Endurance Training ↔ Overtraining & Muscle Loss? Run to Exhaustion & Sympathetic, Medium Intensity Steady State & Parasympathetic, HIIT-Like Training & No Overtraining

HIIT-like 400m sprinting is exhausting, but unlike running to exhaustion and medium intensity steady state cardio it's not going to mess up your nervous system.

Not one but two recent studies confirm what many of us have experienced first hand: Endurance training - specifically during a cut - is a double-edged sword. On the one hand, it's a neat way to augment the energy deficit, when you're dieting and maintain in a eucaloric state, when you're not. On the other hand, however, even moderate endurance training can alter the sympathetic and parasympathetic balance and thus create an imbalance that is characteristic of any form of overtraining.

Speaking of overtraining: As a SuppVersity reader you should actually be aware of the fact that scientists distinguish two different types of overtraining: Sympathetic and parasympathetic overtraining

You can learn more about HIIT, which appears to be less overtraining prone than MISS.

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

Triple Your Energy Exp.

Due to the fact that the symptoms (see Figure 1) closely resemble those Morbus Basedow (engl. Grave's Diseases) and Addison's Disease, respectively, sympathetic and parasympathetic overtraining are also called Basedowoid and Addisinoid overtraining.

Figure 1: Overview of the symptoms of the two major forms of overtraining.

You can see that the symptoms partly overlap. That's yet not the only problem you have if you want to diagnose the type of overtraining. In many resistance trainees, for example, you find either mixed forms or see a transition from classic sympathetic to parasympathetic overtraining over time (assuming the athlete doesn't do anything to normalize his / her sympathetic nervous system function).

There is no formula to calculate how much exercise you can sustain, but I'd suggest you take a look at my previous articles on heart rate variability and overtraining ("Are You Overtraining? Two Scientifically Proven Methods to Test Yourself - Method 1: Heart Rate Variability Analyses" | read more). They will help you to check, where you're at, if you have a baseline reading that was taken, when you've been completely rested  | learn more.

For the average study participant in a recent experiment that was conducted by scientists from the , The 42nd Hospital of PLA, the Xinqiao Hospital and the Chongqing Normal University in China, the duration and intensity of their cardio workouts (running) determined, whether the prescribed workout routines that consisted of ...

• 

  There is such a thing as overtraining, folks | read more

  4 times a week running at 100% of their maximal heart rate until they were exhausted (utmost intensity group)
   
• 30 minutes of running four times per week (moderate intensity group)


• 3 - 5x 1200 m runs per day with a  5-min break every 400 m four times per week (high intensity group)

made them overtrain or not, and whether their para- or sympathetic nervous system was overreacting.

Table 1: Characteristics of study groups at pre and post | Data are means XS± . Pre, pretraining; post, at the end of 8-week training; mid, at the end of 4-week training. Utmost, utmost intensity endurance training; moderate, moderate intensity endurance training; high, high intensity endurance training (Tian. 2014)

The subjects, 72 nonsmoking male students whose characteristics are summarized in Table 1, followed the routine they had been randomized to for 8 weeks. As you can see, there were no statistical significant changes in body composition over the course of the 8-week study. Although, it sould seem that the body fat percentage (I assume BFR is body fat) declined a tad bit more in the high intensity group.

Greater fat loss with HIIT, this wouldn't be a surprise - That's no news for you as a SuppVersity reader. I've repeatedly pointed out that the short intense workouts are more suitable for fat loss; and that not in spite of, but rather because they may burn less body fat during exercise.

If you have no idea what I am talking about, I suggest you take another look at my June 2012 article "Are You Still Burning Calories or Already Losing Fat? Study Shows: 5x15 Min HIIT Reduce Body Fat & Improve Fitness Twice as Effectively as 5x40min of Classic Cardio" (learn more) after you've finished this article.

Where the subjects differed, however, was in their response to the specific aerobic exercise programs they've been assigned to (I will directly quote the results from Tian et al (2014) and briefly comment on each of them):

• Heart rate variability (HRV): No significant changes in HRV parameters were found in all groups at pre and mid. But at post, the moderate intensity group showed more significant increases in RMSSD, PNN50, HF, LF and SDNN (P < 0.05 or 0.01) and much greater reduction in LF/HF than the other two groups (P was 0.033, 0.037 respectively). HFn of the moderate intensity group was significantly higher than that of the utmost intensity group (P = 0.012), while the opposite pattern occurred in LFn and LF/HF of the two groups (P was 0.025, 0.015 respectively).
  
  As you would expect the changes in HRV in the moderate and utmost intensity group reflect increases in parasympathetic and sympathetic nervous system activity, respectively.
• Circadian Changes in Cold Pressor Test (CPT): From pre to post marked differences were not found in SBP and DBP of all groups and their increases. At post HR was much less increased in utmost intensity group during CPT than the other two groups (average P < 0.05).
  
  Next to a high basal heart rate an inhibited increase in heart rate is another characteristic of later stages of sympathetic overtraining.
• Plasma catecholamine (NE & EPI): Norepinephrine (NE) concentration was considerably lower in utmost intensity group than the other two groups (P was 0.001, 0.00 respectively). At post marked inter-group differences were still not found in plasma PEI concentration.
  
  A reduced catecholamine release is a classic characteristic of long(-er) term sympathetic overtraining - a phenomenon, some people may call "adrenal fatique" that occurs after an initial phase of catecholamine overproduction in sympathetic overtraining.

Overall, the results of the study at hand confirm previous research that found associations between classic "moderate intensity" endurance training and parasympathetic dominance (Yamamoto. 2001; Pichot. 2002; Myslivecek. 2002).

For the utmost intensity group, on the other hand, the scientists diagnosed an "over-excited SN [sympathetic nervous system]" (Tian. 2014), which is in contrast to the medium intensity and high intensity group, where the head-up tilt test did not indicate an "impairing effect on autonomic regulation" (Tian. 2014).

What about muscle loss? Oh, yes! I almost forgot that scientists from the University of the Witwatersrand (Oost- huyse. 2014) in South Africa have recently been able to show that 3 h of race- simulated cycling on 4 consecutive days may improve the cyclists' ability to tap into their fat stores as an energy reserve. Unfortuna- tely, it will also lead to a 28-46% greater reliance on endogenous protein catabolism during exercise on day 2-4.

Now, every SuppVersity reader knows that protein catabolism doesn't necessarily translate ot "muscle loss", but for the average 10h of cardio + 20% energy deficit "dieter", it could.

Bottom line: A least in the study at hand, the intense, albeit better short bouts of high intensity exercise in the HIIT-like high intensity group of the study at hand turn out to be the least overtraining prone type of aerobic activity.

Even the classic medium-intensity cardio training appears to be more overtraining-prone, due to the comparatively long duration and the subsequent increase in parasympathetic nervous system activity. If you're looking for a "side-effect free" cardio regimen, 3-5x intervals of 3x400m sprints could be a good way to incorporate cardio training into your exercise routine.

One thing we should keep in mind, though, is that someone who is sympathetically overtraining in the gym with all its negative consequences (see Figure 1) would probably be better of with classic "moderate intensity cardio" to bring up the parasympathetic tone and avoid "weight lifting induced" sympathetic dominance | Comment on Facebook!

References:

• Myslivecek, P.R., Brown, C.A. and Wolfe, L.A. (2002) Effects of Physical Conditioning on Cardiac Autonomic Function in Healthy Middle-Aged Women. Canadian Journal of Applied Physiology, 27, 1-18. 
• Oosthuyse, T., & Avidon, I. (2014). Changes in substrate utilisation and protein catabolism during multiday cycling in well-trained cyclists. Journal of Sports Sciences, (ahead-of-print), 1-11.
• Pichot, V., Busso, T., Roche, F., Garet, M., Costes, F., Duverney, D., Lacour, J.R. and Barthélémy, J.C. (2002) Autonomic Adaptations to Intensive and Overload Training Periods: A Laboratory Study. Medicine & Science in Sports & Exercise, 34, 1660-1066. 
• Tian, Kaixin, et al. "Effect of Endurance Training on the Autonomic Nervous System Function of Young Male." International Journal of Clinical Medicine 5.19 (2014): 1189.
• Yamamoto, K., Miyachi, M., Saitoh, T., Yoshioka, A. and Onodera, S. (2001) Effects of Endurance Training on Resting and Post-Exercise Cardiac Autonomic Control. Medicine & Science in Sports & Exercise, 33, 1496-1502. 

Are You Overtraining? Two Scientifically Proven Methods to Test Yourself - Method 2: ABEL Sport Test. Plus: 54 Item Questionnaire + 8 Additional Clues to Identify Overtraining

Theoretically it's already available for everyone. Costs are yet not the only thing you should keep in mind before you buy into Knight Scientific's overtraining analysis system

I've got plenty of positive, skeptic and euphoric feedback in response to last week's first installment of this two-part series on "proven" methods to test for overtraining syndrome (OTS). Before I tackle method number two in today's second installment, I do thus want to briefly remind you that the HRV method is not going to work, when you are chronically overtrained, already. It's also questionable, whether it will be able to identify parasympathetic overtraining syndrome (POTS). The latter is associated with marked decreases, not increases in the ratio of high / low frequency component (Portier. 2001). In people who train intense and with a high volume this effect can even mask the early increase in sympathetic tone and would thus render the HRV method basically useless.

You can learn more about overtraining at the SuppVersity

Heart Rate Variablity (HRV)

ABEL Sports Test + More

Overtraining & Undereating

Calculate your Energy Intake!

There Are No Magic Macros!

Reinvent Your Training!

More alternative tests / indicators of overtraining:

• increased sensitivity of 5HT receptors ➯ early fatigue (Budgett. 2010)
• free testosterone and testosterone/cortisol ratio higher than 30% (Cunha. 2006)
• increasing serum urea and decreased ammonia at rest w/ identical protein intake, indicative of higher gluconeogenesis from protein (Urhausen. 2002)
• low urinary catecholamines, esp. during night and w/ parasympathetic overtraining (Lehmann. 1992) and low ACTH and/or GH response to maximal exercise (~adrenal fatique; cf. Urhausen. 2002)
• inverse ‘iceberg profile’ in Profile of Mood State (POMS) scale (Morgan. 1987) and messed up sleep (Urhausen. 1998)
• decreased glucose & increased fat oxidation during high intensity exercise (Urhausen. 2002)

None of these markers can serve as a sole marker of overtraining. They can however support conclusions you make based on questionnaires, performance data and HRV analyses.

For method number two, so-called ABEL-Sport Test, these interferences between symathetic (~intensity, short(er) term) and parasympathetic (~volume, long(er) term) overtraining shouldn't be a problem. The test is easy, but it's not free. You will after all have to buy a portable luminometer to measure the optical properties of your blog. In other words, the ...

"[...] test does not measure a single biomarker of OTS [overtraining syndrome] but instead utilises hidden information acquired by circulating leucocytes as they patrol the body spotting pathogens, responding to markers of inflammation (cytokines and chemokines) and other changes in the blood that occur after strenuous exercise." (Knight. 2013)

As J Knight, M Wakeman, J Reeves, who have a vested interest in research into their own products, which have been used by elite and amateur athletes in many different fields and were "successfully used" by Skandia Team GB for two years prior to and in the final run up to the Olympics in Beijing in 2008, when Britain’s squad topped the medal table in the Olympic sailing competition, point out, the test is designed to elicit this "hidden information from the cells" (and I should add "hidden information that requires interpretation"!).

The technology relies on the bioluminescent protein Pholasin. It emits light, when it gets in contact with reactive oxygen specimen (ROS). To test the amount of leucocytes in a 5-20µL sample your blood you do thus just have to react it with Pholasin, activate the ROS response of the leukocytes and measure the light response (Roberts. 1985, 1987; Knight. 1999). By superimposing the results on a set of reference sample curve, Knight et al. are then (that's at least the claim) able to identify various responses during training, "indicating if the athlete is heading towards OTS and identifying infections, superimposed on training curves." (Knight. 2013)

With score way beyond 25 (15 is the first signal of OT), it's usually a good idea to take some time off and re-start your training at a saner intensity / volume - irrespective of ABEL or HRV results.

Stay skeptic! Despite the fact that a very similar technology has already been used in the analyses of the effects of foods and cosmetics, there is as of yet no independent comparison of the accuracy of the interpretation of the leukocyte ROS responsible on which Knight et al. base their assessments of the training status.

The word "interpretation" should have made you sit up: Even if the scientists are able to provide a cost-effective solution for individual hobby athletes, it is not guaranteed that the results are actually going to help you control your training load. Before the beneficial real-world effects Knight et al. observed in sailors, footballers and other athletes are confirmed in a well-controlled study by an independent team of researchers, I would thus suggest you rely on the traditional rules of thumb, your personal training experience, the HRV method and the overtraining questionnaire on the right of this "bottom line".

References:

• Budgett, R., Hiscock, N., Arida, R., & Castell, L. M. (2010). The effects of the 5-HT2C agonist m-chlorophenylpiperazine on elite athletes with unexplained underperformance syndrome (overtraining). British journal of sports medicine, 44(4), 280-283. 
• Cunha, G. D. S., Ribeiro, J. L., & Oliveira, A. R. D. (2006). Overtraining: theories, diagnosis and markers. Revista Brasileira de Medicina do Esporte, 12(5), 297-302.
• Knight, J. (1999). Rapid, simple and sensitive blood biocompatibility tests with the light emitting protein Pholasin®. Proceedings of the TechMed/Medical Device Technology Conference. Advanstar Communications UK Ltd, Chester, 3-17.  
• Knight, J., Wakeman, M., & Reeves, J. (2013). Abel-Sport™ Test For Assessing Over Training Syndrome And Detecting Infection. British journal of sports medicine, 47(17), e4-e4.
• Lehmann, M., Gastmann, U., Petersen, K. G., Bachl, N., Seidel, A., Khalaf, A. N., ... & Keul, J. (1992). Training-overtraining: performance, and hormone levels, after a defined increase in training volume versus intensity in experienced middle-and long-distance runners. British journal of sports medicine, 26(4), 233-242.
• Morgan, W. P., Brown, D. R., Raglin, J. S., O'connor, P. J., & Ellickson, K. A. (1987). Psychological monitoring of overtraining and staleness. British Journal of Sports Medicine, 21(3), 107-114.
• Portier H, Louisy F, Laude D, Berthelot M, Guézennec CY (2001). Intense endurance training on heart rate and blood pressure variability in runners. Medicine and science in sports and exercise, 33(7), 1120-1125.
• Roberts, P. A., Knight, J., & Campbell, A. K. (1985). Pholasin®: a new bioluminescent indicator for cell activation. Biochem. Soc. Trans. 1140, 1139-1140. 
• Roberts, P. A., Knight, J., & Campbell, A. K. (1987). Pholasin®: a bioluminescent indicator for detecting activation of single neutrophils. Anal. Biochem. 160, 139-148.
• Urhausen, A., Gabriel, H. H. W., Weiler, B., & Kindermann, W. (1998). Ergometric and psychological findings during overtraining: a long-term follow-up study in endurance athletes. International journal of sports medicine, 19(2), 114-120.
• Urhausen, A., & Kindermann, W. (2002). Diagnosis of overtraining. Sports medicine, 32(2), 95-102.

Dietary Zinc & Copper Improve Glucose & Lipid Metabolism. High Cortisol Amplitudes Counter Belly Fat. Hypoxic Hearts Love Creatine + Ribose. Apples Counter Cancer & Obesity

I guess this is about as close as we have hitherto gotten to understand why we got fat. Wrt to the hilarious pace at which we got fat and are still getting fatter, we are much better informed though.

After you've learned about the general importance of exercise for your health and a couple of tweaks that may or, as in the case of sugary "energy drink", may not help you maximize the benefits and performance gains on Saturday. The focus of today's SuppVersity article is on the results of non-exercise related studies that highlight non-exercise related confounders of your health.

Before we get to the actual news, I would yet like to invite all of you to take a look back at the increasingly obese history of the US... I suppose those of you who have not yet seen the link on my Facebook wall, will enjoy the animated obesity map in the Atlantic article from April 11. I mean, even if we still don't have anything but over-simplistic cookie-cutter "explanations" of why we get fat, the map shows that we do at least know how fast we got fat!

You don't feel knowing about how fast we got fat is good news? Ok, maybe you'll like one the following results from recent studies better:

• Dietary zinc & copper influence glucose & lipid metabolism in women (Shab-Bidar. 2013) According to a recent study from the Obesity Research Center at Shahid Beheshti University of Medical Sciences in Tehran, Iran, there is a gender specific effect of copper and zinc in the diet on glucose and lipid metabolism of men and women in Iran - statistical significant effects were observed only in women with...

  

  Odds ratios for the MetS and low HDL across quartiles of copper intake (Shab-Bidar. 2013)

  • higher zinc intakes being associated with higher HDL-C, lower triglycerides (TG) and lower 2-hour blood glucose, and 
  • higher copper intake correlating with higher HDL-C, lower fasting blood glucose (FBG), significantly lower TG and a huge 81% reduction in the risk for suffering from metabolic syndrome (highest vs. lowest copper intakes)
  These observations stand in contrast with the current notion of the "bad" copper and the "good" zinc and reamphasize the importance of both nutrients for metabolic health.

  ---

  Remember: Two questions that will still have to be resolved pertain to (a) the gender-specificity of the effects and (b) confounding effects of food quality / choice and thus whether the same beneficial effects would be observed with the standard American diet.
  For both, but espicially for copper a little more than the RDA does not appear to hurt: What's particularly interesting, is that contrary to the zinc intakes in quartile 4 (>14mg/day; RDA 9mg/day) the copper intake in quartile 4 was more than 3x higher than the current RDA for women (0.9 mg). In fact, even the copper intake in the lowest quartile ~1.5mg/day was way above the RDA. If that's something we have to be surprised about is yet questionable, after all, there is not exactly much research on "optimal copper nutrition" (much contrary to zinc, by the way) and the RDA is based on age-old depletion-repletion studies and will thus probably reflect the absolute minimum to maintain "normal" serum levels.

• Evidence from human study: Flat cortisol profile not averages or spikes are associated with increased adiposity and visceral obesity (Sharp. 2013) In their most recent paper that's soon going to be published in the American Journal of Human Biology Dan S. Sharp and his colleagues from the Center for Disease Control and the State University of New York provide conclusive evidence for the irrelevance of mean cortisol levels with respect to the purported negative effects of cortisol on visceral obesity.

  

  Associations between sextiles of within-subjects cortisol standard deviation (SD) in 217 Buffalo policemen and adjusted lean-mass trunk index (Sharp. 2013)

  As the data in the figure above clearly shows, the police officers with the greatest cortisol fluctuations (spikes and troughs) had the highest ratio of lean body mass to trunk mass. It is thus, as the scientists phrase it,
  

  "not the average level of salivary cortisol among 18 specimens on each officer that drives the association; it is the variation among specimens."

  The oral cortisol measures were taken on 3 subsequent days in standardized procedures that involved a venipuncture and a standardized high protein meal as "challenges", on day 1, six measures that were taken by the police officers over the course of the day, on day 2, and series of tests that was taken after a dexamethasone challenge after waking on day 3 (the subjects had ingested 0.5mg of dexamethasone the night before).

  ---

  Bottom line: While the scientists are careful in pointing out that it will still have to be established that the results translate to other populations. The results corroborate the uselessness (if not potential detrimental effects) of "cortisol blockers", I've discussed in my previous in the Science Round Up Seconds on March 29, 2013 (read more).

• Combination of creatine and d-ribose heals damaged, but unscarred rodent-hearts (Caretti. 2013) While the many of the "daggered" claims* on the boxes of various "advanced" creatine products (learn more about their uselessness) are probably a little overblown (*the dagger refers to the "not verified by the FDA"), that's nothing compared to the absolutely disappointing results trainees had with d-ribose. Meanwhile, it seems as if even the last jerk knew that the unbearably sweet simple sugar is nothing worth spending his/her money on.
  
  

  

  Ribose regulates the novo synthesis and restoration nucleotides, can relieve the energy toll of ischemia  and its usefulness in the context of CVD is backed by rodent and human studies (Shecterle. 2011)

  In view of it's physiological role in the recovery of ATP levels (Helsten. 2004), it was assumed that supplementatal D-ribose would ameliorate the ATP depleting effects on exercise and improve endurance in glycolytic and/or long endurance activities, yet...
  

  "[...s]tudies examining the effect of ribose on performance during intense intermittent exercise and rowing have not been able to demonstrate improved performance in humans." (King. 2012)

  Other than the non-existence of side-effects, pertaining studies, which used up to ∼40 g/day, as well as acute and chronic supplementation regimen did  yet not yield any positive results
  
  Now, the aforementioned studies on the ergogenic effects of d-ribose were conducted in healthy individuals, in whom the ATP re-synthesis obviously does not depend (and not even benefit) from the provision of the monosaccharid that was discovered by Emil Fischer in 1891, when he analyzed the carbon structure of gum arabic (Prince. 2012). "Healthy" would yet not be the correct term to describe the rodents in the recently conducted study by Caretti et al. who observed that five week-old mice who were exposed to an atmosphere containing 10% O2 for 10 days in order to induce right ventricle hypertrophy and left ventricle apoptosis did not show any signs of cardiac damage, when they were gavaged creatine + D-ribose, every day.
  
  And while both phenotypes, i.e. the hypertrophy of the right and apoptosis of the left ventricle, were blunted to a certain degree by creatine or d-ribose, only their reversed the pathogenic changes to the heart muscle "almost" completely, by normalizing the expression of AMPK and Akt signaling in the hearts of the rodents.

  ---

  

  Light micrograph of representative nuclear pro-files (background, red = atypical, green = normal nuclei; my emphasis) and volume (%) of atypical cardiac cells in anterior left ventricle of rodents on caffeine + nicotine + ephedrine combo (learn more)

  Bottom line: While they may not be beneficial for the average trainee, people "on" the literally heart-breaking combination of nicotine + caffeine and ephedrine, could be able to reduce their detrimental effects on the heart (learn more), by adding this combination of proven (creatine) and disproven (d-ribose) ergogenics to their supplement regimen. People with sleep-apnea and other conditions which will leave the heart poorly oxygenized for longer time-periods should obviously benefit, as well.
  
  Based on the likewise promising results of previous studies in (human!) subjects with congestive heart failure (e.g. Omran. 2003), a daily dose of 5g d-ribose, along with the tried an proven chronic ingestion of 5g of creatine appears to be a good starting point, until respective human trials have been conducted.

• Further evidence for the "An apple a day..." theory (Rago. 2013) In an allegedly methodically complicated, but very comprehensive analysis of the effects of raw, whole apples on the plasma metabolome of rodents, researchers from the University of Copenhagen found
  

  

  Total antioxidant activity (µmol vitamin C equivalents/g) of various fruits (Boyer. 2004)

  "that the intake of fresh apple in rats has a considerable and specific impact on the plasma metabolite profile, reflecting altered gut microbial metabolism, retarded lipid- and protein catabolism, and lowered metabolic, oxidative and steroid-related stress". (Rago. 2013)

  These results stand in line with the recent observations a group of Spanish researchers made, when they added a polyphenol extract from apples to the chow of rodents on an obesogenic high-fat + high sugar (HFS) diet:
  

  "Our results from histological studies demonstrated that supplementation of HFS with AP markedly reversed the enlargement of adipocyte volume induced by HFS diet intake in the epididymal fat pad, reducing it by almost 28% [...it also] reversed the increase in the population of large epididymal adipocytes, especially with diameters higher than 130m." (Boqu. 2013)

  The visceral specific effects of the apple polyphenols in the Boqué study could thus be interpreted as supportive evidence for the real-world significance of the metabolomic changes Rago et al. observed in the afore-cited study.

  ---

  Bottom line: No reason to be scared of the "high fructose fruit" apple. It comes with all HFCS sweetened beverages don't have. Polyphenols, vitamins, minerals and most importantly a flesh from which the fructose is extracted only slowly. Still, I have to warn you: Apple consumption can have profound beneficial effects on your health, such as (random examples)
  
  •  - 17% colorectal cancer risk (Michels. 2006)
  •  - 37% wheeze risk in your offspring (Willers. 2007)
  •  - 21% reduced risk for cancers of the oral cavity and pharynx (Gallus. 2005)
  •  - 25% reduced risk for oesophagus (Gallus. 2005) 
  •  - 18% / -15% / -9% risk red. for breast / ovary / prostate cancer (Gallus. 2005)
  and obviously the - 15% reduced breast cancer risk, the if you want to avoid these, you should thus better keep obsessing about the high fructose content of apples and stick to sausages and lard ;-)

References:

• Boqué N, de la Iglesia R, de la Garza AL, Milagro FI, Olivares M, Bañuelos O, Soria AC, Rodríguez-Sánchez S, Martínez JA, Campión J. Prevention of diet-induced obesity by apple polyphenols in Wistar rats through regulation of adipocyte gene expression and DNA methylation patterns. Mol Nutr Food Res. 2013 Mar 25.
• Boyer J, Liu RH. Apple phytochemicals and their health benefits. Nutr J. 2004 May 12;3:5.
• Caretti A, Bianciardi P, Marini M, Abruzzo PM, Bolotta A, Terruzzi C, Lucchina F, Samaja M. Supplementation of creatine and ribose prevents apoptosis and right ventricle hypertrophy in hypoxic hearts. Curr Pharm Des. 2013 Apr 10. [Epub ahead of print]  
• Gallus S, Talamini R, Giacosa A, Montella M, Ramazzotti V, Franceschi S, Negri E, La Vecchia C. Does an apple a day keep the oncologist away? Ann Oncol. 2005 Nov;16(11):1841-4. 
• Hellsten Y, Skadhauge L, Bangsbo J. Effect of ribose supplementation on resynthesis of adenine nucleotides after intense intermittent training in humans. Am J Physiol Regul Integr Comp Physiol 2004;286:R182–8.
• Michels KB, Giovannucci E, Chan AT, Singhania R, Fuchs CS, Willett WC. Fruit and vegetable consumption and colorectal adenomas in the Nurses' Health Study. Cancer Res. 2006 Apr 1;66(7):3942-53. PubMed PMID: 16585224.  
• Omran H, Illien S, MacCarter D, St Cyr J, Lüderitz B. D-Ribose improves diastolic function and quality of life in congestive heart failure patients: a prospective feasibility study. Eur J Heart Fail. 2003 Oct;5(5):615-9.  
• Price, NPJ. The Name of the–ose: An Editorial on Carbohydrate Nomenclature. J Glycobiol. 2012; 1(e105).
• Rago D, Kristensen M, Gözde G, Federico M, Morten P, LarsOve D. LC–MS metabolomics approach to investigate the effect of raw apple intake in the rat plasma metabolome. Metabolomics. 2013; 1573-3882.
• Shab-Bidar S, Hosseini-Esfahani F, Mirmiran P, Mehran M, Azizi F. Dietary intakes of zinc and copper and cardiovascular risk factors in Tehranian adults: Tehran Lipid and Glucose Study. Nutrition & Dietetics. 2013
• Sharp DS, Andrew ME, Fekedulegn DB, Burchfiel CM, Violanti JM, Wactawski-Wende J, Miller DB. The cortisol response in policemen: Intraindividual variation, not concentration level, predicts truncal obesity. Am J Hum Biol. 2013 Apr 20.
• Shecterle LM, Wagner S, St Cyr JA. A sugar for congestive heart failure patients. Ther Adv Cardiovasc Dis. 2011 Apr;5(2):95-7.
• Willers SM, Devereux G, Craig LC, McNeill G, Wijga AH, Abou El-Magd W, Turner SW, Helms PJ, Seaton A. Maternal food consumption during pregnancy and asthma, respiratory and atopic symptoms in 5-year-old children. Thorax. 2007 Sep;62(9):773-9. Epub 2007 Mar 27.
   

Science Round-Up 2nds: Intra-/Post Workout Stims, Carbs & Protein and Their Effects on Performance, Hydration, GH, Cortisol, Testosterone & Fatty Acid Oxidation

As mentioned on yesterday's show, small 100kcal packets are as much of a problem as large dinner plates and XXL meals (data based on Coelho do Vale. 2008)

I want to start today's Seconds with a question: How did you like that Carl and I did not rush through the news-lineup as it was the case in previous episodes, but simply took our time to discuss the topics in depth an breadth, yesterday?

Personally, I believe that this is much better than the accumulation of "buzzword" the show had become in the previous weeks due to my "study hunter and gatherer" drive - or, in other words, the mere mass of studies I wanted to pack into the show and Carl's desperate effort to cover them all.

Would you agree? And what other changes / improvements would you like to see in the future? We are open for constructive criticism. You can't improve your game without it.

Let's get to what did not fit into the show, then...

The net result of the spending more time on each and every of the single items, or, to say it in the spirit of yesterday's show, a bit more mindfulness was obviously a much larger amount of Seconds for you to devour today. So, let's not waste any time and get right down to business:

• Is 200mg of caffeine the optimum!?A 2008 study by Beavan et al., which involved 24 professional rugby players who were randomly assigned to receive 0, 200, 400 or 800mg of caffeine 1h before performing a standardized resistance training protocol (Beavan. 2008), found that contrary to what bro-science has been suggesting for years, the ingestion of the high amounts of caffeine (800mg) lead to a profound drop in the testosterone-to-cortisol ratio, while the lower doses of 200mg and 400mg of caffeine only blunted the performance hampering decline of cortisol half-way into the workout, while increasing the testosterone levels by 15%
  Caffeine or pseudoephedrine for performance enhancement? As far as improving you game is concerned, a recent study from the School of Sports Science at the department of Exercise and Health of the University of Western Australia was able to show that you are only wasting your time an money, if you are trying to up your cycling-time trial and thus probably every other HIT performance by ingesting the purported CNS stimulant pseudoephedrine (not to be confused with the "real deal"; cf Spence. 2013).
  
  Contrary to the comparatively low amount of 200mg caffeine, which allowed the 10 well-trained cyclists and triathletes who participated in the study improve their TT times in trial 2 of 3, all of which were performed on th same day, by statistically significant 57s, the ingestion of the WADA banned substance pseudoephedrine at a dosage of 180g would have cost them their license for nothing.

  ---

  Bottom line: Spare yourselves pseudoephedrine and other nasal/sinus decongestant belonging to the the class of phenethylamines and amphetamines (e.g. geranium). Even if others worked (for 1,3-dimethylamine this has never been proven in isolation), the long(er)-term detrimental effects they'll have on your central nervous system really isn't worth it.

• Protein-enhanced Gatorade ain't worth your money -- If you are no ultra-endurance runner or at least marathon runner, you don't need, because you don't benefit intra-workout carbohydrate + electrolyte + protein (CEP) drinks for hydration.
  
  The results of a recent study from the Chinese University of Hong Kong show: A CEP solution containing 42g/L carbohydrate, 21g/L whey protein and 15.3 mmol/L sodium and 2.3 mmol/L potassium does not show "extra benefits for the maintenance of hydration status during 60 min cycling" (Sun. 2013)

• Carbohydrate + protein drinks maximizes GH response to exercise -- Now that you know that it's not worth to guzzle on carbohydrate + electrolyte + protein drinks during a workout for hydration purposes, I guess I should tell you that doing the same (w/out the electrolytes, though), may still provide an athletic / anabolic edge. After all, another recently published study that was conducted at the School of Sport at the Department of Exercise and Health Sciences of the Loughborough University in Leicestershire, U.K (Betts.  2013) shows that the ingestion of a carbohydrate + protein mixture (CHO+PRO: 0.8 g sucrose per kg bod weight per hour + 0.3 g/kg/h whey protein isolate) in the 4h recovery period between two exhaustive treadmill runs at the same intensity augmented the growth hormone response by 60%(!) compared to the ingestion carbohydrate only (0.8 or 1.1g of sucrose /kg per hour).
  

  

  Figure 1: Growth hormone (GH) and cortisol response to 2nd bout of exhaustive treadmill running with either 0.8 or 1.1g of sucrose /kg per hour (CHO, CHO-CHO) or  0.8 g/kg/h sucrose per kg bod weight per hour + 0.3 g/kg/h whey protein isolate (CHO+PRO; cf.

  As the data in figure 1 goes to show you this increase in GH was accompanied by a 23% reduction in cortisol. With both, GH and cortisol being released in response to the depletion of muscle glycogen and impeding low blood glucose levels (Galbo. 1977), you could thus argue that protein (probably by its glucagon promting effects; cf. Claessens. 2008) programs the "anabolic glucose procurement plan".
  

  ---

  Bottom line: Yet another reason for the often touted, yet tried and proven "Bananas + whey" = WIN! And that's not true wrt to the protein anabolic response after a workout, but also in view of the "anabolic" or I should probably say generally more favorable way of glucose procurement during subsequent workouts.

• 

  No, no and no! The ingestion of carbs before a HIIT workout will only increase, not blunt the fatty acid oxidation in the post-workout period.

  Pre-workout carb ingestion does not blunt, but promote fatty acid oxidation after the workout -- In as much as this result may go against common bro-science that you must never consume any carbs before your workout if you are trying to lose body fat, it is actually in line with what I have been preaching before. The beneficial effects of AMPK come with the depletion of ATP and the rise in ADP (~used ATP), not with the constantly depleted ATP stores of a no-carbohydrate + protein only starvation diet. Or put more simply - a constant over-expression of AMPK negates all the benefits of it's cyclic up and down (cf. "The mTOR/AMPK Seesaw"; read more)
  
  While the scientists from the Department of Nutrition & Metabolism at the Faculty of Health and Medical Sciences of the University of Surrey in Guildford, UK, did not observe statistically significant improvements in fatty oxidation due to the small study size (10 healthy untrained females; age 18–22 yr; BMI 22kg/m²), the pronounced decrease in RQ after 8-10x 60 second cycling bouts at 95 % VO2peak separated by 90 seconds recovery at 50 watts in 9 out of 10 participants (see figure 2) does speak itself: "In women, consuming carbohydrate before exercise may potentially be more beneficial for fat oxidation than consuming carbohydrate post-exercise" (Honnor. 2013).
  

  ---

  Bottom line: The results of the study at hand, which stand in line with previous research by Fuchs et al. who presented their research in the Proceedings of the Nutrition Society one year before, re-emphasis the fallacious over-reliance of high fatty oxidation rates during a workout. The max. 60-90min in which you may burn slightly more fat, are simply negligible compared to the much longer post-workout period, where the ingestion of 59 g CHO before a HIIT workout did not blunt but promote fatty acid oxidation.

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Believe it or not, but that's it for today! If you are hungry for more, I suggest you either go to the SuppVersity Facebook Wall or listen to Casual Friday later today... actually, I found Gabriel's name, i.e.  "The Alisa Profumo Show", for the Friday edition of Super Human Radio show quite fitting ;-)

References:

• Beaven CM, Hopkins WG, Hansen KT, Wood MR, Cronin JB, Lowe TE. Dose effect of caffeine on testosterone and cortisol responses to resistance exercise. Int J Sport Nutr Exerc Metab. 2008
  Apr;18(2):131-41.
• Betts JA, Stokes KA, Toone RJ, Williams C. Growth Hormone Responses to Consecutive Exercise Bouts with Ingestion of Carbohydrate plus Protein. Int J Sport Nutr Exerc Metab. 2013 April. 
• Claessens M, Saris WH, van Baak MA. Glucagon and insulin responses after ingestion of different amounts of intact and hydrolysed proteins. Br J Nutr. 2008 Jul;100(1):61-9.
• Coelho do Vale R, Pieters R, Zeelenberg. Flying under the Radar: Perverse Package Size Effects on Consumption Self‐Regulation. Journal of Consumer Research. 2008; 35(3):380-39.
• Fuchs, A. & Young, H. Investigation into gender differences in the effects of feeding around exercise on exercise performance, energy expenditure and substrate utilisation. Proceedings of the Nutrition Society. 2011; 70 (OCE6), E380.
• Galbo H, Richter EA, Hilsted J, Holst JJ, Christensen NJ, Henriksson J. Hormonal regulation during prolonged exercise. Ann N Y Acad Sci. 1977;301:72-80. Review.
• Honnor M, Herdsman M, Collins AL.The effect of food timing on fat oxidation during exercise and resting recovery. Proceedings of the Nutrition Society. 2012; 71 (OCE3), E236 
• Spence A, Sim M, Landers G, Peeling P. A Comparison of Caffeine versus Pseudoephedrine on Cycling Time-Trial Performance. Int J Sport Nutr Exerc Metab. 2013 Apr 9. 
• Sun, F; Li, L; O’Reilly, J; Wong, SH. Effect of carbohydrate-electrolyte-protein solution on hydration. International Journal of Sport Nutrition and Exercise Metabolism. 2013; 23: S1-S15

On Short Notice: Teas & Prostate, Metformin & Amenorrhea, Stevia & High, Omega-3 & Low Cortisol, Aminos & Weight Control, Nordic Hamstring Exercise & 20% More Power!

Image 1: This would be a case where metformin probably won't help you to get your menses back - unless this is just one of your "yous" and you are taking high doses of anti-psychotics, of course.

In view of the fact that I have piled up way more "On Short Notice" items than I can possibly squeeze into one installment, today's news on the right tea (green or black) for prostate cancer, the purported anti-obesity effects of leucine and alanine, which turn out to be inferior to those of whole protein, the anti-amenorrhea and weight loss effects of metformin in women on anti-schizophrenic drug and how this relates to PCOS, the surprising N=1 cortisol-raising, high blood pressure and water retaining effects of stevia, the stress and weight loss reducing effects of omega-3s and high DHA levels in the brain, and an effective yet rarely used hamstring exercise, the "Nordic hamstring exercise", will be complemented by another installment of "On Short Notice" either tomorrow (in case I don't find the time to write the next installment of the Circadian Rhythm Series) or earlier next week... but enough of these organizational matters, let's see what we have in stock, here:

• Differential effects of green and black tea on prostate cancer risk While we are, yet again, only dealing with epidemiological shenanigan in a population living in a, if not the juggernaut of the far east, the >50% increase in hazard risk in the 27,293 men from the Singapore Chinese Health Study Julia A. Montague and her colleagues report for men who drink 1 cup of black tea per day is somewhat alarming (Montague. 2012). The fact that the hazard risk decreases to +17% with more than 2 cups of black tea does yet suggest that this is nothing but a statistic outlier. That said, black tea is (at least based on the results of this study) overall probably as benign as green tea, which is totally devoid of statistical beneficial or detrimental effects on prostate cancer risk in this cohort of normal-weight men in their middle to late 50s.
  This result does by the way not conflict with previous research, which did - if anything - only suggest a "borderline significant" beneficial effect of green tea and absolutely no effect of black tea on prostate cancer risk (Zheng. 2012). Apropos prostate cancer, just in case you missed it I highly suggest you take a look at my brief write-up on the recently published "red meat will give you prostate cancer study" before you decide on whether or not you got to stop eating meat for the sake of your prostate.

• 

  Figure 1: If  ~50g of leucine and alanine /kg chow are good, then 500g of whey are magic; makes you wonder, why you would want to add just one amino acid, instead of more protein, no?

  "Dietary L-leucine and L-alanine supplementation have similar acute effects in the prevention of high-fat diet-induced obesity",  that's the somewhat ill-chose title of a recently published paper by Anne Freudenberg, Klaus J. Petzke, Susanne Klaus from the German Institute of Human Nutrition in Potsdam-Rehbruecke which does not show that the ingestion of l-leucine or alanine, but rather an isocaloric high protein diet version of the high-fat diets the researchers fed their 10-week-old male C57BL/6 mice, prevented them from getting obese (Freudenberg. 2012).
  While the high fat + complete protein mice hardly gained any body fat, the high fat + leucine and high fat + alanine (both diets were "adequate" in protein and contained 100g whey + 60g leucine and 100g whey + 45g alanine, respectively)  got only significantly less fat compared to their peirs on the 100g whey only diet control HFD diet. Now, the high protein mice (500g of whey per kg chow; =5x over baseline) simply consumed less energy, but so did the mice on the leucine and alanine enhanced diets, so that the title of the study is not just misleading, it also disguises the most important result of the study, which is high protein diets keep mice lean.
• "Cure-it-all-drug" metformin helps with anti-psychotic induced amenorrhea and weight gain, as well. If metformin was not (a) no longer protected by patent rights and (b) would not basically work via similar mechanisms as exercise I would really begin to smell fraud over the ever-extending list of pathologies this 1920s medication is good for (this is when it was originally discovered, it took however until 1958 before researchers realized the potentials and a pharma company introduced it to the UK market). New to the list are the negative side-effects women experience in response to anti-psychotic treatments. In a recently documented experiment, 48 women (ages 18-40 years) with amenorrhea and weight gain in response to clozapine, olanzapine, risperidone, or sulpiride (all anti-psychotic drugs administered to treat schizophrenia) received a dose of 1,000mg of the wonder-molecule per day (Wu. 2012). After 2 months 25% of the women had resumed menstruation, after another 2 weeks it were 80% and after 3 months all women were eumenorrheic, again (of the placebo group only 2 resumed menstruating). Instead of gaining another 2kg of body weight, they had lost 2kg and the previously thwarted prolactin, LH, and testosterone levels, as well as the LH/FSH ratio had normalized.
  Probably, some of you may now ask themselves: Will this work for me as well - though I am not taking anti-psychotics? I would love I could answer this question, but aside from polycystic ovarian syndrome (PCOS), where we have a couple of trials in which metformin was used with success (cf. Velazquez. 1998; Bela. 2009; Palomba. 2009), the scientific evidence is scarce and in view of the fact that we know even less about the underlying mechanisms by which risperidone & co cause amenorrhea and weight gain than about the almost magical omnipotence of metformin I honestly can't tell. One thing that comes mind, where metformin is yet very unlikely to of any use is diet or exercise induced amenorrhea (overtraining and undereating), because this form of amenorrhea presents with a totally different hormonal profile, with low levels of basically all reproductive hormones.
• Stevia as cortisol promoter? Case study: Bloating, high blood pressure and malaise in a young previously healthy woman. Before I go on, let me briefly remind you that the events that are described in a recent case report from the University of Iowa Hospitals and Clinics may should be regarded with the degree of caution that is indicated whenever we are talking about case reports, specifically because stevia does actually have a pretty decent safety profile (aside from the occasional allergic reactions you will see with almost every foreign molecule you put into your body, obviously).

  

  Figure 2: If you block the 11bHSD2 enzyme that will convert cortisol into inactive cortisone, you are in trouble and a bloated tummy is certainly your least problem, not because "cortisol is bad", as common sense would dictate, but because not being able to manage it is bad (img. Michael. 2008)

  When a 32 year old Caucasian woman presented with generalized edema (feet, hands and face) that had persisted for over six months at her Dr office and was found to to suffer from pre-hypertension (138/88 mmHg) and hypokalemia (3.4 mM/l) that was brought about by a decline in serum aldosterone and plasma renin activity and corroborated by a concomitant  increase in the plasma cortisol/cortisone ratio, most Dr.'s would probably have thought of licorice intoxication. As it turned out, it were neither the glycyrrizinic acid, not the glycyrrhetinic acid from licorice which brought about these problem, but rather the stevia the lady had been using for over 9 months, now. Obviously, the sweetener (from an undisclosed brand) had blocked the 11 beta-hydroxysteroid dehydrogenase Type 2 (11-beta-HSD 2, see figure 2) enzyme that's responsible for the conversion (="deactivation") of cortisol to cortisone - with all the negative side effects of the subsequent 12x elevation of the ratio of active to inactive corticosteroids (Esmail. 2012).
  Now, I am certainly not suggesting that this is going to happen to everyone, but it could well be that the frequent reports of headaches people are developing after a couple of days "on stevia", could also be related to the effects the sweetener has on people with a certain genetic disposition. So, if you get a headache or start holding water like crazy, when you use stevia / stevia sweetened products, first try using a different brand (there have been issues with toxins in some products), make sure you have a pure stevia sweetener and not one with other sweeteners added (thx. to Amit for the reminder about erythritol that's in many products), switch to another preparation, e.g. from pure stevisoids to a a more "natural" extract and if all that does not help, just turn your back on it - you can live without it, I guarantee ;-)
• Omega-3's modulate adrenal activity What many people know from going overboard on fish oil has now been established in a recently published rodent study by Marie Hennebelle and her French (resident) colleagues (Hennebelle. 2012). The researchers fed a group of rodents a totally ALA free energetically restricted diet to produce male rats with brain phospholipid DHA levels that were 50% lower than those of the normal control. The 6 month-old rodents were then subjected to chronic restraint stress (6 h/d) for 21 days. As expected the rodents on the alpha linolic acid deficient diets had a much harder time coping with the torture they were exposed to and showed higher corticosterone levels, more pronounced behavioral abnomalies and slightly more pronounced weight loss in the 3-4 week of the 1-month experimental period. What's intriguing though is the the remarkable stress resistance (one could also say adrenal hypofunction ;-) in the rodents in a third experimental group, who had received an omega-3 enriched diet that boosted their brain DHA levels to 10% above normal: Compared to both the normal, as well as the omega-3 deprived rodents they had ~30% lower cortisol levels during week two and three of the experiment and lost only 50% of the weight their normal and ALA deprived peers did.
  That this is not necessarily a good thing for everyone is probably nothing I have to tell you. After all, the number of people who are hardly functioning due to over-supplementation with fish oil and (as this study would suggest) below normal stress responses is ever increasing. As with so many nutrients and supplements, it thus comes down to specificity and hitting the right ratios for you as an individual, again. And what's most important: Before you even start thinking about "fixing your adrenals" you should first take a look at the various stressors in your life. After all, the aforementioned fatigue is not simply a result of two much fish oil, but of its combination with a lifestyle which simply requires a robust and healthy cortisol response. You would not smoke weed to calm yourself down minutes before running away from a saber-toothed tiger, either, would you?

• 

  Video 1: These young ladies show you how it's done - well almost, you better go a little slower (click image to watch.

  Scientists confirm efficacy of nordic hamstring exercise - up to +20% increase in peak torque! What? You don't know the nordic hamstring exercise - I bet you do, but probably not by this name. Check out video 1 to the right and you will know what the 18 male players from a club in the English professional soccer leagues (mean±SD; age, 22.9±3.6 years; stature, 1.81±0.08 m; body mass 78.0±9.7 kg) did for 1x 2x5, 2x 2x6, 3x 3x6 and 3x 3x8 (sessions per week x sets x reps) during week 1-4 of the study period to improve their peak torque by up to 21% in all assessment conditions (90-61°, 60-31° and 30-0° of knee extension; cf. Iga. 2012).
  What is yet important is that you stick to an adequate temp and don't mess around and hurt yourself. In the study at hand, the velocity of the movement was standardized to 30°/s. If we assume that you go over the full ROM it must therefore take you 3s until your nose hits the ground (if you are afraid to hurt your nose, you may be interested in the SuppVersity EMG Series and the Best Leg + Hamstring Exercises ;-)

I hope you enjoy this more digestible format, having 20 of these items in one installment is - at least in my view - somewhat beside the point. Not that this would not be possible, but if I go by the average attention span of my real-life students, multiply it by 2x to accommodate for your superior cognitive abilities and personal interest in the topic, it appears prudent to call it a day for today. And if can't stand the 24h for the next SuppVersity news to be released, I suggest you simply like the SuppVersity Facebook Wall, where you will find another seven allegedly shorter news-items... about the wheat-allergens in soap (+ scary pic of what can happen, when you use those), for example or the news photo-based cholesterol test (a photo of your hands is all it takes), which is probably going to give the sales of statins another boost.

References:

• Billa E, Kapolla N, Nicopoulou SC, Koukkou E, Venaki E, Milingos S, Antsaklis A, Adamopoulos DA. Metformin administration was associated with a modification of LH, prolactin, and insulin secretion dynamics in women with polycystic ovarian syndrome. Gynecol Endocrinol 2009; 25:427–434
• Esmail S, Kabadi UM. Edema, Enigma: 11 B-Hydroxysteroid dehydrogenase Type 2 Inhibition by Sweetener “Stevia”. Open Journal of Endocrine and Metabolic Diseases, 2012, 2, 49-52.
• Freudenberg A, Petzke KJ, Klaus S. Dietary L-leucine and L-alanine supplementation have similar acute effects in the prevention of high-fat diet-induced obesity. Amino Acids. 2012 Jul 31.
• Hennebelle M, Balasse L, Latour A, Champeil-Potokar G, Denis S, Lavialle M, Gisquet-Verrier P, Denis I, Vancassel S. Influence of omega-3 Fatty Acid status on the way rats adapt to chronic restraint stress. PLoS One. 2012;7(7):e42142.
• Montague JA, Butler LM, Wu AH, Genkinger JM, Koh WP, Wong AS, Wang R, Yuan JM, Yu MC. Green and black tea intake in relation to prostate cancer risk among Singapore Chinese. Cancer Causes Control. 2012 Aug 3.
• Palomba S, Falbo A, Zullo F, Orio F Jr. Evidence-based and potential benefits of metformin in the polycystic ovary syndrome: a comprehensive review. Endocr Rev 2009; 30:1–50
• Wu RR, Jin H, Gao K, Twamley EW, Ou JJ, Shao P, Wang J, Guo XF, Davis JM, Chan PK, Zhao JP. Metformin for treatment of antipsychotic-induced amenorrhea and weight gain in women with first-episode schizophrenia: a double-blind, randomized, placebo-controlled study. Am J Psychiatry. 2012 Aug 1;169(8):813-21. 
• Velazquez EM, Mendoza S, Hamer T, Sosa F, Glueck CJ. Metformin therapy in polycystic ovary syndrome reduces hyperinsulinemia, insulin resistance, hyperandrogenemia, and systolic blood pressure while facilitating normal menses and pregnancy. Metabolism 1994; 43:647–654
• Zheng J, Yang B, Huang T, Yu Y, Yang J, Li D. Green tea and black tea consumption and prostate cancer risk: an exploratory meta-analysis of observational studies. Nutr Cancer. 2011;63(5):663-72.

Putting Carbs to Good Use: Meta-Review Reports Ergogenic Effect of Carbohydrates in Endurance Athletes

One of the leitmotifs, many of my posts here at the SuppVersity share, is the idea that (almost) everything works for someone. From the feedback I am receiving, from the crowd this blog is attracting, I gather that my general advice against high carbohydrate intake is (as human as that may be) often misinterpreted as "carbs are evil, beware of all carbs"! For the average pizza eating fast-food junkie, this certainly is an adequate message, because even if he believes that carbs are the root of all disease, without a MAJOR change in his dietary habits (I am not talking of ordering the normal, instead of the super size menu at McDonalds, here) he will probably still get way more carbs out of his diet than it would fit his sedentary lifestyle.
If, however you are an athlete or avid gym-goer you may probably already start to notice that following what you took to be a one-solution-fits-it-all recommendation lead to performance decreases, laziness, brainfog, lack of sexual desire, bad sleep and many of the other symptoms you would find, when you googled one of the ambiguous terms "adrenal fatigue" or "general fatigue syndrome"... Carbs are more than just insulin triggers, and fatteners. Glucose is the gasoline in your fuel tank and - most importantly - its the substrate your nervous system thrives on. And while it might not be necessary to eat them, very active (and lean) individuals may derive similar benefits from a moderate carb consumption as the athletes from the 50 studies included in a meta-review by Themesi et al. (Themesi. 2011).

The scientists' results suggest that intake of a <8% carbohydrate beverage (~50-80g) [TT] in the course of an endurance event (≥1 h) significantly "enhances endurance exercise performance in adults" as measured by submaximal exercise performance and time to exhaustion [TTE]:

The ES [effect size] for submaximal exercise followed by TT was significant (ES = 0.53; 95% CI = 0.37–0.69; P < 0.001) as was the ES for TT (ES = 0.30; 95% CI = 0.07–0.53; P = 0.011). The weighted mean improvement in exercise performance favored CHO ingestion (7.5 and 2.0%, respectively). TTE (ES = 0.47; 95% CI = 0.32–0.62; P < 0.001) and submaximal exercise followed by TTE (ES = 0.44; 95% CI = 0.08–0.80; P = 0.017) also showed significant effects, with weighted mean improvements of 15.1 and 54.2%, respectively, with CHO ingestion. Similar trends were evident for subanalyses of studies using only male or trained participants, for exercise of 1–3 h duration, and where CHO and PLA beverages were matched for electrolyte content.

Against this background, can the relevant question really be: "To carb or not to carb?" Probably not. You better follow Vince Andrich's recent advice and ask yourself "Are you working your sugar-bags (muscles) hard enough to earn your fair share of carb intake?" in order to make sure that you use just as much carbs as it takes to optimize performance without compromising health and body composition.