Fructose Impairs Fatty Acid Oxidation: Replacing 26g of Starch and Lactose in low GI Meal by Fructose Decreases Postprandial and Exercise Fatty Acid Oxidation by -21%

Image 1: With just bacon and eggs for breakfast you would not run the "risk" of reducing fatty acid oxidation.

A carby meal, i.e. a meal with a high amount of carbohydrates, right before workout triggers a shift in substrate utilization, i.e. the type of energy resource, your body will use to fuel the subsequent workout, from fats to carbohydrates, right!? But does it make difference whether you eat a Snickers bar or drink a can of Coca Cola, if both contained the same amount of carbs? Or, in other words, does the source and/or the glycemic index of your pre-workout meal have an impact on the respiratory quotient (RQ), which is the quotient of the amount of exhaled CO2 and inhaled oxygen, with higher RQs (towards 1.0) indicating that you are predominantly running on carbs, and low RQs (towards 0.7) indicating that you derive a greater part (not all!) of your energy from fatty acids.

Orange juice with breakfast? Better not...

The question, whether GI and carbohydrate type of a meal would have a significant impact on the postprandial glucose, lactate and free fatty acids levels, as well as the insulin response and the subsequent carbohydrate and fatty acid oxidation in the course of a low intensity 1h walk, has been bothering Feng-Hua Sun and his (or her?) colleagues from the Department of Sports Science and Physical Education at the Chinese University of Hong Kong, too. In a counter-balanced crossover design (>=7 days between trials; identical, recorded diet in the 3 days before each trial), all 10 healthy male subjects reported fasted (10-12h) at the laboratory, where they consumed one out of three meals with identical macronutrient composition, yet varying carbohydrate sources and glycemic indexes (cf. figure 1).

Figure 1: Macronutrient (in g) and ingredient composition of
the three test meals (according to Sun. 2011)

As you can see, the meals have identical caloric values and macronutrient compositions. Unfortunately, the differences between the ingredients go beyond their plain sugar vs. starch vs. fructose content. After all, spaghettis are not rice and milk is not ham ... this is a design flaw, of which I think that it impairs the significance of the results, but hey! At least the Chines have grasped the idea that calorie is not a calorie...

After all participants had finished eating their "delicious" breakfast, they remained seated for another 120min, in the course of which they had to drink 2ml of water per kg of body weight every 30 minutes "to ensure adequate hydration and balance the water content of the meals".

After these sedentary 2 hours, the subjects performed a standardized 5 min warm-up at 40%  of their individual VO2 and then completed 60 min of brisk walking at 50% of their VO2max.

Figure 2: Differential postprandial (2 hours) glucose (left) and insulin (right) response to the three test meals
(data adapted from Sun. 2011)

As you can see in figure 2, there were significant difference in the postprandial (120 min before exercise) glucose and insulin response to the different meals. Yet, while the difference between the low and high GI meals was something you should have expected, judged by the GI, the fructose enriched LGF meal should not have produced greater glucose (+63% area under the curve, cf. figure 2, left, small graph) and insulin (+62% area under the curve, cf. figure 2 right, small graph) responses than the low GI, no fructose meal, which, in fact, had a slightly lower glycemic index.

Figure 3: Postprandial (2 hours) lactate concentration in the 10 subjects after ingestion of the three test meals
(data adapted from Sun. 2011)

What is yet even more striking is the profound increase in lactate concentration during the prostprandial (not the exercise phase) in the subjects who consumed the fructose-containing meal (cf. figure 3). With +211% (lactate AUC) the postprandial lactate concentration in the LGF group is more than 3x higher than in the LG group! A clearcut sign for an increase in hepatic glycolysis and probably part of the reason that we are seeing increased carbohydrate and decreased fatty acid oxidation rates in the course of the subsequent walking exercise (cf. figure 4).

Figure 4: Postprandial, during exercise and total substrate utilization (in g) subsequent to the ingestion of the three different test meals (data adapted from Sun. 2011)

Postprandially, the increase in carbohydrate oxidation is even more pronounced in the LGF group than in the HG (sugar) group. That being said, the total reductions in fatty acid oxidation are -21% for the low GI fructose (LGI) and -23% for the high GI sugar (HG) group and thusly, within their respective statistical margins, identical!

With respect to the underlying reasons of this disadvantageous shifts in substrate utilization, Sun et al. speculate, that the mechanism

[...] behind this may be the reduced hyperglycemia and hyperinsulinaemia during the postprandial period following LGI meal consumption. [...] In addition, it is well known that insulin can suppress the lipolysis. This suppression appears to be long lasting, even when insulin concentration has returned to basal levels.

The last part, here, is of particular interest, because, obviously, after a few minutes of walking and with the increased need for carbohydrates the insulin levels of all subjects (regardless of the composition of their prior meals) dropped to levels ~2-3mU/L. Now the insulin response in the LGF group was still smaller than the one of the high GI (HG) group, so that the scientists assume that the ability of the fructose to bypass first rate-limiting enzymes of glycolosis in the liver, which renders it readily available for oxidation, must explain why the ratio of carbohydrate to fat oxidation was still similarly skewed in both, the low GI, plus fructose, and the high GI groups.

Image 2: I wonder if nutritionists will ever understand that there is difference between fructose powder (left) and an apple (right)

Although these results stand in line with the detrimental effects of fructose sweetened foods, I would still like to see two methodologically flawless studies with a) meal 1 not using different foods (I mentioned that in the 4th paragraph of this post already) and b) fructose from whole fruit and not in the form of the powdered poison Sun et al. just dissolved in water and added to their meals... and you know, in case these studies will be done - sometime in the distant future, when mainstream nutritionists will finally understand that not only is a calorie not a calorie, but that powdered fructose is also not an apple, you will read about that on the SuppVersity, first!

The Acute & 24h Effects of 3 Types of High Intensity Circuit Training on Testosterone & Cortisol in Young Trained Men.

It's obviously to have the 24h effects on testosterone and cortisol than only those measured after the workout , but can we make solid conclusions based on the additional data?

In spite of the fact that the acute testosterone and cortisol response to exercise appears to have little direct effects on the overall training outcome (Schoenfeld. 2013), acute increase in cortisol and reductions in testosterone, i.e. a decrease in the testosterone:cortisol ratio is a classic feature of overtraining and can very well blunt, if not reverse the beneficial effects of exercise on your health and body composition.

Against that background a recent experiment that was conducted by researchers from the University of Chieti-Pescara in Italy could be of great interest to everyone who is performing high intensity interval training on a regular basis. Why?

Well, in contrast to previous studies, Blasio et al. investigated both the acute and 24h effects of a high intensity interval resistance training regimen in trained young men.

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To characterize the effects on heart rate and hormonal responses the subjects, eight trained, healthy trained men (28.61 ±3.51 yrs), performed three different workouts which had the same exercises, the same load and number of repetitions for each exercise, but different exercise order, recovery and speed of execution.

• RANDOM workout: the assigned goal was to complete the assigned repetitions respecting only two duties. The first one was don’t stop until all of the repetitions were completed; the second was that there were no assigned order of execution of exercises and no assigned consecutive repetitions to complete.
  
  Participants were thus free to choose both the order of exercises and number of consecutive repetitions for each exercise (i.e. 2 repetitions of kettlebell swing, 10 repetitions of medicine ball slam, 20 repetitions of squat, 4 repetitions of spin with Bulgarian bag, etc.).
  
  No recovery period was assigned, except the time necessary to move from a station to another, and no speed of execution of exercises was assigned: participants were free to choose the preferred speed. 
• LADDER workout: respecting the following order of execution, kettlebell swing, medicine ball slam, spin with Bulgarian bag, squat, pull-up, burpee, participants had to complete the total repetitions according to a pyramidal scheme (e.g. 1st lap 10 repetitions at each exercise, 2nd lap 9 repetitions at each exercise) until the total number of repetitions of each exercise was executed.
  
  Each lap of the circuit was followed by 1 minute of recovery. No speed of execution of exercises was assigned: participants were free to choose the preferred speed. 
• AS SOON AS POSSIBLE (ASAP) workout : respecting the following order of execution, kettlebel swing, medicine ball slam, spin with Bulgarian bag, squat, pull-up, burpee, participants had to complete the total volume in six laps executed as soon as possible.
  
  During each lap participants had to complete the sixth part of total number of repetitions of each exercise without rest among exercises. Each lap of the circuit was followed by 1 minute of recovery.

Salivary samples were collected before and after each workout, at 11:00 p.m. and at 7:00 a.m. of the following day. Salive was also collected during a non-training day. Similarly, before and after the workout, plasma lactate was measured while a beat-to-beat heart rate recording was executed during each workout. Cortisol (C) and testosterone (T) were measured in salivary samples.

2h before the workouts the subjects who had to abstain from sexual intercourse, stimulants and alcohol from 2 days before to the experimental days and until 9:00 a.m. of the following day, consumed a standardized meal that was lower to 400 and consisted of 33 cl of water, 35 cl of orange juice and two 30 g energy bars (Power Sport Double Use, Enervit, Milan, Italy).

Let's look at the results

While the protocols elicited the same heart rate response (the major part of each workout was spent between 80 and 100% of maximal heart rate, confirming the high cardiovascular intensity of the workouts), they elicited different hormonal and lactate variations with the LADDER workout producing the lowest lactate increase and the RANDOM workout eliciting the highest lactate, cortisol and testosterone increases.

Figure 1: Relative changes in hormone and lactate concentration in response to the workouts (Di Blasio. 2014)

When C was considered in ratio with T no significant differences have been shown among workouts-induced variations. Results of the analysis of covariance, executed on significantly modified variables, confirmed that basal hormonal and lactate values did not influence their variations.

When they studied the effects of workouts on prolonged hormones production (i.e. until the morning following the morning, di Blasio et. al. found that observed that observed that

"C had both time (F=179.723; p < 0.001) and group × time effect (F=10.942; p < 0.001): while during non-training day there is a physiological decline of C production at 11:00 p.m., during training days its decline is not present but seems to have a continuous increase from 7:00 p.m. to 7:00 a.m." (Di Blasio. 2014)

For the testosterone production the authors found both time (F=443.340; p < 0.001) and group × time effect (F=3.254; p=0.008) even if the group × time effect seems determined by the samples collected at 7:00 p.m., so that the effects cannot be ascribed fully / exclusively to the workout.

Figure 2: 23h hormone profile after the RANDOM, LADDER, ASAP workouts on a control day (di Blasio. 2014)

What is most interesting, though, is the cortisol to testosterone ratio. It shows the greatest inter-group differences and could potentially be of great physiological relevance (Crowley. 1996). In that, the LADDER workout has the most negative effect, as it will totally blunt the natural decline of the C:T ratio at noon.

In case you're planning to incorporate circuit training into your schedule, make sure to have a huge chunk of beef after your workouts ;-) - "Post-Workout Steak "Supplementation" (135g of Lean Beef) Augments Improvements in Body Composition In Response to 8 Weeks of Circuit Resistance Training" | more

Bottom line: As usual, it is difficult to interpret the results in order to make concrete practical recommendations. The lactate and hormonal data does yet suggest that the "random" order, i.e. a training that involves a self-selected exercise order and rep speed, as well as little to no rest between exercises is the least, the ladder training, with its decreasing 10, 9, ... rep numbers and one minute rest between each lap of the curcuits is the most metabolically demanding workout.

Whether and to which extend this translates into an increased risk of overtraining, let alone increased muscle and strength gains, on the other hand, remains to be seen. In view of the overall effect on lactate levels and the C:T ratio, though, the study does suggest that you better be careful with high intensity circuit / interval resistance training sessions and give your body adequate time to rest and recover | Comment on Facebook!

References:

• Crowley, Michael A., and Kathleen S. Matt. "Hormonal regulation of skeletal muscle hypertrophy in rats: the testosterone to cortisol ratio." European journal of applied physiology and occupational physiology 73.1-2 (1996): 66-72. 
• Schoenfeld, Brad J. "Postexercise hypertrophic adaptations: a reexamination of the hormone hypothesis and its applicability to resistance training program design." The Journal of Strength & Conditioning Research 27.6 (2013): 1720-1730.

Pyruvate Supplements - Useless as Ergogenic, Surprisingly Effective as Dieting Aid & Body Recompositioning Agent

Pyruvate = Recomp agent, not performance enhancer?

I am not sure if you even remember that pyruvate, which is made from glucose through glycolysis, and can be converted back to carbohydrates (such as glucose) via gluconeogenesis, or to fatty acids through acetyl-CoA, has once been touted as (yet another) "next big thing" by parts of the supplement industry.

The idea was that pyruvic acid could supply energy to working muscles through the citric acid cycle (also known as the Krebs cycle) when oxygen is present (aerobic respiration), and alternatively ferment to produce lactate when oxygen is lacking (fermentation) - this would make it the perfect workout fuel for high intensity exercise, but theory and practice are two very different animals.

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Past studies investigating its efficacy have however yielded mixed results. In the year 2000, Michael A. Morrison , Lawrence L. Spriet , David J. Dyck reported that "oral pyruvate supplementation does not increase blood pyruvate content and does not enhance performance during intense exercise in well-trained cyclists." (Dyck. 2000)

Similarly disappointing results have been reported by Ebersole et al., likewise in the year 2000 for improvements in critical power (there were none) and stand in contrast to observations by JL Ivy who found that pyruvate, when "provided as an oral supplement for several days", whill "enhance aerobic endurance capacity" in rodents (Ivy. 1998) or Stanko et al. who found back in 1990 that feeding  dihydroxyacetone and pyruvate for 7 days  increased  arm  muscle  glucose  extraction  before  and  during exercise,  thereby  enhancing  submaximal  arm  endurance  capacity of (albeit) untrained men.

Weight & amp;fat loss(kg)/4.25-MJ deficit (Stanko. 1995) ➽ Pyuruvate makes dieting more effective.

Previous studies show that Pyruvate propels weight and fat loss: On a standardized 1.015kcal per day diet, subjects lost significantly more weight and body fat, when they received 30 grams of mixed sodium + calcium pyruvate per day. Plus: The pyruvate supplement had protein sparing effects, as well. In spite of the fact that the difference was not statistically significant, the subjects in the pyruvate group lost 5% less lean mass (relative to the total weight loss) than their peers in the placebo group.

Olek, et al. the authors of the most recent pyruvate paper in the open access journal nutrients, were well aware of the fact that pyruvate (PYR), in spite of its importance in energy metabolism, has not been shown to have ergogenic effects after prolonged supplementation. In view of the fact that Morrison et al. indicated that acute oral intake of calcium PYR (Calcium Pyruvate), even at a dose of 25 g, did not modify the PYR concentration in the whole blood or in the plasma, while Olek et al. have previously shown that a single dose of sodium PYR (NaP) does, the researchers from the Gdansk University ofPhysical Education and Sport in Poland decided to re-examine the effect of a single NaP ingestion on blood acid-base status and the exercise metabolism markers.

"Since 0.1 g of sodium bicarbonate per kg of body mass induces metabolic alkalosis 60 min following ingestion [14,15], we hypothesized that a similar NaP treatment before commencing the high intensity physical exertion may change the exercise metabolism." (Olek. 2014)

Nine active, but non-specifically trained, malesubjects (mean ± SEM: 23 ± 1 year old, 1.75 ± 0.02 m height, 72 ± 2 kg body mass) participated in the double-blind, placebo-controlled, crossover study.

"On separate days, the subjects reported to the laboratory in the morning, then rested for 30 min and then ingested placebo or NaP in a random order. In the previous studies the subjects consumed PYR in the amount of ~0.07–0.08 g/kg body mass;  therefore, the subjects in our study ingested NaP in a single dose of 0.1 g/kg body mass (which is ~0.08 g of PYR per kg body mass). " (Olek. 2014)

An hour following the ingestion, the subjects performed the physical exertion. The exercise protocol consisted of 2 min at a power output of 50 W and then for 6 min at a constant power output, corresponding to ~90% O2max. To determine  O2max, participants performed a graded cycle ergometry test on an electromagnetically-braked, cycle ergometer. After an initial warm-up period, the work rate was increased by 25 W/min until volitional exhaustion was achieved.

Figure 1: Lactic acid and blood pH during the placebo (•) and (o) pyruvate trial (Olek. 2014)

As you can see in Figure 1 the lactic acid concentration after the workout was significantly higher in the dotted pyruvate trial. Interestingly, though, the pH and thus the acidity of the blood was only marginally elevated - a clears sign that the buffering function of sodium pyruave Olek et al. had speculated about is real.

Pyruvate as a PGC-alpha driven metabolic engine builder: In view of the fact that high pyruvate levels would usually occur during intense exercise it's no wonder that researchers from Novartis Institutes for BioMedical Research in Cambridge have found that it increases mitochondrial biogenesis in rodent muscle (Wilson. 2007)

Table 1: Gas exchange, ventilation and heart rate responses during and after severe-intensity exercise following placebo and sodium pyruvat eingestion. Values are the means ± SEM (Olek. 2014) | As you can see, there are no asterisks (*) which means: None of the differences reached statistical significance.

A brief glimpse at the measured differences in O2 uptake, CO2 output, minute ventilation, respiratory exchange ratio, and heart rate (see Table 1) does yet reveal that the study at hand generally confirms what previous studies by Ebersole et al (2000) and Morrison et al. (2000)  suggested: In spite of the fact that it would be 100% logical, if we saw performance improvements with pyruvate supplementation, the parameters Olek et al. recorded do not suggest that there were any.

And even when it was administered as creatine pyruvate, Van Schuylenbergh et al. did not find any benefits on cycling performance in a 2003 study.

Bottom line: In spite of the fact that it's physiological function would suggest that supplemental pyruvate should increase exercise performance, there is as of now no good evidence that it will actually do that.

Figure 2: Pyruvate may not improve performance, but it promotes improvements in body composition in dieting overweight men and women (Kalman. 1998).

Against that background you may be interested to hear that several studies suggest that it may not improve performance, but could help you lose weight. The ingestion of pyruvate 6 g/d for 6 weeks, along with regular exercise, for example, has been shown to reduce body fat, increase lean body mass, and improve fatigue and vigor scores in a 6-week, double-masked, placebo-controlled study that was conducted by Douglas Kalman et al. in 1998 to determine the effects of pyruvate supplementation on body weight, body composition, and vigor and fatigue levels in overweight men and women. Quite an impressive result. Specifically if you take into consideration that there were no changes in body composition in the placebo group who followed the same diet and training regimen.

Similar, albeit slightly less pronounced effects have been observed in the absence of dietary restrictions by Koh-Banerjee et al. (2005) and in a low energy + no exercise context by Stanko et al. (1992). Unfortunately, the mechanism(s) remain unclear. As Kalman et al. point out, previous rodent studies would suggest that an increase in insulin sensitivity and glycogen storage and decrease in fatty acid synthesis in fat cells may be at the heart of the effects the researchers observed 15 years ago | Comment on Facebook.

References:

• Ebersole, Kyle T., et al. "The Effect Of Pyruvate Supplementation On Critical Power." The Journal Of Strength & Conditioning Research 14.2 (2000): 132-134.
• Ivy, John L. "Effect of pyruvate and dihydroxyacetone on metabolism and aerobic endurance capacity." Medicine and science in sports and exercise 30.6 (1998): 837-843.
• Kalman, Douglas, et al. "Effect of pyruvate supplementation on body composition and mood." Current Therapeutic Research 59.11 (1998): 793-802.
• Koh-Banerjee, Pauline K., et al. "Effects of calcium pyruvate supplementation during training on body composition, exercise capacity, and metabolic responses to exercise." Nutrition 21.3 (2005): 312-319.
• Morrison, Michael A., Lawrence L. Spriet, and David J. Dyck. "Pyruvate ingestion for 7 days does not improve aerobic performance in well-trained individuals." Journal of Applied Physiology 89.2 (2000): 549-556.
• Stanko, Ronald T., Denise L. Tietze, and Judith E. Arch. "Body composition, energy utilization, and nitrogen metabolism with a 4.25-MJ/d low-energy diet supplemented with pyruvate." The American journal of clinical nutrition 56.4 (1992): 630-635.
• Van Schuylenbergh, Reinout, Marc Van Leemputte, and Peter Hespel. "Effects of oral creatine-pyruvate supplementation in cycling performance." International journal of sports medicine 24.02 (2003): 144-150. 
• Wilson, Leanne, et al. "Pyruvate induces mitochondrial biogenesis by a PGC-1 α-independent mechanism." American Journal of Physiology-Cell Physiology 292.5 (2007): C1599-C1605.

HIITing Diabetes With the Hammer: 20min of Low-Volume High-Intensity Interval Training is Enough! + Metabolic Benefits and Optimum Interval-Format for Healthy People!

Figure 1: Number [in millions!] of prediabetics and diagnosed and undiagnosed diabetics in the USA according to data from the American Diabetic Association from January 2011 (ADA. 2011)

You probably remember Wednesday's news-item on high-intensity interval training (HIIT) for cardiac patients - as it turned out, even 2 weeks after myocardial infarction our central pump needs real exercise to get back in, or to get into even better shape. Today, I do yet want to go beyond infarction patients and address another, ever-growing sub-group of the self-perceived "victims" of the obesity pandemic, the type II diabetics.

About a month ago, J.P. Little and his colleagues from the University of British Columbia Okanagan published a study in the Journal of Applied Physiology (Little. 2011a), the results of which confirm (once again) the unpopular hypothesis that getting your ass off the couch in order to work it off in the gym hard (!) is the only way to treat a (largely) self-induced health condition that is plaguing 8.3% and threatening another quarter (79 million people with pre-diabetes) of the US population (ADA. 2011, cf. figure 1).

In the Little study (pun intended ;-), it took 8 type 2 diabetics no more than 60 minutes of intense exercise at 90% of their maximal heart rate (+another 60 minutes of rest in between intervals) to

[...] rapidly improve glucose control and induce adaptations in skeletal muscle that are linked to improved metabolic health

120 minutes (!) of which only 60 were spent doing 10x60s intervals on a cyclometer brought about changes, no pharmaceutical (or even supplement) will ever produce (without significant side effects). 120 minutes spread across 6 exercise sessions in the course of two weeks, i.e. 3 sessions of 20 minutes per week - probably 20 minutes the majority of the 8 overweight (BMI 32.6kg/m²) diabetics would otherwise have spent on their couch in front of the TV, or - with comparably small benefit - trampling away at 65% of their VO2Max on a recumbent bike. With intervals at 90% of their maximal heart rate, however, the

[...] average 24-h blood glucose concentration was reduced after training (7.6±1.0 vs 6.6±0.7 mmol/L) as were the sum of the 3-h postprandial areas under the glucose curve for breakfast, lunch and dinner (both p<0.05).

More importantly, though, HIIT training set the stage for future improvements by improving the capacity of the trainees mitochondria to handle / burn nutrients, with the >3.5x increase in GLUT-4 acticity indicating a profoundly increased capacity for glucose uptake and the +20% increase in citrate synthase activity indicating an increased capacity for substrate oxidation (energy usage) in the cellular power plants of the 8 diabetics (cf. figure 2).

Figure 2: Improvements citrate synthase, protein content of 70kDA subunit, complex III core 2 protein, complex IV subunit IV, mitofusion 2 and Glut-4 activity - all markers of mitochondrial capacity / efficiency - after 6 sessions of 10x60s cycling at 90% HRmax in 8 diabetic patients (data calculated  based on Little. 2011a).

These improvements, and this is a result from a previous study by Little's group (Little. 2011b), were - at least in part - a result of the effects HIIT has on mitochondrial biogenesis, of which Little et al. found that it is profoundly elevated in the first 24h after the exercise bout (3h post: +70% nuclear PGC-1alpha/Tubulin, 24h post: +60% whole muscle PGC-1alpha/Tubulin; +150% increase in p-p38MAPK) - and all that after a single session of a all 4x30s all-out Wingate cycling tests separated by 4 min of rest).

Now, let me ask you: Do we really ask too much of our fellow (and mostly ridiculously lazy) human being, if we ask them to invest one hour of their life per week to exercise into a, no, their healthier future? I wouldn't think so!

Figure 3: Fat oxidation in kJ per minute during 60 min of cycling at 60% VO2Max before and after 7 sessions of HIIT training in eight healthy, normal-weight recreationally active women (Talanian. 2006).

Metabolic benefits of HIIT training: Now, you may well ask yourself, why you should a give a damn about those changes, well... would it convince you, if I told you that in a 2006 study Talanian et al. were able to show that after 7 sessions of serious HIIT training (10x4 min at 90% HRMax with 2 min rest between intervals) the amount of body fat the eight female study participants burned during cycling at 60% of VO2Max was increased by 36% (Talanian. 2006)? in other words, the HIIT sessions primed the bodies of the "recreatinally active women (22+/-1 yr old, 65.0kg body wt, 2.36l/min VO2peak) to burn more fat during subsequent cycling at the lower end of the "fat-burning zone"! As the data in figure 3 shows, this effect was partly, because the subjects switched more readily into "fat burning mode" - a priming effect from the HIIT sessions.

HIIT, yeah... but how to find the right dosage?

Both the Moholdt, as well as the Little study have shown that it does not take much to induce profound health benefits - but what would be the optimal dosage for YOU, who, as a diligent student of the SuppVersity, are probably (or should I say hopefully) neither an overweight diabetic nor a cardiac patient?

Figure 4: Changes in body weight, body fat (%), peak lactate levels, perceived exertion (RPE) and VO2Max (rel. to body weight) after low intensity continuous training or three different HIIT protocols in recreational cyclists (data calculated based on Seiler. 2011)

Apparently, a group of scientists from Kristinsand (again in Norway, where the descendants of the Vikings obviously are tough enough fore real exercise ;-) asked themselves the exact same question (Seiler. 2011). In the course of a 2 months study they had 29 male and 6 female recreational cyclists, whose VO2Max of 53+/-6 ml*kg/min were ~56% higher than those of the cardiac patients (after the intervention) in the Moholdt study, perform 2 HIIT sessions per week (plus 2-3 weekly low-intensity bouts) of one out of three different interval training programs: 4x4min, 4x8min, or 4x16 min at 94%, 90% or 88% of their respective maximal heart rates.

Hard, but neither torturous, nor time consuming

The results, I have plotted in figure 4, confirm that HIIT must be hard, but neither torturous nor time-consuming. Or as the scientists put it:

The 4x8 min prescription induced greater physiological adaptation than both lower and higher intensity interval programs of 64- and 16-min total duration but was perceived as less stressful than 4x4 min at ~95% HR max . These findings suggest an important interaction between accumulated work duration and work intensity that can be optimized for inducing maximal physiolo gical adaptations at manageable RPE [rates of perceived exertion] in endurance athletes performing interval training.

Image 1: Spinning at ~90% of your max heart rate
would be one way to do 4x8 intervals.

On that note, it may also be interesting that in line with the +91% increase in time to exhaustion Seiler et al. observed in the 4x8 HIIT group (vs. +12% in low intensity and +62% and +63% in 4x16 and 4x4 HIIT programs) and the increased respiratory exchange rate Moholdt et al. observed in their study (cf. Wednesday's news), A.D. Hafstadt and his colleagues from the University of Tromsoe (Hafstadt. 2011) have found in a mouse-model (where cutting out the heart and measuring its weight obviously is not so much of an issue as it would be with human subjects ;-) that despite similar increases in the heart to body weight ratio (+10%), ...

[...] only HIT altered cardiac substrate utilization, as revealed by a 36% increase in glucose oxidation and a concomitant reduction in fatty acid oxidation, [...] improved cardiac efficiency by decreasing work-independent myocardial oxygen consumption and increased cardiac maximal mitochondrial respiratory capacity.

These findings lead the scientists to conclude that "high intensity training is required for induction of changes in cardiac substrate utilization and energetics" and that these improvements may be at the heart (pun intended) of its "superior" ability to increase aerobic capacity - or as, I previously phrased it: HIT, not steady state aerobics, is real cardio training! You would not train a 20inch biceps with blue 2pound sand-filled plastic dumbbells, would you? I think, I will leave it on that, for today and wish you all have an intense weekend (whatever your interpretation of that may be ;-)

Image 2: There is no one-size-fits-it-all HIIT training.

Addendum of 10/01/2011: In the comments area, Oni posted a quite resonable question: "Doesn't HIIT usually employ shorter (1min) intervals? And how could 8 minute intervals, as in the Seiler study be feasible?" The answer to the first question is easy, as we just have to look at the words "high intensity" and "interval training", now obviously no one questions that the regimen Seiler et al. used, had a high intensity (90%) and employed intervals - and I think Oni does not disagree on that, but rather implies that this type of training is too intense and if the subjects had not been recreational cyclists, this could actually have been the case.

On the other hand, the results of the Seiler study also showed that shorter intervals at higher intensity lead (in this subject group) to greater rates of perceived exertion. Now, I dare say that 95% of the trainees who are doing the standard ~1min bouts of all-out exercise - are not going "all out" in the sense that they are scratching their real heart rate max. If they did, I am quite sure they would (in line with the results from the Seiler study) confirm that 8min @90% did not wear them out as much as 1min @100% of ALL OUT exercise at their  max. heart. This leaves the question to be answered, whether 4 intervals à 8 minutes are optimal for everyone? And this is fortunately a question that is easy to be answered... 4x8 is obviously for "advanced" athletes (who have been practicing some type of endurance activity already). From my training experience, I know that untrained (or less trained) trainees sometimes do not even reach "target heart rates ~90%" before they feel so exhausted that they give up.

Image 3: The type of equipment you are using will also have an influence on optimal interval length; doing 8-min all-out intervals on the treadmill certainly are no viable option - even not for highly trained athletes!

So what does that mean for your training, then? If you like doing the all-out (! don't forget to push yourselves!) 1-minute intervals, keep doing them. There are plenty of studies that confirm similarly beneficial effects on mitochondrial biogenesis with these protocols, e.g.

• 7x30s - Psilander. 2010
• 8-12x60s - Little. 2010
• 4x 30s - Giballa. 2009

If, on the other hand, you are an (endurance) athlete wanting to improve your performance, the available data would suggest that intervals in the +4min range would be the way to go (Seiler. 2004; Driller. 2009; Seiler. 2011), as they are more sport-specific. Overall, it is yet always about balancing duration (individual interval length + number of intervals + rest days in-between) vs. intensity (heart rate) to find your optimal HIIT protocol (Gross. 2007; Zuniga. 2011)

22g Baking Soda 60min Before a Old-School 4 x 12RM Leg Workout Allow for a 22 Rep Volume Increase on Hypertrophy Oriented Squat + Leg Press + Leg Extension Quads Routine

Image 1: Squats, 8 x 12, Leg Press 6 x 12, Leg Ext. 6 x 12; that's the Quads routine Serge Nubret trained twice a week in conjunction with chest – it stands out of question that this is the kind of workout that benefits most from an acid buffer like NaHCO(3)!

As a diligent student of the SuppVersity you are no stranger to the ergogenic value of sodium bicarbonate, NaHCO(3) or baking soda, and though I still believe that I have to do a lot of persuading in terms of its stand-alone benefits (click here to read more), many of you will at least have been impressed by its ability to boost the uptake and subsequent performance benefits from creatine supplements (cf. "Supercharging Creatine With Baking Soda"). And while I am not sure if the soon-to-be-published study by Carr et al. will be last straw that's finally going to break your back... ah, I mean your resistance, or I should say, unwillingness to accept that something as cheap and simple as baking soda could outperform 90% of the overpriced supplemental non-starters on the market and will not make you draw water or increase your blood pressure, although it has the bad word "sodium" in its name, I cannot tell, what I can tell you though, is that Benjamin M. Carr and his colleagues from the School of Human Performance and Recreation at the  University of Southern Mississippi in Hattiesburg are spot on, when they say (or write) that their "findings demonstrate ergogenic efficacy for NaHCO(3) during [hypertrophy-type resistance training]" (Kerr. 2012).

The benefits of baking soda start at high intensity aerobic exercise, and end right where your willpower ends ;-)

That baking soda can be an effective ergogenic aid, especially when it comes to high volume workouts has actually long been established. Still many, if not most of the trials involved sprinters or cyclists performing HIIT-esque protocols on the track or cycle ergometer (e.g. 11.5% increase in sprint performance in Price. 2003), whereas researchers such as Portington et al. or Webster et al. totally missed the boat or, I should say, what it means to train, when they had their study participants perform laughable 5 sets of leg presses and measured nothing but a (yet significant) difference in blood pH in response to pre-supplementation (105 min before the test) with sodium bicarbonate (Webster, 1993; Portington. 1998).

Figure 1: Overview of the experimental protocol that was used in the study (based on Carr. 2012)

With four sets of three exercises at the 12RM (not yet Serge Nubret style, I know; see image 1 ;-) and the king of all leg exercises, the squat being one of them, as well as resistance trained study participants who were actually able to lift a weight that would be taxing enough to see a difference, the study design of the Carr study (see figure 1) is yet more of what I would expect to yield results with real world significance for trainees who are not at the gym to chat and show off their latest gymwear, but to train... and as the data in figure 2 goes to show, the results were what these very trainees are looking for:

Figure 2: Lactate, pH, ratio of hydrogen carbonate ions to NaHCO(3) and base excess in blood after, as well as number of total reps performed during the leg workout (data adapted from Carr. 2012)

I freely admit, an overall plus of ~22reps, in other words 1.83 reps per set does not sound like much, but if you think about how long you would have to train to achieve this improvement and/or compare it to the median effect size of weeks of beta alanine supplementation, of which you can hardly say that it was one of the aforementioned supplemental non-starters, and still offers a performance increment of only 2.87% (Hobson. 2012), the 22 +/- 13 reps or 4% increase in total volume the participants in the Carr study achieved within about 2min (by drinking their 22-32g of baking soda) are more than just a bit of alright.

"But isn't the increase in lactate a bad thing?"

"Lactate...?" I knew this would be your next question. I mean it is already hard enough to believe that anything that has the word "sodium" (by the way you Americans are the only ones who don't get that this ought to be "natrium" and not "sodium" ;-) in its name is not per se bad for you, and now the guys in the baking soda group had higher lactate levels!

Image 2: "Cholesterol is the devil and sodium is his little brother!" Everyone who still believes everything the medical orthodoxy says, please raise your hands!

A note on the dangers of "salt": Firstly, baking soda is "only" ~28% sodium, which means that for every 4 grams you ingest you get roughly 1 g of sodium. Secondly, it is arguable how much of the sodium is effectively taken up and will be floating around in your blood. As T. Lakhanisky points out in his dossier for the Belgian government: "The uptake of sodium, via exposure to sodium carbonate, is much less than the uptake of sodium via food. Therefore, sodium carbonate is not expected to be systemically available in the body." (Lakhanisky. 2002) And thirdly, there is more and more evidence that suggests that the chloride rather than the sodium content of common table salt (NaCl = Natrium + Chloride) is the root cause of "sodium induced hypertension" in "sodium sensitive" individuals / animal models. Only recently, a study by Schmidlin et al. showed that chloride loading induced hypertension in the stroke-prone spontaneously hypertensive rat despite profound sodium depletion (Schmidlin. 2010). So, if you asked me, rather than pointing at salt as the #2 on the list of greatest evils (obviously cholesterol is still #1, here) the medical orthodoxy would be better advised to address the imbalances between sodium and potassium (click here to learn more about the ratios), which are so characteristic of the western diet, instead of painting yet another black and white picture where sodium is the bad guy and potassium the dangerous mineral that cannot be sold OTC in dosages >80mg.... but hey, this would be the topic for a whole new blogpost and as gross as it may sound, the chance that you get diarrhea from the baking soda is probably 1000x higher than the remote possibility of increases in blood pressure. A 1990 study by Luft et al. even found that the blood pressure of 10 mildly hypertensive and normal subjects decreased by 5mmHg after 7 days in the course of which they drank 3 liters of sodium bicarbonate containing water per day (Luft. 1990)

Now, you would have reason to be concerned if we were talking about lactic acid, which is basically lactate + a proton (you can also say, lactate is the negative ion of lactate acid if you want to). Contrary to the latter, which increases during exercise when the acid buffer of your musculature is exhausted, lactate is however not just benign, but actually beneficial.

"So lactate is a bonus... really?"

Figure 3: Mean plasma lactate, GH, and prolactin responses to intravenous infusion of 250ml 1M sodium lactate in 7 untrained healthy volunteer; note: the respective increase in GH is more pronounced with natural = exercise induced increases in lactate.

While it's still debated whether lactate is only a beneficial co-factor in the mitochondrial energy chain, as Van Hall proposes in his Y2K review of the research (Van Hall. 2000) or rather a mitochondrial energy substrate in its own right that cannot be used only in the mitochondria of your skeletal and heart muscle but also in your brain, as Pellerin et al. suggest (Pellerin. 2007), it is indisputable that the decreased formation of lactic acid, due to the perseverance of an overall higher alkalinity in the presence of a 4% higher workout volume is a beneficial things. Not the least, by virtue of the its ability to trigger the release of growth hormone (cf. figure 3; Luger. 1992), which could - in conjunction with the increased workout capacity and the supposedly faster post-workout recovery give trainees on a hypertrophy-oriented volume training regimen an edge over the salt-o-phobic competition.

In view of the fact that Carr et al. arrive at the exact same conclusion, before they state that the "ergogenic efficacy" of sodium bicarbonate during "hypertrophy-type resistance exercise" would "warrant further investigation into chronic training applications" (Carr. 2012), we can expect to see a future trial investigating exactly that: How much more will you gain if you repeat this practice for 6-8 weeks? ... I guess, I don't have to tell you that the SuppVersity is going to be the place, where you are going to read about the results of that study, first!

References:

• Carr BM, Webster MJ, Boyd JC, Hudson GM, Scheett TP. Sodium bicarbonate supplementation improves hypertrophy-type resistance exercise performance. Eur J Appl Physiol. 2012 Sep 4.
• Lakhanisky T. Sodium Bicarbonate. OECD SIDS. UNEP Publications. 2002.
• Luger A, Watschinger B, Deuster P, Svoboda T, Clodi M, Chrousos GP. Plasma growth hormone and prolactin responses to graded levels of acute exercise and to a lactate infusion. Neuroendocrinology. 1992 Jul;56(1):112-7.
• Luft FC, Zemel MB, Sowers JA, Fineberg NS, Weinberger MH. Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man. J Hypertens. 1990 Jul;8(7):663-70.
• Pellerin, L., Bouzier- Sore, A.-K., Aubert, A., Serres, S., Merle, M., Costalat, R. & Magistretti, P. 2007. Activity-dependent regulation of energy metabolism by astrocytes: an update. Glia 55, 1251–1262. 
• Price M, Moss P, Rance S. Effects of sodium bicarbonate ingestion on prolonged intermittent exercise. Med Sci Sports Exerc. 2003 Aug;35(8):1303-8. 
• Portington KJ, Pascoe DD, Webster MJ, Anderson LH, Rutland RR, Gladden LB. Effect of induced alkalosis on exhaustive leg press performance. Med Sci Sports Exerc. 1998 Apr;30(4):523-8.
• Schmidlin O, Tanaka M, Sebastian A, Morris RC Jr. Selective chloride loading is pressor in the stroke-prone spontaneously hypertensive rat despite hydrochlorothiazide-induced natriuresis. J Hypertens. 2010 Jan;28(1):87-94.
• Van Hall G. Lactate as a fuel for mitochondrial respiration. Acta Physiol Scand. 2000 Apr;168(4):643-56.

Maximal Intra- & Post-Workout Fat Oxidation With Pause or 90min LISS Between 2x40min Incremental Exercise Bouts?

Image 1: You better don't even think about losing fat, while you cycle!

As a regular reader of the SuppVersity  you know that I don't believe in the idea of "working out to lose fat", at least not if that implies that you would actually try to burn the fat while you are working out ... yeah, right! I am talking about the hilarious concept of the "fat burning zone". I was still amazed, when I came across a paper that's scheduled for the October issue of Journal of Applied Physiology Nutrition and Metabolism (thanks to my friend Sean Casey from CasePerformance, who helped me out on this one) and investigates the effects of two different modes of what initially looked like a novel torture method and then turned out to be somewhat of a comparison of a twice-a-day cardio-workout, as you could perform it during a contest preparation to make weight and it's evil twin brother.

Train insane... and for nothing?

Enough of those metaphors, let's take a closer look at what the 15 healthy, moderately trained male subjects (age 27.4 +/-1; BMI 23.1; body fat 14.4%; fat free mass 63.7kg) were put through (note: all subjects performed both protocols in random order; see figure 1):

Figure 1: Outline of the study protocol; the two trials differed only with respect to the medial part, where the heavy group kept on working out, while the "light" group waited for their second incremental exercise trial.

I guess I don't have to tell you that the upper path, with the additional light intensity steady state exercise in-between was the "evil twin", while the lower one with "only" two bouts of exercise to the anaerobic threshold (when the respiratory ratio RER reaches RER=1) was the lullaby version.

Image 2: Train hard, but make it smart!

Parenteral, ... ah I mean SuppVersital Advisory: Please don't take any of the results or the whole discussion here as an incentive to perform either of these protocols on a daily basis for the rest of your life - especially if the only thing you are allowed to consume during and in between the trial which started at 7-8AM fasted is water (it should be said that this was an experimental necessity here, as everything else would have skewed the results). If you do, I can guarantee that you will be joining the rest of the pack who's sitting in your Dr's complaining about low thyroid, chronic fatigue, or whatever other self-diagnose people who don't want to admit to themselves that they are overtraining will be en vogue then.

So what do you expect the outcome did look like? No, wrong. None of the subjects collapsed... or at least the scientists don't mention that. And let's be honest it's not impossible. I know a couple of people who still believe they had to exercise the fat away who follow a similar protocol ;-) That said, let's see if that's even worth it - I mean do you really burn fat at all when you exhaust yourself like that?

Figure 2: Fat oxidation during the 40min incremental exercise bouts on the cycle ergometer at the beginning (Incr 1) and end (Incr 2) of the trial (data based on Chenevière. 2012)

As the data in figure 2 shows, the answer is straight forward: YES! You do. And surprisingly much, in fact. This is by the way partly mediated by the surprising effect the 90min of LISS had on the "fat max" exercise intensity which is now, in the 2nd incremental exercise trial (Incr 2) 60.9 % of the VOmax, while it is in the "low intensity" trial with the 90min PAUSE instead of LISS at 56.9%. This may sound bad at first, but if you can go faster without shifting to glucose as your preferred fuel this does obviously allow you to burn more fat - and that's exactly what the subjects did during the heavy trial: They derived 9% more of their total energy expenditure from fat and burned 34% more total fat minute per minute - that this would have been meager 8g even if they had been cycling at that high intensity for the whole 45min incremental exercise bout is yet further evidence of the futility of trying to "exercise the fat away"...

So if you can't burn it while you train, what can you do to burn more after you train?

By now, I guess I will have convinced all of you that you won't get ripped by burning an additional 8g of fat while you work out, but what about this EPOC thingy... I mean that "burn fat after you workout concept", what about that? Does it make sense to literally run around all do to make use of that?

Figure 2: Respiratory exchange ratio (lower values = higher percentage of fatty acids oxidized), lactate and heart rate after the second incremental exercise bout (Incr 2; data based on Chenevière. 2012)

Well, if we are honest, the post-exercise data collected right after the incremental exercise bout # (Incr 2, figure 1) is even more disappointing. Ok, the respiratory exchange ratio is minimally, yet statistically significantly lower, but the heart rate the exertion and the lactate levels are much higher. Plus, you cannot tell me that any sane individual would keep on fasting after this torture and in the very same moment you start eating your the "RER advantage" will be lost, anyway.

Image 3: These abs were not sculpted in the "fat burning one"! Click here to read the original article I used this image with, the "Fat Loss Support Routine" from the Step By Step to Your own Workout Routine guide.

So what's the bottom line, here? Aside from another primer on the fallacy of trying to do more, more and once again more, instead of simply getting your diet in check and sticking to it, to lose weight, there is actually a take home message you could derive from the results of this study: Let's assume that - hypothetically, of course - you got to make weight fast and still have more than enough time to recover after this quick weight loss fix before your performance must be back to it's usual heights. In a situation like this, and only as a short time intervention, the additional total energy expenditure during the 90min of LISS and the increased fat oxidation, combined, would make the "evil twin" protocol, with its 2x incremental exercise regimen interspersed by 90min of relatively light cycling in the fasted state, an option, you could even  improve on by replacing the 2x 45 min bouts with 2x20min of HIIT + 2x10min cool-down and guzzling some non-gluconeogenic BCAAs (max. 10g-15g / 45min) while you are putting yourself through this torturous regimen.

References:

• Chenevière X, Borrani F, Droz D, Gojanovic B, Malatesta D. Effects of 2 different prior endurance exercises on whole-body fat oxidation kinetics: light vs. heavy exercise. Appl Physiol Nutr Metab. 2012 Oct;37(5):955-64.

Glutamine, a Better Glucose Source Than Glucose? Can You (Ab-)Use It As an Intra-/Post Workout Supplement? Human Study Suggest: Yes You Can! 8g Will Do the Trick

Could it be better to use glutamine as the main energy source in an intra-workout beverage? Or is the latter superior to glucose, only when it's already to late, meaning only, when you already are hypoglycemic?

I see the irritation on your face. How on earth should glutamine be a better glucose source than glucose: Adel obviously has lost his mind under the pressure of putting out interesting stuff on a daily basis... well, while the latter may be true (how would a sane person do what I do?), I am actually just reformulating the main message of a recently conducted study from the State University of Maringá in Brazil. In the corresponding paper, which was published online in the International Journal of Endocrinology (Nunes Santiago. 2013).

So yes, glutamine is in fact the better glucose...or maybe I should clarify it is a superior source of glucose to promote glycemia recovery after insulin-induced hypoglycemia. In other words, it will help you to lose the dizziness, the tiredness, the shaking and the sweating that are only a handful of the symptoms of low blood sugar (=hypoglycemia) more readily than glucose.

How do the scientists know?

Actually Nunes Santiogo et al. tested not just glucose and glutamine, they also provided their rodents which had been injected with a non-lethal but profoundly hypoglycemic dose of 1U/kg insulin at the beginning of their experiment with either of these substances:

alanine
glutamine, or
saline (control group)
• glucose
• glycerol
• lactate

The dosage was identical (100mg/kg) for all of them, so that we had a "level playing field". Now, if I had not given away all the information right in the headline, you would probably have expected glucose to rule, right?

Figure 1: Glucose (mg/dl) levels after administration of 100mg/kg of saline, glucose (Glu), glycerol (Gly), lactat (Lac), Glutamine (Gln) or alanine (Ala) to hypoglycemic mice (Nunes Santiago. 2013)

What? Your money was on Lactate? Well that's actually a smart choice, as well and shows me that you have been attentive over the past months.

A note on lactate: In view of the results of a recent study that showed that lactate may not be able to completely replace glucose, but can modulate metabolic and neuronal activity in a way that the glucose contribution to brain metabolism under hypoglycemic conditions is restored to levels otherwise only observed at euglycemia (Herzog. 2013), it is likely that it could sooth the symptoms of hypoglycemia without even replenishing blood glucose to normal. Well, as long as it is buffered (NaHCO3 ;-) and is not converted to lactic acid, at least.

Yeah, lactate is an emergency fuel, so it does not seem totally unlikely that it works, but if you take a look at the study outcome in figure 1 you will realize that glutamine was not just a notch, but rather significantly more effective in getting the ~70% reduced glucose levels back up in the normal zone. It's also better than the #1 source of gluconeogenesis alanine, which in turn was still superior to "the real deal", i.e. glucose.

The glucose, diabetics, for example are so desperate to find ("Where's my Snickers?"), when they realize that they are about to go hypo after an insulin injection or workout, on the other hand, brought the levels back up to only 63% and was thus only slightly better than lactate of which I already hinted at in the box to the right that the actual blood sugar levels may not adequately reflect the symptoms, due to it's ability to modulate the energy flux to the brain.

How could that be? Why is glutamine more effective than glucose?

It still sounds odd, I know, so let's see what the scientists have to say about their own results:

"In contrast with rats, oral glutamine showed better glycemia recovery compared with alanine (Figure 1). This difference could be attributed to the possibility that in mice the catabolism of glutamine in the enterocytes is lower than in rats" (Nunes Santiago. 2013)

Now this is a problem, because it makes the usual question of whether or not these results apply to human beings, or not even more difficult to answer. Are we more like rats or rather like mice? And what would be the perfect "blood sugar restoration agent" for us - Glucose or glutamine. I honestly cannot answer this question, but I can still give you a decent bottom line, I guess.

---

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

Bottom line: Irrespective of whether it is "optimal" it is certainly a viable way to keep your glucose up and even replenish your glycogen levels after a workout by supplementing with l-glutamine. In 2005, for example, Iwashita et al. were able to show that 8g of glutamine promote storage of muscle glycogen to an extent similar to 330ml of 8.5% (wt/vol) glucose polymer solution (Bowtell. 1999); and this would not work if the glutamine was not turned into glucose by the liver and transported to the muscle in the blood stream so that it will - at least for as long as it disappeared in the skeletal muscle glycogen stores - also be available for the brain, the heart and all the other organs.


Whether things look different in insulin induced hyperglycemia is questionable, but I tend to think that 99% of you are interested in it's use as a workout / post-workout fuel in exchange for carbs and not so much as a means to save your life, when you you've been overdoing your slin shots.

If that's what you want to do, the optimal strategy would be to combine both. According to Bowtell et al. this will increase the non-oxidative glucose disposal by another +25%. This would also have the advantage that you are not overtaxing the glyconeogenic pathway in the liver. A potential overload of the latter is by the way also the reason why I strongly advise against trying to live off glutamine let alone other not as readily metabolized amino acids as your sole source of glucose (or energy in general).

Additional reads:

• "30g of oral glutamine have similar effects on GLP-1 as 75g of glucose" | read more
• "7 Rarely Thought of Side Effects of High Dose Glutamine" | read more
• "Chronic High Dose BCAA Supplementation Reduces Endurance Performance by 43% Plus: How Ammonia, Glutamine, Arginine & Low Carb Could be Involved" | read more
• "New Role for Glutamine in Protein Synthesis? Study Suggests Direct Effects on Mammalian Target of Rapamycin (mTOR) - EAAs Alone Won't Produce Optimal Results" | read more
• "Use Glutamine to Heal the Gut and Hinder Your Gut Bacteria from Eating Away Your BCAA, Arginine and Other Aminos" | read more

References: 

• Bowtell JL, Gelly K, Jackman ML, Patel A, Simeoni M, Rennie MJ. Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise. J Appl Physiol. 1999 Jun;86(6):1770-7.
• Herzog RI, Jiang L, Herman P, Zhao C, Sanganahalli BG, Mason GF, Hyder F, Rothman DL, Sherwin RS, Behar KL. Lactate preserves neuronal metabolism and function following antecedent recurrent hypoglycemia. J Clin Invest. 2013 May 1;123(5):1988-98. 
• Nunes Santiago A, Ferreira de Godoi-Gazola VA, Milani MF, et al. Oral Glutamine Is Superior Than Oral Glucose to Promote Glycemia Recovery in Mice Submitted to Insulin-Induced Hypoglycemia. International Journal of Endocrinology, vol. 2013, Article ID 841514, 7 pages, 2013.