Cardio & Weights - Mutual Exclusives or Synergists? Two New Studies Suggest: Cardio "Before" and After Workouts Offers More Benefits Than Downsides for Strength & Mass

Could "cardio" really be more than just a necessary evil on your way to a physique like this?

Yesterday testosterone booster (see "Capsaicin or 28-OB...") and today already the next "bro favorite": The never ending debate about "cardio and weights" (or should I rather write "cardio vs. weights"). If you are no newcomer to the SuppVersity you will be aware that this is not the first time, we are tackling this issue (e.g. "Cardio Before or After Weights?" or "Before, After or In-Between"). While most of the previous posts did however deal with the question of "How do I do the least damage to my resistance training, if I want to do cardio, as well". The two studies, I have in stock for you, today, would suggest that this question in and out of itself is quite nonsensical and that the "correct", or at least way more productive question must be: "How can I use cardio to promote my strength and mass gains?"

Curious? All right, let's take a look at what Tufano, Lundberg and their respective coworkers have in stock for you (Tufano. 2013; Lundberg. 2013)

• The Tufano study confirms that doing cardio after an intense leg workout facilitates recovery- A question yet remains: What are the long term consequences? At least as long as you stick to doing just 20 minutes of cardio at 70% of your maximal heart rate, some cycling after a an eccentric leg workout (6 sets of 10 reps of eccentric leg extensions, specifically designed to induce maximal DOMS).
  
  

  

  Figure 1: Isometric strength after eccentric leg extensions in no, low and mean intensity cycling group expressed relative to pre values (Tufano. 2013).

  In the most recent study from the Department of Kinesiology at the Center for Sport Performance of the California State University the 10 women in the medium intensity cycling arm, who had cycled for 20 minutes at 70% of their individual heart rate recovered faster the muscle damaging workout than the women who went home without a "heavy cool down". What's actually even more astonishingly, though is that they also recovered faster than a third group of women who performed the 20min workout at only 30% of their VO2max.
  
  While there were no differences in pain scale or dynamic strength during the 4-day recovery phase, the isometric strength of the women in the 20min @ 70%VO2max arm of the study showed significant super-compensation effects on day 3 and day 4, so that Tufano et al. conclude:
  

  "Enhanced blood perfusion during moderate-intensity aerobic recovery, in conjunction with a short-term training effect, may enhance isometric strength after DOMS. Therefore, moderate intensity aerobic activity is suggested as a recovery method after multiple eccentric muscular actions." (my emphasis in Tufano. 2013)

  That certainly sounds as if another bro-scientific myth was tumbling and about to fall. Still, Tufano et al. are also right to point in the discussion of their results, that we need further research into the chronic effects of moderate-intensity aerobic 'recovery exercise' after resistance training - I mean, who guarantees that doing this after every workout week after week, month after month won't eventally turn against you?

What? You are not interested in recovery, anyway? All you want is grow and you doubt that the small increase is indicative of earlier supercompensation and that strength and grows would be two different pairs of shoes, anyway? Well, in that case here is another pro-cardio study:

• 

  The first important question this study answers is: How do you cycle with just one leg. You see the answer in the small inset of the image above.

  Aerobic before resistance training leads to minor increase in mTOR response and does not seem to hinder muscle gains! This one certainly flies in the face of what you may have been told by credible and less credible experts for your whole life. I mean, if anything, cardio was supposed to keep the gains lean. While the consensus is that it will diminish your gains -- right? Well, according to the latest study from the Mid Sweden University and the venerable Karolinska Institute and University Hospital in Stockholm this could turn out to be just another counterproductive bro-scientific myth: Skipping cardio altogether is not simply bad for your overall health an conditioning, as it would seem, it could even be beneficial for your gains, as well.
  
  To probe the effects of aerobic training on a whole host of hypetrophy and performance related factors, Tommy R. Lundberg and his colleagues recruited 9 physically active men (23+/-1 yr, 18+/-6 cm, and 75+/-6 kg) who "had been involved in recreational aerobic exercise two to three times per
  week and/or habitual RE one to two times per week for more than a year" (Lundberg. 2013) and had them perform a 45-min one-legged cycle ergometry exercise
  

  "The target load was 70% of the Wmax (cadence = 60 rpm). After 40 min, workload was in-creased by +20 W, and subjects were requested to continue until failure to maintain the prescribed cranking cadence, which typically occurred within 1–4 min (2 min 43 s)" (Lundberg. 2013)

  that was followed by 14 maximal concentric–eccentric knee extensions for each leg 6 h later (2 sets, 7 reps, 90s rest; starting with the AE+RE leg).
  

  "Thus, one limb was subjected to aerobic and resistance exercise (AE+RE), and the contralateral limb to resistance exercise (RE) only." (Lundberg. 2013)

  Before, as well as 15 and 180min minutes after the subjects underwent this training sessen, biopsies were taken and the glycogen content, the mRNA levels of vascular endothelial growth factor (EGF), peroxisome proliferator–activated receptor--gamma-coactivator-1 (PPAR-gamma), muscle RING-finger protein-1, atrogin-1 and myostatin, as well as the phosphorylated proteins mammalian target of rapamycin (mTOR), p70S6 kinase, ribosomal protein S6 and eukaryotic elongation factor were  measured. To ensure that no dietary factors would interfere with the results meals had been fully standardized on the day of the testing:
  

  "A standardized meal (pasta, tomato sauce, and juice) consisting of 2.21 g CHO/kg body weight, 22 g protein/kg bw, and 0.04 g fat/kg bw was provided at 8:00 p.m. the night before the experimental day. Subjects also had a standardized breakfast (1.01 g CHO/kg bw, 0.31 g protein / kg bw, and 0.24 g fat / kg bw) 1 h before the aerobic exercise session and lunch (2.02 g CHO/kg bw, 0.62 g protein/kg bw, and 0.49 g fat /kg bw) consumed 3 h before RE. These meals consisted of commercial energy drinks (Ensure Plus; Abbott Laboratories BV, Zwolle, The Netherlands). Water was allowed ad libitum at any time during the intervention." (Lundberg. 2013)

  As nice as it is to see a tightly controlled study, investigating a relevant topic and with trained healthy participant like this, I am really not a fan of these 'compare the left to the right leg' studies. And still, the fact that I am happy about any study into the whereabouts of different training modalities is neverthelsess not the only reason I am not going to beat a dead horse here.

  

  Figure 2: Unilateral peak concentric (CON) and eccentric (ECC) power (W) in knee extension and leg press during the experimental bout; data expressed relative to group baseline (Lundberg. 2013)

  The other and probably more relevant reason is that the data you see in figure 2 as surprising at it may seem  -- I mean who would have thought that the resistance training (RT) only leg would see a greater decline in force production during the experimental bout compared to baseline -- does not look like it had been skewed into this surprising direction by carry-over effect from one leg to the other or systemic factors such as central nervous system fatigue or the depletion of liver glycogen levels.
  
  In particular, we don't see anything of the expected drop in resistance training performance in the AE + RE leg due to the previous cardio workout. Even if it was only small, maybe statistically non-significant, common wisdom would dictate that it should be present! What we are seeing instead, however is a beneficial instead of a detrimental pre-conditioned effect in the 'cardio leg', of which you can hardly argue that it speaks in favor of the hypothesis that doing cardio must necessarily hamper your gains, if you allow enough time and food in between the morning and the evening workouts.
  
  It certainly looks as if the myth of the strength busting effects of any aerobic activity was about to fall and the corresponding protein expressions, the scientists measured before, 15min and 180min after the trial onyl support this notion.
  
  The image that emerges, when you take a closer look at the data in figure 3 is actually quite clear. At "pre" already, i.e. immediately before the resistance training part begins, the 'cardio leg' has and edge over the previously rested leg it won't lose in the course of subsequent hours. After all, despite the fact that at T = 180min some of the values have returned to baseline and/or the levels in the resistance training only leg have caught up, there is never a significant advantage of the resistance training only, over the aerobic + resistance training leg in the whole 3h period (respectively at the three intervals at which the biopsies were conducted).

  

  Figure 3: Selected markers of mitochondrial biogenesis and protein synthesis before during and 15, respectively 180min after the resistance training bout in the AE + RE and the RE only leg (a.u.; data adapted from Lundberg. 2013)

  Personally, I would still not consider these observations conclusive evidence of the superiority of aerobic + strength training in terms of its potential as a muscle builder (that it is a mitochondrial builder stands out of question). What is however undebatable (at least in this particular case), is that doing aerobics earlier in the day and lifting weight later in the day will not have a negative impact on either the performance or the measured markers of the exercise induced growth stimulus the resistance training session will have. It is rather, as the scientists point out that ...
  

  "[...] concurrent exercise elicited greater mTOR and p70S6K phosphorylation compared with RE. Although these differences were modest, if anything, they indicate that translational capacity was reinforced rather than compromisedby the AE + RE intervention. In parallel, myostatin was suppressed for longer time in AE + RE, with no obvious sign of exacerbated protein degradation. Thus, in contrast to the posted hypothesis, it seems that concurrent AE + RE may enhance skeletal muscle anabolic environment." (my emphasis in Lundberg. 2013)

  I guess, there is actually little to add to that, despite the important warning that you must keep an eye on your overall training volume, in case you want to follow this approach. In the end this means that you are switching to a two-times-a-day regimen, which can take its toll not just on the ability of your muscles to adapt and recover, but more importantly on the ability of your central nervous system to cope with this additional stressor. 
  

Can I do HIIT instead? For the first study, the answer probably is no. It makes no sense to use HIIT training as a regenerative means after a workout. For the second study I would guess the answer is yes. After all, the aerobic morning workout was pretty strenuous and glycogen depleting, so I don't see any reason why a brief HIIT training in the 10-20min range would not yield the same if not even better priming effects (cf. "The Anabolic Effects of HIIT" )

Bottom line: I would not say that any of these studies gives you, who are hopefully interested to build muscle and maintain optimal health a free ticket to do as much cardio, whenever you want. What this compilation does yet do, is debunk the myth that you have to become a sedentary slob and discard the cardiovascular and obvious fat loss benefits the implementation of moderate amounts of aerobic training into your regimen will yield just because aerobics will necessarily comprimise your gains, let alone burn away your muscles.

Timed appropriately and used in moderate, instead of excessive amounts, some 'cardio' could in fact offer an overlooked means to provide a greater growth stimulus and promote faster recovery - and that next to all the health- and conditioning related benefits, I guess even the hardcore-bros won't doubt.

References:

• Lundberg TR, Fernandez-Gonzalo R, Gustafsson T, Tesch PA. Aerobic exercise alters skeletal muscle molecular responses to resistance exercise. Med Sci Sports Exerc. 2013 Sep;44(9):1680-8.
• Tufano JJ, Brown LE, Coburn JW, Tsang KK, Cazas VL, Laporta JW. Effect of aerobic recovery intensity on delayed-onset muscle soreness and strength. J Strength Cond Res. 2013 Oct;26(10):2777-82.

8x Increase in "Mitochondria Building" Protein PGC1-Alpha W/ Medium Intensity Exercise in Glycogen Depleted Elite(!) Cyclists: Training Revolution or Recipe for Disaster?

With only 2-7x increases in PGC1-alpha expression HIIT seems to lag behind compared to this "eat low, train low, gain high" strategy, but not every protein essay that glitters in the petri dish will turn into Olympic Gold in the real world ;-)

As a diligent student of the SuppVersity you should by now have at least a preliminary understanding of how the adaptive machine you call your "body" adapts to the various nutritional and physical challenges most people subsume under the all-encompassing and pretty nondescript terms "diet" and "exercise". Against that background it should not really come as a surprise that researchers from the The Swedish School of Sport and Health Science are soon going to publish the data of an experiment that shows that even (you could probably also say, in particular, although respective evidence is still missing) highly trained athletes can benefit from exercising in a glyocogen depleted state - at least if the yardstick you use to measure the "benefits" is an increase in mitochondrial biogenesis (Psilander. 2013).

Train high, eat low (carb), train low and...?

To elicit the differential effects of 6x10 min bouts of cycling at 60% of the individual VO2max (4min of active rest in between) with normal vs. depleted skeletal muscle glycogen stores, Psilander et al. had their 10 highly trained male national elite level competitive road cyclists and mountain bikers (27.8±1.6 years, 74.7±2.0 kg, 183±2 cm, and 4.9±0.1 l/min VO2Max) perform an 8x4min interval training at 88% of their individual VO2Max ~16.5h before they had to report back at the laboratory on the actual testing day (the intervals were seperated by 4min of active rest, i.e. cycling at 100W+).

Figure 1: Graphical outline of the experimental protocol and its effect on the glyocogen stores of the from the vastus lateralis muscle (based on Psilander.. 2013)

The protocol (see figure 1) was repeated twice, with adequate time in-between and in random order, with the subjects consuming water only and low carbohydrate meals

• low carb meals (LC) were eggs and bacon (0.02 g CHO, 0.6 g protein and 0.8 g fat/kg bw) for dinner and breakfast, providing a total of of <0.04 g CHO, 1.2 g protein and 1.6 g fat/kg bw

before the glycogen depleted trial (LC) and high carbohydrate beverages (maltodextrin-dextrose powder Carbo 134 w/ 1.0g CHO/kg bw) + high carbohydrate meals

• high carb meals (HC) were pasta with meat sauce and lemonade for dinner (1.83 g CHO, 0.53 g protein and 0.14 g fat/kg body weight bw) and oatmeal and orange juice (1.54 g CHO, 0.31 g protein and 0.12 g fat/kg bw) for breakfast and additional bananas with beverage 3,5,7 and 8 for a total of 12.6 g CHO, 0.9 g protein and 0.3 g fat/kg bw

before the glycogen repleted trial (HC).

... get impressive increases in PGC1-alpha, but no AMPK response at all!

As the data in figures 1 & 2 goes to show you the nutritional intervention was not without effect the factual glycogen levels (figure 1, right) and the glucose, insulin and fatty acid levels before and after the workout (figure 2) - and, as you would expect it, the corresponding changes in gene and protein expression in the muscle samples the researchers collected approximately 15 min before the depletion (S1) and test exercise (S2), as well as 3 h after the test exercise:

Figure 2: Free fatty acid levels before depletion (S1) and before (S2) and after (S3) exercise trial, as well as PGC1-alpha and p-AMPK expression (data calculated based on Psilander. 2013)

Now what you probably won't have anticipated, though is the absence of the expected p-AMPK response to exercise in the low glycogen (LC) trial.

"The mRNA content of the master regulator of mitochondrial biogenesis (PGC-1a) was not changed 14 h after depletion exercise (pre-test exercise) but was significantly increased 3h after the test exercise in both conditions (Fig.2). The increase was, however, much more pronounced in LG than in NG (8.1-fold vs. 2.5-fold, P<0.01). The mRNA content of two other regulators of mitochondrial biogenesis (PRC and Tfam) also increased significantly but with no difference between conditions (time-dependent effect, Py0.01; [not shown in my graph]). The mRNA content of genes for oxidative metabolism enzymes (PDK4 and COX I) only increased after LG with a significant difference between the two conditions. The mRNA content of CS, Sirt1, NRF1 and PPAR[-delta] did not change under any conditions." (Psilander. 2013)

Almost 8x elevated levels of PGC-alpha but no change in the "fat burning, GLUT-4 pomoter" AMP-activated protein kinase? How can that be? The answer to this question is actually pretty simple: If the phosphorlyation of AMPK changes in response to changes in the ATP to ADP ratio (the name is misleading, here as scientists have initially believed that the main determinant was the ATP to AMP ratio, which is yet not the case), it should be obvious that it won't change, if the ATP levels are already so low that at most the ADP to AMP, but not the already rock bottom ATP do AMP ratio will be changing.

What happens if your body senses that it cannot fuel his energetic demands with glucose?

In the presence of borderline hypoglycemic glucose levels (the normal range starts at 4.4 mmol/L; after the depleted test the subject were at 4.3 mmol/L!) your body would be ill advised to increase glucose uptake. So if this is not an option the only way to make up for the lack of energy are fatty acids. Unfortunately the amount of fatty acids your skeletal muscle can oxidize is strictly rate-limited by your mitochondrial capacity ... now, I am asking you what's the "natural", the logical and in the case of the 10 cyclists in the study at hand also the factual reaction that will get you out of this mess? Right! To build more powerful mitochondria and thus widen the "bottle neck"! And what's going to do just that? Yeah! The ~8x increase in PGC-1alpha expression you see in figure 2. 

Practical implications: From protein essays to results?  

 Now that we have gotten the mechanisms straight, there is but one question we have to answer - what does that mean for you? When and for whom does it make sense to train with depleted gycogen stores? And in an even broader context - what does that tell us about low-carbing and (intermittent) fasting?

1. 

   Before you even consider making this a staple of your regimen, I would encourage you to read the whole SuppVersity Athlete's Triad Series

   Even (or especially?) for trained athletes competing in largely aerobic sports, training in a state of depleted glycogen store can serve as a viable tool to elicit even higher (2-7x; cf. Gibala. 2009, Nordsorg. 2010. Psilander. 2010) increases in increases (8x!) PGC1-alpha and (allegedly) mitochondrial biogenesis as you would see them in response to high intensity interval training at much lower intensities (but correspondingly longer durations). 
2. Training in a fasted state does not per se guarantee / put you at risk of being glycogen depleted, neither does intermittent fasting and or "training on empty". As long as you replete your glycogen stores after your workouts you won't see similarly pronounced increases in PGC1-alpha in response to "regular" aerobic training at a low intensity. You will, on the other hand, still see increases in AMPK and, what's even more important, you will be able to perform at much higher intensities! A fact that is particularly important for the strength trainees out there.
3. While it may make sense on occasion, and merely based on it's beneficial effects on purported  mitochondrial biogenesis (I don't have to remind you that we don't have any information on whether the increase in PGC1-alpha did even translate into an increase in mitochondrial biogenesis in the absence of adequate glycogen / ATP levels!), I want to reemphasize the scientists very hint that "[l]ongitudinal studies examining protein levels and performance are required" before it can be recommended to include this practice as a staple into your routine!

4. 

   Life is to complex for black-and-white thinking, and so are AMPK, mTOR & co! Learn more in the Intermittent Thoughts.

   Long-term exercise in a glycogen-depleted state without adequate carbohydrate intake and thus glycogen repletion is not for nothing one of the causative factors of the athlete's triad (see Part I & II of the SuppVersity Athlete's Triad Series). I would therefore be very surprised if the long-term outcomes of low-carbing + (intermittent) fasting w/out regular glycogen repletion would be anything but negative, regardless of its beneficial effects on PGC1-alpha. After all, the study at hand clearly shows that you will also be missing out on the benefificl effects of increased p-AMPK expression of which you know based on what you have read in the Intermittent Thoughts on Intermittent Fasting Series that it is one of the, if not the central argument in favor of intermittent fasting.

The practical take home message of this study is therefore that exercise + diet induced targeted glycogen depletion before a workout (not via an overnight fast, only; that would leave your muscle glycogen stores largely intact, while your body is burning fat and tapping into your hepatic glycogen reserves) can become one among a whole host of tools in your workout-toolbox. You can use it sporadically, but you should not need another study to be able to predict that the downsides of chronic use are going to outweigh (purported - again, we are measuring markers only, here!) short term benefits.

On a last note: I guess you know that the SuppVersity is the place where you will hear about respective longitudinal data first, right? To make sure you don't miss that I suggest you go to www.facebook.com/SuppVersity like the page or register for updates at twitter.com/ProfDrAndro!

References:

• Gibala MJ, McGee SL, Garnham AP, Howlett KF, Snow RJ, Hargreaves M. Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1alpha in human skeletal muscle. J Appl Physiol. 2009 Mar;106(3):929-34.
• Nordsborg NB, Lundby C, Leick L, Pilegaard H. Relative workload determines exercise-induced increases in PGC-1alpha mRNA. Med Sci Sports Exerc. 2010 Aug;42(8):1477-84.
• Psilander N, Wang L, Westergren J, Tonkonogi M, Sahlin K. Mitochondrial gene expression in elite cyclists: effects of high-intensity interval exercise. Eur J Appl Physiol. 2010 Oct;110(3):597-606. Epub 2010 Jun 23.
• Psilander N, Frank P,  Flockhart M, Sahlin K. Exercise with low glycogen increases PGC-1agene expression in human skeletal muscle. Eur J Appl Physiol. 02 Oct 2013 [ahead of print]

On Short Notice: Red Onions For Glutathion & Jiagulan For Muscle Glycogen, Low Iron & Obesity, Sodium Caprate, Useless Probiotics & Leaky Gut, Perivascular Fat & Heat Shock Proteins for Your Heart & Magnesium vs. Migraine

Image 1: You may already have read it on the SuppVersity Facebook Wall; "Sacrificing sleep in order to study won't improve your college grades..." it could however easily whack your circadian rhythm and give you headaches. If those turn into a migraine, you may be happy to have read about beneficial effects of magnesium on the incidence of these crippling and painful attacks (see last item in this installment of "On Short Notice" ).

In order to avoid having another weekend of "On Short Notice" posts, I decided to post the first collection today, already. The topics are, as usually, only loosely related and I hope that each and everyone of you will find something he or she considers interesting. We'll start out by having a brief look at the amazing antioxidant effects of red onions, and then delve deeper into the connection between obesity and low ferritin levels and a brief reminder that sometimes good things can become bad, if they are not handled properly, next on the list are the tight gut junction opening effects of sodium caprate which may be a good thing if your goal is to increase the bioavailability of berberine, but a very bad thing, if other molecules take the opportunity and pass through the open doors, as we are then going to see Dr. Shirota's probiotics are probably not going to help you avoid this problem and they are certainly not helping patients with metabolic syndrome: The latter is probably also true for PPAR-gamma antagonists, which may help prevent visceral fat accumulation, but could at the same time precipitate to heart disease by decreasing the surprisingly heart-healthy perivascular fat.

Although more of an ergogenic, Gynostemma penthaphylum (aka Jiagulan) is probably a more promising strategy to get in better shape. If it allows you to train harder, it will also allow you to make better use of potential systemic health effects of exercised induced heat shock protein expression... and just in case all that was so much information that you are having a headache once you have arrived at the end of this blogpost, a 500mg dose of magnesium could help you reduce the incidence of migraine attacks by more than 60% whether additional 500mg of carnitine make this treatment even more effective does yet remain to be elucidated!

• Do your liver and body antioxidant system a favor and add a couple of red onions to your diet! That's the straight forward take home message from a recently conducted study by a group of Korean scientists (Lee. 2013). The researchers had investigated  the effect of red onion on the total activity of antioxidant enzymes in 18-week-old Sprague-Dawley rats. To this ends the rodent had been kept on a diet enriched with red onion peel, flesh or both (all pulverized and mixed into the standard chow for a total content of 5g per 100g) for for weeks.

  

  Figure 1: The red onions outperformed easily outperformed their uncolored white brethren and cousin, white onions and garlic, in the in vitro dish and had profound antioxidant boosting effects in the in vivo study (Lee. 2013).

  The results, (a) a significant increase in plasma SOD activity in the red onion peel and red onion (peel + flesh) groups, (b) a significantly higher GPX (enzyme that recycles glutathione) activity in the in the red onion flesh group and (c) a general tendency towards higher catalase and ORAC activity in the livers and profoundly reduced liver malondialdehyde (=marker of lipid peroxidation) levels in the red onion groups provide an in vivo (allegedly only "in rodent vivo" ;-) confirmation of the in vitro data in figure 1 which is - as usual - to be treated with caution before respective experiments in complex, real organisms confirm that they are more than artifacts of the respective essay.
• Low iron (ferritin) associated with obesity in adolescents, but simple eating more iron probably won't solve either the iron deficiency, nor the (central) obesity. That's at least what the results of a recent investigation in normal and fat Greek kids would suggest, after all the fat kids did already consume more iron in their diets than their lean age-mates (Moschonis. 2013).
  What makes this study worth mentioning is the (as usual hasty) conclusion that iron must be a bad guy, when just its mismanagement (probably as a result of adiposity induced liver problems, or, as a handful of older and recent studies would suggest vitamin A deficiency; e.g. Arruda. 2009; Citelli. 2013; Yohsikawa. 2013) is a problem - so don't get fooled, donating blood every other week won't lean healthy people out, it will just drain them out.

• 

  Figure 2: Sodium caprate won't "open" the tight gut junctions for berberine, only, but also for all sorts of other, mostly unwanted junk - self-induced temporary leaky gut so to say!

  Sodium caprate opens tight junctions of the gut and let's berberine in. The consequence is an amplification of the hypoglycemic effects of berberine (Lv. 2013), but at the same time it is likely to amplify the effects of whatever you else put into your mouth or the critters that live in your stomach are pooping out - I guess it should be obvious that I am referring to the LPS assault from your gut microbiome, here and that the potential increase in lipopolysaccharide could well outweigh (in a negative sense) the benefits you would see from an increased bioavailability (~1.5-2.3 fold; cf. Lv. 2010) of berberine.
  
  Against that background I am really not sure how sensible the use of sodium caprate or other "tight junction openers" of natural or pharamacological origin really is. But hey, that's just me - maybe you are less cautious...  if there are not yet any products like that on the market, it probably won't be long until the first "enhanced" berberine appear in the line-ups of the large "health supplement" vendors on the Internet.

• 

  Image 2: Patented lactobacillus strains are all the rave, and probably big business... that does yet not mean that they work - regardless of whether they carry the name of famous Drs or not ;-)

  Probiotic supplements don't cure everything - although many ads may give just this impression. In a recently published study, Swiss researchers were not able to show any beneficial effects of the patented L. casei Shirota strain on the increased gut permeability of 28 patients with metabolic syndrome (Leber. 2013). In the course of the three months study period, it rather exasperated the already elevated C-reactive protein levels, due to liposaccharide leakage through the leaky gut into the system and I bet the only reason that the conclusion states that the dosage may have been too low instead of "this is initial evidence that the use of L. casei Shirota is not useful if  not counter-indicated in to treat gut permeability in patients with MetS", was the financial support by Yakult Europe the patent holder of L. casei Shirota ;-)
• PPAR-gamma ablation leads to loss of perivascular adipose tissue (PVAT). What may at first sound great could in fact be deadly. The recently published results of Chang et al. show quite clearly that non-tissue-specific blockade of the "fat builder" PPAR-gamma (cf. "Tangeritin, Natural Metformin from the Rind of Mandarin Oranges Hits the OFF-Switch on Diet Induced Obesity") is a dangerous undertaking. While keeping the differentiation and growth of body fat at bay, especially in the abdominal region, would be a good thing, the high rate of atherosclerosis among the mice from the laboratories of the University of Michigan confirms that "not all body fat is created evil" (Chang. 2013).

  

  Figure 3: Fitzgibbons et al. were already able to show that the UCP-1 expression, which is a marker of metabolic activity, in PVAT is equally high as in the meanwhile infamous brown adipose tissue. In short - PVAT just like BAT will not just store superfluous lipids, it will also burn them and prevent them from accumulating in the vasculature (Fitzgibbons. 2011)

  As it turned out, PVAT, rather than being proinflammatory and hazardous, actually has a protective function on the vasculature it is sourrounding. In fact, the results Chang et al. are presenting in the latest issue of Circulation suggest the assumption that PVAT is anti-inflammatory and functionally similar to the metabolically active brown adipose tissue that has gotten quite some attention by experts ad laymen as of lat. When it's suddenly missing, the lipids inside the vascular can no longer be cleared into the perivascular adipose tissue where they would be oxidized and disposed of. In addition, the ensuing pro-atherogenic coupled with the absence of PVAT-derived prostacyclin, a prostanoid that's metabolized from endogenous arachidonic acid through the cyclooxygenase (COX) pathway and acts as a potent vasodilator (cf. Ruan. 2010) could thus easily set you up to die before your time - regardless of how lean you may have become...
  And though it is very unlikely that this is going to happen from the use of one of the freely available herbs with anti-PPAR-gamma effects (e.g. tashinones from Salvia miltiorrhiza, or the previously cited tangeritin), it certainly is a good reminder of how fatal our constant black-and-white thinking can be, when it is injudiciously applied to such complex matters as our own body.

• 

  Image 4 (dracoherbs.com): Gynostemma penthaphylum is also known as Jiaogulan, is often mentioned in the same breath with ginseng in TCM

  Gynostemma penthaphylum boosts endurance by ROS scavenging and multiplying skeletal muscle glycogen stores. Not yet another potent anti-oxidant was what I first thought,when I hit upon the soon-to-be published study from Shaanxi Normal University in Xi'an, China, but after taking a closer look it turned out that the way this century old adaptogen that goes by the name jiaogulanin TCM and is an herbaceous vine of the family Cucurbitaceae (cucumber or gourd family) indigenous to the southern reaches of China, northern Vietnam, southern Korea, and Japan, could actually make quite an exciting supplement (Chi. 2013). After all its high ROS(radical oxygen specimen) scavenging abilities are only part of what allowed the rodents in the study by Chi, Tang, Zhang & Zhang that had been treaded with isolated polysaccharides from this plant to go significantly longer during a standardized exercise performance test.
  The more intruiging part of the performance boost, however came from the direct pro-gluconeogenic and glyocogen storage promoting effects of the alpha variety of the three Gynostemma penhaphylum polyssacharides the scientists had extracted. If similar effects would be seen in humans, GP would certainly make a valuable addition to the regimen of anyone who does not just perform 1-rep maxes day in and day out - and let's face it: In view of the fact that the glycogen can't be synthesized from nothing, it could also help to burn body fat, by it's repartitioning effects.

• 

  Figure 4: It would certainly be an unwarranted overgeneralization to ascribe all beneficial effects of exercise to the systemic expression of heat shock proteins. But still, there is increasing evidence that their controlled expression does at least contribute to the numerous beneficial effects exercise has on our brains, hearts and other organs; interestingly these effects are likewise mediated by the breakdown and the protection and "recycling" of organ tissue.

  Will training your biceps, heal your heart and protect your brain!? You probably know that the scientists at the McMaster University have put the myth of the pro-anabolic effects of systemically circulating hormones that are released response to isolated muscle training (eg. "train your legs to increase your testosterone and see your arms grow") at rest, years ago. Now, a study that's soon going to be published in theh Journal of Experimental Biology suggests that testosterone, growth hormone and co. may not be the only molecules we should be looking for, when we talk about possible non-localized effects of exercise (Jammes. 2013). Another class of proteins that has gotten quite some attention esp. in the context of the profound effects of occlusion training, the so-called heat-shock proteins, which are released in response not just to heat, but to exhaustive contractions / trauma / hypoxia / etc., could in fact play a likewise, probably more important role not so much in skeletal muscle growth, maybe, but in the overall systemic response to exhaustive skeletal muscle contractions. 
  After all, Jammes et al. observed a delayed, but significant elevation of non phosphorylated HSP25 and HSP70 in skeletal and respiratory muscles, kidney, and brain. Now, of HSP70, for example, it has long been known that it exerts cardio-protective effects (Martin. 1997). In addition to its anti-apoptotic effects, it does yet also contribute to the proteolysis (=protein breaking) that's a necessary part of the continuous clean-up processes that remove the "junk" and "clutter" (defect protein structures) from your body in order to keep everything functional (Lüders. 2000). Similarly, HSP25 (aka HSPB1) exerts both cytoprotective effects due to its ability to modulate reactive oxygen species and raise glutathione levels, as well as proteolytic effects and is working hand in hand with HSP70 by inhibiting protein aggregation and stabilizing partially denatured proteins, so that they can be refolded by the former. That the latter could be of particular importants in view of the neuroprotective effects of exercise is also supported by a couple of trials in which HSPB1, to be precise, its exogenous administration or endogenous overexpression, have been evaluated as treatment or preventive strategies in ALS (Lou Gehrig's Disease), Huntington's, Parkinson's, Stroke and acute nerve injury (for an overview see table 3 in Brownell. 2013).

• 

  Figure 5: The benefit of l-carnitine is questionable, despite the fact that the serum l-carnitine in the Mg group dropped to a similar extent as in the control group; over time the carnitine depletion could however become important (Tarighat Esfanjani. 2013)

  Headaches? Magnesium and l-carnitin help! At a dosage of 500mg/day magnesium oxide, alone did already have significant beneficial effects on the occurrence of migraine in  106 females and 27 males volunteers who were diagnosed with headache according to the International Headache Society criteria, were between the age of 18 and 55 years old and "had severe and continual headache lasting from 4 to 72 h, unilateral and pulsating headaches with moderate or severe intensity, migraine with or without aura, at least two attacks per month, headaches which were aggravated by routine physical activity and associated with nausea and/or photophobia, and phonophobia" (Tarighat Esfanjani. 2013).
  So, if that sounds like you (I don't hope it does) magnesium should be the least you should take, the additional 500 mg/day L-carnitine is questionable - just as whether ALCAR may have provided greater benefits. Apropos, you do realize that this is neither transdermal nor any fancy chelated magnesium or at least magnesium citrate that did the trick? Yeah, right: The same "worthless" (put name of random nutrition guru, here) mg-oxide you find in the cheapest fizzy tablet from the supermarket did the trick!

If you are now thirsty for more, I suggest you check out the SuppVersity Facebook Wall (which is by the way updated several times a day), like the career-boosting information that sacrificing sleep in order to study is a bad idea, that Caucasians, compared to Asians, lose weight relatively easily, but have a hard time getting rid of their bellies, or, if all that ain't for you, how the wise producers of "functional foods" are planning to add a little wood aka methylcellulose into your yogurts and smoothies to curb the cravings you probably would not have, if they had not removed all the fat from it, before ;-)

 References:

• Brownell SE, Becker RA, Steinman L. The protective and therapeutic function of small heat shock proteins in neurological diseases. Front Immunol. 2013;3:74. Epub 2013 May 1.
• Chang L, Villacorta L, Li R, Hamblin M, Xu W, Dou C, Zhang J, Wu J, Zeng R, Chen YE. Loss of Perivascular Adipose Tissue upon PPARγ Deletion in Smooth Muscle Cells Impairs Intravascular Thermoregulation and Enhances Atherosclerosis. Circulation. 2013 Aug 1. 
• Chi A, Tang L, Zhang J, Zhang K. Chemical Composition of three Ingredients of Polysaccharides from Gynostemma pentaphyllum and Comparison of their Antioxidant Activity in Skeletal Muscle of Exhaustive Exercise Mice. Int J Sport Nutr Exerc Metab. 2013 Aug 14.
• Citelli M, Bittencourt LL, da Silva SV, Pierucci AP, Pedrosa C. Vitamin A Modulates the Expression of Genes Involved in Iron Bioavailability. Biol Trace Elem Res. 2013 Apr 14. 
• Fitzgibbons TP, Kogan S, Aouadi M, Hendricks GM, Straubhaar J, Czech MP. Similarity of mouse perivascular and brown adipose tissues and their resistance to diet-induced inflammation. Am J Physiol Heart Circ Physiol. 2011 Oct;301(4):H1425-37.
• Jammes Y, Steinberg JG, By Y, Brerro-Saby C, Condo J, Olivier M, Guieu R, Delliaux S. Fatiguing stimulation of one skeletal muscle triggers heat shock proteins activation in several rat organs: the role of muscle innervation. J Exp Biol. 2013 Aug 16.  
• Leber B, Tripolt NJ, Blattl D, Eder M, Wascher TC, Pieber TR, Stauber R, Sourij H, Oettl K, Stadlbauer V. The influence of probiotic supplementation on gut permeability in patients with metabolic syndrome: an open label, randomized pilot study. Eur J Clin Nutr. 2013 Aug 8.
• Lee B, Jung JH, Kim HS. Assessment of red onion on antioxidant activity in rat. Food and Chemical Toxicology. August 10, 2013.
• Lüders J, Demand J, Höhfeld J. The ubiquitin-related BAG-1 provides a link between the molecular chaperones Hsc70/Hsp70 and the proteasome. J Biol Chem. 2000 Feb 18;275(7):4613-7. 
• Lv, X.Y., Li, J., Zhang, M., Wang, C.M., Fan, Z., Wang, C.Y., Chen, L., 2010. Enhancement of sodium caprate on intestine absorption and antidiabetic action of berberine. AAPS.PharmSciTech. 11, 372–382. 
• Martin JL, Mestril R, Hilal-Dandan R, Brunton LL, Dillmann WH. Small heat shock proteins and protection against ischemic injury in cardiac myocytes. Circulation. 1997 Dec 16;96(12):4343-8. 
• Moschonis G, Chrousos GP, Lionis C, Mougios V, Manios Y. Association of total body and visceral fat mass with iron deficiency in preadolescents: the Healthy Growth Study. Br J Nutr. 2011 Nov 16:1-10.
• Ruan CH, Dixon RA, Willerson JT, Ruan KH. Prostacyclin therapy for pulmonary arterial hypertension. Tex Heart Inst J. 2010;37(4):391-9. 
• Tarighat Esfanjani A, Mahdavi R, Ebrahimi Mameghani M, Talebi M, Nikniaz Z, Safaiyan A. The Effects of Magnesium, L-: Carnitine, and Concurrent Magnesium-L-: Carnitine Supplementation in Migraine Prophylaxis. Biol Trace Elem Res. 2013 Aug 17. 
• Yoshikava O, Ebata Y, Tsuchiya H, et al. A retinoic acid receptor agonist tamibarotene suppresses iron accumulation in the liver. Obesity. 2013 Aug.
• Zhanga M, Lvc X, Lia J, Menga Z, Wangd Q, Changa W, Lia W, Chena L. Sodium caprate augments the hypoglycemic effect of berberine via AMPK in inhibiting hepatic gluconeogenesis. Molecular and Cellular Endocrinology. 16 August 2013

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.