - an unquestionably reasonable assumption that is also consistent with several other studies assessing the effects of ALA combined with the iron ion, studies which showed among other things blood sugar and blood pressure lowering effects, made hair regrow (Higashikawa. 2013; Rodriguez. 2012; Mingone. 2006; Morokuma. 2008).

Table 1: Total energy, protein, fat, carbohydrate, ALA, and iron intake per day (Masuki. 2015b)

Figure 2: Training days (A), training impulse (B), and training time (C) at total, fast, and slow walking during the supplement intake period. Ratio of subjects performing training to total subjects (D), training impulse (E), and training time (F) at fast walking on each day in the period of supplement intake. *p < 0.05, ***p < .001 compared with the CNT trial.

Figure 3: In a previous study, Masuki et al. have just been able to show that there is a linear inverse relationship between older women's adherence to prescribe walking days (APWD; A) and fast walking time (APFWT; B) over the 22-mo training period with the change in lifestyle-related disease score (ΔLSD score) from baseline to 22 mo (Masuki. 2015a).

Bottom line: As the scientists point out in the conclusion to their paper, the higher training achievements they observed in response to ALA+SFC supplementation as a result of an increased exercise efficiency in older women who - and I'd like to highlight that - had performed habitual training before this study,  is associated with greater improvements in physical fitness and risk factors for lifestyle-related disease (Masuki. 2015a).

Therefore, it is correct that Masuki et al. assume that "this regimen would be useful to help older women continue habitual exercise training and thus improve their health" ... and let's be honest: isn't that what "supplements" are meant to do? | Comment!

• Higashikawa, Fumiko, et al. "5-aminolevulinic acid, a precursor of heme, reduces both fasting and postprandial glucose levels in mildly hyperglycemic subjects." Nutrition 29.7 (2013): 1030-1036.
• Masuki, Shizue, et al. "The factors affecting adherence to a long-term interval walking training program in middle-aged and older people." Journal of Applied Physiology 118.5 (2015a): 595-603.
• Masuki, Shizue, et al. "Impact of 5-aminolevulinic acid with iron supplementation on exercise efficiency and home-based walking training achievement in older women." Journal of Applied Physiology 120.1 (2015b): 87-96.
• Mingone, Christopher J., et al. "Protoporphyrin IX generation from δ-aminolevulinic acid elicits pulmonary artery relaxation and soluble guanylate cyclase activation." American Journal of Physiology-Lung Cellular and Molecular Physiology 291.3 (2006): L337-L344.
• Morokuma, Yuki, et al. "Hair growth stimulatory effect by a combination of 5‐aminolevulinic acid and iron ion." International journal of dermatology 47.12 (2008): 1298-1303.
• Rodriguez, Beatriz L., et al. "Use of the Dietary Supplement 5‐Aminiolevulinic Acid (5‐ALA) and Its Relationship with Glucose Levels and Hemoglobin A1C among Individuals with Prediabetes." Clinical and translational science 5.4 (2012): 314-320.

You knew that all these fat burning high protein foods are high in phosphorus?!

If you're looking for a true fat burner, try coffee ;-)

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Table 1: Overview of the baseline characteristics of the subjects in the placebo and phosphorus group (Ayoub. 2015).

Figure 1: Weight, waist circumference and serum phosphorus levels expressed rel. to baseline (Ayoub. 2015).

Table 2: Changes in subjective appetite scores from baseline to 12 weeks (Ayoub. 2015).

• there's firstly the evidence from observational studies linking high protein, high dairy and high whole grains intakes to reduced risk of overweight and metabolic syndrome - since a high intake of all three of these food groups is also associated with an increased intake of phosphorus, that's the first line of evidence which supports a mechanistic role of increased phosphorus intakes in weight management,
• there's secondly epidemiological evidence showing an inverse association between an individuals phosphorus status and his or her body weight and waist circumference, and 
• there's thirdly the well-known effect of phosphorus on ATP production, especially in the liver, of which previous studies suggest that it regulates afferent neural signals to the central nervous system which will result in a reduction in food intake (Friedman. 2007).

Figure 2: In a previous study the addition of 500mg of phosphorus to a non-caloric or caloric pre-load has already been shown to significantly reduce the food intake during ad-libitum (pizza) lunch (Obeid. 2012).

If you're a loyal SuppVersity, you will probably remember that phosphorus supplements have also been shown to ameliorate the decrease of the active thyroid hormone T3 dieters experience as they progressively reduce their food intake | learn more

Disappointed that it all comes back to eating less, once again? I know the mechanism, a reduction in food intake, is not exactly exciting. It means, after all, that you can still not eat as much junkfood as you want and stay lean if you only supplement with enough phosphorus (in view of the potential diarrhea you may get from very high doses, I suspect you could eat as much as you want... but you certainly don't want to ;-).

With the previously reported beneficial effects of phosphate supplements against the metabolic slow down in response to significantly reduced energy intake, the study at hand does yet contribute another line of evidence that suggests that our diet may eventually not really be so much too high in phosphorus / -phates as we believe it was | Comment!

• Ayoub et al. "Effect of phosphorus supplementation on weight gain and waist circumference of overweight/obese adults: a randomized clinical trial." Nutrition & Diabetes (2015) 5, e189; doi:10.1038/nutd.2015.38.
• Friedman, Mark I. "Obesity and the hepatic control of feeding behavior." Drug News Perspect 20.9 (2007): 573-8.
• Obeid, O. A., S. Dimachkie, and S. Hlais. "Increased phosphorus content of preload suppresses ad libitum energy intake at subsequent meal." International Journal of Obesity 34.9 (2010): 1446-1448.

This study is different from the average "fish oil is good for you" study and that's both refreshing and revealing. Speaking of "fresh" you got a 50/50 chance you buy fresh, not rancid fish oil.

You can learn more about omega-3& co at the SuppVersity

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Figure 1: Relative changes in metabolic parameters at rest and during 30 min of exercise (Logan. 2015).

Figure 2: Graphical overview of the absolute increase in energy expenditure and fat oxidation (Logan. 2015).

So, fish oil is a metbalic activator? Well, at least in this particular group of subjects, there's no debating that the 3g of combined EPA + DHA per day triggered statistically significant and as the data in Figure 2 shows even potentially practically relevant increases in energy expenditure at rest and during exercise.

Suggested Read: "TTA + Fish Oil Revisited - Increased Muscular N-3 Levels Compromise Heart & Skeletal Muscle Performance: 40% Reduced Endurance & 54% Lower Work Capacity in 9 Weeks" | more

As the authors highlight, though, "[f]uture research should also aim to test a greater number of participants and include a longer period of supplementation (ie. 1 yr) to determine whether the increase in metabolic rate results in changes in more robust changes in body composition" (Logan. 2015). In view of the complaints of their subjects who had difficulties stomaching the 5g of total fish oil that were required to achieve the desired dose of EPA + DHA, the scientists also argue that future studies have to investigate solutions that reduce the digestive issues (gastrointestinal discomfort) and whether you even need 3g of EPA + DHA or lower dosages would have the same effect... well, and obviously, it would be interesting to see if similar results could be observed in younger and / or male subjects | Comment on Facebook!

• Logan, Samantha Louise. Physical Activity and Nutrition as Modifiable Lifestyle Factors for Healthy Aging in Older Adults. Diss. The University of Guelph, 2013.

"Shed the fat, keep the muscle!" That's a promise you will find not literally, but analogously in every ad for BCAAs, but do they actually do that? Help you shed fat and retain muscle? Scientific prove to support this claim is, as of yet, missing.

Learn more about amino acid and BCAA supplements at the SuppVersity

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• 14g of Xtend (BCAA) before after workouts or
• 14 g Powerade (CHO) before and after workouts

Table 1: W/ the Harris-Benedict equation you calculate the basal metabolic rate and multiply it with a factor (multiplier) that describes your activity level best to arrive at the "real" estimated energy requirements.

"The caloric-restricted diet was designed as an 8 week “cut diet” for reducing body fat, and used a modified carbohydrate-restricted diet approach (percent of total calories for workout days were 30 % carbohydrates, 35 % protein and 35 % fat and for off days were 25 % carbohydrates, 40 % protein and 35 % fat). Each individual’s daily caloric and macronutrient intake was determined using the Harris Benedict formula with an activity factor of 1.35 (lightly active individual engaging in light exercise 1–3 days/week) for workout days and 1.125 (sedentary individual) for off days" (Dudgeon. 2015).

Table 2: Sample dietary card for a subject during an off, non-workout, day (Dudgeon. 2015).

Figure 1: Pre and post absolute mean body weight, body fat and lean body mass values before and after the 8-week intervention; * p < 0.05 for the difference within groups (no difference between groups | Dudgeon. 2015)

Figure 2: Pre vs. post values for body fat % and lean mass %, the two parameters you would classically use to assess body composition (instead of absolute lean and fat mass); pre-to-post change on top of the post-bars (Dudgeon. 2015).

Whey + Casein - A Superior Post-Workout Shake that Kicks Every Amino Acid Product's Ass | read more

So what do we make of this study? Well, first of all, I would like to come back to something fundamental: This is yet another BCCA study that did not make the practically most relevant comparison of BCAAs and cheap (whey) protein protein supplements, in which BCAAs have hitherto always failed. In my humble opinion that's a problem, after all having a carbohydrate supplement as control in a dieting study is nice, but eventually not relevant for the average trainee who is probably not really considering extra-carbs when he's dieting.  What a real trainee would have been interested in, is whether BCAAs can prevent muscle catabolism to a significantly greater degree than the cheap whey protein he's using anyway...

... and maybe, whether the latter has a similar negative effect on fat loss as the BCAAs in the study at hand - which leads me to the actual take home message of the study, which is, as usually, not as straight forward as the conclusion of the abstract suggested. When all is said and done, the study at hand does after all suggest that someone who is approaching the single-digit body-fat zone, where every gram of muscle that is not lost counts, could benefit from the apparent lean mass protective effects of BCAA the scientists observed in the study at hand. It does yet also indicate that someone who's "making weight" for a competition should take a second look at the data in Figure 1 + 2 and acknowledge that taking a BCAA supplement may be the reason he will fail to achieve his weight loss goal. You don't believe that? Well, let's do some scientifically not exactly kosher extrapolations: If you manage to lose 10 kg in 10 weeks without BCAAs, for example, the data from the study at hand suggests that your weight loss "on BCAAs" over the course of those 10 weeks would be as meager as 434 grams ... whether that's in fact the case (I doubt it ;-) will have to be studied in future studies, just like the effect of BCAAs, citrulline and glutamine, alone and whether using your regular whey protein before and after the workout wouldn't have the exact same, or even better effects | Comment on Facebook!

• Dudgeon, WD; Page Kelly, E; Scheett TP. "In a single-blind, matched group design: branched-chain amino acid supplementation and resistance training maintains lean body mass during a caloric restricted diet." Journal of the International Society of Sports Nutrition  (2016) 13:1.
• Faure, Cécile, et al. "Leucine and citrulline modulate muscle function in malnourished aged rats." Amino acids 42.4 (2012): 1425-1433.
• Moinard, Christophe, and Luc Cynober. "Citrulline: a new player in the control of nitrogen homeostasis." The Journal of nutrition 137.6 (2007): 1621S-1625S.
• Hickson, R. C., S. M. Czerwinski, and L. E. Wegrzyn. "Glutamine prevents downregulation of myosin heavy chain synthesis and muscle atrophy from glucocorticoids." American Journal of Physiology-Endocrinology and Metabolism 268.4 (1995): E730-E734.
• Hickson, Robert C., et al. "Protective effect of glutamine from glucocorticoid-induced muscle atrophy occurs without alterations in circulating insulin-like growth factor (IGF)-I and IGF-binding protein levels." Experimental Biology and Medicine 216.1 (1997): 65-71.
• Salehian, Behrouz, et al. "The effect of glutamine on prevention of glucocorticoid-induced skeletal muscle atrophy is associated with myostatin suppression." Metabolism 55.9 (2006): 1239-1247.
• Ventura, G., et al. "Effect of citrulline on muscle functions during moderate dietary restriction in healthy adult rats." Amino acids 45.5 (2013): 1123-1131.

In contrast to the routines I will discuss in today's SuppVersity feature article (thank you Timo for the inspiration), practicing the ab-pose has not been scientifically proven to help you fix your posture... although, when you look at how it's done, it's certainly not going to make things worse.

Want to include this in your routine, but don't know how? Learn more about exercise order!

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• Figure 1: Scapular retraction (top), external rotation (middle) and shoulder flexion for the lower trapezius (bottom | Kluemper. 2006).

  Scapular retraction - With the shoulder abducted to 90° in the scapular plane, the elbows flexed to 90°, and the forearms horizontal, the subject holds a section of the exercise band between the right and left hands and retracts the scapulae, stretching the band (Figure 1, top). The subject must maintain the original 90° position of the shoulders and elbows and then execute a controlled return to the starting position.
• External rotation - The upper arm is positioned at 90° of shoulder abduction and 90° of elbow flexion. The forearm begins in a horizontal position and externally rotates into a vertical position. The subject then executes a controlled return to the starting position. The exercise band is fixed in front of the subject at approximately waist height at the beginning of the exercise (Figure 1, middle).
• Shoulder flexion for the lower trapezius - With arms flexed to 90°, elbows fully extended, and palms down, the subject flexes the shoulders to 180° against the exercise-band resistance and then executes a controlled return to the starting position. The exercise band is again fixed in front of the subject at approximately waist height for the beginning of this exercise (Figure 1, bottom).

Table 1: Progression of the exercises | at the end of the third week the subjects progressed to the next higher level of resistance using the Theraband® latex band (Kluemper. 2006).

Figure 2: Photos of the stretches for pectoralis major and minor (Kluemper. 2006)

"The first stretch, for anterior chest muscles, required the subject to assume a supine position on a 5-in-diameter foam roll, which runs down the center of the back. The subjectʼs partner grasps the subjectʼs shoulders and slowly presses them down in the direction of the floor until instructed to stop and hold for 30 seconds. This was repeated twice per training session (Figure 2, top). The second stretch for shoulder internal rotators required the subject to assume a kneeling position in front of his or her standing partner and lace his or her fingers behind the head. The partner then reaches in front of the subjectsʼ arms and back behind the subjectʼs scapulae, lacing his or her fingers together, as well. The part ner pulls in a diagonal direction, both up and back from the subjectʼs trunk, until instructed to stop and hold by the subject (Figure 2, bottom). The stretch was held for 30 seconds and repeated twice per training session" (Kluemper. 2006).

Figure 3: The photo on the left shows how the scientists measured how severe the subjects were hunched forward; the graph on the right shows the improvements in posture (reduction = subjects were standing less hunched over) - improvements which reached significance only during the especially important relaxed posture test (Kluemper. 2006).

A 2015 study from the Illinois State University shows that the muscle-energy technique described in this box could be another treatment that can help you reduce your messed up posture by increasing the length of the pectoralis minor and reducing "the hunch" (Laudner. 2015).

Muscle energy techniques - an alternative treatment method? Being passively treated by a physiotherpist appears to be another method that can reduce your postural problems. In a very recent study Laudner, et al. (2015) were able to show that a treatment that involves what the researchers call "muscle energy techniques" will improvements the pectoralis minor length (PML) and forward scapular position in  applied to the pectoralis minor of asymptomatic female swimmers provided - likewise within six weeks. For the MET treatment, participants were asked to lie supine on a standard treatment table with the treatment arm off the table. The treatment arm was then passively moved into horizontal abduction, in line with the pectoralis minor and sternal fibers of the pectoralis major muscle fibers, until the end range of motion was reached.

Due to the possibility of glenohumeral instability among swimmers, the therapists proceeded cautiously in all participants during the MET application. The arm was held at this barrier for 3 seconds. The shoulder was then brought out of the stretch slightly, and the participant was instructed to ‘‘pull against the investigator’s resistance towards the opposite hip.’’ This contraction was performed isometrically with approximately 25% of the participant’s maximal effort for 5 seconds. Immediately after this contraction,  the entire sequence was repeated with the arm again being passively horizontally abducted to the new range of motion.

Figure 4: Overview and description of the exercises in the Lynch study (Lynch. 2010).

"Subjects in the intervention group were trained using an instructional video of the exercises as well as being provided with an illustrated handout. Descriptions of the exercises are shown in tables 2 and 3. Strengthening exercises targeted the periscapular muscles. Stabilisation of the scapula throughout the exercise routine was emphasized during instruction. Subjects performed three sets of 10 repetitions of all strengthening exercises. The stretching portion of the intervention aimed at increasing the flexibility of the pectoralis muscle group and the cervical neck extensors. [...] Subjects logged the number of times the training was performed. Random checks by the investigator were performed to ensure compliance as well as the correct execution of the exercises." (Lynch. 2010).

Figure 5: Changes in forward head angle, shoulder translation and scupalar distance (Lynch. 2015); I deliberately chose the same scale for the primary axis as in Figure 3, even though a direct comparison is not exactly scientific.

A 1990 study by Lo et al. reports that 43.8% of athletes who are competing in sports with upper arm involvement complain about shoulder problems, learn how to fix them in six weeks!

Bottom line: Obviously the way I previously compared the two studies with different subjects and exercises is not exactly scientific - and still, I would be really interested to see a study test my hypothesis that the use of resistance bands and partner assisted stretches would produce greater improvements than body weight exercises and regular stretches, in general.

Until this head-to-head comparison will have been done and my hypothesis will have been confirmed, though, the only thing I can tell you "for sure" is that doing any of the previously outlined exercise + stretching regimes will help you to improve your posture | Comment on Facebook!

• Ghanbari, Ali, et al. "Effect of forward shoulder posture on pulmonary capacities of women." British journal of sports medicine 42.7 (2008): 622-623.
• Kluemper, Mark, Tim Uhl, and Heath Hazelrigg. "Effect of stretching and strengthening shoulder muscles on forward shoulder posture in competitive swimmers." Journal of sport rehabilitation 15.1 (2006): 58.
• Laudner, Kevin G., et al. "Forward Shoulder Posture in Collegiate Swimmers: A Comparative Analysis of Muscle-Energy Techniques." Journal of athletic training 50.11 (2015): 1133-1139.
• Lynch, Stephanie S., et al. "The effects of an exercise intervention on forward head and rounded shoulder postures in elite swimmers." British journal of sports medicine 44.5 (2010): 376-381.