Low Fat Toddler, High Fat Adult?! Intra-Workout Carbs More 'Anabolic' Than Protein!? Iron Prevents Gastric Cancer & Insulin Resistance?! Plus: A Sixpack of Kettlebell Studies

If you want to know exactly how your neighbors or rather your county did, check out the CDC's brand new County Data Interactive Atlas (may take some time to load), select your state and click on your county. Unfortunately, it's not exactly likely that you will be pleasantly surprised after all, places with rates below 6.5% (white on the map) have become rare, while those with 11.2% or more are becoming the norm.

"100%" - In words: One hundred percent, that's the SuppVersity figure of the week and at the same time the rate at which the prevalence of diagnosed diabetes in 14 of the US states grew faster in the years between 1995 and 2000 than previous estimates had predicted. The CDC has published this figure along with more information and the link to their brand new County Data Interactive Atlas in their weekly report on November 15, 2013. The Top 5 offenders on the list that's attached to the report are (1) Oklahoma (226 percent), (2) Kentucky (158 percent), (3) Georgia (145 percent), (4) Alabama (140 percent), and (5) Washington (135 percent).

No reason to worry, though, my American friends! According to their own assessment, the CDC and its partners are working on "a variety of initiatives to prevent type 2 diabetes and to reduce complications in those already diagnosed."... you see,all is going to be good! Your well-meaning government is taking care of the problem ;-)

I guess that's enough sarcasm and useless statistics for the day. Let's get down to some serious On Short Notice business, now. And what would be more obvious than to start with something that's probably still not on the radar of the CDC or any its smart partners over at the NIH who are still promoting a high carb + low fat diet to people who can hardly tolerate the amount of carbohydrates in a TicTac. What I am talking about? The predispositioning effects of a fat-deficient toddler diet...

• Fat loving toddlers grow up to be leaner adults (Rolland-Cachera. 2013) -- To determine whether nutritional intakes in early life are associated with body composition and hormonal status at 20 years, a group of researchers from the University of Paris analyzed data from 73 subjects, who had been part of a two-decade-long prospective study (ELANCE, Etude Longitudinale Alimentation Nutrition Croissance des Enfants).
  
  
  Associations of specific factors that increase the risk of being obese in the kindergarten as based on another study that's also been published ahead of print in the online version of Obesity (Flores. 2013):
  

  • born to an obese mother + 240% risk
  • gestational diabetes and gestational diabetes + 190%
  • drinking tea or coffee between meals before bedtime at 2 years old +230% and drinking sugary beverages at kindergarten age at least weekly + 130%
  • Latino or multiracial + 130% race ethnicity
  • ever-attending center-based daycare -70%
  • eating fruit at least weekly at kindergarten age -70
  • maternal history of a prior newborn birth weight greater than or equal to 4000g -90%

  If you do have or plan to have kids, you should maybe make a mental note on some of these.
  The kids, now all young adults had been examined twice, at the age of 10 months and with 2 years. During the recent followup, the  body weight, height, subscapular and triceps skinfold thicknesses, fat mass (FM), fat-free mass (FFM) and serum leptin concentration of the young adults (now twenty years of age) were recorded in order to identify associations between early nutrition and adult body weight.
  
  The adjusted linear regression models Rolland-Cachera and colleagues used to analyze the data actually showed a couple of significant associations, the first one of which, i.e. the fact thatan increase by 100 kcal in energy intake at 2 years was associated with higher subscapular skinfold thickness (β=6.4%, P=0.002) and higher FFM (0.50 kg, 0.06–0.95, P=0.03) at 20 years, seems to stand in line with the hilarious calories-in-vs-calories-out hypothesis. However, these associations could also be related to the fact that early nutrition will program our satiety response, so that those programmed to be "good eaters" by a less nurturing diet in their earliest childhood will remain "good eaters", even when they switch to the energy-laden standard American diet.
  
  Against that background, the second significant association the researchers observed, i.e. the fact that an increase by 1% energy from fat at 2 years was associated with lower subscapular skinfold thickness (−2.3% SF, −4.41 to −0.18, P=0.03), lower FM (−0.31 kg, −0.60 to −0.01, P=0.04) and lower serum leptin concentration (−0.21 μg l−1, −0.39 to −0.03, P=0.02) at 20 years appears to be even more important. After all, it looks like the Rolland-Cachera et al. had found the first relatively convincing evidence (not proof, yet) for the negative metabolic effect of early low fat diets in human beings:
  

  "Low-fat intake in early life was negatively associated with body fat (particularly at the trunk site) and serum leptin concentration at 20 years, suggesting that early low-fat intake could increase the susceptibility to develop overweight and leptin resistance at later ages. These findings substantiate current recommendations against restricting fat intake in early life and open new directions for investigating the origin of obesity." (Rolland-Cachera. 2013)

  Now let's just hope that scientists are actually tackling these "new directions" and - more importantly - that the respective results are recognized by the public and incorporated into the "dietary guidelines".
• Study suggests: If you could chose only one, your intraworkout nutrition should be a carbohydrate not a protein supplement (Kazemzadeh. 2013) -- This is at least the authors' own interpretation of the results of a recent study that was conducted by three researchers from the Azad University and the Teheran University in Iran.
  
  

  

  Figure 1: Changes in hormone levels from pre to post exercise (Kazemzadeh. 2013). If you focus solely on statistical significance you can be likewise mislead as, when you don't even check whether you findings are significant at all.

  According to the statistically significant part of the hormonal response of the 18-25-year-old subjects (university students who selected physical training course, but had no prior training experience), the consumption of an intra-workout supplement containing either 10 ml/kg of a 6% glucose solution was in fact "less catabolic" than during the same strength training routine with a 0.2 g/kg protein shake (PRO group) as an intra-workout supplement. On paper that's certainly true: The increased insulin response "enhances removal of amino acids and synthesis of proteins after the resistance exercise, on the one hand, and decreases the activity of proteolytic enzymes" (Kazemzadeh. 2013) and the non-existant increase in cortisol is in fact what scientists have long heralded as the goto indicators of anabolism.
  
  
  Note: Just as most of these studies the participants did not consume breakfast before the resistance exercise session, which comprised six selected exercises: The bench press, biceps curl with barbell, side stretch, leg press, knee stretch, knee bending. If the study had been conducted after a regular breakfast ~2-3h before the workout, the study could have yielded totally different effects with respect to both, the blunted insulin, as well as the increased cortisol response. On the other hand, the GH spike in the protein group would most certainly have been lower as well. After all, the latter is - as you may have read in the SuppVersity Facebook News earlier today - basically only a means by which your body taps into its fat reservoirs to satisfy his acute energy demands and not strictly a way to protect lean mass (Gahete. 2013).
  I do still have serious doubts about the real-world significance of the temporary blunt in cortisol. After all, the immediate post-workout response is, in contrary to sustained elevations of cortisol levels for hours or days after a workout, associated with an increase, not a decrease in skeletal muscle hypertrophy (West. 2013) and in essence nothing else, but a physiological adaptation that's necessary to maintain stable blood glucose levels during strenuous workouts and sooth the early burst of inflammation after a workout. Moreover, despite being only borderline significant, only the protein shake did increase growth hormone (p=0.057), testosterone (p=0.52) and IGF-1 (p=0.51) levels during the workout.
  
  This does not necessarily refute the benefits of carbohydrate supplementation during a workout, but if you insist on maximizing gains (not necessarily all lean I would guess) at all costs, it may be wise to consume a slow digesting protein + some fiber-laden carbs like oats 1-2h before a workout, to sip a light carbohydrate + BCCA drink intra- and wash everything down with another shake w/ whey protein and one or two bananas afterwards instead of just drinking some sugar water while you are lifting.
• Iron is a negative predictor of gastric cancer in humans and lowered hemoglobin and hematocrit levels induce insulin in rodents (Cook. 2013; Davis. 2013) -- While the alpha-tocopherol, beta-carotene cancer prevention study was a failure (at least with respect to the expected benefits of the anti-oxidants), there are still a couple of interesting side-findings.
  
  

  

   Meat-Ology: The Link Between Red Meat, Cooking Techniques & Prostate Cancer

  One of these side-findings pertains to the touted effects of increased iron intake on the etiology of gastric cancer, which is simply not existent. According to Cook et al. there were statistically significant negative associations for ferritin in the 2nd, 3rd quartile (-33% risk and -48% risk, respectively) and a borderline significant risk reduction of -31% for overall gastric cancer in the highest quartile (>241 ng/ml) and statistically nonsignificant decreases in gastric cancer risk for total iron, transferrin saturation and total dietary iron intake per 1,000kcal/day in the 2nd-4th quartiles of the respective serum parameters.
  
  That said, subsequent adjustments for H. pylori and then gastric atrophy did not materially affect a majority of the estimates ...
  

      "[...] the only exception was that the relationship  between ferritin and GNCC [Gastric noncardia cancer] was attenuated  There was little evidence for direct associations between iron metrics and H. pylori seropositivity or gastric atrophy (low pepsinogen I)—only serum ferritin appeared to share a relationship with these variables, and this relationship was stronger between ferritin and gastric atrophy." (Cook. 2013)

  So if "red meat is bad for you" it is probably not the iron content of the meat that is responsible for the observed associations of gastric cancer and high red meat intake in some previous studies (cf. WCR Fund. 2011).
  
  And with respect to its effect on glucose metabolism, a recent rodent study has just shown that a reduction in hemoglobin and hematocrit due to a lack of dietary iron does actually impair, not improve glucose management in otherwise healthy rodents fed an iron-deficient diet:
  

  

  Figure 2: Blood glucose, insulin and triglyceride on iron sufficient / deficient high sugar (AIN-76) or high starch (AIN-93) died (Davis. 2013)

  "Hemoglobin and hematocrit were significantly reduced in both ID groups compared to the C  and PF groups. Similarly, animals in the both ID groups exhibited elevated steady-state levels of blood glucose and insulin [...]
  
  [Moreover, hepetic]epatic gene expression analyses revealed a ~4-  and 3-fold increase in the expression of glucokinase and pyruvate dehydrogenase kinase-4 mRNA, respectively, in the ID group on either diet compared to their respective PF [pairfed on iron sufficient diets] counterparts" (Davis. 2013)

  The accompanying negative effects on triglycerides and fatty acid synthesis and storage Davis et al. observed were yet exclusive to the animals who received a high succrose iron-deficient diet.
• Vitamin C, D & E in health not disease - Only alpha-tocopherol shows negative correlation with markers of inflammation (Garcia-Bailo. 2013)-- A very recent study that has been conducted by researchers from the University of Toronto and the University of Guelph did not find any relation between the novel and the old savior of the human race, i.e. vitamin D and C, respectively and expression of inflammatory cytokines.
  
  

  

  Suggested read: "Are Vitamin Supplements Bad For Me (1/2)? The wrong Vitamin E Supplements Increase Cancer Risk."

  Plain Vitamin E in its alpha-tocopherol form, which has almost been written off after the selenium + E (and E only) cancer trials, on the other hand, showed statistically significant correlations with interferon-gamma and RANTES, a pro-inflammatory cytokine that is also known as CCL5 and the acronym for "egulated and normal T cell expressed and secreted" plays an important role in various immune processes, such as recruitment of leukocytes to sites of inflammation and mediating T cell and monocyte traffic. In view of the fact that this cytokine has also been shown to increase angiogenesis and is generally elevated in several inflammatory conditions, including atherosclerosis, these results would suggest that keeping an eye on your E-levels is about as, if not more important for young healthy individuals than vitamin C and D.
  
  If you also consider the fact that IL-1RA (by the way not necessarily inflammatory), interferon gamma, IP-10, PDGF-bb and RANTES were the only out of 27 cytokines the researchers initially measured with high enough concentrations to be detect accurately in the 1007 subjects with a BMI of ~23 and a weekly activity level of ~7Met, these results do also provide substantial evidence that it would probably be worth spending more money on studies that investigate  what it is that makes normal people healthy, instead of spending bazillions of dollars into the 1001st study on how people with XYZ (pt your favorite disease here) have low vitamin D levels *yawn*.

• 

  Check out the Website of the Reigning Canadian Kettlebell Biathlon Champion, Ameer Rosic for some workout videos

  A sixpack of kettlebell studies to remind trainers and trainees, alike, that there are more things you can lift than just dumbbells and barbells (various authors) -- I have never gotten hooked to kettlebells myself and would never agree to exchange my barbells and dumbbells for the finest set of kettlebells for more than one week, but if you take a look at some of the studies that have been published in the past 12 months or so, there is sufficient evidence to suggest that the incorporation of kettlebell workouts into your routine, as a means to provide new muscular and metabolic stimuli, could yield highly beneficial results:
  

  Kettlebell swings restore and enhance back health and function (McGill. 2013) On the basis of electromyography, ground reaction forces (GRFs), and 3D kinematic data the researchers determined that kettlebell swings create a "hip-hinge squat pattern characterized by rapid muscle activation-relaxation cycles of substantial magnitudes (∼50% of a maximal voluntary contraction [MVC] for the low back extensors and 80% MVC for the gluteal muscles with a 16-kg kettlebell) resulting in about 3,200 N of low back compression." The way the swings activate the abs and the unique loading patterns of the posterior shear of the L4 vertebra on L5, which is opposite in polarity to a traditional lift could make it a valuable tool in re- and prehab.	Kettlebell swing training improves maximal and explosive strength (Lake 2013) 21 healthy men  were randomly assigned to either a kettlebell (KB) or jump squat (JS) training twice a week. The KB group performed 12-minute bouts of KB exercise (12 rounds of 30-second exercise, 30-second rest with 12 kg if lower than 70 kg or 16 kg if higher 70 kg). The JS group performed at least 4 sets of 3 JS with the load that maximized peak power—Training volume was altered to accommodate different training loads and ranged from 4 sets of 3 with the heaviest load (60% 1RM) to 8 sets of 6 with the lightest load (0% 1RM). The increase in maximum strength of 9.8%, as well as explosive strength (+19.8%) were identical in both groups
  Kettlebell training has "has potential for improving some components of MetS in middle-aged women." (Moreno. 2011): While the changes the author of the thesis observed in response to 10 weeks twice weekly kettlebell training did not reach statistically significance (probably due to the low subject size of N=6 physically inactive women, mean age (mean age 48.8y, BMI 31.8) the trends in " fasting glucose and body fat were encouraging and suggest that kettlebell training has potential for improving some components of MetS in middle-aged women."	Kettle bell workouts can decrease blood pressure (Douglass. 2013): Eight resistance trained pre-hypertensive and HTN males saw statistically and more importantly clinically significant declines in blood pressure (to normal levels!) in the course of a randomized cross-over designed study which included 12 minutes of continuous two-handed swings (THS), three sets of a 6 exercise circuit (CIR), and a resting control (CON).
  Kettlebell training can improve strength, power and and endurance (Mannocia. 2013):  23 subjects (age 18-72 years) were required to perform a10-week kettlebell training program that took place in a group setting two times per week. Post hoc pairwise comparisons of assessments barbell clean and jerk, barbell bench press, maximal vertical jump, and 450 back extensions performance revealed significant time x group interaction and a main effect (p < 0.05) for the bench press, a trend toward a time x group interaction and a significant main effect for clean and jerk. These observations suggest "that kettlebells may be an effective alternative tool to improve performance in weight- and powerlifting".	10 min of treadmill running may burn more more energy, than a short 10-min kettlebell drill, but pro-anabolic & strength edurance effects speak in favor of 'the bells' (McGill. 2013): Only those who still believe in santa... ah, I mean the calories in vs. out theory of weight loss, will probably care, whether they are burning 12.5 or 17.1kcal/min and therefore this "advantage" would hardly be important even if the participants had not been sprinting part of their 10min on the treadmill just to make sure to achieve the prescriped (identical) rates of perceived exertion. And as usual, there is no reason, why you could not switch back and forth from one "drill" to another.

That's it once more for this week's installment of pretty longish short news. I hope you liked one or another and will see you tomorrow for some more information on the latest and greatest from the world of exercise and nutrition sciences. And just in case you have not seen those already, I guess there are a handful of news on facebook you may be interested in:

• 

  If you just skip the hookers and the transdermal cocaine and take a regular bath, this may speed up your regeneration and propel your gains - if timepoint and temperature are spot on!

  Transdermal 'cocaine' in "bath salt" - 3,4-methylenedioxypyrovalerone (MDPV) in OTC "bath salt" is 10x more potent than cocaine and unquestionably hazardous
• The anti-cancer effect of 'active vitamin B6' - High levels of pyridoxal 5'-phosphate, the active form of vitamin B6 appear to have protective effects against breast cancer... or is it exactly the other way around?
• Bisphenol A is a local fat synthesizer - Study shows how Bisphenol A increases obesity: it ramps up the local cortisol production in adipose tissue and thus 'helps' you stash away more body fat

As usual there is more on facebook and further news to come, but I guess you got other things to do on a Saturday than reading SuppVersity posts all day ;-)

References:

• Cook MB, Kamangar F, Weinstein SJ, Albanes D, Virtamo J, Taylor PR, Abnet CC, Wood RJ, Petty G, Cross AJ, Dawsey SM. Iron in relation to gastric cancer in the alpha-tocopherol, Beta-carotene cancer prevention study. Cancer Epidemiol Biomarkers Prev. 2013 Nov;21(11):2033-42. 
• Davis MR, Hester KK, Shawron KM, Lucas EA, Smith BJ, Clarke SL. Comparisons of the iron deficient metabolic response in rats fed either an AIN-76 or AIN-93 based diet. Nutr Metab (Lond). 2013 Oct 30;9(1):95.
• Douglass, MJ. The blood pressure response of two popular kettlebell routines. M.S. thesis in  Kinesiology (Exercise Science). California State University, Sacramento, 2013.
• Flores G, Lin H. Factors predicting severe childhood obesity in kindergarteners. Int J Obes (Lond). 2013 Nov 13.
• Gahete MD, Córdoba-Chacón J, Luque RM, Kineman RD. The Rise in Growth Hormone during Starvation Does Not Serve to Maintain Glucose Levels or Lean Mass but Is Required for Appropriate Adipose Tissue Response in Female Mice. Endocrinology. 2013 Nov 13.
• García-Bailo B, Roke K, Mutch DM, El-Sohemy A, Badawi A.Association between circulating ascorbic acid, alpha-tocopherol, 25-hydroxyvitamin D, and plasma cytokine concentrations in young adults: a cross-sectional study. Nutrition & Metabolism 2013, 9:102. 
• Hulsey CR, Soto DT, Koch AJ, Mayhew JL. Comparison of kettlebell swings and treadmill running at equivalent rating of perceived exertion values. J Strength Cond Res. 2013 May;26(5):1203-7.
• Kazemzadeh Y, Gaeini A, Abasrashid N. Comparison of the Effect of Consuming Carbohydrate or Protein during Exercise on Hormonal Response. Zahedan Journal of Research in Medical Sciences. 2013; 15(2): 90-93. 
• Lake JP, Lauder MA. Kettlebell swing training improves maximal and explosive strength. J Strength Cond Res. 2013 Aug;26(8):2228-33.
• Moreno KIK. Effects of kettlebell training on metabolic syndrome in women. M.A. Thesis, San Jose State University, 2011, 138 pages.
• McGill SM, Marshall LW. Kettlebell swing, snatch, and bottoms-up carry: back
  and hip muscle activation, motion, and low back loads. J Strength Cond Res. 2013
  Jan;26(1):16-27. 
• Manocchia P, Spierer DK, Lufkin AK, Minichiello J, Castro J. Transference of kettlebell training to strength, power and endurance. J Strength Cond Res. 2013 May 3.
• Rolland-Cachera MF, Maillot M, Deheeger M, Souberbielle JC, Péneau S, Hercberg S. Association of nutrition in early life with body fat and serum leptin at adult age. Int J Obes (Lond). 2013 Nov 13.
• WorldCancer Research Fund/American Institute for Cancer Research. Food, nutrition, physical activity and the prevention of cancer: a global perspective. Washington, DC: AICR; 2007.
• West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Appl Physiol. 2013 Jul;112(7):2693-702. 

700% Increase in Insulin, Elevated Blood Glucose + Identical Cortisol & CK Levels Challenge Usefulness of Intra-Workout High GI Carb Ingestion in Advanced Strength Trainees

Image 1 (IndiaToday): If you insist on ingesting 3x cans (=sugar equivalent of the maltodextrin supplement in the study at hand) of a not-to-be-named energy drink during your workouts and don't die from caffeine poisoning, you may gain more, but I suspect not in those areas, where you ant it ;-)

Whether you should or should not supplement with carbohydrates is a matter of constant debate among strength trainees. While some swear that they cannot perform if they aren’t guzzling a glucose-laden “intra-workout” supplement or energy drink from the supermarket, others prefer to get the lion's share of their carbs from whole foods, settle for BCAAs or plain water as their workout beverage of choice and wash down a sweet ripe banana with a tasty protein shake after their workouts. And while a previous paper by Bird et al. suggested that the former practice, i.e. the ingestion of a carbohydrate supplement (6%, preferably with 6g of EAAs) during your workouts, could significantly blunt the exercise induced cortisol spike (CHO alone -116%, CHO + EAA -112% vs. placebo), a very recent study, which was conducted by a group of scientists from the University Federal of Paraíba in Brazil, yielded very different results (de Oliveira Quirino. 2013)

To carb-guzzle or not that is the question!

Contrary to Bird et al., who had recruited previously untrained subjects for their study, de Oliveira Quirino's team picked 7 healthy young men (BMI 25.4kg/m²; age 27.3y) who had been training for at least 6 months with a minimum 3 resistance training sessions per week – this is important to note, because it should, for most of you, increase the real-world significance of the data, as I assume that many of you will have been following a similar protocol for probably longer than 6 month, already. What may be less in line with your own exercise regimen, though, is the exact training protocol, which comprised ten exercises for the upper limbs, i.e.

bench press, inclined press, dumbbell pullover, back lat pulldown, back lat push-down,

front press, bar-bell curl, pushdown, preacher curl, and lying triceps extension

which were performed for 3 sets of 12-15 reps to voluntary failure (60% RM) and at a cadence of 2-0-2-0 (2s concentric, 2s eccentric; no transition time between phases). Obviously all participants performed this protocol twice (in random order) and with a 96h interval in-between the supplemented (1,080ml of an 8% carbohydrate solution =86.4g of maltodextrine, ingested at regular intervals every two exercises) and the placebo (sucralose) trial.

Figure 1: Plasma glucose levels (in mg/dl) at rest, after the first, second, third, fourth and fifth pair of exercises (left) and increases in insulin and cortisol from pre to post exercise (de Oliveira Quirino. 2013)

As you can see in figure 1 the ingestion of  ~350kcal of readily available energy was more or less unnecessary, as it did not blunt, but rather augment the cortisol response (effect was not statistically significant, though); and that in the presence of profound elevations in blood glucose and insulin levels, and without any effect on circulating creatine kinase levels (a marker of muscle damage, not shown in figure 1).

A "substantial" increase in "anabolic hormone activity"?

Now in the absence of concrete data on protein synthesis / degradation, mTOR activity & co and without any information on confounding factors such as an increased training intensity during the carbohydrate trial, it is difficult to provide a conclusive answer to the initially raised question, whether the provision of fast acting carbohydrates during a strength training session would, as the scientists conclude, provide an "additional [benefit] for those engaged in this type of exercise with the aim of hypertrophy”. After all, it may be correct that the findings of the study …

[…] show that carbohydrate ingestion during the course of a training session comprising resistance exercises does not affect catabolic activity, but does increase substantially anabolic hormone activity. (De Oliveira Quirino. 2013)

but the „anabolic hormone“ the Brazilian scientists are talking about is insulin, which is beyond doubt among the most "anabolic” hormones in our body, but unfortunately, not exactly muscle specific, as it is simply a matter of fact that skeletal muscle is not the only tissue that’s going to benefit from insulin’s facilitative effects on nutrient uptake (Timmerman. 2010). It thus appears more than reasonable to assume that two other major players in the complex orchestrate of our metabolism will avail themselves of the superfluous amount of glucose that would be floating around in our bloodstream if we mimicked the supplementation protocol in the de Oliveira Quirino study. Their names? Your liver and your body fat stores!

So what are the implications?

Image 2: Another recently published study by Wax et al. suggest that slow digesting starches can help to maximize workout intensity and volume (read more in my article for Physique Magazine)

If you are not training fasted (the participants worked out on 11am on both occasions) and/or low-carbing without regular re-feeds, so that you have adequate muscle and liver glycogen stores, when you hit the gym, and you are no rookie anymore (cf. Bird. 2008), so that working out is no longer a totally novel stressor for your body, my personal interpretation of the study data is that you simply don’t need the additional fast acting carbohydrates! Neither to stabilize your blood sugar, nor to ward off any exorbitant increases in cortisol.

And as far as the increase in insulin is concerned, it appears more than questionable whether the latter would actually exert significant additive effects on muscle protein synthesis or could not even negate the nutrient repartitioning effects of your workouts (Poehlman. 2000; Hawley. 2008) by diverting the obviously superfluous energy to places where you’d rather not have them stored ;-)

A note on the "importance" of insulin to build muscle: One of the most comprehensive reviews on the role of insulin in skeletal muscle anabolism states it quite aptly "the full response of translation initiation and protein synthesis to either effector is not observed in the absence of a minimal concentration of insulin", but - and this is important - "the amount of insulin required for the effects is low, and a concentration of the hormone that approximates that observed in fasting animals is sufficient for maximal stimulation." (Kimball. 2002)

Bottom line: Avoid the unnecessary insulin spike from the ingestion of high GI carbs before and/or during a workout, but make sure that you have an ample amount of muscle glycogen before you hit the gym via an adequate total and post-workout carbohydrate intake (the lion's share in form of low GI carbs) and planned carbohydrate re-feeds (esp. for low carbers). This practice will not necessarily augment post-exercise protein synthesis (cf. "Glycogen-Free Muscle Growth"), but it is certainly going to help you to increase or at least maintain your workout intensity and overall training volume (Wax. 2013).

References:

1. Bird SP, Tarpenning KM, Marino FE. Liquid carbohydrate/essential amino acid ingestion during a short-term bout of resistance exercise suppresses myofibrillar protein degradation. Metabolism. 2006 May;55(5):570-7.
2. de Oliveira Quirino EL, da Conceição Rodrigues Gonçalves M, de Oliveira CVC, Porto dos Santos E, Silva AS. Influence of carbohydrate supplementation during resistance training on concentrations of the hormones cortisol and insulin. Sport Sci Health (2013) 7:93–97
3. Hawley JA, Lessard SJ. Exercise training-induced improvements in insulin action. Acta Physiol (Oxf). 2008 Jan;192(1):127-35. Review. 
4. Kimball SR, Farrell PA, Jefferson LS. Invited Review: Role of insulin in translational control of protein synthesis in skeletal muscle by amino acids or exercise. J Appl Physiol. 2002 Sep;93(3):1168-80.
5. Poehlman ET, Dvorak RV, DeNino WF, Brochu M, Ades PA. Effects of resistance training and endurance training on insulin sensitivity in nonobese, young women: a controlled randomized trial. J Clin Endocrinol Metab. 2000 Jul;85(7):2463-8.
6. Timmerman KL, Lee JL, Dreyer HC, Dhanani S, Glynn EL, Fry CS, Drummond MJ, Sheffield-Moore M, Rasmussen BB, Volpi E. Insulin stimulates human skeletal muscle protein synthesis via an indirect mechanism involving endothelial-dependent vasodilation and mammalian target of rapamycin complex 1 signaling. J Clin Endocrinol Metab. 2010 Aug;95(8):3848-57.
7. Wax B, Brown SP, Webb HE, Kavazis AN. Effects of carbohydrate supplementation on force output and time to exhaustion during static leg contractions superimposed with electromyostimulation. J Strength Cond Res. 2013 Jun;26(6):1717-23. 

Post-Workout Glycogen Repletion - The Role of Protein, Leucine, Phenylalanine and Insulin. Plus: Protein & Carbs How Much do You Actually Need After a Workout?

Pascal Behrenbruch, German decathlete and one of those athletes whose performance during a meet will certainly depend on "optimal" glycogen repletion between the different sports.

Within the past couple of weeks I have often talked (on the Science Round-Up) and written (here at the SuppVersity) about the importance of glycogen repletion to maintain optimal exercise performance and stave off the metabolic downregulation that's a characteristic of the nasty combination of overtraining and undereating. The recent post on the anti-plateau effect of sucrose should actually have made it quite clear: Even when you are "just" dieting, you should make it a priority to satisfy your body's desire to have an adequate reserve of glucose in the muscle and more importantly the liver.

But what does that mean? Do you really have to guzzle gallons of sugar water (aka weight gainers) after a workout? Certainly not.

The notion that you need to flood your skeletal muscle tissue with sugar right after the workout and that even showering before you do so would compromise your training success and put you at danger of losing muscle is simply hilarious.

That being said, the results of the latest study from the Institute of Sport at the Carnegie Faculty of the Leeds Metropolitan University in the UK is probably of greater importance to professional athletes like triathletes, decathletes, cyclists, etc. After all, they are the ones for whom immediate glycogen repletion can make the difference between victory and defeat. On the other hand, this does not mean that there wasn't something to be learned from the data Detko et al. gathered by the means of 13C magnetic resonance spectroscopy - after all, they took a different approach to the problem and did - instead of modifying the carbohydrate source - try to elucidate how the addition of protein would influence the restoration of muscle and liver glycogen in the immediate vicinity of a workout (Detko. 2013).

Is there even such a thing as an "optimal PWO glycogen replenisher"?

The quest for the optimal PWO carbohydrate source has long been a quest for the highest GI carbohydrate. Until the low carb craze hit home, the mainstay paradigm of figure, bodybuilding and performance athletes was "the higher the GI, the faster the uptake, the greater the gylcogen (re-)synthesis, the better the results". From a scientific perspective, it has has yet long been refuted that the GI and thus the insulin response a given carbohydrate would elicit was the only determinant of its practical value as a muscle (let alone liver) glycogen replenisher.

Did you know that there is a catalytic dose of ~40g of fructose per day (=6 normal size bananas) that will improve your glucose metabolism? (learn more)

One of my favorite and in fact comparably recent studies that demonstrates the fallacy of using the glycemic index as a gauge for post-workout glycogen replenishment is the 2008 study by Wallis et al. In a well-controlled experiment, the researchers were able to show that a post-workout drink that contained 2:1 glucose to fructose ratio was on par with pure glucose in its ability to replenish the depleted muscle and liver glycogen, when it was consumed right after a standardized glycogen depleting exercise bout (Wallis. 2008). Obviously, this result stands in stark conflict with the "glycemic index (GI) hypothesis". After all, the falsely dreaded fructose, the demon of Dr. Lustig's worst nightmares, has a GI of <20 and thus the lowest glycemic index of all natural sugars.

If the "GI hypothesis" was accurate, fructose should therefore be by far the worst choice for an athlete who wants to replete his / her glycogen stores as fast as possible. That this is not the case, goes to show you that things are - once again - much more complex, than the widely accepted, but overtly simplistic "rules of thumb" would suggest.

Why is the glycemic index a bad avisor, when it comes to PWO glycogen replenishment?

Before we head on to the new data the Detko study has to offer, let's briefly take a look at why the glycemic index does not qualify as a compass to guide us on our quest for the perfect post-workout carbohdydrate source. Don't worry, I am trying to cut myself short, just listing the four most important caveats:

• 

  Table 1: It's rarely talked about, but especially endurance athletes will also benefit from increased intramuscular lipid stores. Therefore the overview of the intramuscular glycogen and lipid storage rates from a 2003 paper by Jacques Décombaz could come especially handy to the marathoners among the SuppVersity readers (Décombaz. 2003)

  Non-insulin-dependent glucose uptake: In the first 30-60min after a workout, for example the GI, i.e. the ability of a given carbohydrate source to trigger an insulin release is negligible, simply because the non-insulin dependent uptake of glucose into the muscle is already maxed out.

• Organ specificity: Contrary to the skeletal muscle tissue, the liver has a is downright dotty about fructose; and the more fructose it takes up, processes it and turns it into glycogen (see pathway, here), the more glucose will remain for your muscles to feast on.

• Ceiling effects: The amount of glycogen your muscles can synthesize is limited to approximately 9–10mmol/kg wet weight (WW). This rate can be sustained by the intake of 1.2g of carbohydrates per kg of body weight - more cannot end up in your muscle, regardless what kind of useless nutrient partitioner the company rep in disguise on your favorite bulletin board may have persuaded you to buy.

• 

  Figure 1: Muscle glycogen content 2h into the recovery period (left) and rise and fall of glucose concentrations after the ingestion of a low and high molecular weight starch immediately after a standardized glycogen depleting exercise bout (Gunnar. 2013)

  Molecular weight and absorption dynamics: While it is obvious that the latter should have a major effect they should (a) interact with the glycemic index (faster appearance in the blood = greater insulin response in healthy individuals) and (b) warrant the use of carbohydrate blends (after all, you don't want to run out, after the intitial spike, right). From my use of the conditional in the previous paragraph you may however already have realized that this assumption is not unambiguously supported by the currently available literature which does support the faster transit times, but not necessarily the purported downstream effects on the repletion of the glycogen stores in exercised muscles.
  In his 2013 thesis, Frances Gunnar from the University of Nottingham, for example, demonstrated that the much praised high molecular weight starch Vitargo(TM) did not yield produce greater increases in post-workout glycogen resynthesis than a low molecular weight counterpart (Gunnar. 2013). On the other hand, we have seminal papers such as the Y2k paper by Piehl et al. that are usually cited in this context (Piehl. 2000) and in which solutions with high molecular carbohydrate sources yielded greater rates of skeletal muscle re-synthesis.

I guess these were more than enough, "on the other hands" as Carl Lenore likes to call these lengthy departures of mine on the weekly SuppVersity Science Round-Up on the Super Human Radio Network from time to time. So let's now finally get to the study at hand.

Protein and galactose? What's that got to do with PWO glycogen repletion?

As I already hinted at in the introduction, the experiment Detko et al. conducted was not designed to compare carbohydrate solution A with carbohydrate solution B. The idea was rather to elucidate whether and by which mechanisms the addition of protein to the a standardized post-workout carbohydrate solution could accelerate the PWO glycogen repletion even further. Accordingly the test solutions the scientists prepared from commercially available raw materials contained either

• maltodextrin + galactose - 0.9 g/kg body mass (BM) maltodextrin + 0.3g/kg BM galactose, or
• maltodextrin + glactose + protein + leicine + phenylalanine - 0.5g/kg maltodectrine, 0.3g/kg galactose, 0.2g/kg whey and 0.1g/kg of each leucine and phenylalanine

As subjects, the scientists selected a total of seven recreationally, yet highly trained male cyclists who had been training for least 10h per week over the least 5 years (mean age: 33y, body weight: 79kg, VO2Max: 58 ml/kg per min).

It would have been more promising to use isoleucine instead of leucine and phenylalanine as "additives" to boost glucose uptake (click here to learn why)

Why would the scientists use galactose, leucine and phenylalanine? According to previous research the combination of maltodextrin + galactose has a slight, but significant advantage over the glucose + fructose combination mentioned earlier in this article. Practically it's unlikely that it will make a significant difference, anyways. After all, the important thing here is that fructose and galactose are preferred glycogen sources of the liver, which is thus not going to "steal" the glucose from the maltodextrin which is supposed to end up in the glycogen stores of the musculature - not the live (Decombaz. 2011).

The addition of leucine and phenylalanine, on the other hand, was supposed to increase the insulin response and thus help to shuttle the glucose into the cells. Needless to say that this is not necessarily a good idea and actually based on the same fallacious notion that insulin would be the main determinant of the rate of glucose replenishment after a workout, right?

In order to prevent differences in the baseline diet to interfere with the study outcome, the participants were not only asked to reproduce their nutrient intake in the days prior to the two testing sessions, they were also provided with standardized meals. which containing 150 g CHO, 67 g PRO and 22 g fat  and had to be consumed on the evening before the tests which consisted of

• 45min of steady state cycling at 70% VO2max,
• 6x1min sprints at 120% of the VO2max (2min recovery at 50% VO2max) and 
• 45min of steady state cycling at 70% VO2max

The steady 2nd state part of the intervention was meant to "further promote [the] depletion of glycogen in type I fibres" and to elicit a "reduction of plasma lactate concentrations at the end of the glycogen-depleting exercise".

"Ok, I got it, what about the supps and the results?"

During the trial the subjects were free to consume as much water as they wanted. Blood samples were drawn at the start, 45min after the intervention and every 30min during the 4h recovery period. The crucial part of the study, the supplementation, took place immediately after the first vastus lateralis scan. The drinks were ingested in a single 400ml bolus and 6 smaller 150ml portions every 30 min (see figure 2, left - small bottles).

Figure 2: Outline of the experimental design (left) and glycogen repletion rates - calculated based on averages for all subjects over the full course of the 4h post-workout window (Detko. 2013)

As you can see in figure 2, the averaged glucose repletion rates were virtually identical with a non-significant, but visible advantage for the muscular glycogen with higher carbohydrate and no protein intake. The result clearly refutes the researchers initial hypothesis that

"[...] the post-exercise ingestion of MD and GAL with PRO and AA would enhance liver and muscle glycogen repletion compared with an isoenergetic MD–GAL formulation." (Detko. 2013)

What's particularly intriguing about this result is that it manifested despite the fact that the large spike in insulin, the researchers had expected in response to the addition of whey and the pro-insulinogenic amino acids leucine and phenylalanine to the mix (see figure 3).

Figure 3: Blood glucose and insulin levels in the post-workout period (my markups in Detko. 2013)

In conjunction with the data about the glucose concentration, which did not crash in response to the insulin spike (this should happen if the equation "more insulin = more glucose uptake = faster glycogen replenishment held) this just confirms that the effects of the carbohydrate, protein and amino acid induced insulin spikes have little to no effect on the rate post-workout glycogen re-synthesis. While previous research suggests that a threshold limit must be maintained to keep the influx of glucose constant after the initial ~30min, this threshold is so low that any special "tactics" to increase the insulinogenic effect of post workout-nutrition appears to be a waste of time.

---

Bottom line: If we follow the Taubsian mantra that insulin is the root cause of all disease, the necessary conclusion we'd have to take away from the results of this study is that you better avoid having protein in your post-workout nutrition and rather resort to carbohydrates alone... just kiddin' ;-) We obviously all know about the benefits the ingestion of a fast digesting protein in the vicinity of workout has on protein synthesis. Simply skipping on the protein fraction of your post-workout shake is therefore not really an option. After all, the transient increase in insulin, as useless as it may be, is probably not going to kill you.

That being said, this is study #2 within no more than a week that questions the usefulness of adding leucine as a free-form amino acid to your supplement stash (compare "Leucine Supplementation Exemplifies Potential Downsides of Non-Specific Insulin Sensitizers"). With ~30g of whey you should have enough readily available amino acids (including leucine!) to kickstart protein synthesis, anywa - plus: contrary to the average study participant in this and similar experiments, you are not going to fast for the next 4h, so that the protein from your next full meal is going to help you keep the plasma amino acid levels steady (Tip: If you cannot have a full meal, afterwards add 20g of casein to the shake).

What happens if you eat 194 bananas in 3 weeks? You will get fit and sick, right? No, false. What actually happens is a reduction in body fat (read more)

With your protein needs taken care of, the only other thing you'll need are some carbohydrates to satisfy your bodies desire to refill its glyocogen stores. Preferably, those carbs come at a ratio of 2g of muscle substrate (=glucose or precursors) to 1g of liver substrate (=fructose or galactose). A banana, a food I have previously recommended as a post workout carbohydrate source, would provide you with 5g of free glucose and 5g of free fructose (per 100g). It does however also contain 5g of starch, 2g of sucrose and 2.5g of fiber, so that you would end up with a 2:1 ratio of glucose (+starch) to fructose and thus "right in the zone" (if you really need to replete your glycogen levels as fast as possible, you will have to resort to non-whole food sources, though).

With 32g of carbs a single large banana (~140g) would get you up to a 1:1 ratio of protein and carbs and thus to the lower end of what I would consider a rational post-workout nutrient mix. If you (a) don't follow that up with a real meal, when you are back from the gym, it is probably smart to double the amount of minimal carbs. While this would be the bare minimum, your diet (low or high carb), the respective carbohydrate allowance (limited to X g of carbs per day), your current goals (cutting or bulking, perfromance of body composition changes) and obviously your individual "carb tolerance" (rule of thumb: the leaner the better) dictate how much you can our rather should add to that to see optimal results. And as the results of the study actually underline, only very few of the SuppVersity readers will have to go past the 1g/kg body weight margin, as long as this is not their only carbohydrate containing meal of the day.

References:

• Décombaz J. Nutrition and recovery of muscle energy stores after exercise. Schweizerische Zeitschrift für Sportmedizin und Sporttraumatologie. 2003; 51 (1): 31–38.
• Décombaz J, Jentjens R, Ith M, Scheurer E, Buehler T, Jeukendrup A, Boesch C. Fructose and galactose enhance postexercise human liver glycogen synthesis. Med Sci Sports Exerc. 2011 Oct;43(10):1964-71.
• Detko E, O'Hara JP, Thelwall PE, Smith FE, Jakovljevic DG, King RF, Trenell MI. Liver and muscle glycogen repletion using 13C magnetic resonance spectroscopy following ingestion of maltodextrin, galactose, protein and amino acids. Br J Nutr. 2013 Feb 6:1-8.
• Gunnar, F. The effects of a high molecular weight glucose polymer on muscle metabolism and exercise performance in humans. Thesis submitted to the University of Nottingham. July 2013. 
• Piehl Aulin K, Söderlund K, Hultman E. Muscle glycogen resynthesis rate in humans after supplementation of drinks containing carbohydrates with low and high molecular masses. Eur J Appl Physiol. 2000 Mar;81(4):346-51.
• Wallis GA, Hulston CJ, Mann CH, Roper HP, Tipton KD, Jeukendrup AE. Postexercise muscle glycogen synthesis with combined glucose and fructose ingestion. Med Sci Sports Exerc. 2008 Oct;40(10):1789-94.

Adelfo Cerame: Intermittent Carbohydrate Modulation as a Stepping Stone Towards an Anatomy Chart Physique

Adelfo's goal is to look like an anatomy chart. Now, I don't know about you, but I have seen dozens of anatomy charts that reveal less details of the human physiology than this side-shot which was taken only three days ago.

If you read the headline of today's SuppVersity article, first, you will already know that this is not day 4 of the SuppVersity Exercise Science Week, but (finally) another of Adelfo Cerame's guestposts, here at the SuppVersity. You don't have to worry, there's going to be at least some exercise science in the SuppVersity Science Round-Up, which does (business as usual) air on 1PM (EST) live! on the Super Human Radio Network. So, if you want to be among the first to hear the latest about

• the ameliorative effect of no more than 3g of glutamine on skeletal muscle damage and reductions in immune functions, when you're training like a maniac (learn more about glutamine)
• the superiority of protein blends with respect to net protein retention and why the way most protein supplementation studies are designed has brought about an overreliance on whey protein and a questionable "post-workout window of opportunity" (suggested read: "Opening the Anabolic Barndoor With the Key of Science")
• what percentage of track and field athletes would consider using performance enhancing drugs, if they had the chance and how side effects and the possibility of being busted would influence their decisions (suggested read: "The Brocebo Effect")
• gluten degrading bacteria most of us already have in heir guts and/or mouths and how they could help fight celiac and co. (learn more about gluten & co)
• the importance of doing both, cardio and weight lifting for anyone who's interested in optimal heart health (suggested read(s): "Weights or Cardio, What Comes First?")
• the fat burning effects of sildenafil and how it's combination with EGCG from green tea may turn viagra into an anti-cancer drug (read more about viagra & natural alternatives)

... the podcast, which will be part of tomorrow's Seconds is not really an option ;-) That being said, I have already taken up way too much room in Adelfo Cerame's SuppVersity guestpost - it's high time to make room at the SuppVersity's "writer's desk" ;-)

Adelfo Cerame is back in the house

Well, after a short hiatus from SuppVersity (a well excused one by the way), I’m back to continue my responsibilities of making my guest blogs every other Thursday anin order to share my experiences with the SuppVersity readers as I continue my journey through the world of fitness, nutrition and physical culture ;-)

For those of you who have not been following Adelfo's blogposts right from the beginning: You can read up on his amazing and truly inspiring story how, he got injured and turned it life around in his very first SuppVersity post.

The reason I have been a bit inconsistent with my guest blogs the past few weeks was - as some of you may rememeber - the final weeks of school before the graduation, when I had to learn, juggle two part time jobs and prepare for my upcoming bodybuilding competition in March '13. Not that I’m complaining, I love what has been put on my plate as of late and I’m definitely not going to take it for granted. Still, I am honestly happy that the storm is over now, that I'm finally done with school and have accomplished a goal that I set for myself 4 years ago, when I realized what my calling was and made the decision to go back to school and finish my degree in nutrition science. So now that school is done I can really focus on personal endeavors and other goals I have in mind. - with the first and most obvious one being the dang overall at the show in Florida, so I can finally earn my pro card to become an IFBB wheelchair pro.

I’ve been chasing this piece of paper for a while now and fell short twice last year to two worthy competitors. And as bad as I want that title, I know it’s not priority and never have and never will hold that title on a pedestal to where it becomes my main focus in life. It's my passion, yeah, but in the end it’s just bodybuilding, and not that important when I compare it to other aspects or priorities in my life…

Don't get it twisted, though! I am a competitor ...

.. and I will bring my “A+” game this March, and feel that I’ve made all the necessary adjustments and right moves to put myself in that position. This year I’ve surrounded myself with a great support system of friends, family, mentors, coaches and teammates that have motivated and pushed me physically and mentally to better myself from last year and to put me in a great position to have a shot at that thing again.

Figure 1: Comparison shot this vs. last contest prep back double biceps(img. Adelfo Cerame. 2013-13)

I’ve noticed some significant changes in my physique this year… I’ve been able to put on a tad bit more size especially in my lower back, I’ve been able to add some thickness to it and just might be able to bring out that Christmas tree that I’ve always been looking for on previous preps.

Full, pumped and yet still more defined - what more can you ask for?

In case you don't remember the full story, here is how Adelfo Cerame finally turned his 3-year love and hate relationship with carbs into a highly appreciated ergogenic & delicious friendship (read more)

The biggest difference that I notice is yet that I’m a lot fuller and that despite the fact that my conditioning is a tad better than at the same timepoint during my last prep. And If you’re wondering what adjustments I’ve made this year to make that difference? I’m guessing it’s the higher amounts of carbohydrates I’m consuming this year. That, and the higher training volume I am thus able to sustain. Combined with an increased frquency in body part specific training and the minimal amount of cardio, I've been doing throughout my prep, I was able to keep my overall carbohydrate intake at 150-200g per day, which is - according to my own previous standards, almost hillariously high. I have to thank my coach Alberto Nunez for convincing me to give this high carb moderate-to-low fat approach a try. It has worked out perfectly and according to Alberto, it's also going to help me finally bring in the conditioning and fullness, I may haave been lacking on my previous shows.

I feel that I’m way ahead of schedule from where I was at last year. And from the conversations that coach Alberto and I had; he told me that we haven’t even begun to get serious yet. Lol. So if that’s the case, then from this point on, I’m pretty curious and excited to see for myself how much further I can push my body so I can really achieve that disgusting anatomy chart look ;-)

"Bring on those homemade cheeseburgers, slow churned ice, and poptart pastries!"

Learn more about the RPE routine Adelfo used earlier in his prep

The picture Adel edited in right on top of the article was taken on Monday, when I was exactly 7 weeks out and on the last couple of days of an intermittent 3-week intensive dig at only 100g of carbs/day coach Alberto put me on. As of Wednesday (yesterday), we have started to slowly bring the carbs back  up on regular days and refeed days (WOOOO!!! Right in time for Superbowl on Sunday). Based on what I gather from the weekly evaluations that I get from Alberto, he feels that my body is lean enough to really benefit from an increase in carbohydrates, which will now after this intermittent low carb period be directed right where they belong - into the muscle! So bring on those homemade cheeseburgers, slow churned ice, and poptart pastries! It’s time to get serious!  Oh… Also bring on the fruits and vegetables! Can’t forget about those!

Well that’s all for this week folks! I’m glad to be back on a more consistent level from now on. And please feel free to leave comments below, positive or negative I will try to respond to all of them! Thanks for your on-going support :-)

Exercise Intensity, Oxidative Damage, Glycogen Depletion and Supercompensation. Plus: Optimal 0-12h Post Workout Glycogen Repletion Protocol For Performance Athletes

Do they train at the right intensity and what is the right intensity? What's right, anyway? Lot's of questions, tons of words, a couple of answers and some interesting revelations in today's 2nd article of the SuppVersity Exercise Science Week.

This is day 2 of the SuppVersity Exercise Science Week -- another day, another news. After you've learned about the various mechanisms by which exercise will induce structural changes to your beer belly, lover handles and other problem and non-problem areas, in yesterday's first article of the SuppVersity Exercise Science Week, today's post does actually pick up on the notion of the superiority of high intensity exercise and takes a look at how low vs. high(er) intensity endurance exercise effects the antioxidant defense system of the body. This will lead us to an issue that was once considered to be a downside of high intensity workouts: their notoriousness to deplete muscle glycogen, of which we now know that it is actually one of their fundamental strengths. When we are done with that, it's about time for the sweet dessert. The latter is going to have three courses and will help you achieve maximal muscle glycogen supercompensation after a workout.

Where does the idea that you better work out at low intensities come from?

I have made it a (enervating?) habit to include a small reminder of the "dark side" the same beneficial exercise stress that elicits muscle gains, fat loss, and improvements in conditioning and overall health can have, whenever you don't allow for adequate recovery and nutrient supply, in almost every of the articles pointing to the superiority of high intensity training vs. training in the comfort zone (click here to read up on a couple of these articles).

Figure 1: A comprehensive study by Carey revealed that the increase in ratio of fat-calories to total energy ependiture, when you train in the "fat burning zone" is 3% for men, 5% for women. The total amount of fat is yet higher above the "zone" and, most importantly, the current research suggests that the glycolytic effect, which is inversely related to the relative fat oxidation, is what triggers most of the beneficial metabolic effects.

The question, how pronounced the differences actually are, on the other hand, is not just rarely addressed here at the SuppVersity, it's also something scientists are still trying to elucidate. Usually you will see creatine kinase, an accepted marker of skeletal muscle damage being accessed before and after a workout, but as I have pointed out in previous articles, my personal experience tells me that an intense strength workout is - despite its ability to increase CK levels in training noops by up to 10,000% (x100, no typo - eg. Sewright. 2008) less prone to send you down into the abyss of the Athlete's Triad, than working out for hours (worst on a daily basis) in the purported fat burning zone, i.e. the target heart rate where you'll satisfy the greatest part of your metabolic demands from body fat and of which Carey has been able to show in "relatively fit" male and female runners that it is at least 30% below the anaerobic threshold (AT: 155Hb/min; Fat Burning Zone: 105Hb/min; cf. Carey. 2009).

Aside from that, Carey's results also support the observation Wilson et al. formulate in their recent review of concurrent training, namely that "most dramatic loss in fat mass occurr[s] from moderately high to very high intensities" (Wilson. 2013). In this context, the scientists' definition of "moderately high" is already way beyond the alleged zone of maximal fat loss. "Dramatic" is by the way also an excellent attribute for the 4.5x higher fat loss effect Wilson et al. computed for the highest vs. medium exercise intensities  (91-100% vs. 61-80% HRMax) based on the data they collected for their review.

"Better fat loss, w/ high intensity, aha... but isn't that at the cost of increased oxidation?"

In view of the fact that will be coming back to the issue of "optimal fat loss" later this week, anyway, I guess it's best we get back to the topic at hand and take a look at the toll endurance workouts at different exercise intensities actually take on your antioxidant defense system. As mentioned before, it is still far from being certain which markers you would actually have to measure to get a clear picture of how much stress and damage a given exercise regimen is inflicting. Compared to the creatine kinase levels, the measurement of markers of the activity and status of the anti-oxidant defense system, which was the main outcome variable in a study by Takahasi et al. does yet appear to be more relevant - if not with respect to exercise performance than certainly with respect to overall and metabolic health.

Figure 2: Changes in myeloperoxidase, heart rate, rate of perceived exertion and trolox equivalent antioxidant capacity (TAEC) in eight healthy and untrained males aged 22.6 ± 1.4 years (mean ± SD), with 67.7 ± 4.1 kg body mass, 175.2 ± 3.7 cm height, and 15.1 ± 2.2% body fat after 20min of exercise at 70%, 100% or 130% of the anaerobic threshold.

On three separate occasions, the Japanese researchers studied the effect of different exercise intensities. The latter ranged from 70% over 100% to 130% of the anaerobic threshold and would thus represent exercising in the "fat burning zone" at moderately high intensities and high intensities.

The first thing the scientists registered was that the pre to post increase in oxidative stress at the low and medium intensities did not even reach statistical significance. The "pro-oxidative" effects of the high intensity trial, on the other hand, were statistically significant. Yet, if you look at the actual data in figure 2, I'd guess that you will - just like me - ask yourselves what all the hoopla was about: The absolute differences are mediocre, at best and their physical not statistical significance is highly questionable; and that's not just because the trolox equivalent antioxidant capacity (TEAC) actually increased from pre to post exercise (from allegedly lower pre levels in the 130% trial than before the other exercise tests.

Training at higher intensities is demanding, yeah... but not overtly demanding!

Now, all these statistical significances were calculated on a pre vs. post basis. Intensity-specific differences on the other hand were not observed. We do therefore have to be cautious not to misinterpret the scientists very own and actually non-judgmental conclusion ...

"We found that plasma concentrations of d-ROMs increased as a result of 20 min of exercise above AT. Exercise above AT also increased enzymatic and nonenzymatic antioxidant capacity. On the other hand, there was no effect after 20 min of exercise at 70–100% AT, suggesting that exercise under the AT level does not produce oxidative stress damage." (Takahashi. 2013)

... as an advice to stick to "exercise under the AT [anaerobic threshold]". There are already way too many people wasting their time on the cross-trainers of this word - don't join them, but don't overexert yourself either.

The "Iranian HIIT Solution" has already proven that a minimalist HIIT regimen in the form of 3x200m sprint sessions per week can make all the difference esp. for someone who has never participated in regular activity before (read more).

A single bout of intense exercise leads to significant improvements in glucose and lipid metabolism in obese individuals, that's the latest result of another very recent study that was conducted at the University of Glasgow (Whyte. 2013). The protocol consisted of nothing more than " four maximal 30-s sprints, with 4.5min recovery between each (HIIT), or a single maximal extended sprint (HIT) matched with HIIT for work done". With 20% higher mean power during the sprints the temporary intensity was higher, in view of the fact that the overall exercise duration was longer and there was no time for in-between sprint glycogen replenishment. Thu it's actually not surprising that the acute increase in insulin sensitivity did reach statistical significance only after the extended sprint session. The overall metabolic benefits (non-significant improvements in glucose and lipid metabolism) on the day after, of which we can assume that they were not brought about by the immediate reduction of muscle glycogen, were identical for both conditions, while the the total and relative increase in fasting fatty oxidation was more pronounced after the HIIT protocol (total: 63% and 38%; relative, based on RER: 11% and 8% ).

Figure 3: Oxidative stress and glycogen depletion are important triggers of the beneficial effects of exercise on glucose metabolism ( (based on Kawanaka. 2013).

If we go a step further and think about whether or not oxidative stress is actually something you would want to avoid at all costs, the figure from Kentaro Kawanaka's recently published alongside review of the regulation of glucose transport in skeletal muscle during and after exercise (see figure 3) can help us make up our minds. If you take a look at my mark-ups it's plain to see that ROS production and the increase in AMP (quasi "used ATP") and decreases in ATP and phosphocreatine (PCr) are major signals for the activation of a hitherto incompletely understood signaling cascade that results in increased glucose uptake by the muscle. That's the same glucose uptake, by the way that makes the most significant difference between the "normal" and, insulin-intolerant individual and makes an ideal stepping stone to full-blown diabesity (=obesity + diabetes type II).

"So, what exactly is the effect size of these improvements? Are the worth the sweating?"

To illustrate the quantity of these effects, Kawanaka uses data from a 2009 study by Koshinaka et al. who subjected rats to an acute bout of 3x20s "high-intensity sprint interal swimming" and measured muscle glycogen levels and glucose transport at different timepoints in the 16h window after the workout.

Figure 4: Insulin and non-insulin stimulated glucose transport in rat epitrochlearis muscle at rest and 4 hours after cessation of HIIT exercise (left); muscle glycogen repletion and supercompensation after a workout (from Kawanaka. 2013 based on Koshinaka. 2009)

If we take into account that 3h(!) of continuous swimming elicited the exact same improvement in glycogen uptake as those 3x20s all out "sprints", I probably don't have to say it "appears" as if the synergistic combination of brief HI(I)T training and an appropriate diet will be more productive than the endless hours on an elliptical way too many (often unfortunately female) trainees are still performing in the desperate hope to finally shed the fat from whatever problem areas they have or believe they'd have.

Glycogen supercompensation: This is how it's done

There is yet more to the Koshinika study than another confirmation of the usefulness of HI(I)T exercise for fat loss, fitness and fabulous health. The data Koshinaka et al. collected does also tell us something about post workout glycogen repletion. Most importantly (at least in my humble opinion) that the first, immediate post-exercise phase is characterized by a rapid non-insulin dependent increase in glucose uptake. The latter is actually just as high (>5µmol/g/20min; respective data is not shown in figure 4) as the maximally measured glucose uptake in phase II, in the course of which the presence of insulin has a dose-dependent beneficial effect on the total amount of glucose that's going to be shuttled into the muscle (see figure 4, left). With phase III being characterized by saturated (in fact more than saturated) glycogen stores, these observations would suggest that an "optimal" glycogen replenishment protocol would look somewhat like this:

When you increase your calorie intake on a bulk, you better go really high carb + low fat, if lean gains are what you're looking for. This is at least what a 2011 study by Mendes-Netto suggests (read more)

1. phase I: immediately post > fast absorbing carbohydrate source -- what's important during the immediate post-workout phase is exclusively the availability of glucose, insulin the presence of extra high insulin levels is more or less unnecessary
2. phase II: post workout phase (<8h) > high GI carbohydrate source -- once the glycogen levels have reached a certain level the supercompensation process requires the presence of additional insulin, therefore your post-workout meal should not be carb-free or extremely low GI
3. phase III: recovery phase (>8h) > low GI carbohydrate source -- the glycogen stores have already reached higher than baseline levels, the presence of high levels of insulin in this phase would be counterproductive as it would actually drive glucose uptake by the adipose, not the muscle tissue

Whether this maximum glycogen repletion protocol does in fact make sense for everyone is yet another question, though. For someone who trains twice a day, like Arnold, it certainly does. The same goes for endurance athletes looking for maximal performance. If Lance Armstrong, for example, would ever be allowed to compete again, he would best go for a fast absorbing carbohydrate source like Vitargo right after the race, a huge bowl of pasta and some sugary grape juice as his first meal after the race and some slow digesting carbs like a couple of bowls of oats later that day to ensure optimal glycogen levels on the next day of the Tour -- what neither Lance nor you should not forget, though, is to add some protein to the equation, even if building muscle is not your goal, the protein will speed up the replenishment of muscle glycogen (Zawadski. 1992)

"But how important is muscle glycogen, anyway?"

For the average trainee it does yet remain questionable whether or not this protocol will actually yield noticeable benefits. While it is important to replete the glycogen stores, the advantages of doing this as fast as possible are actually not really relevant for someone who trains 3-4 times per week in order to promote health, well-being and a leaner, more muscular (but not freakish) physique. Especially with respect to the latter, the majority of the more recent studies clearly suggests that muscle protein synthesis is, in the short run, not impaired by low levels of muscle glycogen (click here to learn more).

What you should never forget, though, is that your body will interpret chronically low muscle and liver glycogen levels as a clear-cut indicator that you're starving. The results are a reduced metabolic rate and the shut down of "auxilliary" and costly bodily functions such as the reproductive machinery, etc. - and we don't want that to happen, right?


References:

• Kawanaka K. Regulation of glucose transport in skeletal muscle during and after exercise. 2013. J Phys Fitness Sports Med, 1(4): 563-572.
• Koshinaka K, Kawasaki E, Hokari F, Kawanaka K. Effect of acute high intensity intermittent swimming on postexercise insulin responsiveness in epitrochlearis of fed rats. Metabolism. 2009; 58: 246-253.
• Takahashi M, Suzuki K, Matoba H, Sakamoto S, Obara S. Effects of different intensities of endurance exercise on oxidative stress and antioxidant capacity. J Phys Fitness Sports Med. 2013 1(1): 183-189.
• Sewright KA, Hubal MJ, Kearns A, Holbrook MT, Clarkson PM. Sex differences in response to maximal eccentric exercise. Med Sci Sports Exerc. 2008 Feb;40(2):242-51.
• Whyte LJ, Ferguson C, Wilson J, Scott RA, Gill JM. Effects of single bout of very high-intensity exercise on metabolic health biomarkers in overweight/obese sedentary men. Metabolism. 2013 Feb;62(2):212-9.
• Wilson JM, Marin PJ, Rhea MR, Wilson SM, Loenneke JP, Anderson JC. Concurrent training: a meta-analysis examining interference of aerobic and resistance exercises. J Strength Cond Res. 2013 Aug;26(8):2293-307. 
• Zawadzki KM, Yaspelkis BB 3rd, Ivy JL. Carbohydrate-protein complex increases the rate of muscle glycogen storage after exercise. J Appl Physiol. 1992 May;72(5):1854-9.