Recomp: Building Muscle + Losing Fat Works W/ Weights, but Won't Boost 'Ur Resting Metabolic Rate Along the Way

Sane caloric deficits (maybe 15-20% and thus more than in the study at hand) + strength training may facilitate recomp = body fat loss + muscle gain/maintenance.

There are even equations which indicate that any increase in lean mass should contribute to measurable increases in your resting metabolic rate aka your "RMR". Being able to build muscle and thus increase your metabolic rate is one of the reasons why everyone (including myself) recommends to hit the weights (not just the cardio apparel) whenever you're trying to shed superfluous body fat.

Now, a recent study from the University of Ottawa clearly suggests that, "despite an increase in fat-free mass [...] 6 months of aerobic, resistance, or combined training [adherence was controlled for] did not increase RMR compared [...] in adolescents with obesity" (Alberga. 2017).

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In view of the energy thirst of your muscle and organ mass (total lean mass) this result seems odd. Needless to say that it is thus worth taking a look at the studies goals and methodology. As far as the first is concerned, the articles write that they started with the (logical) hypothesis that "resistance exercise training performed alone or in combination with aerobic exercise training would increase [the] resting metabolic rate (RMR) relative to aerobic-only and nonexercising control"(Alberga. 2017) groups.

In their subjects, postpubertal adolescents (N = 304) aged 14–18 years with obesity (body mass index (BMI) ≥ 95th percentile) or overweight (BMI ≥ 85th percentile + additional diabetes risk factor(s)), who were randomized to 4 groups for 22 weeks however, the scientists did not observe the expected increase in RMR in response to the four weekly sessions of ...

• Aerobic exercise training - Participants exercised on treadmills, cycle ergometers, and/or elliptical machines at an intensity of 65%–85% of their previously measured HRmax for 20–45 min per session, gradually progressing in intensity and duration until the end of the intervention
• Resistance exercise training - Participants performed up to 3 sets of 7 exercises on resistance machines for 6–15 repetitions of their maximum for 20–45 min per session (supplementary Tables S3, S41). Participants were recommended to rest for 1.5 to 2 min between sets. Intensity of resistance training gradually increased by increasing the load (weight) that adolescents were lifting for a fewer number of repetitions, targeting progressive improvements in muscular strength
• Combined aerobic and resistance exercise training - Participants performed both the Aerobic and the Resistance exercise training components during each exercise session

Working out was yet only one pillar of the subjects' weight/fat loss I plotted in Figure 1. The other pillar was a diet containing 250kcal less than the subjects maintenance diet.

Figure 1: Change in body weight and body fat (left axis) and reduction in energy intake (right axes | Alberga. 2017).

Accordingly, it is not totally surprising that all groups lost weight and more importantly body fat (body composition was measured by a fancy MRI) over the course of the study. 

Figure 2: Changes in muscle mass and resting metabolic rate (Alberga. 2017).

What is surprising, however, is that the intended increases in lean mass did not translate into increased rates of metabolic rate (note: non-adherence cannot explain the difference, the scientists' per-protocol analyses including only participants with ≥70% adherence to our prescribed 4 sessions/week showed the same trends such that there were no between-group differences in fat-free mass and RMR following the 6-month exercise trial).

Do not jump to false black-and-white conclusions: I know, life would be easier if there were just black and white, but it would also be boring without "color" or, as in the case of the effects of lean mass on one's resting energy expenditure, the nuances of relevant vs. irrelevant lean mass gains. There's no doubt about it: Lean mass gains or losses of 10% of the total body weight will have significant beneficial/negative effects on your RMR (the overall effect will yet also depend on fat loss). If you scrutinize the data from the study at hand, the meager 900g of muscle and 1.8 kg of total lean mass the resistance training group added to their overweight frames amounts to only 1-2% of the subjects' total body mass. And still, the scientists are right, when they say that there's a "widespread misperception that resistance training increases RMR through its direct effect on increasing fat-free mass" (Alberga. 2017). It is, and this takes us back to where we have been coming from, more complex than that... but that's a topic for another SuppVersity article and another study with different subjects and greater increases in lean and decreases in fat mass.

As the data from the meta-analysis by Schwartz et al. (Figure 3) shows, that is not really surprising. It is well established that weight loss - albeit in this case in adults and of (in almost all cases) significantly more body mass - will almost linearly reduce subjects' metabolic rate.

Figure 3: Comparison of the mean rate of changes in resting energy expenditure relative to weight loss with different weight-loss interventions in all men and women (n = 2983). * and † indicate significant difference from the diet at P < 0.05 and P < 0.001 respectively (Schwartz. 2010).

Against that background, it is, even though the study at hand proves that the lean mass loss is not primarily responsible for the problem of reduced RMRs, important to point out that the resistance training group lost the most body fat (calculated as difference between total lean mass and total body weight), namely 1.8kg and thus twice as much as the aerobic training group (-1.8kg) and almost thrice as much as the control group (-0.5). This and previous evidence showing that resistance training can ameliorate the reduction in RMR, as well, do thus clearly speak in favor of hitting the weights when trying to shed body fat (or as it happened in this case: "recomp").

What do other studies show: Well, compared to Lazzer et al. who observed decreases in RMR with weight loss in youths on a combined diet (-15-20%) and exercise (2x per week physical education, 2x p. week combined training) intervention, the study at hand is good news for teens trying to shed body fat. With a duration of 9 months and a higher caloric deficit and thus weight loss (-16-18kg), the reason for the RMR reduction in this previous study could indeed be what people often label metabolic damage. Now, what is interesting, is that this "damage" can, once again, not be explained by lean mass losses, because only the girls lost lean mass, while both groups in Lazzer et al. showed sign. reductions in RMR. Similar decreases were observed in other pertinent studies (Foschini. 2010; Inoue. 2015), as well as studies in adults (Bray. 1969; Cameron. 2008, 2010; Doucet. 2000, 2001, 2003; Schwartz. 2010), studies that do yet also indicate that working out while dieting can mitigate this effect.

So is the "do resistance training to build lean mass and lose body fat"-advice bogus? Well, I'd say the study at hand shows that the effect of small increases in lean mass as they were observed in the study at hand have marginal effects on overweight / obese young subjects (that could be different in older subjects, but I honestly doubt that a maximal muscle gain of 0.9kg (in the RT group) would make a measurable, sign. difference in adults and/or people of whom nobody would claim that they were metabolically damaged due to overweight (note: the study does not provide evidence in favor of the theory of metabolic damage).

As the authors point out in their conclusion, their study does yet only confirm that the idea that "resistance training increases RMR through its direct effect on increasing fat-free mass" is a "widespread misperception" - at least if you understand that to be a linear effect that begins with the first lbs of muscle you add to your frame. This does not mean that working out in general and resistance training, in particular, were useless. After all, the real takeaway messages of the study are not just (a) that even a very small caloric deficit (for someone who drinks soft drinks or sweetened coffee, it would often suffice to drop those) can have a significant weight/fat loss effect in the longer run (here 6 months), but also that (b) this effect will be most pronounced (keep in mind that the difference did not reach statistical sign. in the 6 months study period, though) in conjunction with resistance training - in this case even more pronounced than with combined training (1.8kg fat loss vs. 1.2kg fat loss), for which data from Byrne et al. (2001) suggests that its reduced ability to build muscle could be the culprit | Comment on Facebook!

References:

• Bray, GeorgeA. "Effect of caloric restriction on energy expenditure in obese patients." The Lancet 294.7617 (1969): 397-398.
• Byrne, Heidi K., and Jack H. Wilmore. "The relationship of mode and intensity of training on resting metabolic rate in women." International journal of sport nutrition and exercise metabolism 11.1 (2001): 1-14.
• Cameron, Jameason D., et al. "The effects of prolonged caloric restriction leading to weight-loss on food hedonics and reinforcement." Physiology & behavior 94.3 (2008): 474-480.
• Cameron, Jameason D., Marie-Josée Cyr, and Eric Doucet. "Increased meal frequency does not promote greater weight loss in subjects who were prescribed an 8-week equi-energetic energy-restricted diet." British journal of nutrition 103.08 (2010): 1098-1101.
• Doucet, Eric, et al. "Evidence for the existence of adaptive thermogenesis during weight loss." British Journal of Nutrition 85.06 (2001): 715-723.
• Foschini, Denis, et al. "Treatment of obese adolescents: the influence of periodization models and ACE genotype." Obesity 18.4 (2010): 766-772.
• Inoue, Daniela Sayuri, et al. "Linear and undulating periodized strength plus aerobic training promote similar benefits and lead to improvement of insulin resistance on obese adolescents." Journal of Diabetes and its Complications 29.2 (2015): 258-264.
• Lazzer, Stefano, et al. "A Weight Reduction Program Preserves Fat‐Free Mass but Not Metabolic Rate in Obese Adolescents." Obesity research 12.2 (2004): 233-240.
• Schwartz, A., and E. Doucet. "Relative changes in resting energy expenditure during weight loss: a systematic review." obesity reviews 11.7 (2010): 531-547.
• Schwartz, Alexander, et al. "Greater than predicted decrease in resting energy expenditure and weight loss: results from a systematic review." Obesity 20.11 (2012): 2307-2310.

Weight Loss, 'Metabolic Damage' and the Magic of Carbs? Human Study Probes Effects of Carbohydrate Content, GL & GI on Diet-Induced Suppression of Resting Metabolic Rate

Will slimming down from a 120 cm to a 60 cm waist always ruin your metabolic rate and set you up for weight regain or can high GI protect you from yoyoing?

Broscience tells us: "Carb up to preserve your resting metabolic rate." And in fact, there is some scientific evidence that suggests a link between high(er) carbohydrate intakes and increased thyroid function. The same amount of T3 will trigger a sign. higher stimulation of lipolysis and fat oxidation, for example, on high vs. low carb diets (Mariash. 1980). Low carb diets, on the other hand, lead to significant reductions of the active thyroid hormone and increases in the 'thyroid receptor inhibitor' rT3 - even in healthy individuals and if the energy intake is standardizes (Serog. 1982; Ullrich. 1985). So, is broscience right? Well, overfeeding studies show a similar increase in T3 in response to protein, fat and carbohydrates (Danforth Jr. 1979). So refeeds should work, irrespective of their carbohydrate content...

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As you can see, it is hardly possible to confirm or reject the "carb up to prevent metabolic damage" (=prevent the diet induced over-proportional reduction in resting energy expenditure) hypothesis based on the existing evidence. A recent study by J. Philip Karl and colleagues who tried to determine "the effects of diets varying in carbohydrate and glycemic index (GI) on changes in body composition, resting metabolic rate (RMR), and metabolic adaptation during and after weight
loss" (Karl. 2015), however, may yet take us one step further towards rejecting or confirming this commonly heard of idea.

Figure 1: Overview of the key parameters of the study design and dietary composition (Karl. 2015).

In said study, Karl et al. randomly assigned adults with obesity (n = 91) to one of four diet groups for 17 weeks. As you can see in Figure 1, the diets all subjects were provided with differed in percentage energy from carbohydrate (55% or 70% | Figure 1, top-right) and GI (low or high, Figure 1, bottom-right) but were matched for protein, fiber, and energy. The study design itself comprised 5 phases:

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"Phase 1 was a 5-week weight maintenance phase in which weight maintenance energy needs were determined by adjusting provided energy intake to maintain stable weight. Mean Phase 1 energy intake was 12.2 MJ/day with 48% energy provided as carbohydrate, 16% as protein, and 36% as fat. Following Phase 1, participants were randomized by the study statistician to their Phase 2 dietary assignment using computer-generated randomization. The four diets differed in carbohydrate content (55%, ModCarb or 70%, HighCarb of total energy) and dietary GI (less than 60, LowGI or 80, HighGI), and were provided for 12 weeks at 67% of the weight maintenance energy intake determined in Phase 1. 

Participants were allowed to increase their energy intake during Phase 2 by requesting additional, randomization-appropriate foods from the metabolic kitchen if too hungry to be adherent. Phase 3 was a 5-week weight maintenance phase during which food was provided according to randomization. Energy intake during Phase 3 was prescribed to support weight maintenance at the new, lower body weight, and was predicted from body weight and energy intake measured at the end of Phase 2, with adjustment for self-reported physical activity. Phase 4 was a 12- month follow-up period during which participants selected and pre pared their own meals after being provided with instructions on fol lowing the diet to which they were randomized" (Karl. 2015)

To assess the effects of this sequence of induction (weight maintenance), and weight stabilization phases, the body weight, body composition, RMR, and metabolic adaptation (measured RMR vs. predicted resting metabolic rate = RMR) of the middle aged study participants (49-64 years) were measured before and after all phases of the study.

Figure 2: (A) Weight loss and (B) percentage of total weight loss attributable to fat mass and fat free mass while consuming provided-food diets differing in glycemic index (GI) and percent energy from carbohydrate (55%, ModCarb and 70%, HighCarb) for 17 weeks (n = 79). Values are mean 6 SEM. Weight loss analyzed by repeated measures ANCOVA, body composition by two-factor ANOVA. a,bMain effect of time; asignificant decrease from baseline (P < 0.001), bsignificant difference from Phase 2 end (P < 0.001). No diet effects (main effects or interactions) for any comparisons. GI, glycemic index; HighCarb, 70% energy from carbohydrate; ModCarb, 55% energy from carbohydrate (Karl. 2015).

Interestingly, the analysis of this data revealed no significant inter-group differences in terms of any of the relevant study outcomes. Yes, you read me right: This means that neither the GI, nor the GL, nor the carbohydrate content of the diet had statistically significant effects on weight loss, body composition, RMR, or the metabolic adaptation aka "metabolic damage" due to weight loss.

Figure 3: Measured resting metabolic rate as a function of predicted metabolic rate (Karl. 2015). Note: If there was no "metabolic damage", the solid line which represents the ideal body-weight dependent decline of energy expenditure and the dashed line which represents the actual ratio of the measured to the predicted RMR should be congruent.

While there were no inter-group differences and neither the amount or the type of carbohydrates had an effect on the reduction of the metabolic rate, there is still one interesting result you can see in the right graph in Figure 3. Said graph depicts the ratio of the measured to the predicted metabolic rate during the 5-week weight maintenance phase. If you look closely, you will realize that it suggests that having a high predicted RMR, i.e. being heavier, being taller and being more muscular, is associated with a non-significant decline of the non-predicted reduction of the energy expenditure (=metabolic damage) and thus a narrowing of the gap between the solid and dashed line.

"Solid and dashed? I don't get it!"

You're asking how I can support this hypothesis? Well, the dashed line that represents the true ratio of the actual to the predicted RMR approaches the theoretical one (the solid line) for higher RMR values. If this was more than a trend, it would suggest that two things: (a) Losing less weight and thus maintaining a higher predicted metabolic rate protects against metabolic damage (that would be useless). And (b) being tall and muscular and thus having a naturally high(er) predicted RMR can protect you from suffering metabolic damage when you lose weight.

Unfortunately, it's not possible to tell which (if any) of the two options is correct. If I had to make an educated guess, though, I would say it's a combination of both: The weight change of an average 5.5 kg did not wary too much and was withing 95% confidence intervals of [-7.1 kg, -4.6 kg]. In conjunction with individual physiological qualities of people with higher baseline RMRs, it could still explain the narrowing of the gap between predicted and true RMR after dieting.

Figure 4: Changes in body composition (absolute value in kg) after 20 weeks and after weight loss phase 2 (Karl. 2015).

Bottom line: As Karl et al. point out, "neither low-GI relative to high-GI diets nor moderate-carbohydrate relative to high-carbohydrate diets showed differences with respect to effects on changes in body composition or resting metabolism during weight loss when confounding dietary factors were tightly controlled in a study providing all food for 22 weeks" (Karl. 2015).

This does not just go against the mainstream assumption that low GI and/or low(er) carbohydrate diets facilitate weight loss, fat loss and weight maintenance (see data in Figure 4 for an overview of these parameters, it also contradicts the initially mentioned broscientific assumption that carbohydrates, in general, and high GI carbs, in particular, have a protective effect against the unexpected diet-induced reduction of basal energy expenditure many people know as "metabolic damage". If there's anything of which the study at hand suggests that it could protect you from such unexpectedly large decrease in RMR, it's not high GI carby, but rather an already high(er) baseline RMR (see Figure 3).

And what does that tell us? Right! Since a high predicted RMR is a function of (a) being male, (b) being tall, and (c) being muscular, all three attributes may protect you from diet-induced "metabolic damage" | Let me know your thoughts and comment on Facebook!

References:

• Danforth Jr, Elliot, et al. "Dietary-induced alterations in thyroid hormone metabolism during overnutrition." Journal of Clinical Investigation 64.5 (1979): 1336.
• Karl, J. Philip, et al. "Effects of carbohydrate quantity and glycemic index on resting metabolic rate and body composition during weight loss." Obesity 23.11 (2015): 2190-2198.
• Mariash, C. N., et al. "Synergism of thyroid hormone and high carbohydrate diet in the induction of lipogenic enzymes in the rat. Mechanisms and implications." Journal of Clinical Investigation 65.5 (1980): 1126.
• Serog, P., et al. "Effects of slimming and composition of diets on VO2 and thyroid hormones in healthy subjects." The American journal of clinical nutrition 35.1 (1982): 24-35.
• Ullrich, Irma H., Philip J. Peters, and M. J. Albrink. "Effect of low-carbohydrate diets high in either fat or protein on thyroid function, plasma insulin, glucose, and triglycerides in healthy young adults." Journal of the American College of Nutrition 4.4 (1985): 451-459.

Green Tea Supplement Boosts Resting & Exercise-Induced Fatty Acid Oxidation + Energy Expenditure - How Relevant is This for Losing Fat + Will it Impair Training Adaptations

"Yes", GTE will increase your total energy expenditure (TEE) and decrease the ratio of glucose to fat you're burning at rest and during your workouts, but "NO", it won't make your abs appear w/out dietin'.

You will remember that I am not exactly a fan of green tea extracts. In spite of the fact that there are studies that suggest reductions of both thyroid hormone and testosterone production, when you consume high(er) amounts, their anti-inflammatory effects appear to help (obese) people lose weight. In view of the fact that a recent study suggests that this does not interfere with the adaptational response to exercise, like vitamin C + E, for example (learn more), they are thus still among the most promising over-the-counter anti-obesity agents.

With that being said, the increase in fatty oxidation is often mentioned when people try to explain why green tea helps (obese) people lose fat.

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As a SuppVersity reader, however, you know that a mere increase in the use of fats over carbohydrates will not translate into practical weight loss. Against that background it is important to investigate the effects of green tea extracts on both, the respiratory exchange ratio (RER), which is the quotient of glucose / fat that's used to fuel your basal and exercise-induced metabolic demands, as well as their effects on your total energy expenditure.

Luckily, a recent study from the Charles Darwin University and the University of New South Wales in Australia includes both measures of changes in RER, resting energy expenditure (REE) and the total energy expenditure (REE + activity induced energy expenditure).

Figure 1: Diagrammatic representation of the study design. * indicates blood collection. Lactate assessed at *1, *2, *4, *6, *9; catecholamines at *1, *4, *5, and glycerol at *1–*9 (Gahreman. 2015).

But that's not all. The scientists also took a look at the potential mediators of increased energy expenditure and fatty acid use like catecholamines and they did so in normal-weight young women (age: 21.5 +/- 0.5 years; body mass: 65.7 +/- 1.8 kg; BMI: 24.3 +/- 0.4 kg/m²; maximal oxygen consumption; VO2max): 32.1 +/- 1.7 mL/kg/min) and not the usual subjects: Overweight or obese post-menopausal women or male and female patients with type II diabetes.

Yes, it's official: Unlike vitamin C + E, GTE will not impair your gains! Ewa Jówko et al. (2015) were able to show that the consumption green tea extract (GTE) supplements in in dosages of only 245 mg polyphenols (including 200 mg catechins, among them 137 mg epigallocatechin-3-galate) does prevent the oxidative stress induced by repeated cycle sprint tests (RST) in sprinters without hindering the training adaptation in antioxidant enzyme system. What it does not do, either, is to decrease the exercise-induced muscle damage, or improve the sprint performance during the sprinters preparatory phase of their training cycle, though. Needless to say that studies involving different subject groups, dosages and training modalities would be required to eventually confirm that there are no anti-hormetic effects w/ GTE.

I have plotted the most relevant results of experiment the design of which is represented graphically in in Figure 1 for you in Figure 2. Please note that only the changes in VO2 which are indicative of an increased oxidation of fatty acids and the corresponding RER, the quotient of carbohdydrate oxidation and fat oxidation changed significantly.

Figure 2: Response at rest and during and after intermittent sprinting exercise in the green tea and placebo conditions; data expressed as relative differences between GTE and PLA (Gahreman. 2015).

It is thus all the more important to put the effects the consumption of three GTE (250 mg of camellia sinesis extract w/ 187.5 mg polyphenols, 125 mg EGCG) or placebo (cellulose) capsules the day before and one capsule 90 min before a 20-min intermittent sprinting exercise (ISE) cycling protocol consisting of

• a 5-min warm-up at 30 W, and 20 min of ISE on a Monark Ergomedic 839E ergometer at 110 RPM during the sprint phase and 40 RPM during the recovery phase (pedal resistance for the sprint phase was calculated as 60% of each participant’s maximal power output) 
• during which the subjects performed a total of sixty 8-s/12-s bouts totaling 8 min of sprinting and 12 min of easy pedaling recovery 

had on the metabolism of the fourteen untrained non-habitual coffee or green tea drinkers (< 2 cups per day) during the exercise, as well as before and after the ISE protocol:

Table 1: Mean power output, rating of perceived exertion, and lactate response to the sprinting and recovery components of the intermittent sprinting exercise for the placebo and green tea conditions (mean and SEM | Gahrmen. 2015).

• There was a significant increase in fat oxidation post-exercise compared to at rest in the placebo condition (p < 0.01). 
• After GTE ingestion, however, at rest and post-exercise, fat oxidation was significantly greater (p < 0.05) than that after placebo. 
• Plasma glycerol levels at rest and 15 min during post-exercise were significantly higher (p < 0.05) after GTE consumption compared to placebo. 
• There was no significant increase in total energy expenditure during or after exercise, though - that's in line with results Gregersen et al. (2009) generated in a study in normal-weight men, but different from some studies in normal-weight-to-moderately overweight men like Dullo et al. (1999) that report increases in TEE of ~2,8% over both, placebo and caffeine.
• Compared to placebo, plasma catecholamines increased significantly after GTE consumption and 20 min after ISE (p < 0.05 | not shown in Figure 2). 
• The effects are almost certainly not triggered by caffeine, because the capsules contained only 20mg of caffeine and previous studies have shown that only oral dose of more than 100 mg caffeine will elicit a significant increase in thermogenic response (Bracco. 1995; Dulloo. 1998 - suggest that 600-1,000mg/day is necessary for sign. increases in thermogenesis).
• It's also worth noting that there were no significant differences in mean power output, RPE, lactate levels, RPM (Table 1), and HR levels between the GTE and placebo trials. This leaves little doubt that the effects were not mediated by direct ergogenic effects (= higher exercise performance / effort) in response to the GTE supplementation.
• Lastly, it should be said that even though this was not tested in the study at hand, previous clinical trials like Bérubé-Parent et al. (2005) report identical thermogenic effects for low and high dosages of GTE. Thus, simply taking more GTE probably wouldn't have changed the results considerably.

Overall, the results of the study do thus support the ubiquitous claim that the ingestion of green tea extracts can significantly increase the fat oxidation at rest, during and after exercise when compared to placebo. In spite of the fact that the conclusion of the abstract to the study at hand makes it appear as if that was a practically highly relevant finding, there's one question neither the abstract nor the full-text of the paper actually address: Do the increase in fatty oxidation and the (albeit non-significant) increases in total and resting energy expenditure mean that consuming green tea extracts is going to help young, healthy, non-overweight women like the subjects in the study at hand lose body fat?

Figure 3: If you do the math and calculate the difference between the amount of energy the women would spend during a given week with 3x ISE sessions with and without GTE, the results are disappointing: The difference per week amounts to only 105.4kcal (1%), which is very unlikely to have a sign. effect on fat loss (calculated based on data from Gahreman. 2015).

Let's do some math to decide if the changes matter, or not... Ok, if they'd do the same ISE protocol three times a week and the increase in REE and TEE would not change over time, young, lean women who consumed GTE on a daily basis would burn an extra amount of only 105.4/kcal per week. That's a pathetic 1% increase of which I don't have to tell you that it is not only stat. not sign., but also practically irrelevant. In fact, this may well explain why you cannot expect green tea supplements to do the weight loss work for you. With the increases in fatty acid oxidation and energy expenditure being only two items on the list of purported anti-obesity benefits of GTE, the results of the study at hand do yet not necessarily mean that GTE supplements were totally useless. What they do mean, though, is that these supplements won't make young women lose body fat without the help of an energy restricted diet, which is still the indispensable backbone of any fat loss regimen.

In fact, specifically in the obese, the proven anti-inflammatory effects, as well as GTE's ability to reduce the absorption of both carbs and fats and to keep your appetite in check make it a viable addition to a reduced energy intake specifically in obese individuals (Hill. 2007; Rains. 2011). In view of the small increase in REE, but sign. impact on inflammation and glucose / lipid metabolism, specifically in the obese, it is thus  not surprising that meta-analyses report only a marginal association between green tea consumption and body weight on the population level, but significant beneficial effects on weight loss maintenance in overweight subjects after reductions in energy intake (Hursel. 2009) | Comment on Facebook!

References:

• Bérubé-Parent, Sonia, et al. "Effects of encapsulated green tea and Guarana extracts containing a mixture of epigallocatechin-3-gallate and caffeine on 24 h energy expenditure and fat oxidation in men." British Journal of Nutrition 94.03 (2005): 432-436.
• Bracco, David, et al. "Effects of caffeine on energy metabolism, heart rate, and methylxanthine metabolism in lean and obese women." American Journal of Physiology-Endocrinology and Metabolism 269.4 (1995): E671-E678.
• Dulloo, A. G., et al. "Normal caffeine consumption: influence on thermogenesis and daily energy expenditure in lean and postobese human volunteers." The American journal of clinical nutrition 49.1 (1989): 44-50.
• Dulloo, Abdul G., et al. "Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans." The American journal of clinical nutrition 70.6 (1999): 1040-1045.
• Gahreman, Daniel, et al. "Green Tea, Intermittent Sprinting Exercise, and Fat Oxidation." Nutrients 7.7 (2015): 5646-5663.
• Gregersen, Nikolaj T., et al. "Effect of moderate intakes of different tea catechins and caffeine on acute measures of energy metabolism under sedentary conditions." British journal of nutrition 102.08 (2009): 1187-1194.
• Hill, Alison M., et al. "Can EGCG reduce abdominal fat in obese subjects?." Journal of the American College of Nutrition 26.4 (2007): 396S-402S.
• Jówko, Ewa, et al. "The effect of green tea extract supplementation on exercise-induced oxidative stress parameters in male sprinters." European journal of nutrition (2014): 1-9.
• Phung, Olivia J., et al. "Effect of green tea catechins with or without caffeine on anthropometric measures: a systematic review and meta-analysis." The American journal of clinical nutrition 91.1 (2010): 73-81.
• Rains, Tia M., Sanjiv Agarwal, and Kevin C. Maki. "Antiobesity effects of green tea catechins: a mechanistic review." The Journal of nutritional biochemistry 22.1 (2011): 1-7.

High Protein Diet & Weight Maintenance - Same or Different Benefits? High Metabolic Rate, Increased Satiety, Improved Body Composition Confirm: "You Better Eat Your Protein!"

Scientists ask: High protein for weight loss only or also during maintenance phases?

"Relatively high-protein diets are effective for body weight loss, and subsequent weight maintenance," that's the first half-sentence from the abstract of the latest study from the Maastricht University, Maastricht (Martens. 2014). A sentence that continues with a reference to an important limitation of the contemporarily available evidence: "It remains to be shown whether these diets would prevent a positive energy balance."

Therefore, Martens et al. conducted a study that investigated the effects of high vs. low protein diets during weeks of body weight stability [unfortunately, no RDA group (0.8kg/day) ;(].

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In that, the researchers objective was to determine fullness, energy expenditure, and macronutrient balances on a high-protein low-carbohydrate (HPLC) diet compared with a high-carbohydrate low-protein (HCLP) diet at a constant body weight, and to assess whether effects are transient or sustained after 12 weeks.

Figure 1: Comparison of the relative contribution of protein, carbohydrates and fat to the total energy intake (Martens. 2014).

As you can see in Figure 1, the "high protein diet" is not exactly as "high" as many of you may have expected. With only 35% of the total energy of approximately 2,000kcal (on average) and a mean body weight of 66kg, the total protein intake relative to body weight was "only" 1.89g/kg protein.

The changes in body composition did not reach statistical significance, but the way the protein balance went from 4.1 ± 18.8 g/day to −16.4 ± 11.1 g/day within just one week and stagnated at −11.9 ± 14.1 g/day on the low protein diet clearly suggests that eating a diet that contains only 0.38g/kg body weight protein won't be able to sustain the amount of lean mass you need to function properly.

Compared to the low protein diet, where only 5% of the daily energy requirements were covered with high protein foods and thus only 0.38g protein per kg body weight, that's yet still plenty of protein and enough to have significant effects on the

• total energy expenditure (TEE) (P = 0.013), 
• sleeping metabolic rate (SMR) (P = 0.040), and 
• diet-induced thermogenesis (DIT) (P = 0.027) 

of the male and female study participants. Most importantly, the total energy expenditure was maintained only in the high protein diet group (HPLC), while it significantly decreased throughout the intervention period in the high carbohydrate (HCLP) diet group (wk 1: P = 0.002; wk 12: P = 0.001).

Figure 2: Metabolic effects of high vs. low protein diets (baseline vs. 12-week in % | Martens. 2014)

Similarly, the protein balance varied directly according to the amount of protein in the diet, and diverged significantly between the diets (P = 0.001); and last but not least, unsurprisingly the fullness ratings were significantly higher in the HPLC vs. the HCLP diet group at wk 1 (P = 0.034), but not at wk 12.

Figure 3: High vs. low protein diets have opposite effects on hunger, fullness, satiety and desire to eat w/ measurable effects on body comp. that may become sign. after more than 12 weeks (Martens. 2014).

Bottom line: The study at hand provides the missing evidence that high protein diets have similar beneficial effects during weight maintenance phases as they do during weight loss phases.

Most importantly, a high protein intake of (in this case) 1.89g/kg protein will help you to maintain a high energy expenditure and keep you from eating more than you need, due to its beneficial effects on hunger, fullness, satiety and the desire to eat you can see in Figure 3. What? Ah, yes! There were also decrease and increase in fat and lean mass of 3% and 1%, respectively. These changes in favor of the high protein diet did not reach stat. significance over the course of the 12-week study, but are likely to become sign. after longer periods | Comment on Facebook!

References:

• Martens, E. A., et al. "Maintenance of energy expenditure on high-protein vs. high-carbohydrate diets at a constant body weight may prevent a positive energy balance." Clinical Nutrition (2014).

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 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, anyway). 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 ("hunger hormone"), the subjects' post-diet response 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. The fact that this didn't show in the hormonal markers the scientists analyzed may simply be a consequence of choosing the wrong markers. Acetylated ghrelin, for example, would be such an alternative marker... and seeing the cortisol and testosterone would also have been interesting.

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.