Green Tea Lipids + Statins, PWO CHO + Glycogen, Visceral Fat, Heart Health + Anthrax - Research Update July '17

Matcha releases more antioxidants than tea leaves (Fujioka. 2016).

Only recently, you've read the "Caffeine June 2017 Research Update" [(re-)read it] here at the SuppVersity. Some of the effects of green tea have thus already been discussed. After all, caffeine is one of the health-relevant ingredients of tea; it is, however, not the most important one.

As Yuan Fen et al. explain in their latest meta-analysis of the effects of green tea on blood lipids, tea can be classified as green tea, oolong tea or black tea depending on the manufacturing process" (Fen 2017). What exactly it is that mediates the various health benefits of tea (inflammation, hypertension/heart disease, and cancer | Serafini 2011) and their potency may thus differ slightly from tea to tea.

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For example, "green tea is abundant with kaempferol glycosides, while oolong tea contains more quercetin and myricetin glycosides and black tea is rich in quercetin glycosides" (Fen 2017). Most importantly, however, teas contain substances we call catechins, e.g. epigallocatechin gallate (EGCG), epicatechin gallate (ECG), epigallocatechin (EGC), and epicatechin (EC). EGCG is considered to be is the major and functional component (Fen 2017). Accordingly, hitherto published studies tested or ascribed the health effects of green tea to the high relative amount of EGCG. I have thus chosen both studies using real tea and EGCG/catechin supplements for this SuppVersity Research Update:

• Green tea improves your blood lipids like a statin, but without the side-effect-prone mechanism of blocking cholesterol completely (Fen 2017) -- The effects of green tea consumption on lipid metabolism in people with overweight or obesity was the research interest of the previously cited study by Fen et al. in "Molecular Nutrition & Food Research". Based on 21 published RCTs, the scientists calculated that ...

  

  Figure 1: No clear effect on HDL was observed (Fen 2017).

  "[...] green tea significantly decreased plasma total cholesterol (TC) and low-density lipoprotein cholesterol (LDL) levels in overweight or obese people[, in form of a] 3.38mg/dl [reduction] for TC (95% CI: -6.42, -0.33mg/dl) and -5.29mg/dl [reduction] for LDL (95% CI: -7.92, -2.66mg/dl), respectively" (Fen 2017).

  That sounds great, but the absolute change in LDL is small in comparison to the average statin, which achieves reductions of 69.6 mg/dl (Law 2003).

Warning! EGCG may mess with the efficacy of your statins (and other medications): It's important to note, that EGCG acutely reduces the pharmacokinetics of statins. This has been proven only recently (Kim 2017) for rosuvastatin in healthy volunteers, whose systemic exposure to the drug was reduced by a whopping 19% when EGCG and rosuvastatin were co-administered only once. Interestingly enough, though, two weeks of chronic EGCG supplementation abolished this inhibitory effect. Green tea does that by interacting with a range of intestinal and hepatic organic anion transport peptides (OATPs) and we're yet far from understanding all its drug interactions. Proven have been the previously mentioned interaction with rosuvastatin, as well as interactions with the blood pressure medication (beta blocker) nadolol, and another statin, namely simvastatin, where it had, paradoxically, opposing effects and increased the plasma concentration by inhibiting both, intestinal CYP3A4 and P-gp and hepatic OATP1B1 (Werba 2015).

And there's more. In rodents on high cholesterol diets, scientists from the Hebrew University in Jerusalem have recently been able to demonstrate that the effect of green tea polyphenols on bile acid will overload your livers ability to get rid of cholesterol and thus promote non-alcoholic fatty liver disease (Tirosh 2017) - a phenomenon that has already been observed in human beings, too.

• Accordingly, people who actually need statin drugs because they have a genetically high risk of heart disease would be ill advised to try and replace their medications with green tea - not just, but also because "green tea's effect on plasma TG and HDL must be further evaluated by additional high-quality and large-scale RCTs" (Fen 2017) - also to answer, among others, the following question.
  • the differential effects of caffeinated and decaffeinated green tea on triglycerides (↕ for regular ↘ for decaffeinated green tea)
  • differences in health effects in healthy overweight or obese individuals vs. unhealthy overweight or obese individuals (in whom the scientists' subgroup analyses, for example, showed sign. reductions in triglycerides that were not observed in healthy subjects)
  • age-effects that couldn't be analyzed in the current meta-analysis of studies in which people from all age groups (from children to the elderly) participated
  • the seriousness and root cause of side effects, which were transient, but were still reported in four of the twenty-one trials
  For (lean and obese) individuals who are interested in overall heart health and don't have a genetically determined increased risk of heart disease, the 2-4 cups of green tea (or 300-1500mg green tea extract) the subjects in the 21 RCTs certainly are the better choice for cholesterol control - after all, the reduction in total (TC) and low-density cholesterol/lipoproteins (LDL) occurs in the absence of headaches, flushing, weakened and impaired skeletal muscle, diabetes, and liver injury - all repeatedly reported side effects of statin therapy (Mancini 2011; Chaipichit 2015; Castro 2016).

600mg/day Anything Beyond That and EGCG May Mess W/ Your Liver Health! Scientists Propose 300mg/day Limit for EGCS in Food Supplements (read the SuppVersity Facebook News Post from July 2nd, 2017). While evidence that the real deal, i.e. green tea can damage your liver, things look different for supplements with isolated catechins, esp. EGCG.

Dekant et al. recently reviewed the existing literature and came to the conclusion that EGCG has the potential to induce hepatic damage. Based on the finding that "[i]n clinical intervention studies, liver effects were not observed after intakes below 600mg EGCG/person/day," the researchers propose a "tolerable upper intake level of 300mg EGCG/person/day" which would give you "a twofold safety margin" (Dekant 2017).

• New study questions previously reported beneficial effects of green tea on post-exercise glycogen resynthesis, but... (Tsai 2017) -- You will remember my article from last October in which I outlined that "Green Tea Extract Reduces the Amount of Insulin You Need to Store Your PWO Carbs by ~20%" (read it). A recent study in the British Journal of Nutrition does now suggest that these effects may at least be dose-dependent.
  
  Unlike the previously cited study by Martin et al. (2016) used 3x350mg of green tea extract (GTE) for one week, Tsai et al. administered a significantly lower dose of GTE (500 mg/d) for 8 weeks. Furthermore, the scientists used a low-intensity workout and a carbohydrate-enriched meal, instead of a graded exercise and 75g of pure glucose as post-workout (PWO) nutrition.
  

  

  Figure 2: While the study did not confirm the beneficial effects on PWO glucose metabolism, it found a sign. reduced PWO RER (a), i.e. ratio of CHO:FAT oxidation, due to higher fat oxidation rates w/ GTE (Tsai 2017).

  In all honesty, it is thus not surprising that Tsai et al. observed only one significant benefit of GTE supplementation: it increased exercise-induced muscle GLUT type 4 (GLUT4) protein content of the vastus lateralis and the energy reliance on fat oxidation compared with the placebo trial (P<0·05). That there were no differences in blood glucose and insulin responses between the two trials may simply be a function of the comparatively slow rise in blood glucose in response to the test meal with a GI of "only" 76.6 (23.4% lower than glucose).
• Even on a normal diet, green tea prevents visceral adiposity (Raso 2017) -- While we do have dozens of studies showing that green tea alleviates the (visceral) body fat accumulation in response to unhealthy, hypercaloric diets, the latest rodent study by Raso et al. is the first study to investigated the effects of administering green tea as the main source of hydration on visceral fat accumulation in the long run - in human terms 45 years!
  

  

  Figure 3: Changes in relative (per kg body weight) and absolute visceral fat over the course of what would be 45 years in human beings with either water or green tea as the main source of hydration (Raso 2017).

  And the results are, as you can see in Figure 3, quite significant: While all animals, which were young at the beginning of the study, showed a sign. increase in weight and visceral fat over the course of the 18-week study, the visceral fat gains proportional to the weight of the animals were different between the groups. In that, the green tea group had a significantly smaller gain in visceral fat compared to body weight, resulting in a smaller area of visceral fat per kilogram body weight at the end of the experiment compared to the control group (p < 0.01).

Table 1: Research overview (Oz 2017 | free full text)

SuppVersity Suggested Read: "Chronic Inflam-matory Diseases and Green Tea Polyphenols" (free full-text). It is well known that green tea polyphenols (GrTPs) are potent antioxidants with important roles in regulating vital signaling pathways. This review summarizes how they act on transcription nuclear factor-kappa B and related proteins to ameliorate the surge of inflammatory markers like cytokines and production ofcyclooxygenase-2.

• Anthrax? Green tea can kill Bacillus anthracis the etiologic agent of the infamous infective disease anthrax that has been used to threaten people and governments by terrorists before (Falcinelli 2017) -- 10 days, that's the time that you have left on earth if you're infected with anthrax spores, spores that can infect you if you touch infected meat or breath in anthrax spores. The corresponding ease of infection is one the reasons that politicians and researchers fear the possible future use of B. anthracis as a bioterrorism agent.
  

  

  Figure 4: Green tea inhibits growth and kills Bacillus anthracis in Luria Broth. CFU/ml of bacilli grown for 4 h in the presence of 10% black tea or 10% green tea. n = 3. p = 0.08, black tea. *p < 0.01, green tea (Falcinelli 2017)

  This fear has resulted in an impetus to develop more effective protective measures and therapeutics. In their latest study, Falcinelli, et al. show that green tea inhibits the growth of B. anthracis - albeit yet only in vitro.
  
  As you probably already expected, it's epigallocatechin-3-gallate (EGCG) that was shown to be responsible for this activity. Yet even though EGCG was clearly bactericidal against both the attenuated B. anthracis ANR and the virulent, encapsulated strain B. anthracis Ames strain, future studies will have to show if and how green tea and EGCG can be used in human beings to prevent or battle anthrax infections... which reminds me to remind you, that GTE has also been shown to be a useful natural disinfectant able to limit enteric viral contaminations conveyed by food and food-contact surface (Randazzo 2017).

Can green tea "fix" Alzheimer's? Latest review of the efficacy of Epigallocatechin-3-gallate (EGCG from green tea) in the treatment of Alzheimer’s disease says that even though "in recent years, natural compounds, due their antioxidants and anti-inflammatory properties have been largely studied and identified as promising agents for the prevention and treatment of neurodegenerative diseases, including AD," the authors highlight that the "promising results" come exclusively from "pre-clinical" studies, so that "drawn clinical trials are extremely needed" (Cascella 2017) before we can tell how useful EGCG is whether it has preventive effects, only or can also be used to ameliorate if not curative Alzheimer's when someone is already experiencing symptoms.

• Part of the heart health benefits of green tea are not about EGCG and green tea extracts don't help with blood flow either, while real tea does (Lorenz 2017) -- In a randomized crossover study, a single dose of 200 mg EGCG was applied in three different formulas (as green tea beverage, green tea extract (GTE), and isolated EGCG) to 50 healthy men. Flow-mediated dilation (FMD) and endothelial-independent nitro-mediated dilation (NMD) was measured before and two hours after ingestion. Plasma levels of tea compounds were determined after each intervention and correlated with FMD.
  
  

  

  Figure 5: Only green tea increased flow-mediated dilation (FMD). Subjects consumed 200 mg of EGCG as isolated EGCG, GTE, or green tea after fasting overnight. An equal volume of hot water served as control. Green tea significantly increased FMD compared to GTE, EGCG, and water as control. Water slightly decreased FMD, whereas EGCG and GTE had little effects. Data are means ± SEM from n = 50 subjects. All p-values by repeated measures ANOVA followed by post hoc Bonferroni (Lorenz 2017).

  FMD significantly improved after consumption of green tea containing 200 mg EGCG (p < 0.01). However, GTE and EGCG had no significant effect on FMD. NMD did not significantly differ between interventions. EGCG plasma levels were highest after administration of EGCG and lowest after consumption of green tea.
  
  Even though the plasma levels of caffeine increased after green tea consumption, caffeine is not exactly the most likely among the various candidate ingredients that could take EGCG's place as an active ingredient responsible for green tea's (drink) ability to improve flow-mediated dilation. After all, previous studies suggest that coffee rather decreases than increases FMD (Papamichael 2005). Since similar effects have been observed by Heiss et al. in 2007 for a high-flavanol cocoa drink, other phenolic constituents of green tea, which obviously cannot be found in green tea extracts are much likelier candidates.

Hot or not? That could be a matter of health or ah... well almost death ;-) Learn why in my previous article "To Boil or Not to Boil? What's Going to Make Your Tea the Healthiest? Recent Study: It Depends on the Type of Tea"

How do I prepare the healthiest green tea? Now that you've learned that a DIY water-extract from green tea is better than commercially available extracts in pills or capsules (at least for FMD), this question is probably preying on your minds.

The answer to this important question comes from a study that will not be officially published before November this year. A study that shows that increasing the extraction temperature will also increase the polyphenol content of your tea. Thi sin turn enhances not just the antioxidant activity of the brew, it will also boost its ability to inhibit α-glucosidase and α-amylase, in vitro. In vivo, however, green tea steeped at 60°C had significantly stronger glucose uptake inhibitory activity (p<0.05) than green tea that was prepared at 100°C.

The answer to the previously raised question "Hot to brew the perfect tea?" is thus both, context- and, as previously discussed research suggested, also type-dependent | Comment.

References:

• Chaipichit, Nataporn, et al. "Statin adverse effects: patients’ experiences and laboratory monitoring of muscle and liver injuries." International Journal of Clinical Pharmacy 37.2 (2015): 355-364.
• Cascella, Marco, et al. "The efficacy of Epigallocatechin-3-gallate (green tea) in the treatment of Alzheimer’s disease: an overview of pre-clinical studies and translational perspectives in clinical practice." Infectious Agents and Cancer 12.1 (2017): 36.
• Castro, M. Regina, et al. "Statin use, diabetes incidence and overall mortality in normoglycemic and impaired fasting glucose patients." Journal of general internal medicine 31.5 (2016): 502-508.
• Dekant, et al. "Safety assessment of green tea based beverages and dried green tea extracts as nutritional supplements." Toxicol Lett. 2017 Jun 24. pii: S0378-4274(17)30233-3. doi: 10.1016/j.toxlet.2017.06.008. [Epub ahead of print]
• Falcinelli, S.D. et al. "Green tea and epigallocatechin-3-gallate are bactericidal against Bacillus anthracis." FEMS Microbiol Lett. 2017 Jun 12. doi: 10.1093/femsle/fnx127. 
• Fujioka K, et al. "The Powdering Process with a Set of Ceramic Mills for Green Tea Promoted Catechin Extraction and the ROS Inhibition Effect." Molecules. 2016 Apr 11;21(4):474. doi: 10.3390/molecules21040474.
• Heiss, Christian, et al. "Sustained increase in flow-mediated dilation after daily intake of high-flavanol cocoa drink over 1 week." Journal of cardiovascular pharmacology 49.2 (2007): 74-80.
• Kim, Tae-eun, et al. "effect of epigallocatechin-3-gallate, major ingredient of green tea, on the pharmacokinetics of rosuvastatin in healthy volunteers." Drug design, development and therapy 11 (2017): 1409.
• Lorenz, Mario, et al. "Tea-induced improvement of endothelial function in humans: No role for epigallocatechin gallate (EGCG)." Scientific Reports 7 (2017).
• Mancini, GB John, et al. "Diagnosis, prevention, and management of statin adverse effects and intolerance: proceedings of a Canadian Working Group Consensus Conference." Canadian Journal of Cardiology 27.5 (2011): 635-662.
• Papamichael, Chris M., et al. "Effect of coffee on endothelial function in healthy subjects: the role of caffeine." Clinical Science 109.1 (2005): 55-60.
• Randazzo, W. et al. "Effect of green tea extract on enteric viruses and its application as natural sanitizer." Food Microbiol. 2017 Sep;66:150-156. doi: 10.1016/j.fm.2017.04.018. Epub 2017 May 3.
• Raso, et al. "Effects of chronic consumption of green tea on weight and body fat distribution of Wistar rats evaluated by computed tomography." Acta Cir Bras. 2017 May;32(5):342-349. doi: 10.1590/s0102-865020170050000003.
• Serafini, Mauro et al. "Health Benefits of Tea" in Herbal Medicine: Biomolecular and Clinical Aspects. 2nd edition. Benzie IFF, Wachtel-Galor S, editors. Boca Raton (FL): CRC Press/Taylor & Francis; 2011.
• Shahid, Saleem Ullah, et al. "Effect of SORT1, APOB and APOE polymorphisms on LDL-C and coronary heart disease in Pakistani subjects and their comparison with Northwick Park Heart Study II." Lipids in health and disease 15.1 (2016): 83.
• Tehrani, H.G. et al.  "Effect of green tea on metabolic and hormonal aspect of polycystic ovarian syndrome in overweight and obese women suffering from polycystic ovarian syndrome: A clinical trial." J Educ Health Promot. 2017 May 5;6:36. doi: 10.4103/jehp.jehp_67_15. eCollection 2017.
• Tirosh, Oren, et al. "OP-17-Tea Extracts-induced Liver Injury: Lipotoxic Interaction Between Lipids and Polyphenols." Free Radical Biology and Medicine 108 (2017): S8.
• Tsai, et al. "Effect of green tea extract supplementation on glycogen replenishment in exercised human skeletal muscle." Br J Nutr. 2017 Jun 20:1-8. doi: 10.1017/S0007114517001374. [Epub ahead of print]
• Werba, Jose, P et al. "Overview of green tea interaction with cardiovascular drugs." Current pharmaceutical design 21.9 (2015): 1213-1219.

Low(er) Carb Crossfitters May be Missing Out | 11.1% vs. 4% Rep Increase With 6-8g/kg CHO in 12-Min Rohoi Benchmark

If there's one thing all crossfit WODs have in common it's their profoundly anaerobic, meaning glucose burning, nature

I don't care if you love or hate Crossfit. Why's that? "Liking" has nothing to do with science and science tells us that CrossFit is a highly demanding continuously glycogenolytic workout. In other words: while you will be burning fat, as well, the Crossfit workouts are mainly powered by glucose / glycogen.

Accordingly, scientists from the University of New Mexico, the California State and the Kennesaw State University speculated that with glucose / glycogen being the main energy resource crossfitters are using, adequate (or high) carbohydrate intakes may be "even more crucial to performance" for crossfitters than it is for other athletes.

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Now, it is one thing to be able to show that an acute failure of glycogen repletion will acutely impair your performance. performance. It is a whole different thing, however, to assess the long(er)-term effect of the relatively low carbohydrate intake that's still prevalent in the world of crossfitters; a study addressing metabolic and performance variables following CHO manipulation during a CrossFit workout; a study as the one Escobar et al. have recently conducted.

In their 9-day experiment, the scientists investigated the effect of three consecutive days of high CHO intake (6-8 g/kg/day) during a period of training on CrossFit performance and corresponding metabolically-related variables in strength-trained individuals who have previously maintained a moderately-low CHO intake <6 g/kg/d.

The 12-minute Rahoi workout is used as a performance benchmark in the CrossFit community. It involves doing as many  rounds of the above box jump, thruster and bar facing burpee cycle (img from ifailedfran.com)

"CrossFit performance was measured in repetitions completed during a 12 minute CrossFit workout (Rahoi) performed on days 1, 5, and 9. From days 6- 8, the CHO group increased CHO intake from < 6 g/kg/day to 6-8 g/kg/day whereas the C group maintained their current intake of < 6 g/kg/day.

Subjects performed prescribed CrossFit workouts on days 6 and 7, followed by a day of rest prior to the final performance test on day 9. The present design was aimed to mimic a mid CrossFit-training period thereby investigating the effect of CHO intake and performance amidst a period of training.

During performance tests (days 1, 5, 9), in addition to repetitions completed, oxygen consumption (VO2), respiratory exchange ratio (RER), and blood lactate (BL) were measured" (Escobar. 2016).

As the authors point out, there was a main effect for time, meaning that both groups saw an increase in repetitions completed.

What about the "real long term"? Unfortunately, there is only one study that comes remotely close to an actual long-term study. It's Outlaw's et al.'s 2014 study in which crossfitters received 19 g of a pre-workout drink (extracts of pomegranate, tart cherry, green and black tea) 30 minutes before and a post-workout protein (females: 20 g; males: 40 g) and carbohydrate (females: 40 g; males: 80 g) with every workout. A study which found only likely beneficial (74.40%) for increasing power and maintaining VO2MAX (78.16%) during CrossFit-type training... and no, that's it: there ain't more research on CHO modifications and long(er)-term adapation to CrossFit workouts.

The data in Figure 1 tells you, however, "a more notable change was observed in the CHO group (+15.22; +10.9%) vs. that in the baseline sessions" (Escobar. 2016). That the difference didn't reach statistical significance is, as the scientists point out, possibly due to the large standard deviations and the small effect size (.354) in this 9-day study (you cannot expect a huge adaptational response within only what effectively were only 3 days, i.e. days 6-9 during which the subjects consumed their extra-carbs while training on day 6 and 7, rest on day 8 and the re-test on day 9).

Figure 1: Pre- vs. post changes in reps performed, Mean VO2 and respiratory exchange ratio (Escobar. 2016).

Needless to say that we cannot tell if the additional reps will translate to a more rapid adaptational response in form of strength or size gains. What is quite interesting, though, is that the high-CHO group improved their intra-workout fat burning rate (as evidenced by a lower RER) more than the subjects on the moderate carbohydrate diets. Diets of which common wisdom would tell you that their <6g/kg body weight CHO content should favor fatty acid oxidation compared to the 6-8g/kg high carbohydrate intake - that's also interesting, because, in a dietary isocaloric scenario, doing more reps and thus burning more calories at a slightly lower RER should promote not (as many of you  may fear) reduce fat loss. Eventually, future studies will have to show, though, whether this is "just" a transient performance increase due to better.-stocked glycogen stores or a training advantage that could give you the adaptational edge that makes the difference between "making gains" and "making outstanding gains" and thus, eventually, amateur- vs. pro-performance.

The number of studies on CrossFit has increased, but it doesn't match the 15-20x increase in interest Google Trends recorded from 2007 to today; below you will find a brief overview of recent and not so recent study results.

Speaking of gains, can you even make gains on CrossFit or will you just injure yourself? Well, even though the number of studies on CrossFit has been continuously increasing over the decade, what we can tell for sure is this:

• CrossFit-based high-intensity power training improves maximal aerobic fitness and body composition -- in Smith et al. 2013, for example, the male and female subjects lost 4% body fat (from 22%) and 3% (from 26%), respectively, while significantly improving their VO2max - irrespective of their baseline fitness level
• CrossFit workouts are injury-prone - not more injury prone than O-lifting, though -- that's at least what Hak et al. (2013) found; in their 2013 paper they report an injury rate of 3.1 per 1000 hours trained [shoulder (1.18 per 1000 hours training | Summitt. 2016) and spine injuries predominate] - a result that is "similar to that reported in the literature for sports such as Olympic weight-lifting, power-lifting and gymnastics [but] lower than competitive contact sports such as rugby union and rugby league" (Hak. 2013); more recently, Weisenthal, et al. (2014) reported injury rates of approximately 20%, with men being more prone to injuries than women (leave your ego at the door, boys!)
• CrossFit is so successful, because it's motivating -- Katie Heinrich et al. (2014) confirmed that two years ago in a study that compared a CrossFit™ workout to a classic aerobic + resistance training combination and found the former workout to keep people on track, i.e. they maintained their exercise enjoyment and were more likely to intend to continue after the 8-week intervention; and, more recently, Eather et al. (2016) showed that teens love it (rather the teen version), too - a satisfaction score ranging from 4.2 to 4.6 out of 5 points ain't bad, for sure
• CrossFit is not more taxing than running -- at least if we measure "taxing" by the oxidative stress that's generated during a workout, a measure of which Kliszczewicz, et al. (2015) have recently shown that they are similar for treadmill running and crossfitting

Now, this is not a CrossFit advertisment-article, so, I would like to remind you that, even if you're not CrossFitting, an increased or at least adequate carbohydrate intake will have scientifically proven benefits for athletes from various other sports - with the "optimal" intake depending on the pecularities of the sports / training and individual (Jeukendrup. 2014; Pöchmüller. 2016).

Want to put your carbs to good use? Try these "Two Crazy, but Scientifically Proven Workouts if You Want to Gain Muscle While Losing Fat" | more

Crossfitters, is it time to carb up? It's too early to answer this question with a clear "yes" or "no". The study at hand does, however, suggest that the "CrossFit-embraced practice of a moderately-low CHO diets such as the Paleolithic (Paleo) and Zone Diets (40% of daily energy intake)" (Escobar. 2016), may provide adequate CHO intakes during the short run (3 days); in periods of daily or almost daily training that last longer than 3 days, however, the observed trend of decreasing performance gains could be of concern. So, if 5-7 highly glycolytic workouts (CrossFit or not) a week sounds like you, it may at least be worth experimenting with an increased (not necessarily 8g/kg body weight ;-) CHO intake and/or strategic refeeds | Comment!

References:

• Eather, Narelle, Philip James Morgan, and David Revalds Lubans. "Improving health-related fitness in adolescents: the CrossFit Teens™ randomised controlled trial." Journal of sports sciences 34.3 (2016): 209-223.
• Escobar, Kurt A., Jacobo Morales, and Trisha A. VanDusseldorp. "The Effect of a Moderately-low and High Carbohydrate Intake on Crossfit Performance." International Journal of Exercise Science 9.4 (2016): 8.
• Hak, Paul Taro, Emil Hodzovic, and Ben Hickey. "The nature and prevalence of injury during CrossFit training." Journal of strength and conditioning research/National Strength & Conditioning Association (2013).
• Heinrich, Katie M., et al. "High-intensity compared to moderate-intensity training for exercise initiation, enjoyment, adherence, and intentions: an intervention study." BMC Public Health 14.1 (2014): 1.
• Jeukendrup, Asker. "A step towards personalized sports nutrition: carbohydrate intake during exercise." Sports Medicine 44.1 (2014): 25-33.
• Kliszczewicz, Brian, et al. "Acute Exercise and Oxidative Stress: CrossFit™ vs. Treadmill Bout." Journal of human kinetics 47.1 (2015): 81-90.
• Outlaw, Jordan J., et al. "Effects of a pre-and post-workout protein-carbohydrate supplement in trained crossfit individuals." Springerplus 3.1 (2014): 369.
• Pöchmüller, Martin, et al. "A systematic review and meta-analysis of carbohydrate benefits associated with randomized controlled competition-based performance trials." Journal of the International Society of Sports Nutrition 13.1 (2016): 27.
• Smith, Michael M., et al. "Crossfit-based high-intensity power training improves maximal aerobic fitness and body composition." The Journal of Strength & Conditioning Research 27.11 (2013): 3159-3172.
• Summitt, Ryan J., et al. "Shoulder injuries in individuals who participate in crossfit training." Sports Health: A Multidisciplinary Approach (2016): 1941738116666073.
• Weisenthal, Benjamin M., et al. "Injury rate and patterns among CrossFit athletes." Orthopaedic journal of sports medicine 2.4 (2014): 2325967114531177.

Post-Workout Coffee Boosts Glycogen Repletion by Up to 30% and May Even Have Sign. Glucose Partitioning Effects

Yes, I do suggest that it may be beneficial to drink these two and another two cups of coffee w/ lots of sugar after your workout - if you are an athlete, at least.

A delicious and refreshing pre-workout coffee or just plain caffeine from pre-workouts are probably on the supplement list of most of the SuppVersity readers. Whether the same is the case for a post-workout coffee, let alone caffeine tablets, though, is questionable. Just as questionable, as the common belief that you better stay away from coffee at any time after your workouts, by the way.

If you look at the existing literature, the effects of post-workout caffeine ingestion are not exactly an intensely researched area. And still, the evidence does more or less strongly support the notion that a post-workout coffee could be as beneficial as its pre-workout analog - in a different area.

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Caffeine Resis- tance - Does It Even Exist?

Initial evidence that the post-workout ingestion of caffeine may have beneficial effects on post-workout gylcogen resynthesis and thus an important part of the recovery process comes from a 2004 study by Battram et al. (2004). Back in the day, Battram assumed - just like you probably did - that the ingestion of caffeine after prolonged exercise would impede the resynthesis of proglycogen and macroglycogen carbohydrate supplementation in humans.

Figure 1: Total glycogen [proglycogen (PG) macroglycogen (MG)] glycogen concentrations during 5 h of recovery in the placebo trial (A) and caffeine trial (B | Battram. 2004).

As you can easily see if you compare the data in Figure 1 (A) for the placebo trial with the data in Figure 1 (B), which was generated in the trial in which the healthy young men who participated in Battram's study received a whopping dose of 6mg/kg of caffeine, there is no ill effect on post-workout gylcogen resynthesis even with high dose caffeine supplementation.

"In conclusion, Caf ingestion does not impede the resynthesis of PG or MG after an extensive depletion of muscle glycogen and with the provision of exogenous dietary carbohydrate" (Battram. 2004).

As surprising as this may be in view of the inhibitory effect of caffeine on full-body glucose uptake (in Battram's study there was also a significantly higher blood glucose concentration in the caffeine
trial), Battram's results are still no outliers. Rather than that, a follow up study by Pedderson et al. found that, in trained subjects, coingestion of large amounts of Caff (8 mg/kg BM) with CHO has an additive effect on rates of postexercise muscle glycogen accumulation compared with consumption of CHO alone" (Pedderson. 2008).

Even though Beelen's study does not support the the superior effect of caffeine on muscle gylcogen, it does at least show that the effect (if it occurs) would probably be identical for fast- and slow-twitch muscles and thus similarly beneficial for strength and endurance athletes (Beelen. 2011).

So, there is no doubt that this works? Well, as usual, there is doubt. Another 2011 study by Beelen et al. did not find the same increases in glycogen resynthesis. It is well possible, though that this was due to either the fact that they pumped their subjects up with even higher amounts of carbs, though (1mg/kg/h in Pedderson vs. 1.2mg/kg/h in Beelen) and lower amounts of caffeine (15% less). In view of the fact that the exercise protocol used in the study only halved the glyocogen levels of the subjects, while it was reduced by >75% in the Pedderson study, the lack of effect may also be a result of the lack of full glycogen depletion in Beelen's study (unfortunately, the authors don't provide their values only in arbitrary units - that's why I can't tell you with certainty to which degree this may have influenced the results).

In that, it is important to point out that the increased glycogen resynthesis in Pedderson's randomized, double-blind crossover study, in which the young well-trained subjects performed intermittent exhaustive cycling and then consumed a low-CHO meal before they rode until volitional fatigue and consumed either

• CHO [4 g/kg body mass (BM)] alone or
• CHO [4 g/kg body mass (BM)] with Caff (8 mg/kg BM)

at the beginning of the 4 h of passive recovery phase, did not occur at the expense of the restoration of the high energy substrates ATP and PCr (see Figure 2) - since the latter two are especially relevant for people who lift weight, sprint and do other high intensity stuff, there's no reason to believe that the caffeine + sugar post-load was something only endurance athletes could use.

Figure 2: High dose caffeine (8mg/kg) increases glycogen resynthesis after exhausting workouts without having ill effects on the resynthesis of ATP and PCr (Pedderson. 2008).

Apropos "using" this strategy: Another three years later, Taylor et al. (2011) expanded on the results of Battram (2004) and Pedderson (2008) in a study in which they went beyond testing the mere amount of glycogen that was transported into the muscle and evaluated its effect on the subjects' performance in a post-recovery high-intensity interval-running capacity test.

Figure 3: Exercise capacity during the Loughborough Intermittent Shuttle Test for the carbohydrate (CHO), CHO plus caffeine (CHO+CAFF), and water (WAT) trials. Lines represent individual subject responses (Taylor. 2011).

As you can easily see in Figure 3, the HIIT advantage, which was tested 4h after the glycogen-depleting exercise protocol and the ingestion of 1.2g/kg carbohydrate +/- 8mg/kg caffeine via an Intermittent Shuttle Test (LIST) to volitional exhaustion, was about as pronounced as the glycogen-advantage Pedderson et al. observed three years before (albeit with some inter-individual differences).

Why would you say caffeine may have a partitioning effect? The answer is easy: While fat cells need insulin to transform and store significant amounts of glucose, muscle cells don't - specifically after workouts the increase in GLUT-4 receptor expression and glucose uptake occurs largely without requiring insulin as a trigger. Now, caffeine's ill effects on blood glucose are due to its ability to block the insulin signalling via beta-adrenergic activity (Thong. 2002). It should thus reduce the glucose uptake by the fat cells while decreasing the rate, but not the total amount of glucose that is taken up and stored by the muscle... speaking of rate and total amount: This hypothesis is fully in line with the initially cited study by Battram et al. who observed just that: a decreased rate, but identical total increase in muscle glycogen.

So why haven't we been taking our post-workout caffeine for years, now? Well, I guess the reason is that it is not sure how the effects of caffeine on the sympathetic nervous may effect other factors of the recovery process. In view of the fact the central nervous system will be "on fire" after any workout, though, it is questionable whether adding in 400-800mg caffeine will actually affect its recovery.

A better reason for not (yet) subscribing to the post-workout caffeine binges would thus be that (a) few of us actually need to refill their glycogen stores in 4-6h after a workout and that we (b) have no real clue what the mechanism is. If it was actually - as some of the data would suggest - a selective inhibition of fat cell glucose uptake (see box on the right), even those of us who don't have to restore their glycogen stores as fast as possible may see beneficial effects on body composition. If, on the other hand, it works by stimulating the intestinal absorption of glucose, only (cf. Van Nieuwenhoven. 2000), the real world implications for the average trainee would be significantly less pronounced | Comment on Facebook!

References:

• Battram, Danielle S., et al. "Caffeine ingestion does not impede the resynthesis of proglycogen and macroglycogen after prolonged exercise and carbohydrate supplementation in humans." Journal of Applied Physiology 96.3 (2004): 943-950.
• Beelen, Milou, et al. "Impact of caffeine and protein on postexercise muscle glycogen synthesis." Med Sci Sports Exerc 44.4 (2012): 692-700.
• Pedersen, David J., et al. "High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine." Journal of Applied Physiology 105.1 (2008): 7-13.
• Taylor, Conor, et al. "The effect of adding caffeine to postexercise carbohydrate feeding on subsequent high-intensity interval-running capacity compared with carbohydrate alone." International Journal of Sport Nutrition andExercise Metabolism 21.5 (2011): 410.
• Thong, Farah SL, and Terry E. Graham. "Caffeine-induced impairment of glucose tolerance is abolished by β-adrenergic receptor blockade in humans." Journal of applied physiology 92.6 (2002): 2347-2352.
• Van Nieuwenhoven, M. A., R-JM Brummer, and F. Brouns. "Gastrointestinal function during exercise: comparison of water, sports drink, and sports drink with caffeine." Journal of applied physiology 89.3 (2000): 1079-1085.

Nitrate for Muscle+Brain Performance | Walking for Glucose Management | Full Glycogen Stores W/Out Excessive Water Retention | 5x10, 10x10, Cardio How mTOR and Co Respond

If Yap et al. were right and only continuous and not accumulative physical activity mattered, activity trackers like the this would be useless. No one needs a device to remind him of the 30 min of brisk walking he did / skipped today.

In today's installment of SuppVersity "On Short Notice", we're going to take a closer look at a selection of recent papers from the European Journal of Applied Physiology. To be more specific, I will discuss the physiological and psychological effects of dietary nitrate and their potential significance for team athletes. From there we're taking a detour to glycogen resynthesis and its interaction with hydration - a topic that may be highly relevant for bodybuilders and at least interesting for everyone else. Before we then take a departing look at the differential effects of 5x10, 10x10 and endurance exercise on markers of protein synthesis and glucose uptake, we'll spend briefly review the claim that the cumulative physical activity (the one you measure w/ step counters) would lack the characteristic health benefits everyone expects from meeting his daily activity goals.

Read more about exercise-related studies at the SuppVersity

Tri- or Multi-Set Training for Body Recomp.?

Alternating Squat & Blood Pressure - Productive?

Pre-Exhaustion Exhausts Your Growth Potential

Full ROM ➯ Full Gains - Form Counts!

Body Pump, Cardio & Exercise Expenditure

Study Indicates Cut the Volume Make the Gains!

• Dietary nitrate improves sprint performance and cognitive function during prolonged intermittent exercise - While anyone of you should know that nitrate from beetroots can have significant physiological effects, the observations Thompson et al. made in their recent double-blind randomised crossover study are probably real news and above all practically relevant for some of you and/or your clients from various athletic domains (Thompson. 2015).
  
  To investigate the effects of dietary NO3(-) supplementation on exercise performance and cognitive function, the scientists had 16 male team-sport players consume NO3(-)-rich (BR; 140 mL/day; 12.8 mmol of NO3(-)), and NO3(-)-depleted (PL; 140 mL day/1; 0.08 mmol NO3(-)) beetroot juice for 7 days (these are the regular shots you can buy at supplement stores | if you want to drink regular beetroot juice, you need 3-4x the amount). With the nitrate supplement being consumed over a one week period we are thus not talking about the effects of acute, but about the effects of chronic supplementation. Keep that in mind, if you buy one shot and don't feel the results immediately.
  
  On the test day the subjects completed a prolonged intermittent sprint test (IST) protocol (two 40-min "halves" of repeated 2-min blocks consisting of a 6-s "all-out" sprint, 100-s active recovery and 20 s of rest) on a cycle ergometer during which cognitive tasks were simultaneously performed.

  

  Figure 1: Comparison of total work during the sprints and reaction times during cognitive decision making tasks designed to emulate the cognitive tasks during team sports (Thompson. 2015).

  As you can see in Figure 1 both, the total work done during the IST, as well as the reaction times that were measured during cognitive tasks in the second half of the IST, were improved in the beetroot vs. placebo trial.
  
  Even though, the scientists didn't find a difference in response accuracy, the findings are highly relevant for any athlete who has to (a) perform at high intensities, while (b) maintaining optimal cognitive performance and decision-making reaction times. Who is that? Well, I'd say almost every team sport athlete of whom previous studies have shown that his / her cognitive acuity suffers during prolonged intermittent exercise. 
• Extra water is not necessary for optimal glycogen replenishment after workouts - In fact, bodybuilders may want to avoid it... Avoid water? No, I am not saying you should not drink water at all, but if you look at the results of Valentín E. Fernández-Elías' recent "analysis of the relationship between muscle water and glycogen recovery after prolonged exercise in the heat in humans" you will see that too much water in the post-workout window may actually give you the 'watery' look some physique athletes like bodybuilders are trying to avoid.
  
  It is usually stated that glycogen is stored in human muscle bound to water in a proportion of 1:3 to 1:4 g. In their latest study, the scientists from the University of Castilla-La Mancha investigated this proportion in biopsy samples that were taken when their trained subjects recovered from prolonged exercise in the heat:

  "On two occasions, nine aerobically trained subjects (VO2max = 54.4 ± 1.05 mL/kg/min; mean ± SD) dehydrated 4.6 ± 0.2 % by cycling 150 min at 65 % VO2max in a hot-dry environment (33 ± 4 °C). One hour after exercise subjects ingested 250 g of carbohydrates in 400 mL of water (REHLOW) or the same syrup plus water to match fluid losses (i.e., 3170 ± 190 mL; REHFULL). Muscle biopsies were obtained before, 1 and 4 h after exercise" (Fernández-Elías. 2015).

  In contrast to what you may have expected, the muscle glycogen replenishment was not impaired by the lack of water in the REHLOW group. Ok, if you look at the data in Figure 2 right, there is a minimal advantage for the adequate water group, but this advantage is not statistically and almost certainly not practically relevant (79 ± 15 and 87 ± 18 g/kg dry muscle; P = 0.20).
  

  

  Figure 2: Muscle water content before and after dehydrating exercise and after 3 h recovery period (a). Muscle glycogen content before and after dehydrating exercise and after 4 h recovery period (b). Data is presented as mean ± SD. *Different from previous time point. †Different from REHFULL (P < 0.05 | Fernández-Elías. 2015).

  The thing that did differ between the adequat (REHFULL) and the inadequate (REHLOW) hydration trial, however, was the muscle water content which was significantly higher in the REHFULL than in the REHLOW trial (3814 ± 222 vs. 3459 ± 324 g/kg dm, respectively; P < 0.05; ES = 1.06).
  
  

  

  SuppVersity Suggested: "Hydrated or Dumb: Dehydration Affects Brain, Muscle and Other Vital Organs - Plus: 15+ Causes of Dehydration + Can the Color of Your Urine Tell You if You Drink Enough?" After reading this SV Classic and my recent article about the link between dehydration and type II diabetes you will probably stop thinking about using dehydration more than just occasionally.

  What's even more striking is that the scientists analysis of the ratio in which water and glycogen were stored in the two groups showed that subjects in the REHLOW trial stored the glycogen at the minimal 1:3 glycogen : water ratio, while their peers who got plenty of water exhibited a glycogen : water ratio of 1:17. Needless to say that this difference in water storage may be very important for bodybuilders during the last days and hours of their contest prep. In view of the importance of optimal hydration for your health, cognition and the hitherto unproven hypothesis that increases in cellular water may be involved in the hypertophy response to exercise (including the efficacy of creatine | Op‘t Eijnde. 2001), (non-)rehydration practices as they were used in the study at hand are nothing I would generally recommend. 
• Study says: Only continuous, not accumulated 30 min of walking will improve your glucose sensitivity - While step counters suggest that all you have to do to improve your health is to take "X" steps per day, the conclusion of a recent study from the DSO National Laboratories in Singapore refutes the simple and beautiful idea that you can distribute the X number of steps you would usually take during 30 minutes of brisk walking over three or more small "exercise servings" and see the same benefits as you'd see with 30 minutes of continuous brisk walking:

  "These findings demonstrate that 30 min of brisk walking is sufficient to improve insulin sensitivity in healthy, young Asians but only continuous and not accumulated walking provides this benefit. " (Yap. 2015).

  In said study, twenty-five healthy participants (12 males) participated in an oral glucose tolerance test (OGTT) the morning after: (i) accumulating three 10 min bouts of walking the previous evening; (ii) walking continuously for 30 min the previous evening or; (iii) resting the previous evening. Blood samples were taken in the fasted state and for 2 h post-OGTT. The subjects' insulin sensitivity was estimated from fasting blood glucose and insulin using the quantitative insulin sensitivity check index (QUICKI) and in response to the OGTT using an insulin sensitivity index (ISI-Matsuda).
  

  

  Figure 3: Changes in fasting glucose, insulin and insulin sensitivity (QUICKI) the morning after accumulated walking, continuous walking or a rest day; values expressed rel. to sedentary control (Yap. 2015).

  Now, as you've read a few lines above, the scientists say: Only the continuous walking is beneficial. Well, I don't know about you, but if I look at the study results in Figure 1, I wouldn't say that the data suggests that only continuous brisk walking would be beneficial. In fact, the early morning glycemia, which is by the way a pretty stupid measure of glucose tolerance anyway (cortisol rises in the AM and ruins the results), is very similar and the OGTT data in Figure 2 shows no practically relevant effect or difference either.
  

  

  Figure 4: Glucose (a), insulin (b) and insulin sensitivity index (ISI-Matsuda) (c) calculated from an oral glucose tolerance test the morning after three 10 min bouts of accumulated brisk walking, a 30-min continuous brisk walk or resting the previous evening. Values are mean (SD) (n = 25). Main effect of time for glucose (a) and insulin (b) (both P < 0.001). Main effect of trial for ISI-Matsuda (c) with Bonferroni post hoc t tests: accumulated walking vs. continuous walking (P = 1.000); accumulated walking vs. rest (P = 0.204); continuous walking vs. rest (P = 0.081 | Yap. 2015)

  With that being said, you can still rely on your step counter as a guide to a health-relevant amount of activity. What is important is that you get your physical activity in; and not that you do it in a continuous matter (even though that may offer small benefits in the study at hand). Plus, you will remember: Especially for those with some extra-weight on their hips "Increasing Physical Activity Just as Effective as Strength, Endurance or Combined Exercise to Lose Fat and Build Muscle" | re-read the SV article.

Figure 5: Summary of exercise-induced responses in signaling proteins and their selected signaling pathways investigated in the present study. The figure is simplified, and not all the possible connections between the proteins are shown. Signaling proteins are marked according to the present findings of changes from pre-exercise to 30 min post-exercise within the group (Ahtiainen. 2015).

Are you missing something? Yes, the -TOR study. The one with the different exercise types and volume and the effects on the signaling pathways regulating skeletal muscle glucose uptake and protein synthesis after workouts. So why did this interesting paper not get more room? Well, the answer is simple: If you determine only markers of protein synthesis, glucose uptake & co in response to 5 × 10 repetition maximum (RM) resistance exercise (RE) with leg press device (5 × 10 RE; n = 8), 10 × 10 RE (n = 11), and endurance exercise (strenuous 50-min walking with extra load on a treadmill; EE; n = 8) you generate results with little practical relevance. After all, we know that an increase in mTOR phosphorylation does not tell us that the actual protein synthesis let alone the long-term gains increases, as well - since those were not assessed in the Ahtiainen paper, their results are rather of educational than practical value.

The educational value is thus also the reason I still mention the study. I mean, I didn't want to deny you the opportunity of looking at the scientists' excellent "summary of exercise-induced responses in signaling proteins and their selected signaling pathways" in Figure 5 - even though, the cause-and-effect relationships are still 'hypothetical' in parts ;-) | Comment on Facebook!

References:

• Ahtiainen, Juha P., et al. "Exercise type and volume alter signaling pathways regulating skeletal muscle glucose uptake and protein synthesis." European journal of applied physiology (2015): 1-11.
• Fernández-Elías, Valentín E., et al. "Relationship between muscle water and glycogen recovery after prolonged exercise in the heat in humans." European journal of applied physiology (2015): 1-8.
• Op‘t Eijnde, B., et al. "Effect of creatine supplementation on creatine and glycogen content in rat skeletal muscle." Acta physiologica Scandinavica 171.2 (2001): 169-176.
• Thompson, Christopher, et al. "Dietary nitrate improves sprint performance and cognitive function during prolonged intermittent exercise." European journal of applied physiology (2015): 1-10.
• Yap, Mei Chan, Govindasamy Balasekaran, and Stephen F. Burns. "Acute effect of 30 min of accumulated versus continuous brisk walking on insulin sensitivity in young Asian adults." European journal of applied physiology (2015): 1-9.