Fewer Than 1 in 100 People Need More Than 2.4 Times Their Resting Energy Expenditure | Eating More 'll Make You Fat!

Sweet potatoes alone won't cut it for Tour de France Cyclists and people on a North Pole Expedition - the only study subjects who need >5x their RMR.

I assume you won't have the technical equipment to measure your total energy expenditure by the means of doubly labeled water. Accordingly, I would suggest you go back to my recent article about the accuracy of equations to calculate your resting energy expenditure (read it). Once you know that you multiply it by 2.0-2.4 and that's it: You are not going to expend more energy per day, bro...

How do I know? From a recent paper by Klaas R. Westerterp published in the Proceedings of the Nutrition Society (2017). In the paper, he reviewed results from doubly labeled water studies of the total daily energy expenditure (TDEE) under daily living conditions.

What will affect your energy expenditure and how much energy do you expend?

Intermittent Fasting Boosts Energy Exp. (EE)

3 Revelations About EE While Lifting

How Dieting Reduces Your EE via the CNS

Calculate Your RMR Accurately (+Spreadsheet)

Synergistic or Antagonistic for Max EE

Up the Volume to Up Your Energy Expenditure

The goal was to determine the ratio of total daily energy expenditure to the resting metabolic rate, a quantity scientists somewhat misguidingly call the physical activity level (PAL). Since the carbon dioxide production needs interpretation as it critically depends on your substrate utilization (21·1 kJ/l CO2 for carbohydrate oxidation vs. 27·8 kJ/l for CO2 fat oxidation) and can not be 100% accurate unless all relevant dietary information is available.

While the energy equivalent is 23·5 kJ/l for subjects consuming a typical Western diet with 55 % carbohydrate, 15 % protein, and 30 % fat, exercising subjects often consume diets with a large contribution of carbohydrate-rich sports drinks. Accordingly, they will have a correspondingly lower value for the energy equivalent of carbon dioxide of 23·0 kJ/l. As Westertarp points out, "[i]n he Tour de France, the contribution of sports drinks was twice as high, resulting in an energy equivalent of 22·5 kJ/l carbon dioxide" (Westerterp 2017).

Figure 1. Pal value distribution in the general population in men (grey) and women (white) bars as measured in the first two-week doubly-labeled water analysis (left); PAL values decline from age 50+ almost linearly in both older men (dotted line) and older women (solid line | Westerterp 2017).

That does not change the fact that for the average population less than 1% achieve PAL values beyond the 2·00–2·40 of 'high expenders'. What does that mean? Well, if your RMR is 1600kcal, you better be competing in the Tour de France if you want to get away with eating significantly more than 3840kcal per day (note: if you do only slow-paced classic resistance training you won't even get close to that value - any gains you make with 2.4x your RDA will at least in large parts body fat).

The highest ever measured PAL values were observed in Tour de France cyclists (PAL 4.3-5.3 according to Westerterp 1986): Only an expedition to the North-Pole (on foot!) can compete with a similar PAL value of 5.0. But I doubt that many of you will like to copy the exercise protocol of the trekkers, who walked from the northernmost point of Siberia, pulling each a 135 kg sledge with food, fuel and equipment, in the direction of the North Pole and were unable to maintain their body weight despite ample supplies (1kg weight loss every week) - an observation that's in line with the majority of other studies which show that PAL values over the 2.0-2.4 mark are usually associated with an energy deficit.

And no, these values were not observed while dieting. If food intake is restricted, the exercise induced increase in energy expenditure will decrease even further. Plus: The review also shows that "an exercise induced increase in activity energy expenditure can be compensated by a reduction in REE and by a reduction in non-exercise physical activity - especially at a negative energy balance. So...

• you are not going to need more than 2.0-2.4x your RDA per day - unless you're really competing in the Tour de France (see information in the previous red box).
• if you try to surpass this limit by exercising, even more, your resting energy expenditure will decrease (478,011kcal more than the reduction in weight would suggest in Johannsen (2012).

Additionally, in untrained subjects, an exercise-induced increase in activity energy expenditure is compensated by a training-induced increase in exercise efficiency. Which means that

• the more trained you are the less energy you will need for the same amount of exercise

As the data in Figure 1 goes to show you, women are on average less active than men, but their numbers in the high activity group is still higher.

What does previous research say?

Westerterp found only 10 studies that utilized the measurement of PAL to assess the effect of exercise before and during an exercise intervention. The exercise interventions, which lasted for 4-40 weeks, used either aerobic training or resistance training, and were with two to five 40–90 min sessions per week, representative of the physical activity the average gymrat may be accumulating. In view of the fact that all subjects had been sedentary slobs before the intervention, the significance of the measured PAL values of 1·40–1·69 is not clear.

Figure 2: Participating in a half-marathon training will "at best" get you across to the 2.0 PAL mark (Westerterp 1992)

In four of those studies, subjects reached values of 2·00–2·40 for a vigorously active lifestyle, but that required absolutely unrestricted energy intakes. Interestingly enough, the only study that combined exercise interventions with an energy-restricted diet, the extra exercise did not increase the ratio of the total to the resting energy expenditure in the 20 healthy obese women who participated. In none of the ten studies, PAL values over the 2.0-2.4 maximum were reached.

One of the reasons why exercise intervention could fail to improve the PAL values is that people compensate by reducing non-exercise physical activity significantly. Scientific evidence to support this assumption has yet only been observed in studies in elderly individuals and studies that combined exercise with energy restriction.

Click image to open spreadsheet to calculate your RMR; obviously, you will have to change the data at the top

What's the take away: When I look at the interwebs people are bragging with how much they're eating... while I am not saying all of them are lying, I have to warn you, though, you're not Michael Phelps and no matter how much you train, you're not going to get away with 8,000kcal/d - unless you're a Tour de France Cyclist or on a survival trip to the North Pole and thus able to master a PAL value of 5 or more (which would mean that your daily energy requirements are 5x your RMR).

Moreover, Klaas R. Westerterp study suggests that 2.0-2.4 x your resting metabolic rate is where you will end up if you're highly active (within what one would see in non-pro-athletes). Accordingly, most of you will get fat if they consume more than twice their resting metabolic rate - a value you can calculate with the spreadsheet in my previous article about calculating your resting metabolic rate on a daily basis ... sorry, bros! Comment!

References:

• Johannsen, Darcy L., et al. "Metabolic slowing with massive weight loss despite preservation of fat-free mass." The Journal of Clinical Endocrinology & Metabolism 97.7 (2012): 2489-2496.
• Westerterp, K. R., et al. "Use of the doubly labeled water technique in humans during heavy sustained exercise." Journal of Applied Physiology 61.6 (1986): 2162-2167.
• Westerterp, Klaas R., et al. "Long-term effect of physical activity on energy balance and body composition." British Journal of Nutrition 68.1 (1992): 21-30.

Accuracy of Calculated Metabolic Rate in Athletes: Best and Worst Equations are +3% to -17% Off Measured RMR | Plus: Spreadsheet to Calculate Your RMR With Each Equation

Wouldn't it be cool if you could simply plug your computer into a USB-slot at the back of your head to read out your energy status...? Ah, no, it wouldn't! It's already scary enough how much Fitbit, Garmin, and co know about us.

This is by no means the only problem with metabolic research, these days, but it's one that's really getting on my (and probably also your) nerves. It's all about the sick and obese. It is thus no wonder that you will easily find papers that assess how the Nelson, Mifflin, Harris-Benedict and other equations that are commonly used are off wrt the real energy requirements of the average obese type II diabetic. What you'll be hard-pressed to find, though, is data on their accuracy in athletes.

I have addressed this issue before, but with the publication of a recent paper in the Journal of Strength and Conditioning Research there's now more data available than from all the previous studies I've seen.

The effect of lean mass on RMR is often overrated, but you must build muscle to get jacked

Tri- or Multi-Set Training for Body Recomp.?

Alternating Squat & Blood Pressure - Productive?

Pre-Exhaustion Exhausts Your Growth Potential

Exercise not Intensity Variation for Max. Gains

Battle the Rope to Become Ripped and Strong

Study Indicates Cut the Volume Make the Gains!

The purpose of the study was to determine the accuracy of five different resting metabolic rate (RMR) prediction equations in male and female athletes.

• Nelson Equation (cf. Nelson 1991) -- RMR (kcal/day) = 25.80 x Fat-Free mass(kg) + 4.04 x Fat mass(kg)
• Mifflin-St. Jeor Equation (cf. Bullough 1995) -- RMR (kcal/day) = 9.99 x weight(kg) + 6.25 x height(cm) - 4.92 x age + 166 x Sex (males, 1; females, 0) -161 
• Harris-Benedict Equation (cf. Brožek 1963) -- revised equation for men RMR (kcal/day) = 66.47+ 13.75 x Weight(kg) + 5 x Height(cm) – 6.76 x Age(yrs.); for women RMR (kcal/day) = 655.1 + 9.56 x Weight(kg) + 1.85 x Height(cm) – 4.68 x Age(yrs.)
• De Lorenzo Equation (cf. Carpenter 1995) -- RMR (kcal/day) = -857 + 9 x Weight(kg) + 11.7 x Height(cm) 
• Cunningham Equation (cf. Cunningham 1980) -- RMR (kcal/day) = 500 + 22 x Fat-Free mass(kg)

Twenty-two female (19.7± 1.4 yrs.; 166.2 ± 5.5 cm; 63.5 ± 7.3 kg; 49.2 ± 4.3 kg of Fat-Free Mass; 23.4 ± 4.4 BF%) and twenty-eight male (20.2 ± 1.6 yrs.; 181.9 ± 6.1 cm; 94.5 ± 16.2 kg; 79.1 ± 7.2 kg of FFM; 15.1 ± 8.5% BF) athletes were recruited to participate in one day of metabolic testing.

"Assessments comprised RMR measurements via indirect calorimetry and body composition analyses via air displacement plethysmography. One-way repeated measures analysis of variance with follow up paired t-tests were selected to determine differences between indirect calorimetry and five RMR prediction equations. Linear regression analysis was used to assess the accuracy of each RMR prediction method. An alpha level of p < 0.05 was used to determine statistical significance" (Jagim 2017). 

What Andrew R. Jagim and colleagues found is in contrast to what studies in the non-athletic population show (Woolf 2015; Namazi 2016; Willis 2016), which tend to show both, over- and underestimations, depending on the equation that was used.

Figure 1: Measured (bottom) and calculated RMR in men (orange) and women (blue) - the percentages next to the bars are the relative differences between the respective calculation and the actual measurement (Jagim 2017).

In the study at hand, however, "[a]ll of the prediction equations significantly underestimated RMR". Moreover, the scientists found that...

Click image to open spreadsheet to calculate your RMR; obviously, you will have to change the data at the top

• the Cunningham equation had the smallest mean difference (-165 kcals); 
• in males, the Harris-Benedict equation was found to be the best prediction formula with the lowest root mean square prediction error (RMSPE) value of 284 kcals;
• in females, the Cunningham equation was found to be the best prediction equation with the lowest RMSE value of 110 kcals. 

In view of the fact that all of these equations "consistently [...] underestimate[d] RMR in male" athletes and tends to do the same in female athletes, you should exercise caution when you're using them on yourself or clients...

Figure 2: The relationships between constant error (actual – predicted RMR) and average RMR ((measured + predicted)/2) for males (A) (n = 28) and females (B) (n = 21) in the current sample of athletes. The solid line represents mean of constant error. Dashed lines represent ± 1.96 SD of constant error. RMR = resting metabolic rate. *P < 0.05 (Jagim 2017).

...get suspicious if they don't gain in a planned caloric surplus, it could be the way you calculated the energy needs that is messing with the results. And keep in mind: Figure 2 tells you that individuality is still key - eventually, food logging and extrapolating from that will thus always be the most reliable way to estimate the actual energy requirements of an individual.

Now that you "know" how much energy you need, you just have to "get your macros straight" - Luckily, I've got a write-up that will help you do just that within no more than two minutes | read this SuppVersity Classic

Bottom line: Somewhat surprisingly, the often derided Harris-Benedict equation [RMR (kcal/day) = 66.47+ 13.75 x Weight(kg) + 5 x Height(cm) – 6.76 x Age(Yrs.)] delivered the most accurate results for male, while the fat-free mass based Cunningham equation [RMR (kcal/day) = 500 + 22 x Fat-Free mass(kg)] performed best for female athletes.

Neither of them will yet yield absolutely reliable results for a given individual. And you will still have to use a different equation to calculate your actual energy requirements, which are obviously RMR + activity dependent energy expenditure. That's why I stick to my repeatedly phrased recommendation: if you want to know how much you "need", log your food intake over two weight-stable weeks and go from there | Comment on Facebook!

References:

• Brožek, Josef, et al. "Densitometric analysis of body composition: revision of some quantitative assumptions." Annals of the New York Academy of Sciences 110.1 (1963): 113-140.
• Buchholz, Andrea C., Mahroukh Rafii, and Paul B. Pencharz. "Is resting metabolic rate different between men and women?." British Journal of Nutrition 86.6 (2001): 641-646.
• 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.
• Cunningham, John J. "A reanalysis of the factors influencing basal metabolic rate in normal adults." The American journal of clinical nutrition 33.11 (1980): 2372-2374.
• Jagim, Andrew R., et al. "The accuracy of resting metabolic rate prediction equations in athletes." The Journal of Strength & Conditioning Research (2017).
• Namazi, Nazli, et al. "Accuracy of the common predictive equations for estimating resting energy expenditure among normal and overweight girl university students." Journal of the American College of Nutrition 35.2 (2016): 136-142.
• Nelson, Karl M., et al. "Prediction of resting energy expenditure from fat-free mass and fat mass." The American journal of clinical nutrition 56.5 (1992): 848-856.
• Willis, Erik A., et al. "Predicting resting energy expenditure in young adults." Obesity research & clinical practice 10.3 (2016): 304-314.

Women Have a Hard(er) Time Losing Body Fat W/ Exercise 'cause it Increases Their Appetite More Than Men's, Right?

Is she going to binge after this body weight squat workout? Nah, don't worry...

I've repeatedly written about studies that show that the Taubs'ian notion that "exercise is useless because it just makes you hungry" is bullsh*t. It is indeed useless to work out to burn calories, it is yet never useless to work out - even if fat loss, not health or longevity is your goal.

What you should be aware of, though, is that there is a gender bias in the selecting of subjects in health sciences; and since the average subject in nutrition and exercise sciences is male and studies that have enough male and female subjects to identify relevant sex differences are rare, we don't really know if everything that has been "scientifically proven" can also be considered "scientifically proven" for female dieters and/or trainees.

Learn more about the (often ;-) small but significant difference at the SuppVersity

1g PRO per 2g CHO + Circuit T. for Women?

Is the Optimal Exercise Order Sex-Specific?

1-3mg Melatonin Shed Fat W/Out Diet & Exercise

Not Bulky! Lifting Will Make Toned & Strong.

How to Really Train Like a Woman

Sex-Differences in Fat Oxidation - Reviewed

The effects exercise will have on your appetite, for example, is such a research interest that has been investigated mainly in male subjects. As Alice E. Thackray, et al. (2016) point out in their latest paper in Nutrients, ...

"[...] opportunities to examine sex-based differences have been limited, but represent an interesting avenue of inquiry considering postulations that men experience greater weight loss after exercise interventions than women" (Thackray, 2016). 

In other words: While we don't know much, the few things we do know about the sex-specific interaction between exercise and your appetite are enough to draw a handful of practically highly relevant conclusions about optimal exercise and diet regimens for women.

Acute exercise, appetite, and compensation with energy intake - it's primarily individual

Before we delve deeper into sex-differences, though, I would like to remind you that the individual differences in fat and weight loss are not just better studied than those between men and women, they are probably also much more relevant than any sex difference - and that in spite of the fact that the research suggests that they are mediated by the same (individual) differences in compensatory behaviours that negate the exercise-induced energy deficit as the inter-individual differences.

Figure 1: The 2008 study by King et al. shows that (a) the individual differences in appetite are magnitudes larger than the actual effect of exercise and that (b) what the subjects make of it in terms of their effects on the subjects' actual energy intake cannot be predicted based on these subjective changes (King. 2008).

In their 2008 study, for example, King et al. found that the individual propensity to compensate for a reduction in energy intake and/or an increase in expenditure can explain weight loss differences that are larger than 50% - albeit with a standard deviation in the "compensators" that is significantly larger than the total weight loss.

SuppVersity Suggested Article: "Training "On Cycle", Done Right - Women See Much Better Results When Periodization is in Line W/ Menstrual Cycle" | read it

Did you know that women benefit from dieting and training in-sync with their menstrual cycle? I am pretty sure you know that as I've mentioned this before at the SuppVersity and even wrote a whole article about "Training on the Female Cycle"evidence  suggests that compared with untailored programs, synchronising diet and exercise training interventions around the hormonal changes that occur during the menstrual cycle elicits greater weight loss (Geiker, 2016) and improvements in muscle strength (learn more). Yet while we do know how cyclical fluctuations in sex hormones (estrogen and progesterone) alter appetite-regulatory hormone concentrations and energy intake in women (Buffenstein, 1995; Brennan, 2009), however, we don't know their interaction with exercise.

Similar discrepancies were found for the effect on subjective hunger, where the standard deviation of the subjects' hunger on a visual analog scale was ±9.6 mm and thus 240x larger than the average appetite increase of 0.4 mm/day. That's huge and it's quite a pity that the study didn't have enough subjects to conduct a meaningful analysis of the effect of the interactions of the subjects' sex on the increase in hunger the subjects experienced in King's 12-week study over the course of which the subjects trained five times a week without having to adhere to an energy restricted diet.

Men or women - that could still make an important difference

That this analysis could have yielded a significant difference between men and women, however, appears to be refuted by studies like Alajmi, et al. whose healthy male and female subjects had - within the previously described inter-individual differences - identical changes in the concentrations of the hunger-regulating acetylated form of ghrelin in response to 60 min treadmill running at 70% VO2peak (see Figure 2) - and that even though the men burned 57% more energy than the women.

Figure 2: Time-averaged total area under the curve (AUC) for appetite ratings (left); and plasma acylated ghrelin concentrations (right) in the control trial (□), and after 60 minutes on the treadmill at 70% VO2peak (■) in Alajmi's study.

In fact, the data in Figure 2 appears to confirm - for both men and women - the anorexic effect that is often ascribed to exercise. The study by Alajmi et al. is yet only one out of four partly contradictory studies that investigate the sex-based differences in the regulation of appetite in response to acute exercise:

• Kawano, et al. (2012) - The first acute exercise and appetite study that compared men and women was published in Obesity Research & Clinical Practice. The authors reported that 20 min of rope skipping exercise increased ratings of subjective hunger 30 min after exercise in women but not men - quite a surprising result, also because high(er) intensity exercise as rope skipping has been shown to be particularly appetite suppressive in the average (=male) study subject; furthermore, Thackray et al. rightly criticize that the authors did not "control for the potential confounding effects of the menstrual cycle, which represents an important consideration for acute exercise studies comparing men and women" (Thackray. 2016). In this regard, recent studies have given us a few interesting insights (see light blue box). However, whether appetite responses to exercise in women are influenced by the menstrual cycle phase is not known and "represents", as Thackray et al. write "a research avenue to consider in the future".
• Hagobian, et al. (2012) - Scientists from the California Polytechnic State University tested the effects on both appetite and energy intake in 11 men and 10 women exercised for 60 min on a cycle ergometer at 70% VO2peak until 30% of total daily energy expenditure was expended (men, expenditure = 975 ± 195 kcal in 82 ± 13 min; women, expenditure = 713 ± 86 kcal in 84 ± 17 min) in a counterbalanced, crossover study.
  

  

  Figure 2: Energy intake (see captions) and macronutrient composition (graph shows %-ages, the figures indicate the actual intake in g) of the post-workout ad-libitum meal (Hagobian, 2012).

  In line with Alajmi et al. (2012) and in contrast to Kawano et al. (2012), Hagobian et al. (2012) found a sign. reduction in energy intake (P < 0.05) after exercise compared with rest in men (672 ± 827, 1133 ± 619 kcal, respectively) and women (−121 ± 243, 530 ± 233 kcal, respectively). A result the scientists interpret as evidence of the previously cited "effectiveness of acute exercise to suppress relative energy intake regardless of sex" (Hagobian, 2012).
• Bailey, et al (2015) - While the previous studies tested relative intense steady state exercises, a 2015 study from the University of Bedfordshire focused on a very different type of exercise. In fact, the 'exercise intervention' consisting of walking a total of 28 min in form of 2 min bouts every 20 minutes was designed to investigate the effect of daily physical activity on appetite and energy intake in 6 male and 7 female inactive, but otherwise healthy subjects, whose appetite and appetite-regulatory hormones were not affected by the exercise intervention.

You probably already suspect it: intensity is a key regulator of the effects of exercise on subjective appetite, but since I've addressed that before while discussing the sex-differences only superficially, I want to refer you to my previous article and focus on the influence of sex of which separate studies in men and women, respectively appear to suggest that...

• 24h energy intake is unchanged in both, men and women in the few studies that investigated this important parameter in male and female subjects in isolation
• acute energy intake (post exercise) mostly remains the same, often decreases and rarely increases in men and women when studied in isolation
• exercise intensity, that's what evidence suggests modulates the effects on energy intake for both, men and women; in that, low-intensity exercise such as walking appears to be more prone to increase energy intake than high(er) intensity exercise such as jogging or sprinting
• dietary overcompensation, i.e. an extra energy intake that provided more energy than the subjects had burned during their workouts, does not occur in either men nor women
• individuality reduce the validity of the results; as previously pointed out, the appetite response to exercise appears to be highly individual and whether that's due to genetics and/or baseline diet (e.g. low carb vs. low fat, etc.) will have to elucidated in the future 

The one thing that's still left to discuss is the chronic effect of exercise on appetite, hunger, the respective hormones and - most importantly - men's and women's energy intakes.

The effects of chronic exercise

Unfortunately, studies that compared the effects of chronic exercise on appetite and food intake of men and women directly, don't exist. What we do have, though, are studies on both men and women (not adequately powered for comparisons), as well as studies that investigate men and women in isolation. These studies suggest that...

• complex interactions w/ weight loss in both men and women - If weight loss occurs in response to chronic exercise, that's, according to King, et al. (2009), because overweight individuals (men and women) balance any potentially existing increased drive to eat due to the extra energy expenditure with a concomitant increase in the satiety response to a meal (increased insulin sensitivity, decreased acetylated ghrelin, decreased leptin | Martins. 2010 & 2013).
  
  Similarly, Thackray et al. conclude in their previously cited review that this interactive effect between exercise, weight loss and appetite / energy intake also explain the complex alterations in appetite-regulatory hormones, of which they even go so far as to say that they "arise as a secondary consequence to changes in body mass" (Thackray, 2016)
• overall, women are more susceptible to changes in energy balance - In the long-term, it becomes more apparent that women react more sensitive to changes in their energy balance. Comparing studies in men and women (direct comparisons don't exist) suggest that this is why women are more susceptible to perturbations in appetite-regulatory hormones and energy intake.
• exercise is less likely to trigger dietary compensation than energy restriction - In contrast to the initially referenced statement of Gary Taubes, it's dieting that makes you hungry, not exercise in both men (King, 2011) and women (Alajmi, 2016). "Dietary restriction," Thackray et al. explain may simply "represent a greater challenge to appetite regulation and energy balance than exercise".
  
  

  

  Figure 3: The energy intake between men and women differed in a 12-week aerobic exercise training intervention in overweight and obese men (n = 35) and women (n = 72), but the effect on the objectively measured (quantified using laboratory-based test meal days) did not differ between the male and female subjects (Caudwell, 2013)..

  And since we know that women react more sensitive to changes in said energy balance, it is not exactly surprising that individual two separate studies by Stubbs et al. (2002a,b) show that only women will compensate ~33% of the extra energy they expended during seven days of daily moderate- or high-intensity exercise (Stubbs, 2002a), while men didn't change their energy intake, at all (Stubbs, 2002b) - at least if we trust their food logs and the subjects' own scales, because that's what Stubbs et al. used as their data source.
  
  That's a problem, because - as usual - other studies suggest an increased compensation in men or, just as one of the few tightly controlled studies in this field no sex- but sign. indiv. differences (Caudwell, 2013). 

Eventually, the jury is thus still out. While anecdotal evidence suggests and evolutionary considerations, i.e. "that women have evolved to store body fat to preserve energy balance and reproductive function" (Thackray, 2016), could even explain an increased energy expenditure in women, the hard evidence we'd need for a definitive conclusion is simply not there.

Not Exercise, But Dieting Makes You Hungry: Beneficial or No Effects on Appetite of Exercise in Lean & Obese. (Ab-) using Exercise to Make Up For Messy Diets Still a Bad Idea! More...

Don't complain, ladies. Use your energy in the gym! As Thackray et al. point out, most of the more recent experimental work "question[s] the prevailing view that exercise is less effective for inducing weight loss in women, with several studies showing equivalent effects of exercise training on body composition in both sexes when the exercise-induced energy expenditure is matched" (Thackray, 2016) - the latter is obviously rarely the case, after all, women have a lower body weight and a lower lean body mass. So even if they trained at the same intensity as men (which a comparison of the average male to the average female gym-goer suggests they don't), they still wouldn't burn as much energy...

Rather than to complain about how unfair life is when it comes to exercise and fat loss, women should use their energy in the gym and focus on the new research on how training and eating according to their menstrual cycle could augment both, their exercise-induced fat loss and the actually desired changes in body composition | Comment on Facebook!

References:

• Bailey, Daniel P., et al. "Breaking up prolonged sitting time with walking does not affect appetite or gut hormone concentrations but does induce an energy deficit and suppresses postprandial glycaemia in sedentary adults." Applied Physiology, Nutrition, and Metabolism 41.3 (2015): 324-331.
• Brennan, Ixchel M., et al. "Effects of the phases of the menstrual cycle on gastric emptying, glycemia, plasma GLP-1 and insulin, and energy intake in healthy lean women." American Journal of Physiology-Gastrointestinal and Liver Physiology 297.3 (2009): G602-G610.
• Buffenstein, Rochelle, et al. "Food intake and the menstrual cycle: a retrospective analysis, with implications for appetite research." Physiology & behavior 58.6 (1995): 1067-1077.
• Caudwell, Phillipa, et al. "No sex difference in body fat in response to supervised and measured exercise." Medicine & Science in Sports & Exercise 45.2 (2013): 351-358.
• Geiker, Nina RW, et al. "A weight-loss program adapted to the menstrual cycle increases weight loss in healthy, overweight, premenopausal women: a 6-mo randomized controlled trial." The American journal of clinical nutrition (2016): ajcn126565.
• Hagobian, Todd Alan, et al. "Effects of acute exercise on appetite hormones and ad libitum energy intake in men and women." Applied Physiology, Nutrition, and Metabolism 38.999 (2012): 66-72.
• Kawano, Hiroshi, et al. "Appetite after rope skipping may differ between males and females." Obesity research & clinical practice 6.2 (2012): e121-e127.
• King, Neil A., et al. "Individual variability following 12 weeks of supervised exercise: identification and characterization of compensation for exercise-induced weight loss." International Journal of Obesity 32.1 (2008): 177-184.
• King, Neil A., et al. "Dual-process action of exercise on appetite control: increase in orexigenic drive but improvement in meal-induced satiety." The American journal of clinical nutrition 90.4 (2009): 921-927.
• King, James A., et al. "Differential acylated ghrelin, peptide YY3–36, appetite, and food intake responses to equivalent energy deficits created by exercise and food restriction." The Journal of Clinical Endocrinology & Metabolism 96.4 (2011): 1114-1121.
• Martins, Cecilia, et al. "The effects of exercise-induced weight loss on appetite-related peptides and motivation to eat." The Journal of Clinical Endocrinology & Metabolism 95.4 (2010): 1609-1616.
• Martins, Catia, et al. "Effect of chronic exercise on appetite control in overweight and obese individuals." Medicine and science in sports and exercise 45.5 (2013): 805-812.
• Stubbs, R. James, et al. "The effect of graded levels of exercise on energy intake and balance in free-living men, consuming their normal diet." European journal of clinical nutrition 56 (2002a): 129-140.
• Stubbs, R. James, et al. "The effect of graded levels of exercise on energy intake and balance in free-living men, consuming their normal diet." European journal of clinical nutrition 56 (2002b): 129-140.

Fructose - An Update: "Fructose Has Adverse Effects Only Insofar as It Contributes to Excess Calories" Plus: The Role of Exercise + Meta-Analyses on BP, Weight Gain & T2D

It's incredible... for some, but probably not unexpected for most of us that fructose becomes problematic in overfeeding scenarios, only.

Some of you will probably have seen the press release from the St. Michel's Hospital that made it onto all the major science outlets on the Internet and up on Alex' Facebook page, where he tagged me and thus got me interested in a study that claims to provide evidence that: "Fructose does not impact emerging indicator for cardiovascular disease" | read more.

The main goal of the corresponding paper that has been published in the Atherosclerosis earlier this months (Wang. 2014) was to identify and analyze all clinical interventions that investigated the chronic effect of exchanging isocaloric or hypercaloric oral fructose for a reference carbohydrate on postprandial triglycerides.

Update - Coca Cola & Co buy a white slate for their sugar-sweetened beverages (SSB): Shortly after publishing my analysis of the meta-analysis, I hit onto a more recent review that deals with sugar sweetened beverages and the influence sponsors from the industry have on the outcome of corresponding studies and, more importantly (since easier to be biased) reviews. While the main finding of Bes-Rastrollo's et al.'s analysis is that there is a 5x higher likelihood of SSBs being portrayed as benign, when reviews are financed by the industry, the editor of PLoS|One Medicine rightly points out that "[a] major limitation of the study at hand is however that it cannot assess which interpretation of the available evidence is truly accurate" and that "scientists involved in the systematic reviews that reported having no conflict of interest may have had preexisting prejudices that affected their interpretation of their findings". In other words, financed and non-financed research are both biased" (Editorial published with Bes-Rastrollo. 2013 | learn more).

Don't forget: Nobel Laureate Peter Higgs worked with the method on the right: Conclusion first: "There is a boson that mediates gravitational forces" ➲ Years of research: "Heureka!"

It's also important that you realize that meta-analysis such as the one at hand are less prone to bias, than regular reviews (including those of Internet celebrity scientists ;-). This is particularly true, when they are conduced according to the strict criteria of the Cochrane Collaboration (something that applies to Wang et al's analysis). If the you want to pick the results of the meta-analysis at hand apart, you will thus have to (a) prove that they deliberately ignored studies although those complied to the inclusion criteria (selection bias) or (b) that important studies that have been included were so biased that the overall result of the meta-analysis (which is mostly math) gets skewed.

The scientists included ony human trials and the deadline on which they stopped looking for new studies was September 3, 2013. In other words: Wang et al. don't bother us with rodent data with questionable relevance (e.g. rodents on 70% fructose diets) and they include almost alll studies in their review that have been published in the last couple of most... well, assuming they were available on MEDLINE, EMBASE, and in the Cochrane databases and complied to the following criteria:

"We included clinical interventions that investigated the chronic effect of exchanging isocaloric or hypercaloric oral fructose for a reference carbohydrate on postprandial triglycerides in humans. Comparisons were considered “isocaloric”if oral fructose in the fructose arm was exchanged for the reference carbohydrate in the control arm in an iso-energetic and iso-glucidic manner and“hypercaloric” if the oral fructose in the fructose arm was provided as a supplement to the background diet providing excess energy (E) relative to the background diet alone in the control arm. Trials with less than 7 days follow-up, which lacked an adequate carbohydrate control, or administered IV-fructose were excluded" (Wang. 2014)

It's quite funny to see how the 1259 initial hits were decimated in the review process with 111 being identified as duplicates, 270 not being having human, but hairier subjects,  54 being only case studies, 2 being letters in disguise, 280 papers being reviews, 233 papers having only a general CHO arm, 71 studies with intravenous administration, 127 studies with "unsuitable endpoints" (e.g. measuring the effect on exercise performance), 61 having a study duration < 7 days and two simply being irretrievable in full-text form.

Now you may be asking yourselves, why I am bothering you with this!? Right? Well, firstly, I want to give yo an idea of how painful it is to write an objective review of the literature. I realized the same only recently, when I compiled the True or False item on dairy induced reductions in testosterone and its possible carcinogenicity. Secondly mentioning the fact that 1211 articles were excluded in the 1st and 48 articles in the 2nd phase of the review process may help silencing all the fructose haters who read this and consider it the work of diabolical cherry pickers, who have received grants from the devil, i.e. the Coca-Cocal Company and a whole host of other usual and unusual suspects, in the past (read the long list of "competing interests" and don't forget that the study at hand was not funded by any high fructose corn-syrup interest group).

A note on potential bias: As I have pointed out numerous times, already. A "competing interest" is no reason to discard the results of a paper / review altogether. Especially in the case of the latter, you should yet carefully evaluate the scientists interpretation of the reviewed literature, because - consciously or not - those interpretations may well be influenced and the corresponding conclusions biased by a researchers' basic assumptions. Unbiased research is - and I am sorry to say that - an illusion that's never going to manifest in the real world; and that's true irrespective of funding / research grants (Schulz. 1995).

While I do hope t hat I am not implying we were talking about scientific fraud here, you should still keep in mind that information Sievenkemper, who is the "correspond author", i.e. the media guy among the 15 scientists from 12 research institutes in Canada, gave Leslie Shepherd, the author of the the initially mentioned press release (Shepherd. 2013), is not some sort of objectively measured truth (there are philosophers of science who question such a thing does even exist). 

"[F]uctose doesn’t behave any differently than other refined carbohydrates. The increases you see are when fructose provides extra calories." (Sievenkemper in Shepherd. 2013)

The above is his (and his colleagues) professional opinion, of which I seriously doubt that it was consciously influenced by previous research grants or the current financial support from the Canadian Institutes of Health Research and the Calorie Control Council that funded the study at hand.

Effects of hypercaloric diet (+50%) w/ 30% fructose content on triglyceride production and clearance in healthy subjects in the presence and absence of exercise (Egli. 2013)

A minimalist explanation of the results: Based on the way fructose is metabolized (increased triglyceride production, reduced storage in fat cells; cf. Chong. 2007), it is only logical that there is a minimal effect on serum triglycerides. In the absence of a hypercaloric diet, this statistically and physiologically non-significant increase is yet not a threat to your health. Your body will simply use the part of fructose your liver converts to triglycerides as an energy source. Only when the total energy intake is so high that it is no longer necessary / possible to use the trigs as an energy source, the latter will begin to accumulate in the blood and. even worse, in the liver (NAFLD). For you that would mean trouble - unless, of course, you work out and use the superfluous trigs to fuel your workouts (Egli. 2013; figure to the left).

Basically, what the scientists did to form this "professional opinion" was (1) reading the papers several times, (2) weighing them by a set of pre-determined criteria from the Cochrane Handbook for systematic reviews of interventions (Higgins. 2011), (3) filtering out all relevant data, (4) calculating the SMD's (standard mean differences) for pre vs. post intervention triglycerides levels of the average study subject for each individual study, (5) pooling the data in groups (healthy subjects, overweight / obese subjects, diabetics), and finally (6) using the individual weight of the to calculated the SMDs [including 95% confidence intervals] for different subject groups. The results, i.e....

• 

  Complete results (Wang. 2014)

  otherwise health: 0.30 [-0.00, 0.60]; weight 37.8%
• overweight / obese: 0.69 [0.20, 1.19] *; weight: 6.8%
• diabetes: 0.00 [-0.15, 014]; weight: 55.4%

did then 7) serve as the basis for the magic overall SMD of 0.14 and confidence intervals of [-0.02, 0.30] ,which tell you that the 14% increase in triglycerides is statistically not significant (for someone who does not sit around all day, the same can probably be said for the physiological relevance - specifically in view of the fact that we have no reason to believe that this was not a new steady state; or, more straight forward: It's unlikely that the levels kept increasing after a short adaptation phase.

How realistic are these studies, anyway? Currently the dietary fructose intake of the average fructose intake of fructose is estimated to be contribute 10-15% to our dietary energy intake (Vos. 2008). If we do the math on only those two trials with corresponding fructose intakes, i.e. Huttenen et al. (1976; healthy subjects) and Anderson et al.(1989; diabetic subjects), we get a standard mean differences of 0.019 with 95% confidence intervals of [95% CI: -0.32, 0.35]. The 1.9% increase in postprandial triglycerides the researchers detected in these studies is thus physiologically irrelevant  and statistically in- significant.

Bottom line: There is little doubt that the researchers' conclusion that "fructose has adverse effects only insofar as it contributes to excess calories" (Sievenkemper in Shephard. 2013) is supported by ...

1. the absence of differences between diets that delivered up to 25% of the daily energy from fructose or other carbohydrate sources, respectively, as well as
2. the fact that only studies that employed hyper-caloric diets had significant negative effects on the postprandial triglyceride levels (SMD: 0.65 [95% CI: 0.30, 1.01])

Nevertheless, Sievenkemper's comment in the previously cited press release lacks the most important piece of information, i.e. the fact that the potential adverse effects of fructose are not restricted to increases in serum triglycerides and that a similar verdict of acquittal from a peer-reviewed, up-to-date meta-analysis of its effects on the development of NAFLD is still (over-)due.

What we do have, are meta-analysis for it's effects on blood pressure (Ha. 2012), weight gain (Sievenpiper. 2012) and glucose metabolism in diabetics (Cozma. 2013) which argue that replacing glucose with an isocaloric amount of fructose does not affect blood pressure or weight gain and can actually "improve long-term glycemic control, as assessed by glycated blood proteins, without affecting insulin in people with diabetes" (Cozma. 2013).

References:

• Anderson, J. W., Story, L. J., Zettwoch, N. C., Gustafson, N. J., & Jefferson, B. S. (1989). Metabolic effects of fructose supplementation in diabetic individuals. Diabetes Care, 12(5), 337-344.
• Bes-Rastrollo M, Schulze MB, Ruiz-Canela M, Martinez-Gonzalez MA (2013) Financial Conflicts of Interest and Reporting Bias Regarding the Association between Sugar-Sweetened Beverages and Weight Gain: A Systematic Review of Systematic Reviews. PLoS Med 10(12): e1001578.
• Chong, M. F., Fielding, B. A., & Frayn, K. N. (2007). Mechanisms for the acute effect of fructose on postprandial lipemia. The American journal of clinical nutrition, 85(6), 1511-1520.
• Cozma, A. I., Sievenpiper, J. L., de Souza, R. J., Chiavaroli, L., Ha, V., Wang, D. D., ... & Jenkins, D. J. (2012). Effect of Fructose on Glycemic Control in Diabetes A systematic review and meta-analysis of controlled feeding trials. Diabetes care, 35(7), 1611-1620. 
• Egli, L., Lecoultre, V., Theytaz, F., Campos, V., Hodson, L., Schneiter, P., ... & Tappy, L. (2013). Exercise Prevents Fructose-Induced Hypertriglyceridemia in Healthy Young Subjects. Diabetes.
• Ha, V., Sievenpiper, J. L., de Souza, R. J., Chiavaroli, L., Wang, D. D., Cozma, A. I., ... & Jenkins, D. J. (2012). Effect of Fructose on Blood Pressure A Systematic Review and Meta-Analysis of Controlled Feeding Trials. Hypertension, 59(4), 787-795.
• Huttunen, J. K., MÄkinen, K. K., & Scheinin, A. (1976). Turku sugar studies XI: Effects of sucrose, fructose and xylitol diets on glucose, lipid and urate metabolism. Acta Odontologica, 34(6), 345-351.
• Schulz, K. F., Chalmers, I., Hayes, R. J., & Altman, D. G. (1995). Empirical evidence of bias. JAMA: the journal of the American Medical Association, 273(5), 408-412.
• Sievenpiper, J. L., de Souza, R. J., Mirrahimi, A., Matthew, E. Y., Carleton, A. J., Beyene, J., ... & Jenkins, D. J. (2012). Effect of Fructose on Body Weight in Controlled Feeding TrialsA Systematic Review and Meta-analysis. Annals of Internal Medicine, 156(4), 291-304.
• Shepherd, L. (2013)   Researchers say fructose does not impact emerging indicator for cardiovascular disease. St. Michael's | Newsroom | Our News. < http://www.stmichaelshospital.com/media/detail.php?source=hospital_news/2013/20131230_hn > retrieved on Jan. 01 2014.
• Vos, M. B., Kimmons, J. E., Gillespie, C., Welsh, J., & Blanck, H. M. (2008). Dietary fructose consumption among US children and adults: the Third National Health and Nutrition Examination Survey. The Medscape Journal of Medicine, 10(7), 160.
• David Wang, D., Sievenpiper, J. L., de Souza, R. J., Cozma, A. I., Chiavaroli, L., Ha, V., ... & Jenkins, D. J. (2014). Effect of fructose on postprandial triglycerides: A systematic review and meta-analysis of controlled feeding trials. Atherosclerosis, 232(1), 125-133.

Bulking Done Right: What Can the Latest 100 Day +1,000 Kcal/day Overfeeding Study Tell Us About How Baseline Fitness, Fatness, Hormones & More Affect the Outcome

Bulking!? What is it that will keep the veins popping, the waist circumference level and your muscle growing? It is your basal metabolic rate? Your body fat level? Your muscle mass? Your fiber type composition? Or maybe your cardio-respiratory fitness?

If you have listened to the latest installment of the Science Round Up you will know that there is very practical reason why you want to avoid "classic dirty bulking", with an increased formation of body fat: the accompanying changes to the structure of your adipose organ - the increase in adipopocyte number and thus the touted reason for the future weight problems (listen to the show to learn more). But let's phase it a certain degree of "overfeeding" is actually necessary to make gains, so the question, which factors there are to predict the changes in body composition and body energy in response to chronic overfeeding is a question that's of equal importance for the lean physical culturist as it is for the obese child of the fast food generation. And you know what? This is exactly the question a soon-to-be-published paper by scientist from the Pennington Biomedical Research Center and the Laval University is dealing with.

Twin power vs. heterogenity

As Bouchard, Tchernof and Tremblay rightly point out, "human heterogeneity in the response to the much described “obesogenic environment” created by affluent societies represents a critical aspect of the obesity epidemic" (Bouchard. 2013) And while this is certainly right it is, from a scientist's perspective, a huge problem. After all, we want to study the influence of a given parameter in isolation.

Twin studies can provide us with pairs of subjects where these inter-individual differences are minimized and while the focus of previous observational studies has been on the hitherto more or less fruitless and above all practically 100% irrelevant (what does it help you to know that you are "at risk" of getting obese) identification of genotype-overfeeding interaction, Bouchard et al. are

"[...]taking advantage of the extensive panel of pre-overfeeding traits to investigate the most parsimonious predictors of the gains in body mass, FM, FFM, and total body energy (BE), with a particular focus on the partitioning of the energy gains between adipose and lean tissues." (Bouchard. 2013)

The goal is to identify biomarkers of body composition changes in response to chronic overfeeding may allow us to develop new hypotheses about the endogenous (genetic) and environmental causes of human heterogeneity in the response to chronic overfeeding.

Figure 1: Factors that predispose to weight & fat gain on a caloric surplus (adapted from Bouchard. 2013)

In a previously published paper, the researchers have already reported that their subjects, 24 young lean men (12 pairs of identical twins) exhibited individual differences in body weight and composition gains in response to a standardized 353 MJ (84 000 kcal) overfeeding protocol over 100 days

"The mean (+SD) gains in fat mass (FM) and fat-free mass (FFM) were 5.4+1.9 kg and 2.7+1.5 kg for a total body energy (BE) gain of 221+75 MJ representing 63% of the energy surplus consumed." (Buchard. 2013)

In this follow up publication, Buchard et al. were now taking a closer look at the most important baseline correlates of these overfeeding-induced changes with the aim of identifying biomarkers of the response.

"From 16 to 8% body fat" a cross-fitesque training-style may be right for those with high baseline fitness (learn more).

"The subjects were studied eight at a time (four pairs of twins) over a period of 18 months. Subjects were housed in a closed section of a dormitory on the campus of Laval University 24-hour supervision.

Each subject stayed in the unit for 120 days, which included a 14-day baseline observation period, a 3-day pre-overfeeding testing period, a 100-day experimental overfeeding treatment, and a 3-day post-overfeeding testing period." (Buchard. 2013)

Unfortunately, the subjects daily energy expenditure was highly limited, as they were "kept sedentary" except for a supervised 30min walk, over the whole study period, in the course of which their body weight was measured daily, while their body density was assessed on three occasions from a series of underwater weighing tests.

An "intermittent overfeed" protocol

The actual overfeeding protocol comprised a 6-day binge with 1,000 extra kcal per day that was followed by a backlash to the calculated maintenance level on day 7. Thus, subjects overfed during 84 of the 100 day experimental phase.

• the total excess energy intake was 84 000 kcal
• the macronutrient ratio as 15/35/50% for protein, fat and carbs

With the latter certainly not being representative of your diet (at least I would hope so), this is sign #2 (remember: the first part was the non-existent physical activity) that we are dealing with a study targeting the average American and not the extra-ordinary SuppVersity reader and Super Human Radio listener who are spread all across the globe.

Suggested Read: "If You Go 'High Carb', You Better Go Really High! Seven Meals/Day, More than 800g of Carbs, Less Than 50g of Fat & 1000kcal Over Maintenance and Still 'Lean Gains'!" A previous study would suggests: The major downside to the diet the twins were following was the low protein and not the high carbohydrate intake, of which I am sure some of you are now freakin' out in the usual, "But Gary told us that carbs make you fat"-mania

So, while it is obvious that a study on the same subjects, but with different macronutrient ratios (like a lower vs. higher carb intake) and/or an additional exercise component would have told us more about how you can channel your gains into the right direction, I would say that there is more than enough evidence of the superiority of

• a higher protein intake (30g+ of a high EAA protein source w/ every full meal, 15-20g of protein with snacks),
• the usefulness of a sane carbohydrate intake (low GL instead of low carb),
• the avoidance of a skewed n6-PUFA to other dietary fat intake, and 
• an intense, but not overexerting workout routine with a focus on heavy compound lifts, a minimal amount of HIIT and the occasional very low intensity (walking on a treadmill steady state cardio)

when you are about to go on a lean bulk (you overall energy surplus should not exceed 15% in the beginning; and you should go higher only, if this does not bring about any changes).

Now, talking about the study would be pointless, if the only thing to take away from the experiment were recommendations based on papers that were discussed in previous blogposts, right? So what are the new insights this study brings to the table, then?

• Total, not relative, increases in calorie intakes matter: First of all, it is kind of surprising that the changes in body composition did not depend on the pre-overfeeding levels of body weight, FM, BE, and daily caloric intake. In other words, for these lean healthy men, the changes the scientists observed were almost fully determined by the absolute increase in energy consumption - irrespective of how lean they were and even more surprisingly irrespective of whether those 1,000kcal extra were a surplus of 30% or 40% of their baseline energy intakes.
• Muscle has a "repartitioning effect": Contrary to the fat mass, which did not correlate with changes in any of the measured parameters, the scientists observed a statistically significant inverse correlation between the amount of muscle, the subjects were carrying on their frames and the changes in the lean-to-fat mass ratio (r=-0.41; p=0.05) - this means: the more muscle the guys had to begin with the more muscle and less fat they were gaining in response to the 1,000 extra kcal they were consuming.
• RMR and food induced thermic effects don't influence the total gains, but... While neither the resting metabolic rate, nor the thermic effect of food influenced the changes in body weight, FM, FFM, or BE, the thermic effects in the 4h after a meal had a significant and highly beneficial effect on the ratio of muscle to fat, the subjects gained (clear-cut evidence in favor of a high(er) protein diet yielding better results).

• 

  Learn about the fallacies of the training in the "fat burning" zone and why burning fat for fuel does not equate fat loss (read more)

  The respiratory quotient (RQ) did not matter: As a SuppVersity reader you know that the influence of the ratio of carbohydrates to fats, described by the RQ (with an RQ = 1 telling you that someone burns exclusively glucose) on your efforts to cut body fat, is totally overblown. The finding that
  

  "[t]here was no correlation between RQ during the RMR measurement and at various time points of the TEM test with the overfeeding-induced gains in body weight, FM, FFM, or BE." (Bouchard. 2013)

  is perfect evidence that this is also, or I guess I'd better say, "even more so" the case when you are bulking.
• Fitness is a negative predictor of fat gains: In view of the fact that a high VO2max correlates with higher mitochondrial capacities (and often higher muscle mass) it is not surprising that "VO2max per kilogram of body weight was negatively correlated with the gains in body weight,
  FM, and BE, with coefficients ranging from -0.41 to -0.49, all p<0.05" (Bouchard. 2013); and that the overfeeding-induced increases in fat mass relate to those in lean mass were negatively related to baseline VO2max per kilogram of body weight and the maximum O2pulse (r=-0.43; p<0.05)
• A high(er) count of type I fiber count protects against fat gains: In line with the previously mentioned negative correlation between fitness (endurance type) and fat gains, there was a strong trend for the proportion of type I fibers in the vastus lateralis muscle to correlate negatively with (r = -0.40) with fat gains. Accordingly, the oxidative potential of the skeletal muscle, the scientists quantified by assessing the maximal activity of OGDH (Alpha-ketoglutarate dehydrogenase is an enzyme that's involved in the oxidative process by which the citric acid cycle converts fats to energy) in a muscle homogenate, was negatively correlated with the gains in FM, as well as in the FM–to-FFM ratio. According to Bouchard, et al. these correlations ranged from -0.42 to -0.48 (p<0.05).

• 

  Fiber composition of bodybuilders, recreational lifters, endurance rowers and sedentary control; determined via myosin heavy chain (MHC) isoform content of the triceps brachii muscle (data adapted from Jurimäe. 1997; figure originally published as part of the Intermittent Thoughts on Building Muscle)

  A high glycolytic muscle activity predisposes to fat gains: While being a good "fat oxidizer", i.e. someone who is not necessarily oxidizing more fat than glucose, but has the ability to burn fat effectively (high type 1 fiber count, high OGHD activity, see bullet point above) is a plus, the opposite effects were observed in those twins who had a high(er) ratio of PFK to OGDH muscle enzyme activities, which indicates that their muscles have a high glycolytic relative to oxidative potential. Remember: While people with many exclusively fast-twitch type IIb fibers, would fall into this category, bodybuilders don't - they do in fact have an abundance of metabolically flexible type IIx and type I muscle fibers (see figure on the right)
• Thyroid hormones don't matter that much: While they can make all the difference when you are cutting, the basline TSH levels and the subjects response to a TRH challenge (this is test to evaluate, whether the pituitary response to the hormone that will trigger TSH release is normal) did not influence total weight gain, body fat or fat free mass gains. It should be said, though that all subjects were euthyroid and obviously not overtraining (learn why this matters)... well, there is one thing that did show a correlation though: Although it's not quite clear what the implications are, the early 30-45min TSH response during the TRH challenge was correlated positively with the fat mass to fat free mass gains. In other words, the more pronounced the spike in TSH, the more likely you'll gain fat, not muscle. Without seeing the corresponding thyroid response this could yet mean either that the thyroid is sluggish to react, so that the negative feedback takes longer to occur, or that the opposite is the case and a HPTA that produces larger spikes in thyroid metabolism is to blame for the increased propensity for fat gain.
• Plasma glucose and insulin don't matter: We are approaching the end of the list and I have to admit that this is one of the things that kind of surprised me. In the end, the non-significant influence of both basal, as well as glucose stimulated increases in blood glucose and insulin levels had no effect on the overfeeding-induced changes in body weight, fat mass and fat free mass does confirm that "the fattening hormone" and the purported reason "why we are fat" is not an issue for those of us who are lean and healthy and whose body easily manages his glucose levels just the way it is supposed to be.
• The restless ones don't get muscular: The fact that high baseline norepinephrine levels showing a significant negative association (r = -0.41) with increases in fat-free mass should remind you of something I want to scream at 50% of the people emailing me questions like "What happens if I eat another gram of carbs extra?" I can tell you if you are stressing out about these 100% irrelevant details all the time this and the corresponding constant psychological stress is going to do more harm to your progress than eating 200g of carbs extra, folks... but I guess those of you for whom this is an important message will continue to ignore this. So keep freaking out that you missed your macros by a blueberry, today - obviously you must be enjoying it more than the beautiful things in life.
• Leptin and the rest of the hormonal pack: With a positive associated with the changes in body weight and fat mass gains the "fat hormone" (actually it's an adipokine, but since a "hormone" is a signaling molecule produced by an organ and the adipose tissue is imho an organ, it would be valid to call it a hormone), leptin, appears to be a fattening. On the other hand, higher baseline leptin levels are usually the result of higher baseline body fat mass and since fat begets fat, the latter is probably the common determinant. Leptins "good" cousin adiponectin, but also ghrelin and even IGF and hGH were totally void of pro- or anti-obesogenic effects.

Now that you are in the know about how where you are starting from, i.e. how fat you are, how fit you are, how muscular you are, what you muscle structure looks like, etc. a question arises and this question is...

Suggested read: "Building LEAN Muscle Starts With Losing UNHEALTHY Fat" and what you'll have to do first will depend on where are you on the fat/muscle mass (FFMI = weight/height[in m]² from ) continuum from "ripped bodybuilder" to "sumo wrestler" (learn more)

What are the implications: Well, I guess some of you may have expected the usual "eat this", and the notorious "don't eat that", when you read the title of today's SuppVersity article and... be honest (!) - I have already answered this question and told you that a 1,000kcal surplus would be too much for 99% of you to start out with.

When it comes to filter out a conclusion from the parameters the scientists evaluated, however, I still owe you a compre-hensive bottom line  And if you wanted me to formulate it as short and concise as possible it's: Get healthy, fit and lean first, bulk 2nd. Your results depend on it.

References:

• Bouchard, Claude, Andre Tchernof, and Angelo Tremblay. "Predictors of body composition and body energy changes in response to chronic overfeeding." International Journal of Obesity 38.2 (2014): 236-242.

Your Body Knows How Much It Needs: Muscle & Activity Increase, Being Fat Decreases Energy Intake. Argan Oil, A Natty Test Booster (+20%) W/ Melatonin, CoQ10 & More. Pimp Your Workout With Palm Cooling & Heating

It does not always have to be the beach. There are other places to relax and enjoy the summer. And let's be honest anything is better than your computer screen, no?

Alright, we are in for a regular installment of On Short Notice and my figure of the day is 25°C - which goes to tell you that summer is there and I am not about to spend more time than necessary hanging out in front of the computer. A smart move on my part and one I would suggest you simply copy.

And if you have a pre-schooler hanging in front of the computer / TV set next to you, you better make sure you take him / her along with you if you don't want his/her chance of getting fat (beta = 56% for skinfolds) compared to his / her peers with close to zero computer use (Can you imagine that even in 2007 >10% of pre-schoolers were hanging on front of a computer for >1h per day? Mendoza. 2007)

• Body composition and energy expenditure predict energy and macronutrient intake (Weise. 2013) -- Sounds almost to good (and normal) to be true, but the more you burn, the more you eat...
  
  

  

  "Bikini Body Now!", headlines like this and the unfair suggestion that by following diet X or taking supplement Y you would make it onto the cover of a magazine like that are part of the problem why diets fail, people get discouraged and caught in the diet trap. After all, "5% Calorie Restriction & Longterm Dieting Make You Fat and Insulin Resistant. Plus: Model Predicts Weight Loss Based On Number, Weight Lost & Diet Pill Use On Previous Diets" (read more)

  ... well, at least that appears to the case for the 184 participants (73 F/111 M; age 34.5±8.8y; % body fat 31.6±8.1%) of the study at hand, whose fat free mass index, index (FFMI kg*m²), fat mass index (FMI kg*m²), and 24-h energy expenditure (EE, n=127), the scientists from the Obesity and Diabetes Clinical Research Section at the NIDDK-NIH in Phoenix compared to their ad-libitum food intake using a 3d vending machine paradigm and what they found was this:
• the more muscle the subjects had, the more they would eat; and this effect was independent of how much fat the participants were carrying around 
• fat people eat more (on total) and they eat some more protein and significantly more fat
• people with lower muscle and fat mass ate more of their daily allotment in form of cabohydrates, while those with higher fat mass and lean mass availed themselves of more fat than the rest of the pack
• 24h-energy expenditure and fat free mass were associated with higher energy intakes than the standard calculation would tell you, while for being fat the opposite was the case

---

So what's the significance of this data? I guess that'd be the underlying message that we can in fact - to a certain degree - rely on our bodies' bodyweight self-regulation. With dieting and overeating and the consumption of 50% chemical foods the system is yet unfortunately totally out of whack in many of us.  

 

• Argan oil - another natural oil, you may have overlooked so far (Derouiche. 2013; Lopez. 2013) -- You may have heard about Alisa Profumo's secret to beautiful hair, when you listened to yesterday's installment of "Casual Friday" on Super Human Radio, but even if you don't care about hair (or skin; cf. Boucetta. 2013). You may be missing out if you don't use some of the expensive oil that is a staple food in the Moroccan diet, for example.
  
  

  

  Figure 1: The testosterone boosting effect of Argan oil (vs. butter) is not much more pronounced than the one of olive oil, but argan oil gets your testes to produce more T without having to resort to sign. more luteinizing hormone (Derouiche. 2013)

  According to 2013 study by Derouiche et al.  60 young and healthy male volunteers aged between 23 and 40 years old saw increases in testosterone and luteinizing hormone (LH) levels of 19.9% and 18.5% (p < 0.007) after consuming virgin argan oil as their staple fat source after only three weeks. Before the intervention the subjects had been consuming butter to standardize the baseline intake for 2 weeks and were then assigend to either argan or extra virgine olive oil (EVOO). And while the latter produced similar increases in testosterone, the 2x higher increase in LH would suggest that argan oil is the preferable test booster with each addition percent of LH yielding a corresponding increase in testicular testosterone production (higher responsiveness vs. EVOO).
  

  ---

  So what? Ok, obviously there was no effect on body composition in the Derouiche study within three weeks, but in view of the potent antioxidant effects Lopez et. al. ascribe to the CoQ10 and melatonin content and the rest of the antioxidant molecules (tocopherols, polyphenols, etc.; cf. Lopez. 2013), this is one of the cases where you may even expect to see those and general health benefits. 

• Keep your palms cool (or hot?) to lift longer (Kwon. 2013) - Now, years after the release of the original iPhone the combination of "cool" or "hot" and "palm" is no longer equivocal (I guess, some of you won't even know what a Palm was, right?)... but that's a whole different story. Different from the one at hand at least: PALM COOLING! You will have heard about how it is supposed to have relevant ergogenic effects, but let's be honest, does that sound realistic?
  
  A recent study from the Department of Kinesiology at the Washburn University in Kansas certainly makes it appear at least more likely that palm cooling could in fact work.

  

  Figure 2: Effects on muscular activity (left); inter-set volume (reps) and total volume (right; Kwon. 2013)

  What is yet amazing and puts another questionmark behind the recommendation to bring a couple of ice-cubes or a bottle of frozen water to the gym, are the effects of palm heating Robert A. Kwon and his colleagues tested in their 8 female subjects (mean±SD, age = 25±6 yr, height = 160±6 cm, body
  mass = 56±7 kg, 1RM = 52±6 kg, weight training experience = 6±2 yr) who completed 4 sets of 85%  1RM bench press exercise to failure, with 3 min rest intervals, as well. After all,
  

  "PC repetitions were significantly higher than TN during the 2nd set and PH repetitions were significantly higher than TN during the 4th set. Total exercise volume-load (kg) for both PC (1387±358) and PH (1349±267) were significantly higher than TN (1187±262)."

  So that the actual and unexpected question is not, whether you want to modulate the temperature of your palms, but rather which direction would be best... upwards or downwards?
  

  ---

  Further research is warranted - both in men, as well as with longer (=more realistic workouts) and different exercises. The finding that palm heating can increase strength endurance on the latter sets could even indicate that you got to bring two Thermos bottles, one with ice and another with hot water in your gym bad ;-)
  

---

Alright, that's it for this beautiful Saturday. Have a nice weekend everyone and read you ... or is it read me - whatever (!?), just briefly check out the most recent facebook news

• 

  All teas, green, black, white, ... have some effect on weight gain  (read more). It does yet appear as if those are most pronounced in the sick and obese, where they are a simple result of the health benefits of GTE & co (learn why)

  Organically grown vs. conventional green tea - The organic version has a "significantly higher" anti-oxidant activity (read more)
• Choline Better than viagra: 1.3g choline per day turn 79-year old man into a sex maniac within 6 weeks (read more)
• Coffee in the eyes? Not really, but in rodents, caffeine eye-drops protect the eye from UVB radiation (read more)
• Michael Douglas, Cancer & HPV - Irrespective of whether the rumors about the actor having cancer due to his love for oral sex are true or false, the corresponding study showing that people will now be more willing to vaccinate, is already out there (read more)

and enjoy your day. And don't worry, there will be more from the peculiar terrain, where bro- and pro-science meet, tomorrow.

References:

• Boucetta KQ, Charrouf Z, Aguenaou H, Derouiche A, Bensouda Y. Does Argan oil have a moisturizing effect on the skin of postmenopausal women? Skin Res Technol. 2013 Mar 26. 
• Kwon YS, Robergs RA, Mermier CM, Schneider SM, Gurney AB. Palm Cooling And Heating Delays Fatigue During Resistance Exercise In Women. J Strength Cond Res. 2013 May 29. 
• López LC, Cabrera-Vique C, Venegas C, García-Corzo L, Luna-Sánchez M, Acuña-Castroviejo D, Escames G. Argan oil-contained antioxidants for human mitochondria. Nat Prod Commun. 2013 Jan;8(1):47-50. 
• Mendoza JA, Zimmerman FJ, Christakis DA. Television viewing, computer use, obesity, and adiposity in US preschool children. Int J Behav Nutr Phys Act. 2007 Sep 25;4:44.
• Weise CM, Hohenadel MG, Krakoff J, Votruba SB. Body Composition and Energy Expenditure Predict Ad-Libitum Food and Macronutrient Intake in Humans. Int J Obes (Lond). 2013 May 23.