Update on GAINZ: More Muscle & Strength W/ Exercises You Like | Deadlifting Unshoed NO Power Booster | 50% Sugar NOT Anti-Anabolic | Cryotherapy NO Recovery Boost

No, bro - Losing your shoes won't allow you to magically lift thrice your BW when your current 1-RM is only twice your BW.

Who would have thought that? If trained subjects are allowed to chose their 'favorite' exercises (or those they deem most productive) they gain 63% more lean mass in a realistic 9-week study (difference short of sign., though). I guess compared to this result from a recent study from the University of Tampa, the realizations that deadlifting unshoed doesn't seem to provide a systematic benefit, that sugar does not - if protein intake is adequate - negatively affect anabolism, and that local cryotherapy doesn't just threaten the adaptational processes that occur after your workouts are rather expected results... results that were IMHO still worth summarizing in this October 2017 Suppversity "Update on GAINZ" ;-)

If you want to update YOUR gains, try creatine-monohydrate - safe and proven!

Creatine Doubles 'Ur GainZ!

Creatine Loading = Unnecessary

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1st Benefits of Creatine-HCL

The Real Bioavai-lability of Crea

Anti-Cre GAA Better Than Cre?

• Deadlifting unshod changes rate of force development and the medio-lateral center of pressure - albeit with unclear effects on deadlift performance (Hammer 2017).
  
  "While the unshod condition may have produced changes in RFD and ML-COP compared with the shod condition, there is only limited evidence in the current study to support this lifting technique for the conventional deadlift," that's the unfortunately very unspecific conclusion of a recent study in the Journal of Strength and Conditioning Research. Before I am going to tell you that the authors are right, though, "[f]urther investigation is required to clarify any possible implications of this result and its benefit to lifters", let's at least check out what Mark E. Hammer et al. did, observed, and concluded.
  
  For their study, the scientists recruited 10 strong male participants (mean ± SD, age = 27.0 ± 5.8 years; weight = 78.7 ± 11.5 kg; deadlift = 155.8 ± 25.8 kg) with a minimum training history of 2 years. A counterbalanced, crossover experimental design was used with different loads (60% and 80% 1RM). Four sets of four repetitions were prescribed per session with two sets per shoe and with each shoe condition involving one set per load.

  

  Figure 1: Overview of the study results; all values expressed relative to 60% 1RM shoed; statistically significant effects of wearing / not wearing shoes were observed only where %-ages given (Hammer 2017).

  Peak vertical force (PF), rate of force development (RFD), time to peak force (TPF), anterior posterior (COP-AP) and medio-lateral (COP-ML) center of pressure excursion, and barbell peak power (PP) data were recorded during all repetitions. Except for RFD (F = 6.389; p = 0.045; ƞp2 = 0.516) and ML-COP (F = 6.696; p = 0.041; ƞp2 = 0.527), there were no other significant main effects of shoe.
  
  What did matter, obviously, was the load; with significant main effects for PF (p < 0.05), COP-AP (p = 0.011), TPF (p = 0.018) and COP AP (p = 0.011), but there was no interaction between session, shoe and load (p range from 0.944 to 0.086).
  
  So what's the verdict, then? Eventually, we do thus arrive at the previously cited conclusion that "[f]urther investigation is required to clarify any possible implications of this result and its benefit to lifters." That's bad? Well, not really. If you personally like deadlifting without shoes, the study at hand does at least tell you that it doesn't mess with your power... you don't get why one would do that? Well as Hammer et al. point out, it's an "observed practice within the strength and conditioning field" to lose your shoes, because people expect that being unshod during the deadlift exercise can significantly improve your deadlifting performance... for the average experienced deadlifters, this is probably not the case; with the inter-personal differences Hammer et al. observed, though, it may work for you, personally, though.

• No ill effects of sugar-overfeeding w/ amounts equivalent to 50% of the daily energy requirements on protein anabolism in (young healthy) men and women if protein intake is adequate (Jegatheesan 2017).
  
  The dreaded reduction in IGF-1 and leucine and protein synthesis from sugar overfeeding, here an extra 50% of the subjects (12 healthy young male and female volunteers ) daily requirements (this means if you need 2000kcal, you got to eat 1000kcal extra... from 125g of pure sugar).
  
  French and Swiss scientists observed the "low protein" phenomenon, when they supplemented compared diets that were already high in carbohydrates (45% starch) with tons of sugar (delivering a 50% kcal surplus) and either 37.5% lipid and 7.5% protein (HSLP) or 15% lipid and 30% protein (HSHP) for 7-days and analyzed and compared fasting and postprandial plasma insulin, glucagon, and IGF1 concentrations were assessed before and after each intervention, and fasting plasma AAs level.

  "The increase in Ala elicited by sucrose overfeeding was blunted with HSHP (249 ± 18 vs 386 ± 11 μM, p < 0.001) compared to HSLP (251 ± 20 vs 464 ± 33 μM). Leu concentration decreased (130 ± 4 vs 116 ± 5 μM) after HSLP, but not after HSHP (139 ± 6 vs 140 ± 7 μM). Compared to HSLP, plasma BCAA, Phe, Tyr, and Pro were significantly higher with HSHP than HSLP. Fasting IGF1 concentration increased (174 ± 18 vs 208 ± 15 μg/dl) after HSHP and decreased (212 ± 13 vs 173 ± 12 μg/dl) after HSLP (p = 0.04)" (Jegatheesan 2017).

  So what's the verdict, then? As previously highlighted, the results clearly indicate that "sucrose overfeeding decreases IGF1 and Leu level [only] when associated with a LP [low protein] intake" (Jegatheesan 2017). No reason to go overboard on sugar, but at least an 'all-clear' for the occasional CHO refeed.

• Local cryotherapy is ineffective in accelerating recovery from exercise-induced muscle damage on biceps brachii (Lima 2017)
  
  From previous articles at the SuppVersity, you know that cryotherapy can impair the long-time size and strength gains of athletes. Against that background, it is all the more problematic that cryotherapy does not, as most people assume, accelerate recovery from every form of exercise-induced muscle damage ... no matter what.
  
  The reality of a recent study in nineteen untrained women proves this assumption wrong. After having performed an eccentric protocol of damage induction (2 sets of 10 repetitions) in both arms, the cryotherapy was applied for 20 min, twice per day, for 4 days following the eccentric exercise. Randomly, one of the subject’s arms was assigned as intervention and received cryotherapy, the opposite arm served as control. As muscle damage indirect markers, we collected muscle thickness, and echo intensity, delayed onset muscle soreness, and peak torque at baseline (PRE), and at 24, 48, 72, and 96 h.
  

  

  Figure 2: Neither the most important (=strength/torque) nor the auxiliary marker DOMs improved (Lima 2017).

  The muscle soreness markers increased in both, the experimental and the control arms, significantly compared to the PRE value at 24, 48, and 72 h. In a similar vein, the peak Torque of both experimental and control arm was significantly reduced and the scientists didn't find changes in any of the indirect markers of muscle damage between arms at any moment (p > 0.05).
  
  So what's the verdict, then? While they do risk a long(er) term reduction in gains in strength and size. Rookies will not be able to control their muscle soreness or improve their exercise recovery with local cryotherapy.

• More than 60% increase in average lean mass gains when experienced trainees are allowed to auto-regulate (=self-select) exercises (Rauch 2017).
  
  In contrast to previous studies on auto-regulation of training parameters, the study at hand did not allow its subjects, N=32 strength-trained volunteers, who were able to squat and bench 1.75 and 1.3 times their body mass, did not primarily address quantitative resistance training variables (e.g., volume, intensity, rest interval), but allowed the subjects to modify their exercise selection - a qualitative variable about which there is, according to Rauch et al. "a paucity of data" (Rauch 2017).
  
  Dietary intake was monitored using MyFitnessPal, subjects consumed used a pre-workout (Dymatize M.Pact) and 25g of whey (Dymatize Elite Whey Protein, 4g leucine) before and after workouts, respectively. Total protein intake was required to be >1.5g/kg per day if any subject’s protein intake fell short of this goal, they were given additional nutritional guidance from a certified sports nutritionist. Body composition was assessed using DXA.
  
  The workout the subjects had to follow was a full body-training regimen (3d per week, 9 weeks total). Each workout consisted of six different exercises. A 90-120 second rest interval was allowed between sets while two minutes were respected between exercises.
  

  "A daily undulating periodization model was implemented for both groups as follows: Day 1: 6-8RM, Day 2: 12- 14RM and Day 3: 18-20RM. The training regimen was divided into three mesocycles, the number of sets progressed in each mesocycle; Mesocycle 1: four sets per exercise, Mesocycle 2: five sets per exercise, and Mesocycle 3: six sets per compound exercise and five sets per accessory exercise. [...] Four certified strength and conditioning specialist were present for every training session, providing verbal encouragement and ensuring the proper amount of sets and repetitions were being performed" (Rauch 2017).

  The only difference between conditions was the exercises performed. The fixed exercise selection group (FES) group was handed a workout sheet with seven predetermined exercises.

  

  Table 1: Overview of the fixed exercise order and selection in the FES group (Rauch 2017).

  The auto-regulatory exercise selection (AES) group, on the other hand, was handed a workout sheet in which they had to select one exercise per muscle group... a small change that made a significant differences you can see in Figure 3  (note: with 15 dropouts, the scientists had to resort to a 95% confidence analysis to establish potential inter-group differences, though):
  

  

  Figure 3: Workout volume(s) and strength parameters in the 17 out of initially 32 trained subjects (>3y experience) who made it through the 9-week study without falling off the wagon (Rauch 2017)

  With the total volume load being significantly higher during mesocycle 2 and 3 when the subjects were allowed to auto-select their exercises (AES: 573,288kg ± 67,505, FES: 464,600 ± 95,595, p=0.0240), it is also not exactly completely surprising that the intra-group confidence interval analysis (95%CIdiff | analysis for conducted only within groups, because the inter-group difference was too small) Rauch et al. conducted suggests that only AES significantly increased LBM (AES: 2.47%, ES: 0.35, 95% CIdiff [0.030kg: 3.197kg], FES: 1.37 %, ES: 0.21, 95% CIdiff [-0.500kg: 2.475kg]) - the relative difference in changes in lean mass between treatments was 63% (1.6 kg vs. 0.98 kg), practically relevant, but statistically not significant (probably at least also because 15 subjects dropped out for unknown reasons).

  

  Figure 4: The changes in lean mass show a clear advantage for the AES group - in particularly in view of the fact that only one subject in the AES group (vs. 4 in FES) lost lean mass over the 9-wk period (Rauch 2017).

  We are, after all, talking about already trained individuals who are not going to pack on slabs of muscles within 8 weeks and for whom Figueiredo et al. (2017) have only recently pointed out that 'more helps more' - with the currently available evidence not suggesting a high likelihood of overtraining and reduced gains w/ increasing volume.
  
  Significant effects on bench-press strength (95% confidence analysis) were likewise observed only for the AES group (AES: 6.48%, ES: 0.50, 95% CIdiff [0.312kg: 11.42kg; FES: 5.14%, ES: 0.43 95%CIdiff [-0.311kg: 11.42kg]) while for back squats the 1RM responses were similar between groups, (AES: 9.55%, ES: 0.76 95% CIdiff [0.04kg: 28.37kg], FES: 11.54%, ES: 0.80, 95%CIdiff [1.8kg: 28.5kg]).
  
  So what's the verdict, then? It remains to be seen if the significant increase in training volume was a physiological or psychological effect. What seems to be certain, however, is that it's the mechanism which eventually drove the increase in lean mass and bench press gains in the AES group... a result that clearly refutes the over-generalized notion that the "exercises you tend to avoid will build the most muscle" (broscience).
  
  In that it may be worth mentioning and important to point out that (a) the effect on training volume occurred only in the 2nd and 3rd mesocycle, i.e. when the subjects' volume was already high, and that (b) the average lean mass increase of 1.6kg (see Figure 4) may not seem like much, but you should keep in mind that the guys in the study have been busting their a%% on the grind for years. So you cannot expect newbie gains of 2lbs per week. Plus: Only one subject in the AES group, but four subjects in the FES group actually lost muscle mass over the course of the 9-wk study period... makes you wonder if the inter-group difference had achieved significance if all N=32 subjects had made it from week one to week nine (15 dropped out and thus reduced the statistical power of the study significantly).

Even if done 5x/wk "weights" won't trigger the female athlete triad - that's your beloved "cardio", ladies.

You still want more? Well, what about this one, then: Ikezoe, et al. (2017) report in their latest paper in the Journal of Strength and Conditioning Research (once again) that low load high rep training will produce the same gains as high load low rep training - this time, albeit even if the subjects didn't go to failure... cool? Well, not really: the subjects were, after all, untrained. Just like most subjects in studies like these. Schoenfeld et al.'s 2016 meta-analysis highlighted that and a "trend [...] for superiority of heavy loading" in their latest meta-analysis (2016): " | Comment on Facebook!

References:

• Figueiredo, V. C., de Salles, B. F., & Trajano, G. S. (2017). Volume for Muscle Hypertrophy and Health Outcomes: The Most Effective Variable in Resistance Training. Sports Medicine, 1-7.
• Hammer, M. E., Meir, R., Whitting, J., & Crowley-McHatten, Z. (2017). Shod versus barefoot effects on force and power development during a conventional deadlift. Footwear Science, 9(suppl. 1), 99.
• Ikezoe, T., Kobayashi, T., Nakamura, M., & Ichihashi, N. (2017). Effects of low-load, higher-repetition versus high-load, lower-repetition resistance training not performed to failure on muscle strength, mass, and echo intensity in healthy young men: a time-course study. The Journal of Strength & Conditioning Research.
• Jegatheesan, P., Surowska, A., Campos, V., Cros, J., Stefanoni, N., Rey, V., ... & Tappy, L. (2017). MON-P291: Dietary Protein Content Modulates the Amino-Acid and IGF1 Responses to Sucrose Overfeeding in Humans. Clinical Nutrition, 36, S285-S286.
• Lima, et al. (2017) "Local cryotherapy is ineffective in accelerating recovery from exercise-induced muscle damage on biceps brachii." Sport Sciences for Health. August, Volume 13, Issue 2, pp 287–293
• Rauch, J. T., Ugrinowitsch, C., Barakat, C. I., Alvarez, M. R., Brummert, D. L., Aube, D. W., ... & De Souza, E. O. (2017). Auto-regulated exercise selection training regimen produces small increases in lean body mass and maximal strength adaptations in strength-trained individuals. The Journal of Strength & Conditioning Research.
• Schoenfeld, B. J., Wilson, J. M., Lowery, R. P., & Krieger, J. W. (2016). Muscular adaptations in low-versus high-load resistance training: A meta-analysis. European journal of sport science, 16(1), 1-10.

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).

The effect on RMR may be small, but you must build muscle if your goal's 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!

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.

Ramadan Fasting Studies Showing Fat, but no Muscle Loss Support Benefits of 'Lean Gains'-Style Intermittent Fasting

Remember, Ramadan fasting is not about eating healthy or dieting, after sundown most Muslims consume at least as much energy as on a non-fasting day.

While scientists usually refer to alternate-day fasting as "intermittent fasting", the average fitness enthusiasts will think of Martin Berkhan's "lean gains" protocol, when he or she hears the words "intermittent fasting" - a protocol that involves fasting for minimally 16h and eating for maximally 8h and is thus somewhat similar to the "eat only after sundown" protocol Muslims follow during Ramadan.

Against that background, it makes sense to assume that the two dozen of peer-reviewed Ramadan fasting studies from the Middle East and the Muslim part of Asia provide an (albeit often uncontrolled) model for intermittent fasting.

Do you have to worry about fasting when your're dieting!?

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Habits Determine Effects of Fasting

Breaking the Fast & the Brain

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review

If we assume that this premise is true, a recent study from the Dr. Cipto Mangunkusumo General Hospital at the Universitas Indonesia, provides intriguing insights into the lean mass conserving effects of "intermittent fasting".

The study aimed to evaluate the effect of Ramadan fasting on body composition in healthy Indonesian medical staff. To this ends, Ari Fahrial Syam et al. (2016) recorded the body composition of healthy medical staff  members of the Dr. Cipto Mangunkusumo General Hospital before, during and after Ramadan fasting in 2013 (August to October).

Figure 1: Changes in body composition during the 28-day Ramadan fast (Syam. 2016).

In conjunction with data on the energy intake of the forty-three subjects, the data the scientists gathered appear to confirm what the proponents and followers of the "lean gains" variety of intermittent fasting say: You will lose body fat, but not muscle and that without significant reductions in energy intake.

According to 24h food recalls, the subjects didn't change their energy intake during Ramadan. The fat loss can thus not be explained by the induction of a caloric deficit.

Yes, the body composition was assessed by BIA, but ... while body impedance analysis (BIA) may not the best method to assess the %fa and % lean mas of trained athletes, but has been shown to have a high accuracy and reliability in "normal" people. Similarly, the 24-hour food recalls that were used to evaluate the subjects' dietary intake are often a bit off, but that's the case for both pre- and post-assessments, which is why it is reasonable to assume that there was indeed no significant change in total energy intake. This doesn't change, though that it's a pity that the scientists don't provide information about individual nutrients intakes. Previous studies suggest increased protein intakes during Ramadan fasting (Frost. 1987; El Ati. 1995) - a potentially highly relevant increase, obviously.

One thing Syam's study adds to the table, however, is that (a) the weight you will lose is not just body fat, it's also a lot of water and even bone (see Figure 1) and that (b) your (fat) weight will bounce back, within 4-5 weeks when you return to your usual eating habits.

Table 1: Overview of pertinent research comparing the results of the study at hand to previous studies (Syam. 2016).

As the research overview in Table 1 shows, some, but not all of the (side) effects are actual news. Hossini et al. (2013), for example, didn't observe changes in mineral or water content. The initially highlighted lack of protein / muscle loss, on the other hand, was observed in all three studies in which the exact body composition was measured. It is thus not unreasonable to assume that this is a characteristic feature of pertinent "intermittent fasting" protocols.

Fears about fat gain are likewise unwarranted | learn more

Bottom line: Don't get all excited, even if the 24h food recall were accurate and the fat loss occurred in the absence of reductions in food intake, the fat loss was statistically significant, but with less than 500g practically negligible.

The more important message of the study at hand is thus that intermittent fasting doesn't trigger a loss of muscle mass - a fear that is still prevalent, especially in male members of the fitness community | Comment!

References:

• El Ati, Jalila, C. H. I. R. A. Z. Beji, and J. A. B. E. R. Danguir. "Increased fat oxidation during Ramadan fasting in healthy women: an adaptative mechanism for body-weight maintenance." The American journal of clinical nutrition 62.2 (1995): 302-307.
• Frost, G., and S. Pirani. "Meal frequency and nutritional intake during Ramadan: a pilot study." Human nutrition. Applied nutrition 41.1 (1987): 47-50.
• Hosseini, Seyyed Reza Attarzadeh, et al. "The effect of ramadan fasting and physical activity on body composition, serum osmolarity levels and some parameters of electrolytes in females." International Journal of Endocrinology and Metabolism 11.2 (2013): 88.
• Faris Mohammed Ahmed, et al. "Impact of Ramadan Intermittent Fasting on Oxidative Stress Measured by Urinary 15-F2t-Isoprostane." Journal of Nutrition and Metabolism 2012 (2012).
• Norouzy, A., et al. "Effect of fasting In Ramadan on body composition and nutritional intake: a prospective study." Journal of Human Nutrition and Dietetics 26.s1 (2013): 97-104.
• Sadiya, Amena, et al. "Effect of Ramadan fasting on metabolic markers, body composition, and dietary intake in Emiratis of Ajman (UAE) with metabolic syndrome." Diabetes, metabolic syndrome and obesity: targets and therapy 4 (2011): 409.
• Syam, Ari Fahrial, et al. "Ramadan Fasting Decreases Body Fat but Not Protein Mass." International Journal of Endocrinology and Metabolism 14.1 (2016).

High Dose NSAID Boosts Muscle Gains in Elderly Men - 11% Increase in Type II Fiber Size, Type I Grew Only 'on' Tylenol

Are NSAIDs over-the-counter anabolics from the pharmacy next door?

Even though this is not the first SuppVersity article about the effects of NSAIDs or COX-inhibitors like Aspirin, Tylenol, Pain-Eze and co., I would like to highlight one again that the existing evidence suggests differential effects in young(er) vs. old(er) individuals, with the former seeing no or detrimental and the latter no or beneficial effects when using NSAIDs during resistance training regimen.

It is thus neither guaranteed, nor likely that a young man or woman would see the same 28% extra-increase in type I fiber and 11% extra-increase in type II fiber diameter, Trappe et al. describe in their soon-to-be-published paper in the journal of the Gerontological Society of America (Trappe. 2016).

The link to hormesis research is far from being straight-forward

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Vit C+E Impair Muscle Gains in Older Men

C+E Useless or Detrimental for Healthy People

Vitamin C and Glucose Management?

Antiox. & Health Benefits Don't Correlate

I do understand, though that the numbers still got your attention. Well, let's take a close look at how the researchers got to these impressive results. It all started with previous research that suggested that common cyclooxygenase (COX)-inhibiting drugs enhance resistance exercise induced muscle mass and strength gains in older individuals.

Unfortunately, the results of the few studies we have, are conflicting (Schoenfeld. 2012; see Table 1) - with one showing benefits and two showing no effect at all. The purpose of Trappe's latest study was thus to (a) simply gather more evidence and (b) investigate the mechanism behind the changes that were observed in previous studies. Or, as the scientists put it "whether the underlying mechanism regulating this effect was specific to Type I or Type II muscle fibers" (Trappe. 2016).

Table 1: Summary of human studies investigating the effect of nonsteroidal anti-inflammatory
drug consumption on muscle hypertrophy (Schoenfeld. 2012).

To this ends, the scientists obtained muscle biopsies from the vastus lateralis of healthy older men who consumed either a placebo (n = 8; 64±2 years) or COX inhibitor (acetaminophen, 4 gram/day; n = 7; 64±1 years | compliance was monitored by researchers, when tablets were taken at the lab or camera when taken at home) during a standardized 12 weeks resistance training program (only the knee-extensor was trained - albeit on 3 days/week) the scientists describe as follows:

"All participants completed a progressive resistance exercise training program of bilateral knee extension that was designed to hypertrophy and strengthen the m. quadriceps femoris, using a protocol employed for several previous investigations in our laboratory. Each participant was scheduled for resistance training three times per week over the 12 weeks for a total of 36 sessions on an isotonic knee extension device (Cybex Eagle, Medway, MA). All sessions were supervised by a member of the research team. Each session was separated by at least 1 day and consisted of 5 minutes of light cycling (828E, Monark Exercise AB, Vansbro, Sweden), two sets of five knee extensions at a light weight, followed by three sets of 10 repetitions with 2 minutes of rest between sets. Training intensity was based on each individual’s one repetition maximum (1RM) and adjusted during the training based on each individual’s training session per formance and biweekly 1RM" (Trappe. 2016).

The compliance of the subjects of this double-blinded study is described as excellent. Therefore, we can assume that the significance of the results of the scientists' analysis of muscle samples that were examined for Type I and II fiber cross-sectional area, capillarization, and metabolic enzyme activities (glycogen phosphorylase, citrate synthase, β-hydroxyacyl-CoA-dehydrogenase) is high.

Figure 1: Pre-/post comparison on fiber (according to fiber type) and muscle size (Trappe. 2016).

Obviously, the most important results of these analysis have been mentioned before: While the type I fiber size did not change with training in the placebo group (304±590 μm²), it increased by a statistically significant and practically relevant 28% in the COX inhibitor group (1,388±760 μm²).

Schematic of the prostaglandin (PG) producing cyclooxygenase (COX) pathway and specific receptors that influence growth and atrophy in skeletal muscle (Trappe. 2013b).

How do COX inhibitors promote hypertrophy? As Trappe et al. point out "[e]vidence from the larger cohort suggests that the augmented muscle growth was primarily mediated by a reduction in intramuscular PGE2 and resultant PGE2 receptor downstream signaling effects (Standley. 2013; Trappe. 2013a,b). Specifically, the COX inhibitor appeared to reduce the negative effects of PGE2 on protein synthesis and degradation, working through established myokines and other cellular regulators of protein turnover. The myocellular findings from the current study suggest that these effects were more pronounced in the Type I fibers, possibly due to a more active PGE2/COX pathway in this fiber type" (Trappe. 2016).

In addition, the authors point out that previous evidence suggests an "additional mechanism for the COX inhibitor–induced supplemental growth, working through PGF2α receptor and protein synthesis upregulation" (Trappe. 2016; referring to Trappe. 2013a,b).

For the type II fibers, both groups recorded significant increases in fiber size. With "only" 26%, the gains of the subjects in the the placebo group (1,432±499 μm2, p < .05) were yet measurably lower than those in the COX inhibitor group whose vastus lateralis type II muscle fiber size increased by 37% (1,825±400 μm², p < .05). In view of the overall benefits the COX group saw, it is thus hardly surprising that the subjects consuming the COX inhibitor recorded significantly greater total muscle CSA gains (see Figure 1, right | note: only the total mass gain was sign. different between groups).

Figure 2: Change in fiber type–independent (A) and fiber type–specific (B) muscle capillarization from the beginning to the end of the 12-week resistance exercise training and drug interventions. CCEF = capillaries in contact with each fiber; CSA = cross-sectional area. *p < .05 vs pre. **p < .1 vs pre.

While enzyme activity (not shown in Figure 2) and capillarization were generally maintained in the placebo group, the capillary to fiber ratio of the subjects in the COX inhibitor group increased by an albeit only borderline significant 24% (p < .1). The citrate synthase activity, on the other hand, increased statistically significantly, but by "only" 18% (p < .05). These differential changes in citrate synthase (important for fat oxidation and endurance) and muscle capillarization further underline the beneficial effects of NSAIDs on the adapatational response to exercise in the elderly.

Figure 2: Two out of three studies find that NSAIDs blunt the satellite cell response to resistance training young people | A: Number of Pax7 cells expressed per number of myonuclei (in %) in muscle biopsies (vastus lateralis muscles) obtained before (pre) and 8 days after maximal eccentric exercise (no block and NSAID); B: Immunohistochemical staining with the use of Pax7 antibody to identify satellite cells on a muscle cross-section (7 m) taken 8 days after exercise (from Mikkelsen. 2009).

Bottom line: There's no reason to doubt the scientists' conclusion that "COX inhibitor consumption during resistance exercise in older individuals enhances myocellular growth, and this effect is more pronounced in Type I muscle fibers" (Trappe. 2016). It is important however, that their results apply only to healthy elderly individuals.

Why only in the elderly? Well based on previous research, there's in fact good reason to doubt that similar benefits would have been observed in younger individuals. The hitherto published results in young people are mixed. A possible explanation for that would be the previously observed "impairment of satellite cell activity" (Schoenfeld. 2012) in response to chronic NSAID consumption - a side effect that may turn out to be detrimental in the long(er)-term, because unlike older individuals, in whom the satellite cell function is compromised, already (Thornell. 2011), young people's long-term gains appear to rely on the myostatin lowering recruitement of additional myonuclei.

Overall, the potential negative effects on satellite cell activity and thus long-term muscle growth, the lack of convincing evidence of benefits in younger individuals and, for young and old alike, the negative side effects of chronic NSAID use on your tendons, gut, kidney and other organs are three good reasons I certainly don't advise to seriously consider "supplementing" NSAIDs daily to augment your muscle gains | Comment on Facebook!

References:

• Mikkelsen, U. R., et al. "Local NSAID infusion inhibits satellite cell proliferation in human skeletal muscle after eccentric exercise." Journal of applied physiology 107.5 (2009): 1600-1611.
• Schoenfeld, Brad J. "The Use of Nonsteroidal anti-inflammatory drugs for exercise-induced muscle damage." Sports medicine 42.12 (2012): 1017-1028.
• Standley, R. A., et al. "Prostaglandin E 2 induces transcription of skeletal muscle mass regulators interleukin-6 and muscle RING finger-1 in humans." Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA) 88.5 (2013): 361-364.
• Trappe, Todd A., and Sophia Z. Liu. "Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise." Journal of Applied Physiology 115.6 (2013a): 909-919.
• Trappe, Todd A., et al. "Prostaglandin and myokine involvement in the cyclooxygenase-inhibiting drug enhancement of skeletal muscle adaptations to resistance exercise in older adults." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304.3 (2013b): R198-R205.
• Trappe, Todd A., et al. "COX Inhibitor Influence on Skeletal Muscle Fiber Size and Metabolic Adaptations to Resistance Exercise in Older Adults." J Gerontol A Biol Sci Med Sci (2016): Advance Access publication January 27, 2016.
• Thornell, Lars-Eric. "Sarcopenic obesity: satellite cells in the aging muscle." Current Opinion in Clinical Nutrition & Metabolic Care 14.1 (2011): 22-27.

Intermittent Fasting Works, But is It Better Than "Regular" Dieting? What Do the Latest Reviews / Meta-Analyses Say?

Don't eat unless this brunette,... ah, I mean her clock tells you to eat. That's intermittent fasting (IF) - well, at least one out of at least three versions of eating by the clock people call "intermittent fasting". Needless to say that this doesn't make it much easier to decide if IF works or not.

It has been some time since I wrote about "Intermittent Fasting" ("lean gains"-style, i.e. eat in a 6h-8h window everyday), "Fasting" (don't eat at all) and "Alternate Day Fasting" (eat very little / usually ~800kcal one day / and normal the next one, repeat). Against that background it is worth devoting a whole SuppVersity Research Update to the latest studies and reviews of IF and ADF.

In the corresponding papers, Tinsley and La Bounty review the "effects of intermittent fasting on body composition and clinical health markers in humans", Varady et al. discuss "the determinants of weight loss success with alternate day fasting" and Seimon et al. address the question whether "intermittent diets provide physiological benefits over continuous diets for weight loss?", as part of a short report in form of a systematic review of clinical trials.

So, where do I start? I guess it would be best to build the article around the most extensive and for many of you probably most interesting analysis by Seimon et al. that's about to be published in one of the next issues of Molecular and Cellular Endocrinology: "Do intermittent diets provide physiological benefits over continuous diets for weight loss? A systematic review of clinical trials" (Seimon. 2015)

Do you have to worry about muscle loss and metabolic damage, when you're fasting?

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Habits Determine Effects of Fasting

Breaking the Fast & the Brain

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review

Usually I don't do this, but in view of the tons of articles I have already written about Intermittent Fasting, I feel like it is possible to start with the conclusion which says that "[i]ntermittent fasting thus represents a valid – albeit apparently not superior – option to continuous energy restriction for weight loss." Accordingly, the question I still owe you an answer to is "WHY?", i.e.: "What makes intermittent fasting 'a valid' weight loss strategy?", and "Why is it 'valid - albeit nor superior'?" Well, the answers to these questions are neither straight forward nor can they be answered objectively. As every review and/or meta-analysis, Seimon's paper ends with the researchers' subjective interpretation of selected, objective data. Data from a total of 40 publications involving humans of any age or body mass index that had undergone a diet involving intermittent energy restriction, 12 with direct comparison to continuous energy restriction. What all of these studies have in common is that they measured one or more of the following variables: Body weight, body mass index, or body composition before and at the end of energy restriction.

Table 1: The Aguin study is one out of many that shows that both intermittent and chronic energy restriction work and produce statistically (see p-values) identical changes in body composition, size and relevant markers of lipid and glucose metabolism (Arguin. 2012)

What they did not share, though, was the type of "Intermittent Fasting". Practically speaking, this means that 31 of the 40 publications "involved ‘intermittent fasting’ of 1-7-day periods of severe energy restriction" - were thus rather "fasting" or "alternate day fasting" than classic "intermittent fasting" studies. More specifically: Seimon et al. also included studies like Arguin et al. (2012) in which the subjects were either dieting for 15 weeks at a moderate energy restriction or for 3 cycles of 5 week at higher energy deficits were interspersed by 3 cycles of 5 weeks on a calorically sufficient diet and the results were compared after each intervention, as well as one year thereafter. These obviously more important parameters are summarized in Table 1, and they don't show any inter-group differences.

How much weight / fat loss and health improvements can you expect? While the Seimon study is excellent for detail, Tinsley's and La Bounty's short review features the more concise overview of the figures - albeit with the same general message, i.e. "intermittent fasting (in the broadest sense) works, but whether it's more effective than continuous energy reductions must be determined on an individual level". This does not negate that (a) alternate-day fasting trials of 3 to 12 weeks in duration appear to be effective at reducing body weight ( 3%–7%), body fat ( 3–5.5 kg), total cholesterol ( 10%–21%), and triglycerides ( 14%–42%) in normal-weight, overweight, and obese humans, and (b) that whole-day fasting trials lasting 12 to 24 weeks also reduce body weight ( 3%–9%) and body fat, and favorably improve blood lipids ( 5%–20% reduction in total cholesterol and 17%–50% reduction in triglycerides). Research on time-restricted feeding aka "lean gains"-style intermittent fasting, on the other hand, is still "too limited" (ibid.) to draw clear conclusions.

Now, while the Arguin study is not correctly summarized in the tabular overview of all studies they reviewed, the most important information, i.e. the fact that the cyclic diet does not provide any significant advantages or disadvatages over continuous dieting is true. Based on the meta-analysis by Seimon et al., the following take-home messages can be stated:

• The drop out rates were comparable for interventions involving intermittent energy restrictions (IER) and continuous energy restrictions (CER).
• Significant reductions in body weight, size (waist, hip, etc.) and adiposity can be achieved with both intermittent energy restrictions (IER) and continuous energy restrictions (CER).
• If we go by weight loss which happens to be the most frequently measured study outcome in Seimon's selection of studies, the results are comparable for IER and CER.

• 

  Study suggests: Your goals may determine whether a low or high fat diet is the better basis for your alternate day fasting fat loss diet | more

  A reduced drive to eat, on the other hand, appears to be a unique advantage of intermittent energy restrictions, where eating very little for a fixed time period appeared to be easier to handle for the subjects then the grazing that's part of many CER interventions.
  
  This is an important results, after all, one of the mainstream arguments against intermittent or alternate day fasting is that they will trigger an overcompensation on the (re-)feeding day - a phenomenon that was not observed.
  
  On the contrary, "participants only consuming an average of 95% of their calculated energy needs on feed days" (Seimon. 2015). This is particularly noteworthy because "this apparent suppression of the drive to eat occurred despite decreased circulating levels of the appetite-reducing hormone, leptin, following IER" (Seimon. 2015). Whether this is related to an increase in ketone bodies in the IER studies that was non-existent or less pronounced in the CER trials will still have to be elucidated, though.
• A trend towards mood disturbance, tension, anger and confusion was observed in only one study. A study by Hussin et al. (2013) that was done in aging normal-weight men and the results of which stand in contrast to what Johnson et al. found in overweight subjects in 2007.
  

  

  Figure 1: Intermittent energy restrictions (IER) appear to be better suited for the obese, whose mood improves during th fast, while the mood of lean subjects decreases sign. (Hussin, 2013 & Johnson. 2007).

  In conjunction with the increased drop-out rates in Hussin's study, we may argue that a lack of triglyceride and FFA releasing adipose tissue may make IER interventions harder to adhere to - probably, because of a simple lack of available energy during the fast.

• 

  So, "Intermittent Fasting Does Now Make You Fat"? Do the Facebook Posts Lie? Not Necessarily, but Many People Forget that IF Works Only if it Reduces Your Energy Intake | more

  In view of the sign. reductions in leptin in IER interventions it is hardly surprising that Seimon et al. didn't find convincing evidence that IER would ameliorate the reduction in resting metabolic rate that's an inevitable (temporary) side effect of any dieting regimen.
  
  One (de Groot. 1989) out of three studies that made a direct comparison between the two even found a further reduction in resting metabolic rate (RER) in the IER group, the others found no difference (Hill. 1989; Harvie. 2011; Arguin. 2012). Overall, it would yet appear as if any potentially existing difference was negligible.
  
  Other metabolic adaptations such as a reduced IGF1 production were observed only in trials where the subjects fasted with liquid meals (Kroeger. 2012).
• No difference and on average comparable improvements in glucose homeostasis were observed in the 20 studies that tested respective parameters in detail. While there are individual studies that suggest advantages for one or another method, the overall picture that emerges is that there are no systematic differences - a conclusion that would also explain the - in parts - contradictory results from pertinent studies.
• Lastly, it must not go unmentioned that the addition of exercise to IER will make it - just as it is the case for CER, by the way - more effective and will thus shed more fat (and maintain more lean mass) than IER alone.
  

  

  Figure 2: The combination of alternate day fasting and exercise reduces uncontrolled and emotional eating in 64 obese subjects over the course of a 12-week study (Bhutani. 2013).

  Somewhat surprising, but in view of the overall anti-appetite effect of fasting not impossible is that the combination of exercise with IER also reduced the subjects' craving for uncontrolled and emotional overeating (Bhutani. 2013).

In view of the fact that only 12 of the 40 publications included in Seimon's review directly compared IER with CER, it is yet important to remember that we are far from being able to tell who will benefit most and who least from "intermittent fasting" (in the broadest sense). If you review the above summary of the results, you will yet have to agree that it would appear as if men and women who still have a ton of weight to lose could fare better with intermittent or alternate day fasting, while lean individuals may, but don't necessarily have to struggle with the lack of readily available energy during the fast.

Figure 3: While race matters and Caucasians appear to do much better on alternate day fasting regimen, the baseline body weight (and BMI | not shown) doesn't make a difference in the 4 ADF trials Varady et al. reviewed (2015).

At least in the 8-week ADF studies Varady et al. reviewed in their previously mentioned short report in Obesity Research and Clinical Practice, however, the initial body weight was not a good predictor of weight loss success. Rather than that, "[s]ubjects aged 50—59 y achieved greater (P = 0.01) weight loss than other age groups" and "Caucasian subjects achieved greater (P = 0.03) weight loss than other races" (Varady. 2015) with the alternate day (ADF) version of "intermittent fasting".

With only 5 out of the 40 studies in Seimon's review having a follow-up and no follow-up in any of the ADF studies in the previously cited short report by Varady et al. (2015), the long-term benefits or detriments must be considered largely under-researched, at the moment, too.

Evidence From the Metabolic Ward: 1.6-2.4g/kg Protein Turn Short Term Weight Loss Intervention into a Fat Loss Diet. 1.6g/kg not 2.4g/kg Offers Optimal Muscle Protection | learn more!

So what's the verdict then? Well, firstly: Intermittent fasting works. It's not exactly well-researched, though. Accordingly, it is difficult to say (a) who would benefit most  / least, (b) which form of intermittent fasting ("lean gains" 6-8h window everyday vs. alternate day vs. total fasting) works best and (c) how (a) and (b) interact with with each other: It is for example well possible that the discrepancy between the effect on appetite in lean vs. obese individuals I highlighted in the main body body of this article occurs only with simple (as in Hussin. 2013), yet not with more complex methods of fasting as ADF or the 6-8h fasting window at a freely chosen point in time.

Overall, the best advise I can give you is thus to try if and which type of intermittent fasting works for you. What I cannot recommend is any form of extended fasting, where you are consuming very low amounts of energy (like 400-600kcal) for more than just one day. In addition, you want to make sure to lift weight and consume enough (~1.5g/kg) protein even on fasting days to conserve lean muscle mass | Comment on Facebook!

References:

• Arguin, Hélene, et al. "Short-and long-term effects of continuous versus intermittent restrictive diet approaches on body composition and the metabolic profile in overweight and obese postmenopausal women: a pilot study." Menopause 19.8 (2012): 870-876.
• Bhutani, Surabhi, et al. "Effect of exercising while fasting on eating behaviors and food intake." J Int Soc Sports Nutr 10.1 (2013): 50.
• de Groot, Lisette CPGM, et al. "Adaptation of energy metabolism of overweight women to alternating and continuous low energy intake." The American journal of clinical nutrition 50.6 (1989): 1314-1323.
• Harvie, Michelle N., et al. "The effects of intermittent or continuous energy restriction on weight loss and metabolic disease risk markers: a randomized trial in young overweight women." International journal of obesity 35.5 (2011): 714-727.
• Hill, James O., et al. "Evaluation of an alternating-calorie diet with and without exercise in the treatment of obesity." The American journal of clinical nutrition 50.2 (1989): 248-254.
• Hussin, N. M., et al. "Efficacy of fasting and calorie restriction (FCR) on mood and depression among ageing men." The journal of nutrition, health & aging 17.8 (2013): 674-680.
• Johnson, James B., et al. "Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma." Free Radical Biology and Medicine 42.5 (2007): 665-674.
• Seimon, Radhika V., et al. "Do intermittent diets provide physiological benefits over continuous diets for weight loss? A systematic review of clinical trials." Molecular and Cellular Endocrinology (2015).
• Varady, Krista A., et al. "Determinants of weight loss success with alternate day fasting." Obesity Research & Clinical Practice (2015).