Appetite Short News: Pavlovian Conditioning at Work in the Obese | Polydextrose as a Satiety Promoter | Parents, Just Like Their Kids, Fall for All the Tricks of the Food Industry

Too lean for Pavlovian Conditioning.

In today's "appetizing" installment of the short news, I have picked three of the latest publications from the scientific journal Appetite, of which I thought that they were newsworthy. In that, I cover the Pavlovian Conditioning of overweight individuals, the benefits of polydextrose on appetite control and the way product labels fool parents and children into buying unhealthy foods.

I have to admit: It's not all practically applicable, but who knows maybe you can use it to smart-ass during the holidays. Or maybe you bake some polydextrose enhanced super-satiating cookies for your family, ha?

More facts for your smart-ass sessions on the holidays ;-)

Bugs Dictate What You Crave

Sweeteners & Your Gut

Foods, Not Ma- cros for the Gut

Lactulose For Gut & Health

Probiotics Don't Cut Body Fat

The Macrobiotic MaPi2.0 Diet

• Hedonic food cue conditioning in the obese: You know the story about Pavlov's dog starting to salivate, when the bell rang that would usually accompany his next feeding?
  
  Well, a recent study confirms that something very similar is at work in obese, but not lean subjects. While the former remain calm and cool to a visual cue that had previously been given alongside some tasty chocolate milk, the latter began to swallow, a reliable sign of increased salivation. As the scientists from the Allaint International University in San Diego say, these "
  

  are the first results to show differential acquisition of Pavlovian conditioned responding in overweight individuals compared to lean individuals" (Meyer. 2014)

  The fact that the conditioning worked was yet not the only significant finding, Meyer et al. made. They also observed that hedonic food stimuli were significantly more effective 'conditioners' in the obese than neutral stimuli.
  
  Practically speaking the observations the researchers from the Allaint International University in San Diego made, may partly explain the difficulties obese individuals who may have been conditioned / conditioned themselves to hedonic food stimuli for their whole lives have when it comes to controlling their energy intake.
• Polydextrose as a satiety promoter: In their meta-analysis of the current literature on the effects of polydextrose on energy intake, researchers from the US and Finland found that...
  
  • polydextrose consumed with a mid-morning snack reduces energy intake (EI) at lunch time.
  • this reduction in EI at lunch time occurs in a dose-dependent manner.
  • but the energy intake during the rest of the day did not show any difference
  Now this probably wouldn't be newsworthy, then, if a a regression model had not been able to confirm a dose-dependent effect on the reduction of daily energy intake.

Added polydextrose reduces the insulin response to milk (Lummela. 2009)

What exactly is polydextrose? Polydextrose is a glucose polymer that is completely soluble in water. As a food additive it offers the texture of sucrose but provides only 25% of the equivalent energy, or 4 kJ/g. It has been approved for use in foods in over 60 nations and is recognized as a dietary fiber in more than 20 countries (FAO/WHO, 2009). Next to the reduced energy content it has another benefits of the fibrous substance is that its addition to foods like milk can reduce the insulinogenic response to this meals significantly - even in healthy individuals (Lummela. 2009).

• More specifically, the meta-analysis was able to show that the dose of polydextrose consumed correlated significantly with the reduction of nergy intake at lunch (−0.67 Polydextrose (g/day) | 80% correlation; P < 0.01), due to which the energy intake was reduced by 1% per 2.86g of polydextrose per day.
  
  As Ibarra et al. point out, the sex-specific results are consistent with results for the whole group - the effect is thus similarly pronounced in both men and women. Accordingly, the meta-analysis "supports the notion that the consumption of polydextrose reduces voluntary energy intake at a subsequent meal" and that "this reduction in energy intake occurs in a dose-dependent manner" (Ibarra. 2014).
• Parents of preschool children make (non-)sense of front-of-package visuals and claims on food - A recent study from the Colorado State University and the University of Illinois at Urbana-Champaign investigated what parents make of the colorful packaging of foods their kids like to buy and found that most of them tend to "accept misleading front-of-package claims when making quick food decisions" (Abrams. 2014).
  
  

  

  Parents fall for unwarranted claims, and misleading images children for cartoons.

  While playful visuals appeal to children, parents associate them with junk food. That does yet not mean that they would not fall for health claims, realistic graphics, and natural claims which make them classify the junkfoods that were investigated in the study at hand as healthier.
  
  Fruit graphics in particular were misunderstood to indicate that the respective foods actually contained fruit, when they were simply meant to communicate flavors, instead. Against that background it's not surprising that the unsettling result of this study in 28 women and 2 men revealed that "[parents may make unhealthy food choices as a result of front-of-package information" (Abrams. 2014).

Intensity is key to reduce the exercise induced increase in appetite | more

Bottom line: I understand very well that for most of you only news item #2 is of practical value. Item #1, on the other hand, is rather a description of the misery than a solution and #3 is something that you as a SuppVersity reader probably knew, already... that being said, simply adding more polydextrose to the foods dumb parents buy for their kids because there are fruits on the packaging is not going to help their kids becoming overweight adults who begin to salivate, whenever they see the right food cues. A long-term solution to the problem would thus have to start with the production of healthier foods by the food industry and the education of the public who would then no longer fall for the unwarranted health claims on the packaging of children and adult food products | Comment on Facebook!

References:

• Abrams, Katie M., Caitlin Evans, and Brittany RL Duff. "Ignorance is bliss: how parents of preschool children make sense of front-of-package visuals and claims on food." Appetite (2014).
• Ibarra, Alvin, et al. "Effects of polydextrose on different levels of energy intake: a systematic review and meta-analysis." Appetite (2014).
• Lummela, Netta, et al. "Effects of a fibre-enriched milk drink on insulin and glucose levels in healthy subjects." Nutrition journal 8.1 (2009): 45.
• Meyer, Monica D., et al. "Pavlovian conditioning to hedonic food cues in overweight and lean individuals." Appetite (2014).

Sucralose, Hazardous or Innocent? Part II: Appetite, Gut Health & Food Reward | Sucralose, Gluttony & Adiposity?

Plain mineral water is still the best thing to quench your thirst.

Today we are going to continue our thorough, educated reading of the recently published overview over the biological issues with sucrolase, a "popular" artificial sweetener most of you will probably know by its brand name Splenda. The focus of part I of this series was on the potential pro-diabetic effects of this agent that belongs to a class of molecules that has originally been hailed as a solution to the diabetes problem (it goes without saying that I am talking about artificial sweeteners here, right?). In a way we are thus only continuing the discussion, when we are trying to verify Schiffman's & Rother's argument that the consumption of sucralose is associated with an increase in obesity risk... or, put more simply that using sucralose is going to make you fat, not lean.

The good old "energy in" vs. "energy out" argument

As SuppVersity readers you are well aware that the oversimplified concept of an "energy balance" is fundamentally flawed. My recent post "Anorexia study suggests: Your body can easily reduce its resting metabolic rate by 10%" in the SuppVersity Facebook News is only one out of thousands of scientific papers you could quote to point out that replacing 420kcal of energy from pure sugar, i.e. three cans of regular coke, with its diet variety is not going to produce a net weight, let alone fat loss of 420g per week (suggested read: "Busting the 3,500kcal = 1lbs Weight Loss Myth!" | learn more).

This is part II of a multi-part series:

Sucralose, insulin, glucose, GLP-1

Appetite, Obesity & Gut Health

Cancer, Drug & Hormone Interact.

I know that Mark Sisson likes to says this, but this website is not written by a machine, but by a man who has the same "short" 24h days you have... basically, what I am trying to say is that I had to split this review of the review into a "trilogy" - and be honest, you wouldn't want an article thrice as long as this one, would you?

Thus being "in the know", you can only shake your head, when you read how Schiffman and Rother (ab-)use a recent study by Ruyter et al. (2012) to support the non-significant, not sufficiently differentiated data from epidemiological studies which inform us that obese people are more likely to consume artificial sweetened products than lean ones, to subliminally imply that artificial sweeteners would not help, in some cases even hinder weight loss.

"In an 18-mo trial with children, participants were randomly assigned to receive an 8-oz can per day of either a noncalorically sweetened or a sugarsweetened beverage that provided 104 kcal (de Ruyter et al., 2012). [...] The calorie consumption from these beverages was 46,627 kcal greater for children in the sugar-sweetened group than in the sucralose-sweetened group (5.8 × 77.3 × 104). In spite of this highly significant difference in calories consumed from the beverages, the total weight gain over this 18-mo study was only 1 kg greater for children in the sugar-sweetened group compared to sucralose group. No explanation was provided to account for the small difference in weight gain given the large difference in caloric consumption from the beverages." (Schiffman. 2013)

Despite the fact that Schiffman & Rother acknowledge that the scientists would not have been able to detect, if the children who consumed the sugar-sweetened beverages compensated by reducing their food intake, the reviewers fail to point out that neither this, nor the second "evidence" they cite, a 2-year study by Ebbeling et al. (2012), where Schiffman & Rother simply ignore the fact that the mere provision of diet sodas to the families of the adolescent subjects did reduce the weight gain in the active intervention period (1st year, see Figure 1, below), would confirm a negative real-world effect on body weight.

Figure 1: Change in body fat percentage (vs. basleline) of adolescents during the intervention & follow up period in the Ebbeling study (2012), of which the reviewers only cite the results of the follow up.

Let's be honest: If you actually take a look at the results from the Ebbeling study (Figure 1), you will have to concede that this study refutes the claim that artificial sweeteners make you fat. During the active treatment period, in the course of which the adolescent participants were...

• 

  "What Really Happens, When Nutrition Science Meets Real Life" | more

  ... supplied with noncaloric beverages (e.g., bottled water and “diet” beverages for the whole family) every 2 weeks, getting monthly motivational telephone calls with parents (30 minutes per call), 
• ... having three check-in visits with participants (20 minutes per visit), and 
• ... receiving written intervention messages with instructions to drink the delivered beverages and not to buy or drink sugar-sweetened beverages, were mailed to participants

...they do exactly what we originally expected them to do: They ameliorate the body fat gain in the adolescent subjects. In other words: As long as respective products are available, and dietary adherence is encourages, replacing regular sugar sweetened with artificial sweetened or unsweetened beverages can have a significant ameliorative effect on the body fat gains of adolescents - irrespective of the fact that they were obviously free to compensate with chocolate, cookies, etc..

Contemporary evidence from RCTs suggest either no, or beneficial effects

If you follow Schiffman's and Rother's lead and discard potential differences between sucrose and other sweeteners, acknowledge the fact that the results from previous rodent experiments have repeatedly failed to translate to human beings and take into account that this data is "inconsistent and conflicting" (Schiffman. 2013), anyways, you will be hard pressed to find arguments to support the claim that artificial sweeteners could hinder weight loss.

"No-Carb Foods, Artificial Sweeteners & The Cravings" | more

Potential mechanisms for the obesogenic effects: In a very detailed review Mattes & Popkin list a whole host of hypothesis ranging from the disproven stimulation of insulin and differences in the GLP-1 response, over osmotic effects and increase food palatability, up to the "Zero sugar, great, I'll have 10 instead of one of those cookies!" effect and the development of an extremely sweet tooth. What's important, though, is that none of this mechanisms is "supported by the available evidence, although some warrant further consideration" (Mattes. 2009).

In fact, the vast majority of RCTs clearly supports the assumption that non-nutritive sweeteners (NNS), artificial or not, promote weight loss and blunt weight (re-)gain (De la Hunty. 2006; Bellisle. 2007). The argument that these effects do satisfy the calories in vs. calories out hypothesis is pathetic, to say the least. Even a 100% controlled diet won't comply to an equation that is about as accurate as "1+2=343". We can thus register that:

1. There is ample evidence to support the beneficial effects of artificial sweeteners (including sucralose) as a tool during controlled dietary interventions.
2. There is insufficient evidence to support the claim that their regular consumption has a negative effect on body weight.

With respect to (2) we would even have to say that the limited amount of useful* evidence we have would rather suggest beneficial than detrimental effects (*a 'useful' study is not a study that tells me that obese individuals are more likely to consume artificially sweetened products than lean ones like the often cited epidemiological data). This is particularly true, for controlled interventions where sugar-sweetened beverages were replaced by their artificially sweetened counterparts.

The great unknown: Hunger, appetite and food reward

If data on the real-world effects of sucralose consumption on body weight gain is "scarce", consistent, experimentally verified hypotheses that would explain the potential underlying mechanism are quasi non-existent... or, I should clarify: They are still in their infancy. Against that background it's quite astonishing that more and more people appear to take it for granted that the consumption of artificially sweetened foods will mess with both, (a) your ability to control your energy intake and (b) the hedonistic response you derive from foods.

Table 1: Sweetness, dose to stimulate the sweet taste receptor (EC50; based on Matsuda. 2011) and correlation of sweetness and EC-50 value.

It goes without saying that there is no sucralose-specifc data out there, but the decrease in hypothalamic sweet taste receptor density I mentioned in the first installment of this series is something I'd expect to see in response to all artificial sweeteners that make it across the blood brain barrier (Note: Even Schiffman & Rother acknowledge that we do not know if they even do that!) - probably "sweetness" dependent,  by the way.  This would imply that sucralose would be the worst, cyclamate the least offender among the common artificial sweeteners in Table 1. With a sweetness that's 300x higher than that of sucrose, stevia would end up being the "(un?)happy medium".

Despite the fact that Schiffman & Rother don't really address this issue in their paper, I still want want to address the practical and thus relevant aspect of the various proposed theories for potential sweetener-induced increases in energy consumption.

Figure 2: Mean effective change in energy intake (%) in RCTs investigating the degree of energy compensation in response to the provision of artificial sweetened products (De la Hunty. 2006)

As the data from De La Hunty's 2006 meta-analysis of 32 study outcomes in Figure 2 clearly demonstrates, there is a statistically highly significant (p < 0.001) trend towards reduced energy consumption in the RCT [randomized controlled trial]. In that, the degree of compensation for the sudden energy reduction due to ingestion of calorically less dense, since artificially sweetened product ranged from statistically non-significant 18% to statistically highly significant 86% in trials such as Porikos et al. (1982), where 6 men lost and gained 0.8kg of body weight within 2x12 days in a metabolic ward on artificially sweetened and sucrose sweetened ad-libitum diets, respectively.

Non-nutritive sweetener (NNS) intake 1965-2004 (Mattes. 2009)

So, sweeteners can't ever make you hungry? I would not necessary subscribe to this idea. While the consumption of artificial sweetened foods as part of your regular diet, e.g. diet coke with your dinner, does not seem to be a problem, Mattes & Popkin (2009) rightly point out that "non-energy-yielding products may heighten appetite", when they are not "ingested in conjunction with other energy sources". So, if you are guzzling diet coke all day, this may very well trigger binge eating. With an ever increasing consumption of sweeteners from partially / totally artificially sweetened beverages (see table to the left), this could thus well be part of our obesity problem.

Just like the previously discussed (relatively short term) effects on insulin, GLP-1 and co, the #2 on the list of most frequently heard objections against the use of artificial sweeteners, i.e. dietary overcompensation, does thus appear to have little basis in fact. What we do not know, though, is whether the results will be identical for all types of sweeteners, or whether sucralose may be the toxic (this aspect will be covered in the next installment) or gut microbiome disrupting exception to the rule.

Sucralose induces changes in the gut microbiome

The last issue I want to address in this second installment of the "Sucralose, Hazardous or Innocent Trilogy" will thus revolve around the question, whether a modulatory effect of sucralose on the microbial composition of your gut could induce potential negative long-term effects that would not show up in the hitherto discussed RCTs.

Under the headline "Effect of Sucralose on the Number and Relative Proportions of Different Intestinal Bacterial Types", Schiffman & Rother argue that it has long been known that bacteria from the oral cavity and soil cannot use sucralose as a growth substrate. If the same was true for the bacteria in our guts the replacement of regular sugar with sucralose would thus starve our (beneficial) subtenants.

Table 2: Differences (%) in bacterial counts in feces of rodents on diets containing what in human terms would be ~14mg, 43mg, 71mg and 156mg of sucralose per day after 12 weeks treatment and 12 weeks into "recovery" (Abou-Donia. 2008)

Based on the fecal bacterial count of rodents on diets that would be equivalent to 14mg, 43mg, 71mg and 156mg of sucralose per day in human beings (see Table 2), Schiffman & Rother argue that chronic (12-week) ingestion of relatively low amounts of sucralose (a single can of Diet Crush Cream Soda, for example, has 42mg of sucralose) lead to highly significant reductions in the numbers of total anaerobes, bifidobacteria, lactobacilli, Bacteroides, clostridia, and total aerobic bacteria.

In view of the fact that Abou-Donia et al. (2008) observed the most significant losses in bifido- and lactobacillus strains, i.e. those strains that have repeatedly been implicated as the driving forces of the beneficial health effects of probiotic supplementation, this and not the previously discussed pro-diabesity effects should be the point where people start to freak out.

Table 4: Other sweeteners are preferred food for certain bacteria and may also alter the gut microbiome (Payne. 2012).

This is particularly true if you take into account that at least part of the beneficial effects of lactobacilli may be related to their ability to keep the number of enterobacteria, a large family of Gram-negative bacteria that includes both harmless symbionts, as well as a whole host of familiar pathogens, such as Salmonella, Escherichia coli, Yersinia pestis, Klebsiella and Shigella, Proteus, Enterobacter, Serratia, and Citrobacter in check (Liévin-Le Moal. 2006) - exactly those bacteria, which produce the nasty lipo polysaccharides (LPS) that have been associated with inflammation and its downstream metabolic effects, such as obesity, diabetes, heart disease, gastrointestinal cancer etc. and, as the data in Table 2 tells you. Now, unfortunately, the these villains are all part only type of bacteria that was not significantly decimated by the sucralose challenge.

As Schiffman et al. point out these reductions are not, as Brusick et al. (2009) suggest simply a result of "normal variation". In fact, the probability to see a similar random reduction in bifidobacterial count occur "naturally"within 12 weeks would be 1/5000. It is thus more than just unlikely that the71.9%, 76%, and 77.7% reductions in bifidobacteria counts Abou-Donia et al. observed at dosages of 3.3, 5.5, and 11 mg/kg/d were coincidental.

Prebiotics, anyone? In view of the alleged neg. effects on your gut microbiome, you may feel inclined to increase your prebiotic intake. If that's the case, this top 10 list of food items with prebiotic fiber contents of up to 65% of total weight may help:

1. Chicory root - 65%
2. Jerusalem artichoke - 32%
3. Dandelion greens - 24%
4. Garlic - 18%
5. Leek - 12%
6. Onion - 9% 
7. Cooked Onion - 5% 
8. Asparagus - 5% 
9. Wheat bran - 5% 
10. Banana - 1% 

Remember: These are the "richest" not necessary the "best" sources ;-)

If there is reason to be concerned it's about your gut health and its downstream metabolic effects: In view of the important role of bacteroides for the health of the intestinal eco-system (Lee. 2013) and their persistent reduction even after the 12-week recovery period, the selective antibiotic activity of sucralose is as of now the by far most disconcerting negative health effect discussed in this series.

If the changes Abou-Donia et al. observed in their rodent studies were to be confirmed in human studies, where the subjects consumed a balanced whole foods diet with a high prebiotic content. The profound changes the researchers from the Duke University Medical Center report in their paper from September 2008 would be reason enough to revise my previous conclusions about a potential contribution of sucrose to the diabesity (=obesity + diabetes) epidemic.

In fact, a revision of the potential long(er) term downstream effects of sucralose on your metabolic health could be all the more indicated, if it turns out that the alleged toxic and endocrine-disrupting effects I will discuss in the next installment of this series turn out to be substantiated, as well.

Reference:

• Abou-Donia, M. B., El-Masry, E. M., Abdel-Rahman, A. A., McLendon, R. E., & Schiffman, S. S. (2008). Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats. Journal of Toxicology and Environmental Health, Part A, 71(21), 1415-1429.
• Bellisle, F., & Drewnowski, A. (2007). Intense sweeteners, energy intake and the control of body weight. European Journal of Clinical Nutrition, 61(6), 691-700.
• De la Hunty, A., Gibson, S., & Ashwell, M. (2006). A review of the effectiveness of aspartame in helping with weight control. Nutrition Bulletin, 31(2), 115-128.
• de Ruyter, J. C., Olthof, M. R., Seidell, J. C., & Katan, M. B. (2012). A trial of sugar-free or sugar-sweetened beverages and body weight in children. New England Journal of Medicine, 367(15), 1397-1406.
• Ebbeling, C. B., Feldman, H. A., Chomitz, V. R., Antonelli, T. A., Gortmaker, S. L., Osganian, S. K., & Ludwig, D. S. (2012). A randomized trial of sugar-sweetened beverages and adolescent body weight. New England Journal of Medicine, 367(15), 1407-1416.
• Liévin-Le Moal, V., & Servin, A. L. (2006). The front line of enteric host defense against unwelcome intrusion of harmful microorganisms: mucins, antimicrobial peptides, and microbiota. Clinical Microbiology Reviews, 19(2), 315-337.
• Mattes, R. D. (1996). Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrate in fluids. Physiology & Behavior, 59(1), 179-187.
• Mattes, R. D., & Popkin, B. M. (2009). Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms. The American journal of clinical nutrition, 89(1), 1-14.
• Payne, A. N., Chassard, C., & Lacroix, C. (2012). Gut microbial adaptation to dietary consumption of fructose, artificial sweeteners and sugar alcohols: implications for host–microbe interactions contributing to obesity. Obesity Reviews, 13(9), 799-809.
• Porikos, K. P., Hesser, M. F., & Van Itallie, T. B. (1982). Caloric regulation in normal-weight men maintained on a palatable diet of concentional foods. Physiology & behavior, 29(2), 293-300.
• Schiffman, S. S., & Rother, K. I. (2013). Sucralose, A Synthetic Organochlorine Sweetener: Overview Of Biological Issues. Journal of Toxicology and Environmental Health, Part B, 16(7), 399-451. 

High Energy Flux, A New Determinant of Successful Weight Loss? Eat More, Train More, Lose More? Increased Resting Metabolic Rate & Satiety, Decreased Hunger While Dieting!

Always hungry? Can't lose weight? "Train more and eat more" (not less!) could be the solution.

A recent thesis from Rebecca Foright, highlights that a high energy flux state characterized by high daily energy expenditure (resulting from increased physical activity) with matching high energy intake (high calorie throughput) may attenuate the weight loss-induced energy gap by reducing hunger and ameliorate the otherwise diet-related reduction in resting metabolic rate.

Foright recruited recruited eleven obese study participants from the Colorado State University community and surrounding areas to test her "exercise more, eat more, lose more (easily)" hypothesis.

The enrollment criteria included: BMI between 30-43 kg/m², age 18-55 years, weight stable over the prior 12 months, desire to lose weight, and ability to exercise as assessed by electrocardiogram (ECG), resting blood pressure and a normal incremental exercise test to exhaustion with simultaneous ECG. Exclusionary criteria included: pregnancy or breastfeeding, smoking, use of medication known to affect appetite or metabolism (including but not limited to antidepressants and statins), or prior surgery for weight loss. In short, most of the participants were what we today call "healthy obese."
"The approach used in this study was a within-subjects cross-over experimental design to test the effect of high and low flux states following weight loss on resting metabolic rate and perceptions of hunger and satiety."

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The study protocol was divided into four distinct phases: (1) baseline testing phase prior to weight loss; (2) weight loss phase induced by a hypocaloric diet over the course of several months; (3) weight maintenance phase in which subjects were maintained at the reduced weight for 3 weeks; and (4) experimental phase in which measures were obtained of subjects’ resting metabolic rates, fasting and post-prandial perceived hunger and satiety, fasting and post-prandial circulating glucose, insulin, and PYY concentrations, and ad libitum food intake on the 5th day following low flux and high flux phase conditions, respectively, completed in random order with a three-day washout period in between (see Figure 1).

Figure 1: Experimental Timeline | #Order of Low Flux and High Flux were randomly assigned (Foright. 2014).

During the low flux condition subjects remained sedentary for four consecutive days. All food was provided so that energy intakes were adjusted to maintain energy balance.

• resting metabolic rate (RMR) measurements on day 1-4 of the low flux phase
• caloric intake was adjusted according to RMR everyday
• subjects were fed standardized meals with a macro composition of 50/35/15 (carbohydrate/fat/protein) and an energy intake that was 1.3x the RMR
• subjects had to refrain from physical activity (>3,000 steps per day)
• at the end of day 5 the subjects completed a hunger/satiety questionnaire used to assess general feelings of hunger/satiety over the prior four days of the low flux condition

During the high flux condition subjects exercised on four consecutive days (approximately 500 net exercise kcal expenditure at 60% V02 max) and were fed additional food necessary to maintain energy balance.

• resting metabolic rate (RMR) measurements on day 1-4 of the low flux phase
• caloric intake was adjusted according to RMR everyday
• subjects were fed standardized meals with a macro composition of 50/35/15 (carbohydrate/fat/protein) and an energy intake that was 1.7x the RMR
• subjects were given pedometers and had to achieve at least 7,500 steps per day
• subjects exercised at 60% of their VO2max to burn 500kcal
• at the end of day 5 the subjects completed a hunger/satiety questionnaire used to assess general feelings of hunger/satiety over the prior four days of the low flux condition

Overall, a testing week consisted of two baseline days and 5 high/low energy flux days. In that, three identical experimental days were used to examine possible differences in perceptions of hunger and satiety, blood glucose, insulin, and PYY in response to breakfast preload, and ad libitum intake from a meal buffet.

Note: The caloric deficit that was designed to produce a 7% weight loss over the course of the 12-16 week long weight loss phase was identical in the undulating high and low energy flux phases of the study. The results are thus not a consequence of the increase in energy intake during the high flux phase (in fact the opposite was the case in some subjects, anway). The extra calories were after all burned again during the four exercise days.

"Now what is particularly interesting about the study is that the researchers did not content themselves with measuring the acute effects of high vs. low energy fluxes. They also investigated what happened after the 12-16 week weight loss phase.

To minimize the acute effects attributable to the dynamic phase of weight loss on metabolic rate and on hunger and circulating appetitive hormone concentrations, subjects were maintained at the seven percent lower body weight for a three-week period prior to the start of the low and high flux conditions. During these three weeks subjects reported to the KANC every three days to monitor weight and minimize weight fluctuations. Subjects were instructed to consume a slightly increased kcalorie intake compared to the weight loss phase to maintain weight" (Foright. 2014).

Put simply, the scientists wanted to know, whether the effects of high vs. low energy flux dieting would influence a dieters ability to lose weight and maintain the newly achieved weight.

Figure 2: Weight loss and energy flux where exactly as the scientists had planned (Foright. 2014)

As you can see, the average weight loss was almost identical to the targeted 7% (de facto "only" 6.9%). Similarly,

[...a]s designed, the energy intake for high flux (x±SD: 3,191±587 kcal/d) was significantly greater (p < 0.001) than for low flux (x±SD: 2,449±406 kcal/d) (Figure 2, right). In accord with the study design, there was no difference in macronutrient composition between the two conditions (data not shown)" (Foright. 2014).

Now all that would be pointless if both groups lost weight similarly effortlessly. In reality, though, On the subjects were significantly more hungry and felt less satiated at the end of each of the days during low flux.

Figure 3: As you see, the mean difference was already huge. It was more than huge in in
the subject who saw the greatest benefit (Foright. 2014).

On the other hand, they were significantly more full at the end of each of the days during high flux (p=0.015). There was a strong trend for the subjects to exhibit greater hunger throughout the day during low compared to high flux (p=0.09).

RMR increases sign. in trained but not untrained subjects in a high energy flux state - no training, no difference between the two groups - the energy balance was identical in both conditions (Bullough. 1995)

No, this is not an outlier study: In 1995 Bullough et al. were already able to show that the resting metabolic rate on diet + exercise regimen that established an identical energy balance was greater in trained than in untrained subjects only when trained subjects were in HF. As Bullough et al. point out "[t]hese data indicate that RMR is influenced by exercise, energy intake, and their interaction and suggest that higher RMR in trained vs untrained individuals results from acute effects of HF rather than from a chronic adaptation to exercise training." (Bullough. 1995) Bell et al. on the other hand found that "[m]aintenance of high energy flux via regular exercise may be an effective strategy for maintaining energy expenditure and preventing age-associated obesity" (Bell. 2013).

And Goran et al. (1994) found that "RMR can be elevated during a state of energy balance when energy flux is increased," and that the "magnitude of adaptive change in RMR is similar in response to increased EI [energy intake] and/or PA [physical activity]." 

Figure 4: The subject who saw the greatest satiety benefit in the high flux phase was also the one that consumed the most energy on the low flux condition - even more than on the high flux condition (Foright. 2014)

Interestingly, the subject who saw the largest benefit (see Figure 3) was also the guy or gal who consumed the most energy in the low flux condition (orange line in Figure 4).

So what about the health markers?

The  fasting insulin decreased following weight loss and was significantly lower on the LF (8.3±1.1 µU/ml) and HF (6.4±0.8 µU/ml) experimental days compared to the pre-weight loss baseline (11.8±0.6 µU/ml). In other words, while both groups saw significant increases in insulin sensitivity due to dieting, the effects were (unsurprisingly) significantly more pronounced during the high energy flux (=exercise phase).

In contrast to what the significant differences in hunger ratings would suggest, there were no general differences in fasting PYY (the satiety hormone) concentrations among pre-weight loss, low and high flux conditions respectively.

Figure 5: Insulin and PYY levels of the subjects in the high and low flux phases over the course of the day (2014).

If you look at the data in Figure 5, it's obvious that the PYY levels were in fact lower in the high flux condition - from 180-360 minutes in the high flux condition compared to the baseline (pre-weight loss) and low flux, to be precise.

Figure 6: Average resting metabolic rate at baseline and across 5 days of low and high flux (Foright. 2014)

So what? Beneficial, not beneficial, or not sure? In spite of the absence of significant differences in PYY, the post-diet response of the subjects clearly indicates that the energy deficit was easier to tolerate in the high flux phases.

The slightly, but significantly higher resting metabolic rate during the high flux phases further underlines that there is a benefit of eating more and training more and the absence of corresponding evidence from any of the hormonal markers measured may simply be related to a "bad" choice of markers. If the researchers had determined the level of the hunger hormone ghrelin, instes, it may well have been that we would have had a physiological explanation for the "hunger difference".

The way it is, we still have the decreased subjective hunger, increased subjective satiety and increased RMR which speak in favor of the high flux state dieting. What we do not know, though, is whether the effects will be the same in athletic (vs. sedentary) subjects [based on my personal experience we will!] and whether they can be maintained for say 4 weeks instead of four days | Comment on Facebook!

References:

• Bell, Christopher, et al. "High energy flux mediates the tonically augmented β-adrenergic support of resting metabolic rate in habitually exercising older adults." The Journal of Clinical Endocrinology & Metabolism 89.7 (2004): 3573-3578.
• Bullough, Richard C., et al. "Interaction of acute changes in exercise energy expenditure and energy intake on resting metabolic rate." The American journal of clinical nutrition 61.3 (1995): 473-481.
• Foright, Rebecca. A high energy flux state attenuates the weight loss-induced energy gap by acutely decreasing hunger and increasing satiety and resting metabolic rate. Diss. Colorado State University, 2014.
• Goran, Miachel I., et al. "Effects of increased energy intake and/or physical activity on energy expenditure in young healthy men." Journal of Applied Physiology 77.1 (1994): 366-372.
• Rarick, Kevin R., et al. "Energy flux, more so than energy balance, protein intake, or fitness level, influences insulin-like growth factor-I system responses during 7 days of increased physical activity." Journal of Applied Physiology 103.5 (2007): 1613-1621.

The Healthy Taste of Olive Oil. Would the Flavor Be Enough to Induce At Least Some of Its Health & Satiety Effects? Plus: Cholesterol Control - Pomace vs. Refined Olive Oil

What about an EVOO perfume, then?

I know, it sounds crazy, but in view of what you've learned in previous articles here at the SuppVersity about sweet taste receptors (learn more) and their far-reaching influence on our metabolism, it does not appear to far-fetched to assume that there is a receptor that "tastes" the flavor-active compounds of olive oil that's responsible for some of its beneficial health effects - right?

I guess, Sabine Frank and almost a dozen of other scientists from Germany and Austria must have had a similar idea, when they came up with the research question of their most recent study.

Olive oil flavored yoghurt?! Really?

I suppose, olive oil flavored, or, more specifically, low-fat yogurt mixed with a fat-free aroma extract from olive oil may not sound appealing to the average Western customer, but it would certainly deserve the label "functional food":

Figure 1: Only the olive oil enhanced yogurt will also enhance the activity of the frontal operculum (Frank. 2013)

As you can see in Figure 1, it's a functional food that has a statistically highly significant effect on the cerebral blood flow in the frontal operculum 30 and 120 min after a meal: This and the increased activity in the anterior insula of which the scientists found that it correlated positively with the postprandial change in bloos glucose change in the 11 healthy male subjects of the study, clearly suggest: The taste of olive oil alone has significant effects on the blood flow in parts of the brain that are involved in the control of energy intake and metabolic rate.

"What is the "frontal opercular" and why would I care about its blood supply?"

If the subheading to this paragraphs describes what you are thinking right now, it's about time to take a look at the little information we have about the frontal operculum:

• 

  Suggested read: "Pimp My Olive Oil! When Virgin is not Phenol-Rich Enough: The Pharmacokinetics of Phenol-Enriched Virgin Olive Oil." | read more

  We know from previous studies that the frontal operculum (FP) is sensitive to food intake.
• The study at hand shows that the FP does not care about caloric values (the yogurts were isocaloric).
• In task-related studies, the frontal operculum as part of the primary taste cortex, has shown pronounced activation to visual food cues and anticipation of food intake.
• The activation of the frontal operculum appears to control the "this smells good" or "this looks good, I must have it" response that makes weight loss so difficult.
• There is a telling relation between the sensitivity of the frontal operculum and the BMI of a person (Batterink. 2010; Yokum. 2011)
• Earlier fMRI studies showed that oral delivery of a drop of fat leads to an immediate increase in insular and frontal opercular activity, which suggests that there are "fat taste receptors" somewhere in the oral cavity or digestive tract that are wired to the the frontal perculum (Small. 2012).

Now, in context of the results of the study at hand, it is obviously the last of these points, which is particularly interesting. The discovery Frank et al. made would after all suggest that we can get satisfactory "fat effect" without the fat - simply by having the right "aroma."

Figure 2: Modulating effect of the minor components of pomace olive oil (POMACE) on lipid composition in 10 healthy young men (Cabello-Moruno. 2013) - severs as illustration for the importance of the "non-fat" components for our health.

Frank et al. also point out that the fact that they measured the CBF not immediately but 30 min and 120 min after the consumption of the yogurt would make it quite unlikely that they had mistaken an acute aroma response for what they believe is the "association with fat" - in other words, the researchers believe that the ingestion of the olive oil flavor components "modifies later responses to achieve an appropriate sensory control." Effects just as we know them from glucose and artificial sweeteners which "prepare" the body to release insulin.

Per capita consumption of vegetable oils and fats in selected European countries in 2009 (Eurostat. 2011)

Bottom line: I guess it is too early to say, whether and what kind of applications the said olive oil extract could have in the future. What the study does however show is that focusing on macros and even micronutrients, only, is insufficient.

In fact, the "ideal" diet, with the perfect macros and 100% adherence could in the end turn out to produce inferior results to a "sub-optimal", but tasty diet with olive oil and other aromas triggering all-sorts of still to be elucidated beneficial downstream effects on our physiology and psychology.

Reference: 

• Batterink L, Yokum S, Stice E. Body mass correlates inversely with inhibitory control in response to food among adolescent girls: an fMRI study. Neuroimage 2010;52:1696–703.
• Cabello-Moruno R, Martinez-Force E, Montero E, Perona JS. Minor components of olive oil facilitate the triglyceride clearance from postprandial lipoproteins in a polarity-dependent manner in healthy men. Nutrition Research. Oct. 2013 [accepted manuscript]
• Small DM, Green BG. A proposed model of a flavor modality. In: Murray MM, Wallace MT, eds. The neural bases of multisensory processes. Boca Raton, FL: 2012
• Yokum S, Ng J, Stice E. Attentional bias to food images associated with elevated weight and future weight gain: an FMRI study. Obesity (Silver Spring) 2011;19:1775–83.

Health & Exercise Quickie: Vitamin D Deficiency, Taurine & Glycine. Multiple Sclerosis & Epstein-Barr. Paracetamol & Muscle Gains. Gender & Fatigue from Workouts. HIIT, LISS & Appetite. Plus: Scientists Debate: Light vs. Heavy Weights

While there is a positive trend in the percentage of US adults who meet the 2008 federal physical activity guidelines according to which they have to "devote at least 150 minutes/week to moderate, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination", the number of people who have gotten the message that a combination of both strength and aerobic training (red line) is much more efficient than doing just aerobics (blue line) remains the same (CDC. 2012)

48%! That's the SuppVersity figure of the week and the percentage of US adults aged 18 and over who met the 2008 federal physical activity guidelines for aerobic activity in 2012 - that's 5% more than in 1997. It would be better to see it up in the 75%+ region, but it's nice to see that more and more people are devoting at least 150min/week to moderate intensity exercise, or 75 minutes/week to vigorous intensity exercise, or an equivalent combination.

What's not so nice is that people are still way too focused on aerobics and the number of US citizens that's combining resistance and aerobic training to reach their exercise goals is stagnating below 20%. Moreover, best-agers and baby boomers, who would probably benefit even more from some weight lifting than the 36% of the young men (age 18-24) who make up the lion's share of the 'real' physical culturists who know about the importance of both, 'weights' and 'cardio', are - if they work out at all - still sticking to the tried and disproven LISS only regimen.

On Short Notice, today: A Health & Exercise Quickie

Apropos "LISS" as the headline of today's On Short Notice news quickie already gave away, light intensity steady state aerobic training aka LISS is one of the exercise related topics today. We will however start out with the health related news... and don't wonder that the first post is about polar bear health. I promise you will be intrigued, when you've read it ;-)

• 'Westernized' polar bears' bones look as if they would need vitamin D supplements, in reality all they are probably missing is sufficient taurine in their diet. I don't know but maybe you've asked yourself before: "How on earth can a white bear survive in the Arctic, when his nose is the only part of his skin that's exposed to the sun and would thus be able to produce vitamin?" (Please mind that this is not a serious question ;-) He eats his vitamin D!
  
  

  

  Scientists speculate: Their cousins in captivity suffer from rickets and fractures due to secondary vitamin D deficiency in consequence of insufficient taurine intake.

  Ok, first question first answer, but what about question #2: "How come that the clubs of his brethren and cousins in captivity get rickets and fractures as if they were vitamin D deficient, although they get the exact same amount of vitamin D from mother's milk and their later diet (sometimes the latter is even supplemented) as their wild counterparts?" Answer? No idea? Well, if you ask the researchers from the The University of Tennessee Health Science Center the answer is (Cheesney. 2009): A lack of taurine in the diet.
  
  Taurine plays a fundamentally important role in the conjugation of ursodeoxycholic acid to TUDCA and facilitates the uptake of fatty acids and fat soluble vitamins. With insufficient taurine in the diet polar beers (and human beings) can probably drink as much vitamin D in olive oil or whatever other fat base they deem more appropriate then dry tabs without any effects on their 25-OHD => calcitonin levels and consequently bone health (suggested read "Fat D-Ficiency! Study Shows, Even 50.000 IU of Vitamin D3 Useless, When You Ingest It Without Fat").
  
  Moreover, a recent guinea pig study from Department of Internal Medicine at the Medical College of the National Cheng Kung University suggests that glycine could be another 'pro vitamin D amino acid' due to its beneficial effect on the liver and subsequent protection of disturbances in vitamin D metabolism and low 25-OHD levels (Chen. 2008) - now, what if any of these, i.e. taurine or glycine, or simply insufficient bile acid, which incidentally depends on the consumption of the "bad, bad" cholesterol (cf. Kern. 1994), is the actual reason of the rampant vitamin D deficiency in our meat-, fat- and cholesterol-o-phobic societies?
• "Low vitamin D and remote EBV infection may be associated with clinical MS breakthrough within 2-3 years." (Décard. 2012) Usually I don't simply copy the study titles, but this one says it all. Even before the first symptoms of multiple sclerosis occur, i.e. in the so-called pre-CIS (=clinically isolated syndrome) interval, patients with quiescent multiple sclerosis have 50% lower 25OHD levels than their healthy peers and - what could actually be the causal factor, here - three times higher Epstein-Barr specific IgG levels (EBNA1). Can these observations a group of scientists from the Department of Neurology at the St. Josef-Hospital of the Ruhr-University Bochum in Bochum, German, really be mere coincidence?
  
  

  

  Figure 1: While it would be best never to be infected with Epstein-Barr your risk of EP-related MS is more than twice as high if you are exposed late (Ascherio. 2010)

  At least as far as the Epstein-Barr relation goes the answer of a 2010 review of the literature would be 'no, probably no coincidence' (Ascherio. 2010). It appears to be established that Epstein-Barr (EB) plays a pivotal role in the etiology of MS. Based on the observation that people without EB are virtually MS free, and the fact that their own previous research has clearly shown that late infections with EP increase your risk to develop MS by more than 2x (compared to people who have been exposed in childhood; see figure 1), Ascherio et al. argue that it is very unlikely that EP is not at least the trigger, if not the ultimate cause of MS.
  
  The scientists also refer to the hygiene hypothesis which has been advanced by other authors before, unfortunately, however, getting rid of the 'cleanliness' and exposing your immune system to the training it needs by exposing yourself to the virus at an earlier age, is of little use, if not totally stupid. After all it would only reduce your risk to develop MS to a level that's still more than 1,000% higher than in people who have never been exposed to the virus in the first place (see figure 1).
  
  Due to the inconclusive data on the long and short term effects of Epstein-Barr infections on the B-cell and T lymphocyte response, the Ascherio et al. are not yet sure about the exact mechanism by which EP stimulates, triggers or drives the development of MS. All that can be said with relative certainty is that Epstein-Bar infections contribute to the increase in multiple sclerosis. Aside from the previously mentioned correlations the mere fact that those regions of the world where Epstein-Barr is quasi non-existent are virtually MS free is probably the best evidence of its involvement in autoimmune attacks on your brain. So if you want to protect yourself you better make sure you don't get infected!  Since EP is part of the herpes family and transmitted via saliva this is unfortunately not exactly easy...

• 

  Figure 2: Overall there is no statistical significant downside to chronic paracetamol supplementation, but there is a slight advantage for the NSAID free group in term of increases in lower body strength - the time course (not shown) of the strength gains was by the way identical for both groups, as well (Jankowski. 2012)

  Paracetamol does not interfere with muscle gains in elderly men. The issue whether or not NSAIDs will interfere with resistance training induced gains in skeletal muscle is certainly relevant for everyone. If there is one group of people for whom it could be of paramount importance, though, this would be the men and women in their best ages (>50 years) who have finally realized that muscle is not just metabolic currency, but a true life insurance.
  
  Against that background the most recent results from the College of Nursing at the University of Colorado Anschutz Medical Campus may be important news (Jankowski. 2012). I mean, if the use of N-acetyl-4-amniphenol (ACET) aka paracetamol would hamper or even forestall muscle gains, the training efforts of the men and women who take ACET would be to no avail.
  
  Now the good news is that the chronic use of paracetamol at a daily dose of 1,000mg did not reduce the lean mass gains in the 17 men (age >50y) who actually participated (instead of giving up) in all of the 3-5 days A/B resistance training sessions
  
  • workout A: R three sets of lateral pull down, bench ress, hip abduction and adduction, biceps curls, seated row, and ssisted chin ups
  • workout B: overhead press, leg press, triceps xtension, knee extension and flexion, heel raise, and shoulder external rotation
  • warm up / cool down: 10 min warm-up on the treadmill, a stair climing intermezzo after the first warm up sets and another 10 min cool down
  that were performed with at 80% of the 1-RM and with at least 1 day off in-between over a period of 16 weeks.
  
  
  The chronic ingestion of paracetamol is not advisable regardless of its negligible detrimental effects on skeletal muscle gain. Only recently, Kane et al. have shown that older people in are particularly prone to the hepatoxic effects of this (imho falsely OTC available) NSAID (Kane. 2012). If there is no way around it, because you cannot stand the pain, a safer (at least for the liver) and more effective medical approach could be the combination of tramadol (75 mg), a weak opioid analgesic, with low dose of paracetamol (325-650mg, max!; cf. Pergollizzi. 2012).
  In as much as the nonexistent negative effects are good news, they are likewise strange news, because according to the expression of proteins involved in the protein synthetic response to exercise, it should actually have hampered the gains:
  

  "[...] in the ACET group that the expressions of the anabolic gene p70S6K and the catabolic gene MAFbx were significantly reduced at week 16 of PRT. Given that the increases in FFM in response to PRT were not significantly different between the groups, it is possible that the suppression of catabolic signaling was sufficient to offset reductions in anabolic signaling in the ACET group." (Jankowski. 2012)

  As the authors point out future studies will have to elucidate the exact mechanism this at first sight contradictory results.
  
  In the mean time Jankowski et al. do yet speculate that the loss of prostaglandin signalling and supsequent increases in p70S6K, the protein that's responsible for muscle protein synthesis may be countered by the normalizing effects paracetamol exerts on the expression of Akt, the ameliorative effect on the overexpression of nitric oxide synthase (iNOS) and the reduction of the age-relatedly increased myocyte apoptosis.
  

• 

  Compared to Hope Solo or Serena Williams Olympian Brian Lochte, is probably a weakling - of course only as far as the fatigabilty of his skeletal muscle is concerned - as far as the risk do develop the Athlete's Triad is concerned, this may yet be advantage.

  Men and women tire differently - men (once more ;-) the weaker sex Let's face it guys,  we are weaklings. At least this is what Beth W. Glace and her colleagues from the Nicholas Institute of Sports Medicine and Athletic Trauma at the Lenox Hill Hospital in New York report in their latest paper. Other than the quadriceps muscles of our significant others, our muscles fatigue after 2h of cycling with intermittent one minute sprints every 20 minutes.
  
  In women, in this particular case just like their male counterparts trained cyclists or triathletes with a training load of at least 100km per week, on the other hand, it's solely the central nervous system fatigue that will keep them from cycling 'forever'. Unfair, right? Us men have to battle both, central as well as local muscular (=peripheral) fatigue.
  
  Now what seems nothing but advantageous can however turn against you. In a way the low fatigability of female muscle is also part of the reason why are way more susceptible to the athlete's triad (click here to learn more) than men: They are simply able to work their CNS into the ground, because their peripheral musculature is less prone to exhaustion.
• Recent study puts question mark behind assumed appetite reducing benefit of HIIT sprints vs. classic aerobics - but does that mean that aerobics is the way to go? Not yet in press, but already intriguing are the results of a recent study by  Kevin Deighton et al. from the School of Sport at the Loughborough University who say that they found that ...
  

  "[a]n acute bout of endurance exercise resulted in lower appetite perceptions in the hours after exercise than sprint interval exercise and induced a greater 24 h energy deficit due to higher energy expenditure during exercise" (Deighton. 2012)

  

  Figure 3: Intentionally or not, based on the conclusion of the abstract you would probably not have expected to see these results (data adapted from Deighton. 2012)

  Now this sentence from the abstract certainly suggests that sprinting would have nothing but negative effects. The actual data you see in figure 3 does yet tell you something different. The sprinters may have had increased ghrelin and lower PYY levels with the expected downstream effects on perceived hunger, but this did not translate into significant differences in food intake. In other words, even longish sprint exercises like the ones in the study at hand won't put you at danger of overeating - despite transient increases in ghrelin levels.
  
  In fact, the increased ghrelin amplitude can actually be an advantage (see August 04, 2012) and the calories in vs. out calculation the scientists do is so irrelevant to the real world health and body composition effects of exercise that I refuse to repeat it here ("No, you cannot eat that extra piece of layer cake because you ran on the treadmill earlier today" ;-)
  
  In the end, comparisons like this always suggest you had to choose between doing one or another mode of "cardio", when a combination of both, i.e. cycling HIIT and LISS, yet not both in one session, would be the most productive way to go. And no, Mr. Taubes, none of them is "just going to make you hungry" (see "Every Dog Has His Day: Dr. Oz Was Right, Exercise Does Not "Just Make You Hungry", But Reduces Energy Intake!")
  
• Researchers debate the "low vs. high weight" conundrum. In the editorial to the next issue of the Journal of Applied Physiology Mark D. Schuenke, Jennifer Herman, and Robert S. Staron reject the criticism they received from Nicolas Burd et al. for the pro heavy weights arguments they put forward in their recently published study on the effects of high vs. low weight training (Schuenke. 2012a; covered on the SuppVersity on October 01, 2012). Now while this back and forth between the two groups does not deliver any new data, I believe that it is still interesting and highly educative to see how science is actually a matter of negotiated not set truths. So, let's see how Schuenke et al. respond to Burd's assertion that ...
  

  

  Figure 4: Changes in body composition (left) and changes in muscle fiber cross-sectional area in response do different training regimen (Schuenke. 2012a; this study was discussed here on the SuppVersity on October 01, 2012)

  "[t]he authors’ views continue to contribute to a resistance training doctrine that is incorrect, most notably the belief that heavier weights are better concept. This conclusion is likely due to the relative dearth of quality studies assessing the hypertrophy potential of lower load resistance training paradigms, in contrast to the large number of studies employing ‘traditional’ resistance training intensities (*70 % of maximal strength).

  Clearly, evidence exists to support the concept that light(er) loads can support training-induced muscle hypertrophy both independently and by comparison to heavy loads. We would propose that so long as the stimulus is an overload, performed with high effort (fatigue), and progressive then even the most seasoned lifters would see progression,  at the very least no regression, in strength or muscle mass." (Burd. 2012)

  I will briefly summarize the most important points the researchers from the University of New England College of Osteopathic bring forward to defend their "go heavy or go home" argumentation:
  
  • The list of previous studies which confirm the the efficacy of training with high(er) weight for "optimal" gains in hypertrophy and strength is extensive.
  • Low load training is not as Burd et al. suggest "simply a milder form of low-load blood flow restrictive exercise", of which the researchers state that it is "interesting".
  • Schuenke et al. specifically refer to a Y2k study by Takadara et al. which shows that without the cuffs light loads don't build anything (Takadara. 2000).
  • The researchers point out that the claim by Burd et al. that "maximal muscle fiber activation can be achieved in any circumstance as long as the effort is to failure is unwarranted and unsubstantiated".
  • The study by Mitchel et al. Bird et al. cite to prove their hypothesis may not report significant differences between knee extensions performed at 30 % of 1RM for 3 sets, 80 % of 1RM for 1 set, or 80 % of 1RM for 3 sets as far as the isometric strength and hypertrophy between the three types of training are concerned, but
    

    "[t]his result is not surprising considering the following: (1) no control group was used, (2) each subject trained each limb using a different protocol (cross-over effect), (3) only one single-joint exercise was used (low volume versus a much higher volume of training used, for example, in Schuenke et al.: 3 sets each of leg press, squat, and knee extension), and (4) only fiber types I and II were delineated (severely limiting interpretation of the results).

    In that the last parentheses is obviously another direct criticism of what Schuenke would probably call "cherry picking" studies and specific results to support an unwarranted hypothesis.
  Based on this line of argumentation, Schuenke et al. conclude their deliberations on the note:
  

  

  One should not forget that it's not only about light vs. heavy, but in as much about appropriate and inappropriate weights. If you go by the quantity of the evidence there is however no debating that those weights are too light - probably even for a Lady in her best years.

  "Low-load training appears to have some merit. How-ever, our data support the use of high-load, high-intensity resistance training to maximize fiber hypertrophy and strength. In addition, heavy loading of the muscle has an impact on bone and other connective tissues which are minimized/lacking using low-load training. Finally, Burd et al. appear to oversimplify the field of exercise physiol-ogy. To claim that any training load (light or heavy) con-fers the same physiological adaptations as long as the end point is volitional failure is shortsighted and similar to claiming that running for any distance or time will elicit the same effects as long as fatigue is reached." (Schuenke. 2012)

  If you asked me, both are right. While I personally tend to agree with Schuenke, the main reason that I do is that the heavy weights approach is tried and proven, while - just as Burd says - the sceintific evidence pertaining to low weights is scarce and ambiguous and the anecdotal evidence from 'big guys' is non-existent. I am still curious about the next move(s) on both sides of this divide. And by the way, conflicts like these have always been among the driving forces of scientific progress, so I am pretty sure that we as trainees can only benefit from this debate as well as potential follow-up studies, both groups will feel inclined to conduct in order to 'prove' their point.

That's all for today! I hope you enjoyed the stay, all have electricity and an intact water supply ... I mean it's nice if you have a fully charged iPhone to get your daily dose of SuppVersity news, but even I have to concede that some other things in live are way more elementary.

References

• Ascherio A, Munger KL. Epstein-barr virus infection and multiple sclerosis: a review. J Neuroimmune Pharmacol. 2010 Sep;5(3):271-7.
• Burd NA, Moore DR, Mitchell CJ, Phillips SM. Big claims for big weights but with little evidence. Eur J Appl Physiol. 2012 Oct 20. 
• CDC. Early Release of Selected Estimates Based on Data From the January–March 2012 National Health Interview Survey. September 2012
• Chen CY, Wang BT, Wu ZC, Yu WT, Lin PJ, Tsai WL, Shiesh SC. Glycine ameliorates liver injury and vitamin D deficiency induced by bile duct ligation. Clin Chim Acta. 2012 Oct 23-
• Chesney RW, Hedberg GE, Rogers QR, Dierenfeld ES, Hollis BE, Derocher A, Andersen M. Does taurine deficiency cause metabolic bone disease and rickets in polar bear cubs raised in captivity? Adv Exp Med Biol. 2009;643:325-31.
• Deighton K, Barry R, Connon CE, Stensel DJ. Appetite, gut hormone and energy intake responses to low volume sprint interval and traditional endurance exercise. Eur J Appl Physiol. 2012 Oct 31.
• Décard BF, von Ahsen N, Grunwald T, Streit F, Stroet A, Niggemeier P, Schottstedt V, Riggert J, Gold R, Chan A. Low vitamin D and elevated immunoreactivity against Epstein-Barr virus before first clinical manifestation of multiple sclerosis. J Neurol Neurosurg Psychiatry. 2012 Aug 11.
• Kane A, Mitchell SJ, Carroll PR, Matthews S, Hilmer SN. Characteristics of older and younger patients with suspected paracetamol toxicity. Australas J Ageing. 2012 Sep;31(3):190-3.
• Kern F Jr. Effects of dietary cholesterol on cholesterol and bile acid homeostasis in patients with cholesterol gallstones. J Clin Invest. 1994 Mar;93(3):1186-94.
• Kappenstein O, Vieth B, Luch A, Pfaff K. Toxicologically relevant phthalates in food. EXS. 2012;101:87-106.
• Pergolizzi JV Jr, van de Laar M, Langford R, Mellinghoff HU, Merchante IM, Nalamachu S, O'Brien J, Perrot S, Raffa RB. Tramadol/paracetamol fixed-dose combination in the treatment of moderate to severe pain. J Pain Res. 2012;5:327-46.
• Schuenke MD, Herman JR, Gliders RM, Hagerman FC, Hikida RS, Rana SR, Ragg KE, Staron RS. Early-phase muscular adaptations in response to slow-speed versus traditional resistance-training regimens. Eur J Appl Physiol. 2012a Oct;112(10):3585-95.
• Schuenke MD, Herman J, Staron RS. Preponderance of evidence proves "big" weights optimize hypertrophic and strength adaptations. Eur J Appl Physiol. 2012b Oct 25.
• Sioen I, Fierens T, Van Holderbeke M, Geerts L, Bellemans M, De Maeyer M, Servaes K, Vanermen G, Boon PE, De Henauw S. Phthalates dietary exposure and food sources for Belgian preschool children and adults. Environ Int. 2012 Nov 1;48:102-8.
• Takarada Y, Takazawa H, Sato Y, Takebayashi S, Tanaka Y, Ishii N. Effects of resistance exercise combined with moderate vascular occlusion on muscular function in humans. J Appl Physiol. 2000; 88:2097–2106.