Meal Timing, Glycemic Index & Load: Human Study Probes Whether "Hitting Your Macros" Really is All That Counts

High or low GI, carbs in the morning or in the evning, cookies and dingdongs or all bran. So many questions and way too many answers from rodent studies or studies in obese diabetics... but what are Mr. and Mrs. Healthy Average Joe supposed to do?

In a recently published paper, Linda M. Morgan, JiangWen Shi, Shelagh M. Hampton and Gary Frost take yet another look on a concept that has lost much of the momentum it had only a decade ago: The GI and / or GL paradigm (GI: glycemic index (abstract unit); GL: glycemic load, i.e. GI / actual amount of food) and combines another paradigm, which is still gathering momentum within the medical science community - the issue of nutrient timing, in order to answer the following questions:

• Will a large evening energy and carbohydrate load cause an increase in postprandial glucose that is comparable to the same amount of energy and carbohydrates in the morning?
• Will a high glycaemic excursions in the evening be ameliorated by decreasing the glycaemic index (GI) of the meal?

Or put simply: Does carbohydrate and energy timing make a difference and can this difference be mitigated by chosing the "right", i.e. low glycemic carbs (e.g. sweet potato vs. white bread)?

White bread king or all-bran pauper - is that  the question?

To answer this world-shattering question and actually prove their hypothesis that both, i.e. having carbs in the evening and having those in the form of high glycemic index foods, will have negative consequences on postprandial glycemia, the scientists picked six healthy volunteers (four females, two males; mean age 30 +/- 4.3 years, BMI 21·6 +/- 1.3 kg/m²) and randomly assigned them to a follow one of the four following dietary protocols:

• Low GI (average GI = 34), with the majority of energy load consumed in the morning (LGI-am)
• Low GI, with the majority of energy load consumed in the evening (LGI-pm)
• High GI (average GI = 84), with the majority of energy load consumed in the morning (HGI-am)
• High GI, with the majority of energy load consumed in the evening (HGI-pm)

with identical energy content of approx. 8368 kJ (2000 kcal) for the whole day on four individual intervention days with a minimum of 7 days between each of the tests. Breakfast was given at 09.30 hours, lunch at 13.30 hours and the evening meal at 20.30 hours - subjects were at the laboratory for the whole day. Blood samples were taken 2h postprandial and blood glucose levels were monitored continuously via a "MiniMed continuous glucose monitoring system" that senses interstitial glucose by electrochemical detection in subcutaneous interstitial fluid in 5 min intervals.

Figure 1: Composition of the two test diets (low GI, blue; high GI read) and individual macronutrient breakdown of the test meals the subjects consumed on two seperate occasions (based on Morgan. 2013)

It does not take a nutrition expert to see that despite the obvious differences with respect to the glycemic index and load, even the allegedly healthy low GI diet with all-bran for dinner* and a macronutrient composition 72% carbohydrates 14% protein and 14% fat is not exactly what the latest research would suggest to be a healthy, let alone a "physique enhancing" diet.

*note: The scientists probably chose similar foods for breakfast and dinner, because the study design required those to be exchangeable.

Against that background it is still astonishing how much of a difference...

• 99% higher fiber content,
• -60% lower glycemic index (GI), and
• -63% lower glycemic load (GL)

... actually make when it comes to the effect of isocaloric meals with identical macronutrient compositions (see figure 1, right):

Figure 2: Total area under the curve for interstitial glucose (0–20 h), postprandial plasma insulin, TAG (**mind the text for info a potential typo, here) and NEFA (0–2 h after each meal) in six healthy volunteers following either a high-glycaemic index (HGI) or a low-glycaemic index (LGI) diet, with most of the energy consumed either early (LGI-am, HGI-am) or late (LGI-pm, HGI-pm); all values expressed relative to respective statistical mean (data calculated based on Morgan. 2013)

I guess I don't have to tell you that the image that emerges here stands in line with the as of late largely ignored glycemic index paradigm the underlying message of which is: It is not simply the amount of sugar you eat,  but rather how fast / hard it hits your blood stream that determines it's impact of on your glucose metabolism. And with respect to the latter, the researchers remark:

"Glucose and insulin responses showed broadly similar patterns. Both meal timing and quality of carbohydrate affected postprandial glucose and insulin responses (P < 0.01). The area under the glucose and insulin response curves was greatest for the HGI-pm meal regimen. The HGI-pm meal regimen produced a significantly greater postprandial area under the glucose curve than for any of the other three meal regimens (P < 0.05). The postprandial area under the insulin curve was significantly greater than both the LGI regimens (P < 0•05). Postprandial insulin resistance measured by homeostatic model assessment was also significantly greater for the HGI-pm meal than for the two LGI meals (P < 0•05)."

However, since Morgan, Shi, Hampton and Frost also state that "[p]ostprandial TAG and NEFA levels were not affected by meal timing or carbohydrate quality", I do suspect that there is a typo in table 3 of the original study, where it says that the TAG would be 5.04 mmol/l x h (probably is 6.04) and thus more than 15% lower than the average (TAG levels and insulin resistance usually go hand in hand, so it is really very unlikely that the 5.04 mmol/l x h is correct).

So what's the take home message here?

The only question that still has to be answered would be "King or pauper? At least with regard to the former, the best thing I can to is to suggest you read both the posts on "Breaking the Fast" and the "Carbs Past 6PM Posts"  (Part 1 & Part 2). When you have done that your perspective on the importance of breakfast and the purported fallacy of having a large dinner should already have changed. The things that are still left to do is not fool yourself into the false belief that you can pound whatever junk you want (as long as it fits your macros). As the glucose curve of the high GI arms (light color) in the figure above goes to show you, your body won't be happy when you get your "carb macros" from sugary junk.

Stick to starchy (or "save carbs", if you will) and fruit. Use veggies to fill you up. Use coconut & olive oil and the fats that are already in your meats, fish and dairy products to achieve baseline fat intake of at least 40-50g (all together). Aim for a 100-120g carbohydrate basis, diverge towards the lower side, when your body fat is high, you can't train or you're dieting and towards the higher side, when you are already very lean, have a high training volume, or are trying to build muscle. Complement that with min. 20g of quality protein with each meal. Don't deprive yourself on any nutrient completely and ramp up the total amount of food (at the given ratio) to fulfill your energy requirements.

In that, avoid processed food sand rely on whole foods, whenever possible (>90%),. Use food supplements* only where it makes sense, e.g. a protein shake post workout (*creatine for example would not be a "food supplement", since you can NEVER get the amounts that are necessary to supersaturate your stores from meat alone) and don't forget to live about all that "dieting" and thinking about the best ways to eat, please!

So if we assume that my assumption with respect to the triglyceride values in the originally published study are correct and we are simply dealing with a typo here, the next questions which arise here, are...

1. What is / are the reason/s that the lipid metabolism did not suffer?
2. How reliable is the HOMA-PP, i.e. the postprandial assessment of insulin sensitivity via the homeostasis model assessment? 
3. What does all this mean for you? Does meal timing not make a difference and are macros all that counts? 

As far as (1) goes, the answer is pretty simple: With a diet that was that low in fat and not overabundant in energy (2,000kcal for both diets) any potential the negative downsides on lipid metabolism will take their time to show. The acute ingestion of three high GI meals on a single day or modifications in their distribution across the day won't have much of an effect in healthy individuals, such as the four women and two men in the study at hand (in diabetics and especially patients with NAFLD things will probably look different, though).

The absence of changes in lipid metabolism after one day on high vs. low GI diets w/ different meal timing patterns yields answer #1 to question (3): If you are healthy the occasional day with junk food won't hurt you as long as you keep the total amount of energy at bay and jump back on the "healthy diet" wagon the very next day.

On the other hand, if only a single day of high GI food consumption can have such a pronounced impact on the postprandial HOMA levels, this raises the question how reliable this "long term measure" of glucose sensitivity actually is. Obviously, you should not go to the doctor's office and have your HOMA measured, at a morning after a day with three SuperSize Meals from McDonalds (even if you have been fasting after supper at night before, as the participants in the study at hand did) - unless you want a prescription for meformin, of course ;-)

It would however be likewise unwise to "do everything right" for three (maybe even just one day) before you head to the doctor to get blood drawn, just to be able to rejoice over a HOMA reading that does by no means represent your "normal" insulin sensitivity. This may make your doctor happy and spare you getting ticked off, but could have you run around pre-diabetic unnoticed for months if not years - maybe so long until the first irreversible damage has already been done.

The high susceptibility of HOMA measures to acute dietary modifications yields answer #2 to question (3): If you want know where you stand, don't make last minute changes to your diet before you get blood drawn. After all, the 90:10 rule (better 95:5 rule ;-) applies both ways - the 90/95 days of consistent eating patterns will decide whether you are lean, muscular and above all healthy or fat, undermuscled and sick.


References:

• Morgan LM, Shi JW, Hampton SM, Frost G. Effect of meal timing and glycaemic index on glucose control and insulin secretion in healthy volunteers. Br J Nutr. 2013 Oct;108(7):1286-91.

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. 

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.