Exercise, the Healthiest Snack! Study Shows More Than 10% Reduction in 3h Post-Prandial Blood Glucose Levels W/ Intense Exercise (Cardio + Weights) Before Each Meal

That's how your healthy "exercise snack" could look like - just make sure your boss knows that you're doing it to make sure you stay healthy and don't miss a day at the office ;-)

Do you think about having a Snickers® bar right now? Why don't you go and work out instead? Sounds crazy? I know, but a recent study from the School of Physical Education at the faculty for Sport and Exercise Sciences of the University of Otago says: "Dosing exercise as brief, intense ‘exercise snacks’ before main meals is a time-efficient and effective approach to improve glycaemic control in individuals with insulin resistance." (Francois. 2014)

Now the obvious questions are (1) what exactly is a "brief, intense exercise snack" and (2) what can you expect from having it before a meal?

By using HIIT you can achieve similar results as in the study at hand

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To answer these questions we have to take a closer look at the experimental protocol the scientists used. In order to investigate whether three small doses of intense exercise before meals (aka ‘exercise snacking’) would result in better postprandial blood glucose control than a single bout of (energy-matched) prolonged, continuous, moderate-intensity exercise in individuals with insulin resistance, Francois et al. had their, 16 volunteers who met the inclusion criteria of being aged 18–55 years and not being medicated for blood glucose or high blood pressure participate in all of the following experimental conditions:

• 

  SuppVersity Suggested Read: Short Bursts of High Intensity Circuit + Plyometric Training Keeps Blood Sugar "In the Zone" - No Matter If Your Parents Were Obese Diabetics, Or Lean Athletes | Learn more about the effects of HIIT on blood sugar control @ www.suppversity.com!

  Traditional continuous exercise (CONT) -- Participants com pleted one 30 min bout of treadmill walking at a moderate intensity (60% HRmax) 30 min before their evening meal (dinner) in accordance with current physical activity guide lines (WHO. 2010). Every 5 min, HR (Polar S810i; Polar Electro, Kempele, Finland) was measured, a rating of perceived exer tion (RPE, using the BORG 6-20 scale) was made and the work rate was adjusted accordingly.
• Exercise snacking (ES) -- Six 1 min work bouts, consisting of walking at 90% HRmaxwith 1 min recovery (slow walk) between each, were completed 30 min before breakfast, lunch and dinner. The total energy cost for CONT and ES were matched (based on metabolic calculations inV˙O2max test). The exercise was undertaken on an incline treadmill, with HR and RPE measured at the end of each interval.
• Composite exercise snacking (CES) -- Six 1 min work bouts alternating between walking and resistance-based exercise were performed, with 1 min recovery between each bout, 30 min before breakfast, lunch and dinner. The total number of 1 min work bouts balanced the ES regime. The resistance based exercise bouts were undertaken using resistance bands (as many reps as possible within 60 s), and walking was at 90% HRmax on an incline treadmill, with HR and RPE measured at the end of each interval. The resistance-band exercises worked the musculature of the arms, back and core. All exercise sessions included a 5min warm-up period and a 3 min cool-down period at a self-selected intensity on a treadmill.

To ensure an equal playing ground for all three types of "snacks", the timing of the three meals was identical between the three exercise trials.

Table 1: Total daily macronutrient intake for the participants’first experimental trial (Francois. 2014)

"For their first trial, participants consumed their habitual diet under free-living conditions while completing a 5-day dietary log. The diet was then replicated for the second and third trials, so that timing, composition and quantity of all food and drink consumed were matched between the three trials. Subsequent dietary analysis (Kai-culator Enhanced 2010 Food Composition Database v0.43; Dunedin, New Zealand) for the main days of interest is shown in Table 1. Physical activity levels for the three trials were monitored using pedometers and activity logs." (Francois. 2014)

As you can see in Figure 1, the exercise snacking protocols lowered the mean postprandial glucose (PPG) following breakfast (by 1.0±0.9 mmol/l [mean ±SD]) and dinner (by 0.5±0.8 mmol/l) but not following lunch (−0.0±0.7 mmol/l). Previous studies with somewhat more intense regimen showed improvement irrespective of the time of the day (Devlin. 1985), though. If you don't stick to running 1.2k, but hop on a treadmill for 3-5 sets of 1 min all out running or a tabata style workout, you should see improvements on every meal.

Figure 1: The 3 h PPG AUC for breakfast (a), lunch (b) and dinner (c) on the exercise day for CONT, ES and CES trials. Data are means ± SD,n=9. *p<0.05 for ES vs CONT for breakfast and dinner PPG AUC (Francois. 2014)

The interaction between meal and exercise was, as the scientists point out, quadratic-by-time (p=0.05), with the highest PPG concentration, and reduction with exercise, observed in the morning and evening, and the lowest after lunch. In contrast, CONT had no effect on 3 h mean PPG at any time point (bearing in mind that CONT also served as a control condition for breakfast PPG and lunch PPG on the exercise day).

Figure 2: Over the whole 24h the reduction in blood glucose was most pronounced in the "composite" exer- cise snacking trial, where the subjects performed a combination of aerobic and resistance exercise ~30 min be- fore their three meals (Francois. 2014)

Bottom line: If you snack, you better do it intensely. Intensely as in "heavy", not as in "super sweet". So forget about the initially mentioned snickers or whatever other dietary snack may have been on your mind. Grab some resistance bands and get out and run to the next best green area to show the slackers why you're lean and fit and not fat and sick ;-)

Before you get all fired up for the idea of "exercise snacking", I would yet like to remind you that it may not be feasible before each and every of your meals. So, be careful not to obsess about being able to eat only after a mini-workout, ah... exercise snack. Why? Well, it's a pretty short way from dedication to obsession and "having to work out before every meal" is a first and huge step towards an eating disorder that will make your life more miserable, but not of healthier | Comment on Facebook.

References:

• Devlin, J. T., and E. S. Horton. "Effects of prior high-intensity exercise on glucose metabolism in normal and insulin-resistant men." Diabetes 34.10 (1985): 973-979.
• Francois, Monique E., et al. "‘Exercise snacks’ before meals: a novel strategy to improve glycaemic control in individuals with insulin resistance." Diabetologia (2014): 1-9.
• World Health Organization. "Global recommendations on physical activity for health." (2010).

Vitamins B1, B2, B5 & B6 & Glucose Management | Part VII of the "There is More To Glucose Control Than Low Carb"- Series. Any Real Benefit From Supplementing With "Bs"

Funny or obscene? A woman w/ low vitamin B and thus fortified cornflakes is among the "top images" Google will show you, when you search for B-vits

There is an often overlooked reason I am addressing thiamin (B1), riboflavin (B2), panthotenic acid (B5) and pyridoxine (B6) in one installment of the "There is More to Glucose Control Than Carbohydrates"-Series (read previous installments): They are all necessary to store glycogen in the liver (Supplee. 1942).

In general, a whole foods diet, as recommended in previous SuppVersity articles will easily cover the B-vitamin needs of the average sedentary and physically active individual - in spite of minimally increased requirements for B2 & B6, in particular (Manore. 2000; Woolf. 2008).

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As a SuppVersity reader you do yet know that "adequate" and optimal intakes can differ significantly and the fact that the provision of additional B-vitamins does not have ergogenic effects does not exclude the possibility that it may have beneficial effects on blood glucose management.

The initially mentioned inability to convert glucose to glycogen and to store the latter in the liver, for example, would already set you up to increases in blood glucose levels. The latter will in turn increase the urinary loos of the water-soluble vitamins, so that a deficiency in one of the initially named B-vitamins could trigger a whole "pro-diabetic" cascade that leaves the by then (pre-)diabetic individual deficient even in those of the B-vitamins of which he or she is actually getting enough from his or her diet (+ supplements).

Annual spending Alzheimer patients >65y in the US from 2010 to 2050 (projection, in billion U.S. dollars;  Alzheimer's Association. 2010)

This article is exclusively about the beneficial effects of b-vitamins on glucose control: The conclusions I draw based on the evidence presented in this article do not affect potential cognitive benefits from "optimal" (=within the RDA) intakes of B-vitamins (in particularly folate, and B-12, which are not part of this overview, anyway) in the young (Herbison. 2012) and old , where they are furthermore "confined to participants with high homocysteine (above the median, 11 µmol/L) and that, in these participants, a causal Bayesian network analysis indicates the following chain of events: B vitamins lower homocysteine, which directly leads to a decrease in GM atrophy, thereby slowing cognitive decline" (Douaud. 2013).

Conclusive evidence for anti-diabetic or insulin-sensitizing effects of B-vitamin supplements is yet still scarce. Even the notion that (pre-)diabetics suffer from low levels of the said B-vitamins is still controversial. This does not mean, though, that there were no promising study results I could report. For thiamine, for example, ...

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  Figure 1: Effects of lipophilic thiamine on HbA1c (top) and insulin requirements (bottom) of type I diabetics (Valerio. 1999(

  Valerio et al. report that the provision of a lipophilic form of thiamine (benzoyloxymethyl-thiamin) at 50mg/day lead to improvements in HbA1c and reduced insulin requirements in children with type I diabetes (Valerio. 1999) - the difference between the active and the placebo arm of the study did yet not reach statistical significance
• Obrenovich et al. report in a 2003 that thiamine, or rather benfothiamine bocks the oxidative damage due to the presence of excessive amounts of glucose in the blood of a rodent model of diabetes - their results have been replicated in human studies by Stirban et al. an other researchers several times over the past decade (Stirban. 2006)

Corresponding evidence for riboflavin is hard to find. While there are studies that suggest the presence of reduced levels of this b-vitamin in both type I and type II diabetics, direct beneficial effects of vitamin B2 supplementation on glucose management have not been reported.

A very similar picture, i.e. reduced levels in type II diabetics, but no reports of direct metabolic benefits from the provision of supplemental vitamin B5 from randomized controlled human trials, emerges if you do a database search for panthotenic acid.

Figure 1: 2h glucose and insulin response to oral glucose tolerance test before (white) and after 25 days of B5 depletion (red), as well as during B5 refeed (violet) in a healthy male subjects (Bean. 1995)

The results of a study from the mid 1950s, when scientists still put healthy individuals on nutritionally deficient diets still indicate. After 25 days without significant amounts of panthotenic acid in the diet, the subjects' insulin sensitivity was notably compromised (Figure 1, red) and was not normalized within only 10 days on a diet with 133x the normal amount of panthotenic acid (Figure 1, violet).

Mind the vitamin <> vitamin interactions: Even if there is no reason for high dose pantothenic acid supplementation to inhibit the cellular uptake of glucose directly, it's well possible that it messes with glucose metabolism via interactions with other water solube vitamins like vitamin B6 aka pyridoxin, the excretion of which is increasing, whenever the intake of panthothenic acid exceeds an (in humans undetermined) sane threshold.

In fact, the extreme elevation of the insulin levels in the "reload phase" would rather suggest that extreme amount of vitamin B5 will compromise, not improve your insulin sensitivity - contrary to edema, severe fatigue, joint pains, reduced protein metabolism, reduced phosphorus, raised VLDL triglycerides, calcification (from calcium pantothenate), dehydration, gastrointestinal symptoms, and depression, a decreased insulin sensitivity is yet not on the "official list of side effects"* of high panthotenic acid intakes (*by "official" I refer to the lists everyone copies ad pastes from the major health information outlets on the Internet).

And what about B6? It's in all my supplements, so it must be good!

If I had to write the bottom line to today's installment of the "There is More to Glucose Control Than Carbohydrates" series now, it would probably be very short and certainly very disappointing for the various supplement junkies out there. Luckily (?) there is still one of the B-vitamins missing: Pyridoxine or vitamin B6 - and you should expect the only B-vitamin that can produce severe toxic effects when it is consumed in very high amounts chronically (peripheral nerve damage) should be able to bring about at least minimal increases in insulin sensitivity / cellular glucose uptake, as well, right?

Well, unfortunately, that's not the case. In 1980, already, a group of scientists from the Gandhi Medical College Hospital in India were able to show that the provision of 40mg of pyrodixine per day had "did not bring about any significant alterations in either the oral glucose tolerance or the insulin response to glucose" in thirteen adult maturity-onset diabetics - and that in spite of the fact that 7 of them were actually vitamin B6 deficient!

Mind the "hidden" B-sources: If you are still concerned that you may not be getting your Bs in, you are probably an OTC supplement junkie. In that case I suggest you briefly take a look at the pre-workout, post- workout and whatever other products in your stack... what? Oh, they all contain 10x the RDA and more of these B-vitamins - that's surprising, right?

A major disappointment? Although this article focused exclusively on the benefits of the water-soluble B-vitamins on glucose control, the results are still paradigmatic for the overall "potency" of vitamin-B-supplements. They are all the rage, but the benefits are overblown, in many cases simply non-existent.

If we discard the well established beneficial effects of benfothiamine on the side-effects of elevated blood glucose levels, and the highly disputed benefits of pyridoxine in diabetic peripheral neuropathies (alleviation of sympthoms, no change in nerve damage; Bernstein. 1988 & 1990), there is actually no reason to even consider taking extra amounts of any or all of these vitamins if you are (a) no diabetic and (b) no junk food eater - and let's be honest, if either (a) or (b) applies you have got more important issues to deal with than potentially suboptimal B-vitamin intakes and their effects on glucose tolerance.

Reference:

• Bean, William B., et al. "Pantothenic acid deficiency induced in human subjects." Journal of Clinical Investigation 34.7 Pt 1 (1955): 1073. 
• Bernstein, A. L., and C. S. Lobitz. "A clinical and electrophysiologic study of the treatment of painful diabetic neuropathies with pyridoxine." Current topics in nutrition and disease (USA) (1988).
• Bernstein, Allan L. "Vitamin B6 in clinical neurology." Annals of the New York Academy of Sciences 585.1 (1990): 250-260.
• Herbison, Carly E., et al. "Low intake of B-vitamins is associated with poor adolescent mental health and behaviour." Preventive medicine 55.6 (2012): 634-638.
• Manore, Melinda M. "Effect of physical activity on thiamine, riboflavin, and vitamin B-6 requirements." The American journal of clinical nutrition 72.2 (2000): 598s-606s.
• Supplee, G. C., R. C. Bender, and Z. M. Hanford. "Interrelated vitamin requirements. The influence of thiamin, riboflavin, pantothenic acid and vitamin B6 on liver glycogen reserves." Journal of the American Pharmaceutical Association 31.7 (1942): 194-198.
• Valerio, G., et al. "Lipophilic thiamine treatment in long-standing insulin-dependent diabetes mellitus." Acta diabetologica 36.1-2 (1999): 73-76.

Polydextrose and Resistant Maltodextrin as Dieting Aids W/ GLP-1 Boosting & Appetite Reducing Effects: 7% Reduced Energy Intake per 10g/day of Polydextrose in Clinical Trials

Many of them look like powder sugar, but they are much more. Novel food ingredients like polydextrose or resistant maltodextrin may help us to slow the progression of obesity, but they won't solve the global obesity problems.

Whenever we are talking about resistant starches, we are not actually interested in the starches themselves, but rather in what happens after they are digested by the bacteria in our guts. The result of this process are short-chain fatty acids. These specific fatty acids interact with receptors in the digestive tract which in turn trigger the release of GLP-1, of which you as a SuppVersity reader have long known that it is of paramount importance for glucose and weight control (learn more).

Next to naturally occuring resistant starches in foods like cooled potatoes or green bananas and relative expensive high molecular weight designer starches, polydextrose and resistant maltodextrose constitute two promising food ingredients of which researchers believe that they may help us to keep the obesity epidemic at bay.

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Resistant maltodextrin (RMD) is a water-soluble, non-viscous and non-digestible saccharide. Like polydextrose, resistant maltodextrin has previously been reported to improve the glycaemic response (12,13) and postprandial TAG elevation (14), and also promotes mineral absorption (15). The mechanisms involved in the improvement of glucose tolerance, however, are poorly understood.

Accordingly, the goal of Tohru Hira et al.'s latest study was to examine whether these effects that have been observed in both human and rodent studies, previously, could be mediated by changes in plasma GLP-1 levels and GLP-1 production in the small and large intestines.

Figure 1: Glucose levels after glucose load (A), changes in glucose (B) and total GLP-1 and active GLP-1 levels (C, D) with different amounts of resistant maltodextrin or fructo-oligosaccharides in the diet of the rodents (Hira. 2015).

If you've read the introductory paragraph of this article, you will not be surprised to see that the data from the Hokkaido University in Japan shows that the ingestion of resistant maltodextrin lead to dose-dependent (more = better) increases in GLP-1 in the blood (Figure 1, C-D) and the intestine (not shown), as well as corresponding improvements in glucose control (Figure 1, A-B).

Do not make the fatal mistake to believe that increasing your resistant starch intake alone will help you lose weight. Unless the increases in GLP-1 make you eat less food, you will -just like the rodents in the study at hand- not lose a single pound of body fat. In addition, polydextrose and probably also resistant maltodextrin - like many of the sugar replacements - has the nasty side effect of giving you the run if you consume high doses in isolation (Flood. 2004). So, if you want to use them, use them wisely.

In that, it is particularly important that the benefits the healthy rodents derived from the ingestion of resistant maltodextrin was significantly more pronounced than the benefits of fructo-oligosaccharides which have likewise been hailed as potential obesity preventers (Arora. 2013).

Speaking of obesity preventers,...

you are probably already wondering about the other "obesity preventer" I mentioned in the headline: Polydextrose, a a glucose polymer that is completely soluble in water and is used asa food additive to give foods the texture of sucrose at 75% lower calories in over 60 countries.

The effects and potential benefits this agent which is usually labeled as "fiber" on the label of commercially produced foods have recently been reviewed by scientists from the St Luke’s Roosevelt Hospital Center in New York (Ibarra. 2015). As of now, we know from several individual studies that polydextrose has the ability to reduce energy intake, but until now, no one had systematically reviewed the disparate evidence on this topic.

Figure 2: Calculated slopes of the effects of adding polydextrose to the diets of men and women on their food intake at lunch (left) and over 24h (right) - individual study results are represented as dots (Ibarra. 2015).

With the study by Ibarra et al. (2015) this review is now available and it shows significant effects on food intake at lunch (Figure 2, left) and total 24h food intake (Figure 2, right). Only the food intake at dinner was not significantly influenced in the few hitherto existing amply controlled clinical human trials (not shown in Figure 2).

A closer look at the data in Figure 2 does also show that there was - just like it was the case for the GLP-1 response to resistant maltodextrin ingestion in the Hira study - a dose-dependent increase in satiety with the ingestion of only 25g of polydextrose per day being able to reduce the total 24h food intake by more than 12%! Based on linear regression analysis the Ibarra et al. calculated the average decrease in food intake over 24h to be 3.8% and 2.3% per 10 gram of polydextrose consumed in men and women respectively. Significantly more pronounced effects were observed in studies investigating the effects of polydextrose ingestion at breakfast on food intake during an ad-libitum lunch which was reduced 7% and 5.7% per 10g in men and women.

According to the first meta-analysis of the existing human clinical trials consuming 10g of polydextrose per day leads will significantly decrease the food intake. The data does yet also show: Women benefit to a lesser degree than men.

Bottom line: There is little doubt that the consumption of increased amounts of resistant starches and more specifically GLP-1 boosting and appetite reducing resistant maltodextrin and polydextrose may help you to lose / control the amount of body fat you are carrying.

It is unrealistic, however, to assume that adding 20g of either of the agents to your diet would be sufficient to trigger significant fat loss in the absence of other lifestyle changes. It is furthermore interesting to observe that - once more - women appear to benefit less from the appetite reducing effects of these agent and that despite the fact that the relative contribution of 20g of these agents to the total food intake of a woman is lower than it would be for a man who obviously consumes more food | Comment on Facebook!

References:

• Arora, Tulika, Satvinder Singh, and Raj Kumar Sharma. "Probiotics: Interaction with gut microbiome and antiobesity potential." Nutrition 29.4 (2013): 591-596.
• Flood, M. T., M. H. Auerbach, and S. A. S. Craig. "A review of the clinical toleration studies of polydextrose in food." Food and chemical toxicology 42.9 (2004): 1531-1542.
• Hira, Tohru, et al. "Resistant maltodextrin promotes fasting glucagon-like peptide-1 secretion and production together with glucose tolerance in rats." British Journal of Nutrition (2015): 1-9.
• Ibarra, Alvin, et al. "Effects of polydextrose on different levels of energy intake. A systematic review and meta-analysis." Appetite 87 (2015): 30-37.