Dieting Down to ~10% Body Fat for Women: Contest Prep Study - Deficits, Muscles, Hormones and the Yo-Yo Effect

This would unquestionably be at the lower end of contest BF% levels (avg. 12%) the women in this study achieved,

The number of studies on fitness and bodybuilding competitions is limited. Probably you will remember my previous discussions of the paper/s by Rossow, et al. ("Natural bodybuilding competition preparation and recovery: a 12-month case study." | 2013) Kistler, et al. ("Case Study: Natural Bodybuilding Contest Preparation." International Journal of Sport Nutrition and Exercise Metabolism", 2014), and Robinson et al. ("A nutrition and conditioning intervention for natural bodybuilding contest preparation: case study" | 2015). And yes, three is not just the number of studies that I've covered at the SuppVersity, it's also the number of decently recent studies dabbling with dieting down for a contest in one of the "physique sports".

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Speaking of fitness, ... you probably already guessed it: There's study #4 by Juha J. Hulmi, et al. (2017). The study that was conducted by researchers from Finland and Estonia has the telling title "The Effects of Intensive Weight Reduction on Body Composition and Serum Hormones in Female Fitness Competitors" and was, as its authors point out, designed at least partly in response to the "worries about the potential negative consequences of popular fat loss regimens for aesthetic purposes in normal weight females have been surfacing in the media" (Hulmi. 2017).

Since longitudinal studies investigating these kinds of diets are lacking, Hulmi et al. studied the effects of a 4-month fat-loss diet in 50 (initially) normal weight females competing in fitness sports. This means we are dealing with a large-scale observational study, not an experimental study in which parameters such as the daily or weekly caloric deficit, the protein intake or related variables were set by the researchers. Rather than that, the 27 females (27.2 ± 4.1 years | 15 newbies, 12 women who had competed before) who dieted for ~4 months, and their 23 (27.7 ± 3.7 years) peers, who were acting as weight-stable controls, managed their diet and exercise regimen as they saw fit (note: with only 3 dropouts from the diet group and 6 from the control group the adherence was pretty good).

Figure 1: The experimental design of the study. Two representative participants are shown from each group. The pre to mid time period lasted ∼20 weeks during which the participants decreased their energy intake and the amount of exercise, whereas the controls maintained their activity levels and nutrient intake. The mid to post period lasting ∼18 weeks was a recovery period with increased energy intake back toward the baseline levels in the diet participants, whereas the controls maintained their energy intake and exercise levels (Hulmi. 2017).

You can take a glimpse both the design and the results in Figure 1. The subjects' body composition was assessed on separate test with the DEXA test being done on empty (that makes the test more reliable, because it's not going to be tricked by overstocked glycogen levels). The exercise performance tests, on the other hand, took place after the subjects' had a standardized breakfasts, because the dieters would otherwise have underperformed due to their low energy intake in the later phase of the dieting period - a period during which the subjects maintained not identical, but similar resistance training and cardio regimen (quoting from the FT | my emphasis):

• Resistance training: Split routines were used for resistance training by all competitors in the diet group meaning that they focused on single muscle groups per session as is often the case also in bodybuilders (Hackett et al., 2013). The main muscle groups trained included thighs, hamstrings, buttocks, chest, shoulders, arms, upper and lower back, calves, and abdominals. Dividing training into separate body parts per session did not differ significantly throughout the training. At baseline the 3-, 4-, 5-, and 6-split training was used by 3, 10, 13, and 1 of the 27 participants, respectively, while the same numbers were during the diet on average 5, 8, 14, and 0 and during the recovery period 7, 8, 12, and 0. In addition, the competitors also practiced their posing routines. Training sessions lasted between 40 and 90min. 
• Cardio: Aerobic training for the participants was almost uniquely either high-intensity interval training (HIT) with a bicycle, cross trainer or other gym equipment or both HIT and steady-state low to medium intensity aerobics (usually walking/running or with cross trainer). During the competition week the participants did not report doing HIT, but instead lower intensity aerobics. Typical HIT-exercise was 10–25 min in total including high intensity 15–45s intervals with 30–60s of recovery between the sets. Steady state lower intensity aerobics was typically 30–60 min in duration. Part of the females completed their aerobic training mainly together with their resistance exercise workouts while most of the participants completed also separate aerobic workouts, especially during the diet.

As the authors point out, there was a tapering period (learn more) during which total training load is typically slightly decreased and carbohydrate and total energy intakes are increased toward the baseline levels, in the last week of the contest prep.

Why would you taper before the competition? A competitor would probably answer that he, or, as in this case, she, did not "want to come in flat". Accordingly you taper, i.e. reduce the training intensity and (re-)introduce carbs into your diet to restore muscle glycogen and get rid of the "flat" look of which Hulmi et al. argue that it will "occur with low carbohydrate diets as ∼2.7g of water per each gram of glycogen is stored in skeletal muscle" (Hulmi. 2017).

Speaking of the subjects' energy deficit. The latter was - as it is currently in vogue - achieved almost solely by a drastic reduction in carbohydrate intake while keeping protein intakes high and fat intakes moderate. You can see the result in form of a diet that lacked, during contest prep/dieting, ca. 20% of the habitual energy intake of the subjects in my plot in Figure 2 reduced (see Figure 6 for data on the energy balance, i.e. calories in vs. calories out from exercise = cardio + weights).

Figure 2: Energy intake expressed as protein, carbohydrates and fats rel. to body weight (g/kg | Hulmi. 2017).

With these dietary changes and the increase in aerobic exercises aka "cardio", the subjects achieved body fat reductions of ~12% and a ∼35–50% decrease in fat mass (DXA, bioimpedance, skinfolds, P < 0.001) during the dieting phase.

Table 1: Tabular overview of the exercise levels in the diet and control groups; learn more about METs (Hulmi. 2017).

As you can see in Table 1, the latter, i.e. the aerobic workload did indeed increase significantly, while the subject's maintained their resistance training volume fairly stable [ 4.7 ± 0.7 (diet group) and 3.9 ± 1.9 (controls) METs] - until the tapering week, which may now give you the false impression that volume and/or intensity were reduced during the dieting phase:

• lower body muscles were trained during the diet 1.4 ± 0.5 times per week, and 
• upper body muscle groups were trained 1.1 ± 0.3 times per week, 

as part of the previously hinted at split design. That allowed for 4.9 ± 2.9 extra cardio sessions per week (that's an increase of +27% | P < 0.05) that came mostly from an increased amount of steady state aerobics "in several subjects" (I interpret this as "the majority increased the steady-state, only a few the HIIT volume). During the recovery period, the subjects' cardio frequency dropped down to 2.3 ± 1.9 times per week - both, cardio and resistance training were yet never skipped completely.

Figure 3: Changes in body composition; for fat and lean mass I used the average of all three measuring methods, i.e. DXA, body impedance and skinfold; * p < 0.05 and *** p < 0.001 (Hulmi. 2017)

The fact that the women kept training after the contest is important, when it comes to the interpretation of the actual study results, which include the following observations:

• 

  Figure 4: Changes in hormone levels; surprisingly, the cortisol levels (not shown) did not change - not even non-significantly at any time-point; *–*** is significant (p < 0.05–< 0.001) difference to Pre and #–### is significant (p < 0.05–< 0.001) difference between the groups in the change (Hulmi. 2017).

  a weight reduction of -12% of their initial weight and a loss of 35-50% body fat according to DXA, bioimpedance, and skinfold measurements -- the exact figures are -23.1 ± 5.6 to -12.7 ± 4.0% (DXA), from -19.7 ± 4.2 to -11.6 ± 3.9% (bioimpedance), and from -25.2 ± 3.0 to -18.3 ± 2.7% (skinfolds) -- in this context it may be worth mentioning that the women lost abdominal fat in particular, with the DXA scan indicating a -60% reduction in visceral fat 
• a small decrease in lean mass (bioimpedance and skinfolds) and in vastus lateralis muscle cross-sectional area (ultrasound) were observed in diet (P < 0.05) -- in that, it is certainly interesting that the scientists found that some competitors even managed to gain lean mass during the contest prep
• the total bone mass decreased by −1.3 ± 1.8% (DXA) in the competitors, 
• the subject's leg strength, measured as the isometric maximal strength and explosive strength of their leg extensors remained unchanged during dieting, their bench press performance, on the other hand, declined,
• a sign. changes in the hormonal system with decreased serum concentrations of leptin, triiodothyronine (T3), testosterone (P < 0.001), and estradiol (P < 0.01) coinciding with an increased incidence of menstrual irregularities (P < 0.05), 
• the surprisingly small (and non-significant) changes in mood-related parameters of which only the subjects' vigor showed a significant decline during the pre-contest phase,
• the normalization of all body weight/composition parameters and all hormones except T3 and testosterone which did not fully recover during the 3–4 month recovery period

Whether or not the small reduction of T3 is enough to produce what people refer to as "metabolic damage" is not clear. On the one hand, the small reduction in fT3 you can also see in Figure 5, would suggest that at least some of the subjects' (N=1...27) metabolisms were running slower than before.

Figure 5: Active thyroid hormone (fT3) concentration at baseline (pre), before the contest (mid) and after recovery (post). The number at the x-axis depicts participant numbers ordered based on the pre-value (Hulmi. 2017).

On the other hand, the subjects' body weight did not yo-yo back up to levels sign. above those they had before the contest, one may assume that this was not the case. After all, all women ate just as much as before the contest and did even less, not more cardio. This, in turn, translates into a 16% increase in their energy balance in the recovery (vs. baseline, see Figure 6) phase.

Now, the question is: What can we learn from this study? If you're looking for information about the "best contest prep diet" or the "ideal workout, volume or intensity for your contest prep training", you will be disappointed to hear that a study with a single dieting group that did not even intend to compare different approaches to contest prep cannot help you to answer these unquestionably important questions (note: since "best" is always individual, I'd say you cannot answer them with certainty, anyway).

Figure 6: It is important to note that the subjects' energy balance was 16% above baseline during the recovery phase when the difference between their energy intake and total ex. induced expenditure was 1471.82 kcal (vs. 1209.60 kcal at baseline). And still, they did not become fatter, but simply returned to their previous body fat levels; the figures beneath the bars indicate the daily energy balance calculated based on data from Hulmi et al by subtracting the exercise-induced energy-expenditure (cardio + weights) from the dietary intake(s).

What the study can tell us - and that's, when all is said and done, eventually even more important - are that (a) using a relatively large caloric deficit (-22.5% as calculated for Figure 6) women can shed up to 50% body fat without losing sign. amounts of lean mass if they force their bodies to keep the muscle by strength training and fuel the protein synthesis that's responsible for conservation of muscle tissue with adequate protein intakes (previous studies on starvation diets show lean mass decreases of 6-28% | Keys. 1950; Dulloo. 1996); (b) the endocrine changes in form of reduced leptin, estradiol, testosterone and T3 levels, as well as the regularity of your menses will recover without medical intervention (albeit with a delay for fT3 and testosterone in some, but not all subjects); (c) there's no classic yo-yo effect which would imply a body fat super compensation during the recovery phase (otherwise the women would have ended up with more fat than before the competition), when the restoration of a pre-contest energy content and the concomitant decline of the subjects' exercise-induced energy expenditure in response to the reduced volume of 'cardio' (ca. 36%) | Comment!

References:

• Dulloo, Abdul G., J. Jacquet, and Lucien Girardier. "Autoregulation of body composition during weight recovery in human: the Minnesota Experiment revisited." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 20.5 (1996): 393-405.
• Hulmi, Juha J., et al. "The effects of intensive weight reduction on body composition and serum hormones in female fitness competitors." Frontiers in Physiology 7 (2017): 689.
• Keys, Ancel, et al. "The biology of human starvation.(2 vols)." (1950).

Three Eggs a Day = Doping for Your Heart Health: Larger LDL & HDL, Increased Efflux and Transport + More Benefits

Don't miss out on a long-neglected superfood. With the latest study from the University of Connecticut the evidence of beneficial (heart-)health effects of increased egg consumption keep accumulating - and this time, we are up to three eggs per day in healthy subjects.

The latest study from the University of Connecticut adds to the previously discussed health benefits of eggs. Starting with the important and scientifically warranted premise that HDL function may be more important than HDL concentration in determining risk for cardiovascular disease, the authors Diana M DiMarco, Gregory H Norris, Courtney L Millar, Christopher N Blesso, and Maria Luz Fernandez conducted a study to confirm and quantify the previously observed increases in HDL and LDL particle size, LCATactivity, and plasma apoAII and carotenoid concentrations in unhealthy populations, in a group of 40 men and women 40 men and women [age 18–30 y, BMI (in kg/m²) 18.5–29.9] who were - hopefully just like you - perfectly healthy.

Whole eggs are also an excellent source of dietary protein

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Before the dietary intervention began, the participants underwent a 2-wk washout period, during which 0 eggs/d were consumed. This baseline period was followed up by sequentially increasing intake of 1, 2, and then 3 eggs/d (large, grade A, white purchased at local supermarkets) for 4 wk each; and before you ask: no they were not told to either hard-boil, soft-boil, fry or scramble them.

Figure 1: Overview of the intake sequence (DiMarco. 2017).

Aside from egg intake, participants were instructed to maintain their normal dietary habits throughout the study. The effects were then accessed based on fasting plasma (30 mL) that was collected at the end of each dietary period, and serum (10 mL) that was collected after intake of 1, 2, and 3 eggs/d.

Figure 1: LDL and HDL particle sizes; note: to make the figure more legible and the ratios easier to recognize, I converted the LDL values to nmol/dL (that's 1/10 of nmol/L as it is still used for HDL | diMarco. 2017)

The scientists' analysis of their results showed nothing but benefits with increasing intakes of eggs:

• 

  Figure 2: The antioxidant concentration in the subject's plasma increased linearly w/ every egg.

  improvements in particle size in form of increased largeLDL (21–37%) and large HDL (6–13%) particle concentrations in the subjects' blood,
• improved levels cholesterol efflux and HDL transport due to higher plasma apoAI (9–15% efflux) and lecithin-cholesterol acyltransferase aka LCAT activity (5–15% transport),
• increased antioxidant defenses as can be seen in the 11% increase in apoAII (P < 0.05), the anti-oxidant, cardioprotective cousin of apoAI, and a 20–31% increase in plasma lutein and zeaxanthin (P < 0.05, see Figure 2)

In that, it is probably worth pointing out that more helped more, significantly benefit of the highest number of eggs (i.e. of 3 vs. 1-2 eggs) was yet only observed for the subjects' PON-1 levels, i.e. the levels of an enzyme that's responsible for hydrolyzing organophosphate pesticides and nerve gasses and has been shown to be a powerful anti-atherosclerotic (=protection against cardiovascular disease) component of high-density lipoprotein (HDL | Getz. 2004).

It's not just high levels of small LDL or, even worse, VLDL cholesterol that is a problem you cannot ignore. Recent research shows: The same can be the case for low cholesterol, too. The dreaded lipid transporter is essential for normal immune health | more

From Villain to Savior? We have been told for decades that cholesterol was killing us. As it turns out, that was wrong. It would be a mistake, however, to go from "cholesterol kills" to "cholesterol does not matter at all", overnight. After all, the cholesterol hypothesis of heart disease has not been completely falsified. Rather than that, it has been refined with particle sizes, ratios of LDL/HDL, HDL/triglycerides, apoA-X levels, etc; and if you include these variables in your assessment of the health effects of eggs, the small increase in LDL and total cholesterol, of which Ancel Keys still believed that it would kill you, is significantly less important for the heart health of people who don't belong to a genetically determined risk group than the beneficial effects on these parameters.

What the egg intake did not do, was to affect the cholesteryl ester transfer protein (CETP) activity. This may seem bad in view of the fact that one of the functions of CETP is to exchange the cholesterol esther load from VLDL and LDL for that from HDL, but scientific evidence that more CETP would increase your life expectancy or decrease your heart disease risk is not available.

Figure 3: Just as in previous studies, there was a correlation between increased ApoA-I concentrations (DiMarco. 2017) and the number of large HDL particles - both have been associated w/ reduced heart disease risk.

What we do know, however, is that rare mutations leading to a significantly reduced function of CETP have been linked to accelerated atherosclerosis. While a polymorphism (I405V) of the CETP gene leading to lower serum levels has been linked to exceptional longevity (Barzilai. 2003) and to metabolic response to nutritional intervention (Darabi. 2009). Since the same mutation will yet also increases the prevalence of coronary heart disease in patients with hypertriglyceridemia, I guess it's actually good news that CETP didn't change over the course of the 3x4-week intervention, of which I should probably mention that it was funded by the Egg Nutrition Center.

Is the fact that the study was funded by the Egg Nutrition Center bad news? Probably not, after all, it is very unlikely that the scientists would have gotten public funding for a study in (a) healthy subjects that (b) served its subjects three eggs a day, not per week as it has been done in most of the previous experiments. Plus: Their conclusion, which is where you will usually find evidence of a bias if there is one, is neither exaggerating nor misrepresenting their findings: "Overall, intake of ≲3 eggs/d favored a less atherogenic LDL particle profile, improved HDL function, and increased plasma antioxidants in young, healthy adults" (DiMarco. 2017).

Three whole eggs also deliver the most effective "dose" of  egg yolk to improve your triglycerides ↓ and LDL ↓ but HDL ↑ | more

So, what should I remember? It's not just that you can have your egg(s) and still be healthy, it's rather that you can have your (at least three) eggs (per day) and thus be healthy - heart-healthy, as this particular study with its improvements in particle sizes (those have been linked to reduced risk of heart disease - 55% reduced w/ fluffy LDL in Lamarche. 2001; and Williams et al. (2012) show that a higher concentration of the larger, more buoyant HDL is closely associated with decreased CVD risk), cholesterol efflux and transport, as well as the total antioxidant status of the subjects' blood shows.

I agree, it would be nice to have a 12-months extension to the study, but eventually it is very unlikely that the medium-term benefits would turn into downsides in the long run. Against that background, I personally am more disappointed that we still don't have the study/-ies to access any potential differences in the health effects of soft- vs. hard-boiled, scrambled and fried eggs. Based on what you've learned about oxysterols in my old article on cholesterol oxidation during cooking, though, you are better off if the yolk is still soft... and let's be honest: it's also tastier | Comment!

References:

• Barzilai, Nir, et al. "Unique lipoprotein phenotype and genotype associated with exceptional longevity." Jama 290.15 (2003): 2030-2040.
• Darabi, M., et al. "Cholesteryl ester transfer protein I405V polymorphism influences apolipoprotein AI response to a change in dietary fatty acid composition." Hormone and metabolic research 41.07 (2009): 554-558.
• DiMarco, et al. "Intake of up to 3 Eggs per Day Is Associated with Changes in HDL Function and Increased Plasma Antioxidants in Healthy, Young Adults." American Society for Nutrition (2017). jn241877
• Getz, Godfrey S., and Catherine A. Reardon. "Paraoxonase, a cardioprotective enzyme: continuing issues." Current opinion in lipidology 15.3 (2004): 261-267.
• Kapourchali, Fatemeh Ramezani, et al. "The Role of Dietary Cholesterol in Lipoprotein Metabolism and Related Metabolic Abnormalities: A Mini-review." Critical reviews in food science and nutrition just-accepted (2015): 00-00.
• Lamarche, Benoit, et al. "A prospective, population-based study of low density lipoprotein particle size as a risk factor for ischemic heart disease in men." The Canadian journal of cardiology 17.8 (2001): 859-865.
• Williams, Paul T., et al. "The effects of weight loss by exercise or by dieting on plasma high-density lipoprotein (HDL) levels in men with low, intermediate, and normal-to-high HDL at baseline." Metabolism 43.7 (1994): 917-924.
• Williams, Paul T. "Fifty-three year follow-up of coronary heart disease versus HDL2 and other lipoproteins in Gofman's Livermore Cohort." Journal of lipid research 53.2 (2012): 266-272.

Adaptation to Intermittent Ramadan Fasting Takes Time, but Eventually Mood, Fatigue, and the Quality of Life Improve

No, it wasn't a button like this which made the subjects happy.

It took some time, yeah, but after a few weeks the participants, students of the Hannover Medical School, where the trial was conducted actually felt better, not - as the scientists who conducted this Ramadan fasting study had expected - worse than without their religious fasting.

But let's not go too fast, here. The subjects had volunteered to participate in the study and were non-randomly assigned to a fasting (FG) and a non-fasting (NFG) group (according to their individual plans | Nugraha. 2016).

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To be eligible into the FG, participants had to: (1) be healthy, (2) be older than 18 years of age, (3) intend to fast the whole month of Ramadan, (4) have fasted during Ramadan at least once before, (5) understand the German or English language. For the NFG, all subjects had to meet the criteria of the FG, except that they would not be fasting. Furthermore (and that's IMHO a pity) The NFG participants were assessed only at T1 and T3. That's in contrast to their peers in FG, where participants were assessed at four different points: one week before Ramadan (T1), mid-Ramadan (T2), the last days of Ramadan (T3), and one week after Ramadan (T4).

Figure 1: While the perceived fatigue of the subjects skyrocketed in the early phase of the Ramadan fast, it dropped during the latter phase and achieved an all-time low in the post-Ramadan week (this peak is missing from the fatigue severity score that kept declining continuously | not shown in Figure 1). The subjects' overall mental health, on the other hand, improved, but without a significant treatment effect due to religious fasting (Nugraha. 2016).

Unfortunately, the lower "resolution" in the NFG group, makes it impossible to directly compare the mood and QoL progression over time.

Examples of effects of intermittent fasting on different organ systems.

More fasting news: 48h of fasting make young weight lifters more aggressive and jumpstart their parasympathetic activity, as well as prefrontal-cortex-related cognitive functions, such as mental flexibility and set-shifting (Solianik. 2016). In young women (mean age 25 years) fasting leads to increased irritability, bit also to positive affective experiences of increased sense of achievement, reward, pride, and control (Watkins. 2016). Furthermore, more and more studies seem to confirm that the health benefits of intermittent fasting (in its various forms) do not depend on weight loss (Aksungar. 2016) and comprise a long list that goes way beyond the things Mattson et al. summarized graphically in the figure to the right:

Limit inflammation, reduced oxidative stress and cellular damage, improved circulating glucose, reduced blood pressure, alteration in IGF-1 levels, improve metabolic efficiency and body composition, including significant reduction in body fat and weight in obese individuals, reduced LDL and total cholesterol levels, prevention or reversal of type 2 diabetes, as well as slow its progression, improved immune function, and shift stem cells from a dormant state to state of self-renewal, improved pancreatic function, insulin and leptin levels and insulin/leptin sensitivity, normalized ghrelin levels, reproduction of some of the cardiovascular benefits associated with physical exercise, protection against cardiovascular disease, modulation of the levels of visceral fat, boost of mitochondrial energy efficiency and protection of striatal neurons against mitochondrial toxicity, elimination of sugar cravings as the body adapts to burning fat instead of sugar, promotion of human growth hormone production (HGH), lower triglyceride levels, elevated production of brain-derived neurotropic factor (BDNF), stimulation of neurogenesis and triggering of brain chemicals that protect against changes associated with Alzheimer’s and Parkinson’s disease, enhanced dopamine overflow in striatum, attenuated age-related decrease in cardiac synaptic terminal norepinephrine uptake, attenuation of age-related loss of cortical dendritic spines, protection against seizure-induced hippocampal damage, memory impairment and focal ischemic brain injury, enhanced learning and motor function in models of aging, slow age-related loss of spiral ganglion neurons while aging, and the list will probably expand further in the years to come (Uher. 2016).

What the data I've plotted for your in Figure 1 still tells you is that the subject's perceived level of fatigue skyrocketed in the initial phase of Ramadan fasting and improved to sub-control levels at the end and one week after Ramadan fasting. At the same time their mental health scores improved, albeit not significantly.

Figure 2: Mood and sleepiness show a similar pattern over the course of the trial (Nugraha. 2016).

Similar trends were observed for the subjects' mood and their sleepiness scores, which were  was measured by using the Epworth Sleepiness Scale (ESS), a self-administered questionnaire with 8 questions that are rated on a 4-point scale (0–3) to yield a score ranging from 0 to 24, with higher scores indicating that person's average propensity of daytime sleepiness increased.

Table 1: Body composition before, during, and after Ramadan (Nugraha. 2016).

The effects on the subject's body composition are significantly less obvious. There were no significant differences in all parameters at both T1 and T3 when comparing FG and NFG. Plus: the way the figures "evolved" make me question the accuracy of the InBody machine (InBody 230; Model MW160, Korea) the scientists used.

Figure 3: Genotype-specific effects of modified fasting (total energy intake <350 kcal/day) on the mood of 108 subjects (Michalsen. 2010). Note: Even though the TT group saw no significant increase in mood, their mood levels did eventually improve - it just took longer than it did for subjects with the CC and CT allele.

So what do you have to remember? The study at hand proves that there is indeed something people often call an "induction phase", i.e. a phase during which your body has to get accustomed to the new meal timing. After that, however, Ramadan (=intermittent fasting from dusk till dawn) shares the same mood improving effects Michalsen, et al. (2010) and Fond et al. (2013) ascribe to prolonged fasting, which is associated with increased brain availability of serotonin, endogenous opioids, and endocannabinoids.

Whether and to which extent you will benefit, however, may depend on your individual gene set with a 2009 study by Michalsen, et al. (see Figure 3) indicating that your individual GNB3 C825T polymorphism determines whether and how fast your mood benefits from fasting | Comment!

References:

• Aksungar, Fehime Benli, et al. "Comparison of intermittent fasting versus caloric restriction in obese subjects: A two year follow-up." The journal of nutrition, health & aging (2016): 1-5.
• Fond, Guillaume, et al. "Fasting in mood disorders: neurobiology and effectiveness. A review of the literature." Psychiatry research 209.3 (2013): 253-258.
• Mattson, Mark P., Valter D. Longo, and Michelle Harvie. "Impact of Intermittent Fasting on Health and Disease Processes." Ageing Research Reviews (2016).
• Michalsen, Andreas, et al. "Hunger and mood during extended fasting are dependent on the GNB3 C825T polymorphism." Annals of Nutrition and Metabolism 54.3 (2009): 184-188.
• Michalsen, Andreas. "Prolonged fasting as a method of mood enhancement in chronic pain syndromes: a review of clinical evidence and mechanisms." Current pain and headache reports 14.2 (2010): 80-87.
• Nugraha, et al. "Effect of Ramadan fasting on fatigue, mood, sleepiness, and health-related quality of life of healthy young men in summer time in Germany: A prospective controlled study."Appetite - Available online 24 December 2016 | In Press, Accepted Manuscript 
• Solianik, Rima, et al. "Effect of 48 h Fasting on Autonomic Function, Brain Activity, Cognition, and Mood in Amateur Weight Lifters." BioMed Research International 2016 (2016).
• Uher, Ivan, et al. "Intermittent fasting and its influence on health." Physical Activity Review 4 (2016): 184-191.
• Watkins, Ellen, and Lucy Serpell. "The psychological effects of short-term fasting in healthy women." Frontiers in Nutrition 3 (2016).

Put Up or Shut Up! How Effective is Caffeine for Gymrats, Self-Proclaimed Bodybuilders & Lifting Weights, in General?

Let's be honest: The authors exaggerate when they call the subjects 'bodybuilders'

Yes, there are dozens, no, I guess hundreds of studies investigating the effects of caffeine in (a) various groups of people (from the obese sedentary slob to the Olympian gold medallist) and (b) a vast range of contexts from the sit-to-stand test in the elderly to the effects of repeated caffeine consumption on high intensity performance (the results are interesting, by the way | learn more). What is surprisingly hard to find, however, are studies that deal with bodybuilding and caffeine which are not case reports of how some bro poisoned himself with an overdose of straight caffeine or caffeine-containing fat burners.

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In this regard, a recent study by Hamid Arazi, Nazanin Dehlavinejad, and Roghayyeh Gholizadeh sticks out. Published late 2016 in the Turkish Journal of Kinesiology (Arazi. 2016), even though it is obviously not the only study evaluating the effects of caffeine or, and those studies are more frequent, the effects of caffeine + a plethora of other ingredients in kitchen-sink "pump" or "pre-workout" supplement in gymrats. Since a comparison of these results is (a) not necessary bodybuilding-specific and will yield conflicting results, the authors decided to conduct a

"[...] study aimed to investigate the acute effect of moderate amount of consumption of caffeine 6 mg per kg of body weight on maximal strength, repetition sustainability and training volume in the upper and lower body of novice bodybuilders" (Arazi. 2016).

Fifteen males' healthy gymrats - I guess eventually we have to admit that these "novice bodybuilders" are not Mr. Olympia, yet - who had resistance training between 6 months to a year participated voluntarily in this study.

Figure 1: Subject characteristics - note: while the study calls them "novice bodybuilders" (Arazi. 2016), we should be honest and admit that we are more or less talking about the average gymrat or "total beginner bodybuilder", here.

Subjects' characteristics are presented in Table 1. All were healthy non-smokers and did neither suffer from diseases nor consume products that would mess with the results of the study.
After 24h of caffeine abstinence, the subjects reported to the lab, where they ingested were randomized (double-blind method) to consume

• caffeine (gelatin capsules containing 6mg/kg) supplements or 
• placebo (maltodextrin) supplements,

each with 200 ml of water. To ensure that the caffeine levels would peak, the authors had their subjects wait an hour before the actual test was performed (that's somewhat debatable, because the athletes reported to the lab fasted, so that peak levels may have been reached earlier, but alas | learn more):

"Subjects performed special warm-up activities for 15 minutes. Then, they did one repetition maximum test (1RM) in bench press (as especial upper body exercise) and leg press (as original lower body exercise) with 3-minute rest intervals in the range of 3 to 5 attempts. After 5 minutes of rest, subjects carried out bench press and leg press 5 times with 80% of one repetition maximum with maximum possible repeat until exhaustion with 3 minutes' rest between sets" (Arazi. 2016). 

This testing procedure was repeated twice separated by an interval of one week and the analysis of the results is quite telling.

This cannot be the only study on so-called "bodybuilders"! Well, if we are talking "caffeine, only," it is. There is yet an interesting paper on ephedrine + caffeine by Haghagi, et al. (Haghagi. 2014), which found that, in 12 male bodybuilders (mean age: 24.41±4.42 years, height: 174.83±3.61 cm and weight: 75.67±8.05 kg) training without a supplement (Con), Ephedrine ((E), 0.8 mg/kg); caffeine ((C), 6 mg/kg), a combination of E + C (0.8 mg/kg + 6 mg/kg), or placebo all yielded significant increases in lower body strength (P<0.05) and upper body endurance (P<0.05). Since the FT is not available online, I cannot tell you how large the inter-group differences were - with no differences being reported in the sloppily written abstract, they were presumably not sign., though.

Figure 1: Relative changes in strength and # reps to failure on bench and leg press w/ and w/out caffeine (Arazi. 2016).

As you can see in Figure 1, the t-test confirms that the subjects' bench press and leg press muscle strength significantly increased in the caffeine condition compared to placebo. Furthermore, all the depicted changes in strength and strength endurance (as evidenced by the increased repetition sustainability in the fourth and fifth set) reached statistical significance.

Table 2: Work volume from the first to the fifth (mean ± SD; *=sign. adv. for caffeine | Arazi. 2016)

It is thus not exactly surprising that the work volume was higher for the two last sets; that it was also higher for the initial sets (see Table 2), on the other hand, shows that the, seen as an average, not exactly impressive 4-6% strength increase is pronounced enough to allow for a significantly enhanced training volume, of which the latest reviews (e.g. Schoenfeld et al. 2016) show that it may, within certain limits, be the main determinant of your gains.

Not Getting into Ketosis? Try Plain Old Caffeine to Double Your AM Ketone Levels | learn more.

So, caffeine works, right? In the study at hand, it sure did. And with related studies by Duncan et al. (2009 | previously resistance trained subjects) and Hudson et al. (2008 | rookies with only 8 weeks of training experience) produced similar (as those that were observed in the study at hand) increases in leg press and bench press performance, respectively. Significant increases in training performance, only for the legs, though, were also reported in Astorino et al. (2011) whose trained subjects did yet suffer from caffeine withdrawal when they had to abstain from the "drug" in the days before testing - which can obviously have negatively affected their performance and thus leveled any benefits.

In contrast to what you could assume, by the way, the effects are not necessarily going to be more pronounced in female trainees: In fact, Goldstein et al. (2010) examined the effect of caffeine (6mg/kg) on the performance of 15 women with a six-months history training and found no increase in strength endurance (but a sign. increase in max strength). A fact of which Arazi, et al. (2016) speculate that it could be the result of an increased metabolism of caffeine during strenuous exercise in women vs. men (Sinclair. 2000). It is likewise worth noting that the majority of studies shows that habitual usage is no obstacle to the performance benefits of caffeine - this goes for the effect on tetanic force (Tarnopolsky. 2000), the rate of fat to carbohydrate oxidation (RER | the jitters due to extreme epinephrine spikes will disappear, though | Bangsbo. 1992). There is, however, evidence that chronic use can, maybe by accelerating the metabolism of caffeine, diminish the endurance gains as it was observed by Fisher, et al. as early as in 1987.

With that being said, the optimal dosage for resistance training ranges from 4-6 mg/kg body weight. Timing is an issue and depends on whether you're taking it on empty or not, but I previously discussed that in the caffeine-article of the "When Timing Matters"-series. So I suggest you read that first before asking about optimal caffeine timing on Facebook!

References:

• Arazi, Hamid, Nazanin Dehlavinejad, and Roghayyeh Gholizadeh. "The acute effect of caffeine supplementation on strength, repetition sustainability and work volume of novice bodybuilders." Turkish Journal of Kinesiology 2.3 (2016): 43-48.
• Astorino, T. A., et al. "Effect of acute caffeine ingestion on EPOC after intense resistance training." J Sports Med Phys Fitness 51.1 (2011): 11-7.
• Bangsbo, Jens, et al. "Acute and habitual caffeine ingestion and metabolic responses to steady-state exercise." Journal of Applied Physiology 72.4 (1992): 1297-1303.
• Duncan, Michael J., Mark Lyons, and Joanne Hankey. "Placebo effects of caffeine on short-term resistance exercise to failure." Int J Sports Phys Perf 4 (2009): 244-253.
• Fisher, S. M., et al. "Influence of caffeine on exercise performance in habitual caffeine users." International journal of sports medicine 7.05 (1986): 276-280.
• Goldstein, Erica, et al. "Caffeine enhances upper body strength in resistance-trained women." Journal of the International Society of Sports Nutrition 7.1 (2010): 1.
• Haghighi, Amirhosein, Kia Ali Heshmati, and Kakhak Seyed Alireza Hosseini. "The Effect Of Caffeine and Ephedrine Supplement and Their Combination on Maximal Strength and Muscular Endurance In Male Bodybuilders." (2014): 89-107.
• Hudson, Geoffrey M., et al. "Effects of caffeine and aspirin on light resistance training performance, perceived exertion, and pain perception." The Journal of Strength & Conditioning Research 22.6 (2008): 1950-1957.
• Schoenfeld, Brad J., Dan Ogborn, and James W. Krieger. "Dose-response relationship between weekly resistance training volume and increases in muscle mass: A systematic review and meta-analysis." Journal of Sports Sciences (2016): 1-10.
• Sinclair, C. J. D., and J. D. Geiger. "Caffeine use in sports: a pharmacological review." Journal of Sports Medicine and Physical Fitness 40.1 (2000): 71.
• Tarnopolsky, Mark, and Cynthia Cupido. "Caffeine potentiates low frequency skeletal muscle force in habitual and nonhabitual caffeine consumers." Journal of applied physiology 89.5 (2000): 1719-1724.