Two-Year Study Seems to Suggest: 'Ketogenic Diet' Doubles Weight, Triples Fat Loss vs. Std. Diet, but in Reality...

This is not a photo of the "ketogenic diet" meals the subjects were served in exactly 2 out of 24 months of the study... and the supple-ments they were taking to make up for nutrional deficits are also missin'

There are two reasons why the number of studies on the long-term effects of ketogenic diets on health and body composition is still limited. The obvious reason is that it takes time to conduct these studies. This is yet not the full truth, though. After all, conducting a "low fat"-diet study will also take time and we have hundreds of long-term studies, here.

Unfortunately, this is where reason #2 comes into play: Not too long ago you would probably have had problems to get funding and/or to even get past the ethics committee of your institution with a study in which overweight or obese subjects were supposed to be exposed to a "high fat" and or "high protein" diet that could "jeopardize their health".

You know, high-protein diets are safer than people say, but there are things to remember...

Practical Protein Oxidation 101

5x More Than the FDA Allows!

More Protein ≠ More Satiety

Protein Oxidation = Health Threat

Protein Timing DOES Matter!

More Protein = More Liver Fat?

Over the past decade, however, the number of low carb dieters and researchers who back the notion of "eating more fat to lose fat" has been growing continuously. You cannot say that the tides are turning, yet, but the existing experimental evidence which shows that low carb or ketogenic diets are effective, at least in the short to medium term, as a tool to fight obesity (Bueno. 2013) is convincing enough to get permission and financing (in this case by a Spanish protein supplement producer who funded the study and supplied the protein powder used in the study) for long-term keto studies.

Against that background, the latest study by Basilio Moreno et al. (2016) would not be an exception to the role but still one out of a selected few studies that assessed the effects of a ketogenic diet on glycemia, lipidemia and body composition (esp. visceral fat) over 2 years and compared the outcomes to both, a non-dieting control and a regular low calorie control group (LC), the scientists describe as follows (Moreno. 2016):

• Low-calorie control (LC) - The standard LC diet was an equilibrated diet that had a caloric value 10 % below the total metabolic expenditure of each individual. The total metabolic expenditure was calculated from the basal metabolic expenditure (based on the formula FAO/WHO/UN) multiplied by the coefficient of activity, which was calculated according to the physical activity of each participant. The calories provided to this group ranged between 1400 and 1800 kcal/day. The ratio of macronutrients provided was 45–55 % carbohydrates, 15–25 % proteins, and 25–35 % fat  in addition to a recommended intake of 20–40 g/day of fiber in the form of vegetables and fruits. A ratio exchange model was followed
• Very low-calorie ketogenic diet (VLCK) - The VLCK diet group followed a diet according to a commercial weight loss program (Pronokal method) based on a high biological value protein preparations diet and natural foods. Each protein preparation contained 15 g of protein, 4 g of carbohydrates, and 3 g of fat, and provided 90–100 kcal. This method has three stages: the active stage, the re-education stage, and the maintenance stage (Fig. 1). The active stage consists of a very low-calorie diet (600–800 kcal/day) that is low in carbohydrates (< 50 g daily from vegetables) and lipids (only 10 g of olive oil per day). The amount of high biological value proteins ranges between 0.8 and 1.2 g per each kg of ideal body weight, to ensure that it meets minimal body requirements and prevents the loss of lean mass. This method produces three ketogenic phases. In phase 1, the patients eat high biological value protein preparations five times a day, and vegetables with a low glycemic index. In phase 2, one of the protein servings is substituted with a natural protein (e.g., meat or fish) either at lunch or at dinner. In phase 3, a second serving of a low-fat natural protein replaces the second serving of a biological protein preparation.
  

  

  Figure 1: Dietary intervention for the VLCK diet. The duration of the different stages depends on the targets and the clinical decision of the physician in charge. The duration of stage 1, i.e., on ketosis, was less than 2 months, stage 2 ranged from 5–6 months and stage 3 was until 24 months (Moreno. 2016).

  Throughout these ketogenic phases, supplements of vitamins and minerals, such as K, Na, Mg, Ca, and omega-3 fatty acids, were provided in accordance with international recom-mendations. This active stage is maintained until the patient achieves most of the weight loss target, ideally 80 %. While the ketogenic phases were variable in time depending on the individual and the weight loss target, they lasted between 45–60 days in total.
  
  In the re-education stage, the ketogenic phases were ended by the physician in charge of the patient based on the amount of weight lost, and a low-calorie diet was initiated. At this point, the patients underwent a progressive incorporation of different food groups and participated in a program of alimentary re-education to guarantee the long-term maintenance of the weight lost (Fig. 1). The maintenance stage, which lasted 2 years, consisted of an eating plan balanced in carbohydrates, protein, and fat. Depending on the individual, the calories consumed ranged between 1500 and 2000 kcal/day, and the target was to maintain the lost weight and promote a healthy lifestyle.

If you take a closer look at the information about the diets of the LC and VLCK group, however, you will realize that this is not a ketogenic diet as you would (rightly) expect it to be used in a study that uses the phrase "ketogenic diet" in the title, already (that's the case for all stages of the intervention, even though it is visible in Figure 1 only in stage 2+3). Rather than that, stage 1 of the intervention makes use of a supplement supported starvation diet that induced a "mild ketosis" (because of its lack of energy, not a high fat and low carbohydrate content). This stage is then followed by an 8-month transition diet (that's not ketogenic either) and a 14-months regular diet follow-up and thus no fair comparison of the two diet concepts (keto vs. mixed or low-fat diet). Eventually, the diets differed not just in their nutrient composition but represent completely different dieting philosophies:

• VLCK - "cut rapid- and severely and try to maintain afterward" 
• LC - "lose weight slowly & continuously w/ lifestyle change + minimal deficit"  

Against that background and in view of the fact that the LC "control" diet was on top of that exactly what (hopefully) no SuppVersity reader would ever do to lose body fat (too little energy from protein and a deficit of only 10%, of which previous studies show that it is more than just suboptimal for weight loss - especially in the obese), you should keep this 'lack of equal playing fields' in mind, when evaluating the differential effects of the diets on the 45 of initially 79 patients (mean age 45 years; mean BMI 35 kg/m², mean waist circ. 110 cm) from the Obesity Unit at the Hospital Gregorio Marañon of Madrid who enrolled in Moreno's study.

Figure 2: Evolution of weight loss after initiation of treatment and during 24 months of follow-up. Data from the completers groups are presented and the data obtained through the ITT analysis are also shown. LOC last observation carried forward, BOC basal observation carried forward, MI multiple imputations. *p < 0.001 difference between groups; ¥ < 0.001 differences with respect to baseline values (Moreno. 2016).

The fact that the VLCK patients lost significantly more weight, and even twice the amount of weight the LC group lost, can, for the previously mentioned reasons, hardly be considered surprising. After all, the subjects in the VLCK group were in a hell of a lot greater deficit. And that was not just the case in the initial ~2 month starvation phase, but also during the major part of the 5-6 months-long "dietary re-education" stage towards the end of which the subjects' weight started to increase again and that despite the fact that they were still consuming much less energy than their peers in the LC group.

Don't be tricked by misinterpretations of this study! I am not sure if this is / was on purpose, but by not comparing the prescribed energy intake the LC and VLCK group anywhere in the paper, the scientists made their study extremely open to being misinterpreted by people with an agenda.

Estimated mean cumulative energy intake in the LC and VLCK groups over those 8 months of the study during which the subjects actually lose weight and cor-responding deficits in % (the figures are based on the assumption that the subjects needed only 1800 kcal per day for weight maintenance) if that was more, the VLCK advantage would increase significantly).

Even if we assume for simplicity a mean dietary intake of 1,800 kcal at maintenance - which is a rather conservative estimate in view of the fact that the subjects were 'heavy' and of both male and female sex - the LC group (~388,800 kcal in the first 8 months) would have been consuming approximately 56% more energy than the VLCK group (~249,000 kcal in the first 8 months). If you still insist that the study shows the superiority of low carb dieting, you must not have read the full-text and/or ignored the scientists' own conclusion which reads "a very low-calorie-ketogenic diet was effective 24 months later, with a decrease in visceral adipose tissue and a reduction in the individual burden of disease" and says nothing of a superiority of one diet over the other (for a good reason).

The reason it is still worth to take a look at the graphs in Figure 3 is thus not to see how well a "ketogenic diet" works (in fact, by know you should have realized that a "ketogenic diet" as you probably had it in mind when you first read about this study here or elsewhere was not even involved in this study) compared to a "regular" diet. No, the reason is to see how well the commercial PronoKal® program, which - and you got to really scrutinize the "privacy policy" small print at the PronoKal® website to find that out - happens to be belong to Protein Supplies the sponsor of the study, did in comparison to wasting one's time with the worst imaginable but still often recommended weight loss approach you will find.

Figure 3: Lean body mass (LBM) and fat mass (FBM) loss in the two groups over time (Moreno. 2016).

So, "yes!", the program worked, but how impressive is a 19.1 kg fat loss on a 42%+ (see red box) deficit you run over an 8-months period (the must be said for the reduction in visceral fat, which is particularly highlighted in both and abstract of the full-text and the reason the main reason the scientists hail the PronoKal® program as being effective to "reduce the disease burden") ?

Still impressive? Ok. So how practically relevant is it if we all know that this diet is not sustainable and it takes only 14 months on a still very strict "balanced maintenance diet" to regain 10.3 kg of the 19.1kg (i.e. 54%) without regaining any of the previously lost lean body mass? I refuse to answer this question, but I think I have given you all the information that's necessary to answer it for yourselves.

It's not that VLCK diets would not have benefits. I have even written extensively about them in previous articles. Articles such as "450-700kcal/day Diet Cuts 7% Body Fat in 3 Weeks - Only if You go Keto, Though, it Will also Increase Lean Mass by 4%" (read the full article) - That they double the weight loss, however, is unheard of in fair and well-designed scientific studies.

Bottom line: I think I have said enough about the study at hand for you to realize that it does not show the superiority of low carb or ketogenic dieting in either the short or long term. Rather than that it is yet another example, where only a close analysis of the full-text will prevent you from falling for accidental or purposeful misinterpretations of scientific research... sponsored scientific research, in the case of which I cannot avoid the impression that it may have looked differently if the scientists' goal had not been "to evaluate the long-term effect of a VLCK diet as part of a commercial weight loss program (Pronokal method), compared with a standard LC diet on decreasing adiposity in obese patients" (Moreno. 2016), but to simply conduct the study we are all waiting for: a fair and controlled (not observational) comparison of the efficacy of effectively designed whole-food based energy-equated ketogenic vs. regular diets in the long run (ideally 24 months+) | Comment on Facebook!

References:

• Bueno, Nassib Bezerra, et al. "Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials." British Journal of Nutrition 110.07 (2013): 1178-1187.
• Moreno, Basilio, et al. "Obesity treatment by very low-calorie-ketogenic diet at two years: reduction in visceral fat and on the burden of disease." Endocrine (2016): 1-10.

Take Control of Your Cortisol Levels - Use These 5x Stress-Modulating Diet, Lifestyle & Supplementation Rules Wisely

Always remember: You want to control cortisol, not eradicate it if you want to melt away your belly fat, beat your personal bests and feel just great!

As a SuppVersity reader, you belong to the chosen few who know that cortisol is not the villain as which it is stigmatized in the fitness industry (obviously to sell supplements | learn more). Rather than being "bad" or "good", cortisol, a glucocorticoid, i.e. a hormone that keeps your blood glucose stable, and potent anti-inflammatory agent, is more vital than any "vitamin" - in spite of not having the magic "vita" in its name.

Whether the effects of this vital adrenal hormone are going to be "bad" or "good" for you, depends mostly on whether it rises and falls according to its natural 24-h rhythm or is chronically low (often labeled adrenal insufficiency) or chronically high.

If you want to mess with your cortisol rhythm overtraining is exactly what you "need"!

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Now your diet alone will probably not suffice to induce one or the other state of chronically messed up cortisol (unless you eat (a) almost nothing while training like a maniac for weeks ⇉ low cortisol; or (b) too much of a typically Western diet ⇉ high cortisol). And yet, it is still a good idea to know more about the diet ⇆ cortisol interaction(s) to be able to maintain hormonal homeostasis, and the SuppVersity is obviously the right place to learn all about it.

Figure 1: Overview of the three areas of your physiology that are directly affected by the levels and rhythm of cortisol.

With the ever-increasing number of "functional" foods boasting of being able to modify health-relevant parameters, including your cortisol level and thus your ability to, through its
multipronged action, stabilize or mess with your blood levels of glucose, to stimulate your tissue's
regenerative processes and to inhibit inflammation in each and every organ of your body.

Figure 2: This is how cortisol is "made" in your body (Stachowicz. 2016). In theory, you can influence its concentration by modifying this cascade at any point.

As Stachowicz, et al. point out in a recent review of the literature they published in the peer-reviewed journal Eur Food Res Technol (Stachowicz. 2016), diet is obviously not the only factor that influences our cortisol levels. Of at least as much importance are "[f]actors like stressful work, personal problems, [and] intensive training" , which "can lead to long-term sustained, excessive concentration of this hormone, affecting formation of metabolic disorders such as insulin resistance, increased blood pressure, abnormal bone regeneration and collagen synthesis or calcium deficiency in the organism" (ibid.). Against that background, it is hardly surprising that various groups of the society try to modulate their cortisol levels in ways they consider healthy (again: low is not healthy!) by supplementing or eating / avoiding certain foods that contain nutrients which regulate steroid hormones homeostasis.

In the short term, e.g. strategic overreaching, your body can cope with the exercise induced release of cortisol, but when over-reaching becomes over-training you run the risk of plumetting into the deep dark valley of unsurmountable fatigue.

Excursion - Exercise and cortisol: Athletes experience substantial increases of cortisol and adrenaline during intense workouts. That's normal and even necessary to (a) keep your blood glucose levels stable and (b) train at high(est) intensities. In fact, studies have shown that in athletes with higher motivation and orientation on the success, levels of these hormones were higher than those of other players. As Stachowicz, et al. point out "[t]hey also generally achieve better results" (Obmiński. 2009). On the other hand, studies show that people who experience mental fatigue experience limited activity of pituitary gland and sympathetic nervous system - in other words low cortisol levels (or rather the absence of appropriate spikes in response to e.g. exercise and other stressors).

And that rightly so! After all, Stachowicz et al. (2016) rightly point out, a "balanced diet with optional supplementation is one of the important factors determining the high physical and mental capacity of organism" (ibid) - and this goes for everyone from the frail elderly over the hobby- and pro-athletes to the stressed manager or teacher, who are all "particularly exposed to abnormal secretion, metabolism and transport of hormones, including cortisol" (ibid.) - people who will probably know about the effects of chronic stress:

"It was shown that in stressful situations appetite for sweet and fat meals rises, probably because of their high rewarding character (Zellner. 2005). Consumption of meals induces [an] increase in cortisol level. This response is strongly marked in men than in women. Influence of kind of macronutrients in taken food on cortisol concentration was investigated in many [types of research], but the results are not clear" (Stachowicz. 2016). 

One of the best known (and most logical) effectors of cortisol production is the content and type of carbohydrates in your diet - especially if you're not a sedentary slob; after all, cortisol's main function as a glucocorticoid is to counter hypoglycemia.

• Rule #1 (esp. for easily fatigued athletes) - Eat enough (or no) carbs: Eat either no carbs at all (ketogenic diet) or enough carbs before, during and after training to prevent hypoglycemic conditions (click here to learn why this will also help to stay lean) and thus an abnormally high intra- and post-workout spike of hydrocortisone in blood while the consumption of liquids (studies show that this takes some carbs, i.e. 7% vs. just 1.5% in the intra-workout beverage | cf. Ihalainen, 2014 vs. Caris, 2014).
• Rule #2 - Don't believe everything the supplement industry claims: As Stachowicz et al. rightly point out, the impact of around training protein, glutamine, arginine or branched-chain amino acids (BCAA), on the other hand, "is not clear and requires testing on large groups of athletes of various disciplines" (Stachowicz. 2016).
  
  What has been shown to work is tryptophan, which is a precursor of serotonin, that will effectively ameliorate the cortisol level increase, during and after workouts, but its potential side effects (esp. performance decrements) have not been well-studied, yet. The same must be said of phosphatidylserine and phosphatidic acid, which have been shown to (a) normalize the stress reactivity of hypothalamus-pituaryadrenal-axis in chronically stressed men and to reduce the cortisol response to exercise in a sponsored trial in which it was administered at dosages of 400 mg/day for 6 weeks - the total number of studies to support PS as a useful supplement for anyone from manager to athlete and from elderly to toddler, however is low; oftentimes, there's sponsorship involved and long-term studies or studies that would evaluate the effect of cortisol control on the adaptational response to exercise are missing.
• Rule #3 - Don't overrate its benefits but get enough protein (1.6-2.2 g/kg per day): As explained in rule #2, there's no evidence that simply adding more protein to your diet is going to help you control cortisol. In fact, eating too much protein and too little fat and carbs may chronically elevate the glucocorticoid, because it has to keep the production of glucose from amino acids in the liver, i.e. gluconeogenesis, working. That adequate protein intakes are necessary, on the other hand, is a logical consequence of the role of serine, taurine, and other amino acids play in the control of the balance and optimal function of your hypothalamus-pituitary-adrenal-axis.
• Rule #4 - Optimize your sleep by sleep hygiene and (optional) supplements: By optimizing your sleep you can restore a normal and healthy circadian rhythm and thus battle what makes cortisol a problem for so many in our society directly. How's that? Well, as previously highlighted, it's not the cortisol spikes you experience in the AM and during and after workouts, but chronically elevated (or depleted) levels of cortisol and spikes that occur untimely (e.g. the "2AM wake-up call", when your cortisol rises way too early and you cannot sleep longer than until 1-3 AM).
  

  

  Figure 3: Optimal sleep, melatonin and cortisol patterns are mutually dependent in health and disease - if you mess up one with the way you behave / live and/or supplements you mess up all (Glickman. 2010).

  Next to using earplugs, a blindfold (or curtains to make sure light doesn't disturb your sleep), reducing your (blue) light exposure in the evening, and using a non-stressing alarm to tell you that it's time to go to bed, a sleep tracker to access whether your intervention is successful, your circadian rhythm restoration program may involve: (1) no caffeine, coffee, or other stimulants in the 6h window before bed (some people will have to extend this window even further); (2) GABA at doses of 100-500mg before bed (don't take more or you may faint); if you cannot tolerate GABA, try taurine, instead, it will also enter the brain and act on the GABA receptor (Song. 2003); (3) melatonin at dosages you will have to figure out yourself (start with 1-3mg and ramp up until you sleep well and wake up refreshed, not groggy, which is usually a side effect of taking (a) too much or (b) the by no means recommendable time-released melatonin preparations).  
• Rule #5 - Strategically supplement with... In contrast to the previous rules, rule #5 is "optional" or facilitative. There's mixed evidence for some vitamins, namely vitamin C (500-1000 mg), vitamin E (400 IU+), vitamin D (>2,000 IU), as well as high doses of vitamin B1, B2, and niacin, which are involved in metabolism and production of cortisol, can lower the glucocorticoid response to exercise. 

  

  Figure 4: Sign. associations between PWO hormone levels and lean mass, as well as fiber size, increases (West. 2012) - they exist, but the largest and best study to investigate them clearly shows: It's cortisol that predicts lean mass gains (left) and GH that predicts the growth of individual fibers. High post-workout testosterone, however, predicts ... nothing (learn more) .

  At least for the former (vitamin C and vitamin E), however, it has also been shown that it will impair the exercise-induced adaptational processes, i.e. improved conditioning, muscle strength, and size when taken chronically. No wonder, if you think about the previously outlined beneficial effects of your body's most potent anti-inflammatory homrone, cortisol, (see Figure 4, too) on the regenerative process after workouts.
  
  The beneficial effects of a natural (controlled) cortisol response to exercise are something you should also keep in mind when using magnesium supplements which have been shown to blunt the cortisol increase to physical exercise in Golf et al. (1984) 32 years ago. Since newer studies were not generally able to confirm Golf's findings, though, I wouldn't be too afraid of (or rely too much on) magnesium's ability to lower your cortisol levels in non-(mg)-deficiency situations. That's particularly true in view of the fact that Cinar et al. saw a sign. increase in cortisol in response to a similar combination of magnesium supplementation (10 mg/kg b.w.) and physical activity in 2008. Stachowicz, et al. are thus right to point out that "[t]he impact of magnesium supplementation on cortisol levels in athletes is not clear and needs further investigation" (Stachowicz. 2016).
  

  

  Figure 5: While we do have evidence that boron will have opposing effects (vs. magnesium or the previously mentioned vitamins on cortisol), the existing evidence is far from being conclusive (Naghii. 2011).

  The same must be said of the cortisol modulating effects of a former star on the bodybuilding supplement sky that has been largely forgotten today: boron. While Naghii et al. (2011) confirmed relatively recently that a daily morning use of preparation containing 11.6 mg of boron, just after 1 week, results in increase in cortisol and free testosterone, dihydrotestosterone (DHT) and vitamin D while decreasing estradiol levels, we are far from being able to call boron a proven ergogenic - also because its long-term benefits appeared to be zero in most exercise-related long-term studies with relevant outcome parameters (not hormones, but gainz in performance, size or strength). The same must be said of fish oil, which has been shown to reduce perceived stress, green tea (EGCG), which is supposed to inhibit the activity of 11β-hydroxysteroid dehydrogenase type 1 that converts cortisone to cortisol, and betaine with one study backing its anti-cortisol effect in trained individuals (Apicella. 2013).
  
  Long-term data assessing its safety, and potential detrimental effects on testosterone is also lacking on the effectiveness of licorice, one of the few supplements of which we have reliable evidence that it affects (increases) cortisol. 

Cardio - Only significantly "too much" can hurt your circadian cortisol rhythm, but if it does, it trigger muscle loss, fatique and (in a caloric surplus) even fat gain | learn more.

So what's the verdict? Get your ducks in a row by following rules #1-4. If you still feel (or even better have evidence from multiple cortisol swap tests in 24h) that you cortisol rhythm is messed up (see Figure 3 for what you should look out), try using supplements like magnesium, green tea or b-vitamins to lower and boron or licorice to increase it strategically.

Needless to say that the latter will require proper timing with the supplements that lower cortisol being taken at times when you want cortisol to decrease (PM) and supplements that increase the glucocorticoid being taken at times when you want it to increase.

Why the timing? If you'd read the whole article and not just the bottom line you wouldn't be asking that, because you'd should know by now that you want a natural cycle of peaks and troughs, not chronically high or low levels (don't use supplements that block your body's ability to activate / deactivate cortisone <> cortisol completely, unless you've good medical reasons, to) of this important adrenal glucoregulatory + anti-inflammatory hormone  | Comment!

References:

• Caris, Aline V., et al. "Carbohydrate and glutamine supplementation modulates the Th1/Th2 balance after exercise performed at a simulated altitude of 4500 m." Nutrition 30.11 (2014): 1331-1336.
• Cinar, Vedat, et al. "Adrenocorticotropic hormone and cortisol levels in athletes and sedentary subjects at rest and exhaustion: effects of magnesium supplementation." Biological trace element research 121.3 (2008): 215-220.
• Glickman, Gena. "Circadian rhythms and sleep in children with autism." Neuroscience & Biobehavioral Reviews 34.5 (2010): 755-768.
• Golf, S. W., et al. "Plasma aldosterone, cortisol and electrolyte concentrations in physical exercise after magnesium supplementation." Clinical Chemistry and Laboratory Medicine 22.11 (1984): 717-722.
• Hellhammer, Juliane, et al. "A soy-based phosphatidylserine/phosphatidic acid complex (PAS) normalizes the stress reactivity of hypothalamus-pituitary-adrenal-axis in chronically stressed male subjects: a randomized, placebo-controlled study." Lipids in health and disease 13.1 (2014): 1.
• Ihalainen, Johanna K., et al. "Effects of Carbohydrate Ingestion on Acute Leukocyte, Cortisol, and Interleukin-6 Response in High-Intensity Long-Distance Running." The Journal of Strength & Conditioning Research 28.10 (2014): 2786-2792.
• Naghii, Mohammad Reza, et al. "Comparative effects of daily and weekly boron supplementation on plasma steroid hormones and proinflammatory cytokines." Journal of Trace Elements in Medicine and Biology 25.1 (2011): 54-58.
• Obmiński, Zbigniew. "Pre-And Post-Start Hormone Levels In Blood As An Indicator Of Psycho-Physiological Load With Junior Judo Competitors." Polish Journal of Sport & Tourism 16.3 (2009).
• Stachowicz, Marta, and Anna Lebiedzińska. "The effect of diet components on the level of cortisol." European Food Research and Technology (2016): 1-9.
• Song, Zhilin, and Glenn I. Hatton. "Taurine and the control of basal hormone release from rat neurohypophysis." Experimental neurology 183.2 (2003): 330-337.
• Zellner, Debra A., et al. "Food selection changes under stress." Physiology & Behavior 87.4 (2006): 789-793.

Intermittent Fasting + Resistance Training: 1st 8-Wk Human Study to Provide Modest Evidence of Benefits During Cuts

You have heard me argue based on theoretical considerations before that "intermittent fasting" is probably best used during cuts, not during "bulks" - the results of the study at hand, even though they may not show stat. sign. inter-group differences, support this suggestion.

You will be surprised, but the latest article Tinsley et al. (2016) published in the European Journal of Sport Science is indeed the very first study to investigate the effects of time-restricted feeding (TRF) "on nutrient intake, body composition, and strength" when they are combined with a standardized resistance training regimen.

That's too good to be true? Well, wait until you've learned more about the methodology and results, but it is indeed cool that someone finally studied the effects of what the majority of people think of if you talk about "intermittent fasting" (that's in contrast to scientists who often think of alternative day fasting when they hear "intermittent fasting, the benefits of which I have discussed only recently, read more).

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

Breakfast and Circadian Rhythm

Does Meal Timing Matter?

Habits Determine Effects of Fasting

Fasting Works for Obese, Too!?

Does the Break- Fast-Myth Break?

Breakfast? (Un?) Biased Review

The subjects were recreationally active, but probably less active than the average SuppVersity reader (because they hadn't been following a consistent RT programme over the previous three months). The study was a randomized controlled 8-week trial that did or didn't involve time-restricted feeding (TRF, 4h eating, 20h fasting window) and identical resistance training (RT) programs:

"The RT programme for both groups consisted of three nonconsecutive days per week of training performed at the gym of the participant’s choice. Participants alternated between upper and lower body workouts. The upper body workout consisted of barbell bench press, seated row machine, dumbbell shoulder press, lat pulldown machine, dumbbell biceps curls, and triceps extension machine. The lower body workout consisted of barbell squat or hip sled machine, lunges with dumbbells, leg curl machine, leg extension machine, and calf raise machine.

Participants who were unfamiliar with the RT exercises were instructed regarding the proper execution of each exercise. Participants were also instructed to utilize a weight that elicited muscular failure after 8–12 repetitions and to adjust the weight as necessary to meet this criterion. Four sets of each exercise were performed and a 90- second rest period between sets was assigned (Tinsley. 2016; my emphasis).

The variables the scientists tracked were, as previously mentioned, the subjects' individual nutrient intakes (as reported in a repeated four-day dietary record) and changes in body composition (X-ray absorptiometry using a "Hologic Discovery W" device for whole-body scans; muscle size was assessed by ultra-sound measurements) and muscular strength (assessed by obtaining the 1-repetition maximum (1-RM) using the hip sled and barbell bench press exercises).

How long did they fast? 20h? Isn't that too much? With a feeding window of 4 hours (at any time between 4PM and midnight | as in Kelly, 2007), the TRF(=IF) regimen in the study at hand is significantly shorter than that in the average IF-dieter who will probably use 6-8h fasting windows... whether the results would be fundamentally different for these shorter fasting windows of 16-18h would have significantly changed the outcome is questionable, also because the subjects fasted only on non-workout days and were allowed to eat ad-libitum on the three days on which they performed RT. Thus, further research is obviously warranted (see bottom line for suggestions).

The reasons that the results are still relevant and worth reporting are (a) they are the first of their kind and (b) it is unlikely that the effect of intermittent fasting is different for people with different training status. What may difference is the baseline response to resistance training, but that's the same for both groups (you can also argue that the response will change over time which is why it is great that the study lasted eight, not just two weeks).

IF cuts energy intake, but not body fat? True, if we focus on statistically sign.

As you can see in Figure 1, the TRF reduced energy intake did, as SuppVersity readers will have expected the reduction in daily energy intake of the subjects by ∼650 kcal per day (see Figure in the bottom line for information on the "macros") - you can only eat so much in a given time-frame and four hours are not long. What may be more interesting than the reduction in energy intake you've expected based on previous research.

Figure 1: Relative changes in body composition; none reached sign. inter-group diff., d-values indicate effect sizes which show a trend towards fat loss and lean & fat mass gains in the TRF and control group, respectively (Tinsley. 2016).

Against that background, it is quite surprising that the TRF regimen did not significantly affect the total body composition - especially the amount of body fat. In that, it is possible that this was just because the study duration was too short, but eventually 4 weeks of being in a caloric deficit should suffice. Eventually, however, the body fat (total mass and %) reduction in TRF shows that (cf. Figure 1) what's missing is only the statistical significance of the difference (and that's nor really a wonder with only N = 28 subjects in total and thus only n = 14 subjects in each group). This in turn which raises the question(s): (A) Was there a reduction in physical activity in TRF that of which we could assume that it compensated maybe 200-300kcal of the ~650kcal deficit? And (B) how accurate the 4-day food logs reflected the energy intake over the two 4-week periods during which they were recorded.

Similar questions and that criticism of the methodology can be brought forward for the lack of significant difference in the increase in cross-sectional area of the biceps brachii and rectus femoris in the two groups. If we look closely at these values and take the effect size data (values over the bars) instead of the p-values for the absolute gains as our yardstick, there is evidence that the TRF regimen impaired the lean mass gains (+2.3 kg, d = 0.25) and upper and lower body muscular endurance increases (not shown in Figure 1) that were brought about by the standardized resistance training protocol both groups followed for 8 weeks.

The lack of protein in the TRF group (0.88g/kg vs. 1.3g/kg) could be a reason for the lack of muscle gains.

So, the study had no results we can use? Not really, but there's certainly reason for further research, because (a) it would be nice to ascertain that the extent of the caloric deficit was in fact -33% (that's neither unlikely nor unheard of, but it is important enough to ask for a more rigid control) and to (b) evaluate whether the 20h fasting window was simply too large. Especially the last-mentioned follow-up study which ideally should involve a control (no fasting), a 16h- and 18h-fasting window could yield very interesting results, after all studies show that significant protein breakdown will occur only after >18h of fasting and last for ~another 24h before the body starts to react to conserve lean mass (reduced RMR, etc.).

What would be similarly interesting, though, would be having a standardized, prescribed protein intake in both groups. With "only" 72 and 81 g of protein per day in the first and second four weeks, respectively the TRF group consumed not just much less protein than the control group (107 and 97 | that's not sign. less, though due to high inter-personal variation); with only 0.88 g/kg they also consumed way less protein than any reasonable recommendation for resistance trainees [~1.6-2.2 g/kg] would suggest.

Overall, the study at hand is thus the first study to investigate the interaction between intermittent fasting and resistance training. The results appear to confirm what I have repeatedly written in the past, i.e. "intermittent fasting" is great for cutting (and potentially "recomp", i.e. losing fat while maintaining lean mass and thus improving your body composition), not so good for gaining weight, but - for the previously outlined reasons - it is not the study to yield final insights into how good / bad it actually is for these purposes and how it compares to alternate-day-fasting that produced impressive weight or rather fat loss in a very recent study | Comment on Facebook!

References:

• Kelly, Caleb J. "A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults." The American journal of clinical nutrition 86.4 (2007): 1254-1255.
• Tinsley, Grant M., et al. "Time-restricted feeding in young men performing resistance training: A randomized controlled trial†." European Journal of Sport Science (2016): 1-8.

What's the Optimal HIIT Protocol for Trained Individuals? 48 x 10s or 8 x 60s for Conditioning + Improved Body Comp.?

Cycling and sprinting (running) are not your only options when doing HIIT. An intense plyometric or other body-weight based workouts can be done in an "80-95% for 10-60s" vs. "running on the spot for 20-120s" or with kettle-bells workout, as well. Be creative...

HIIT is "the hit" in the fitness world. And though it has been a hit for years, now, nobody seems to know how it is done "correctly", or, should I say, optimally!? How's that? Well, as in so many areas of this field, there's simply too little scientific data to make science-based recommendations that are "bulletproof" in the literal, not the new nutrition-and-fitness-craze sense of the word.

With their latest paper, scientists from China are trying to change just that (Chia-Lun. 2016). They set out to compare the effects of a matched-volume HIIT protocols w/ 10s or 60s all-out exercise and identical work-to-rest ratios (1:2) on - a comparison that has, believe it or not, not yet been done!

You can learn more about HIIT at the SuppVersity

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

Triple Your Energy Exp.

What did they want to do? Well, let's recap: The idea is that the researchers from the National Sun YatSen University and the National Taiwan Normal University will have 42 young, healthy, recreationally active male university students (at least 3x training per week), who are HIIT beginners, though, do work-equated HIIT protocols. And while the authors confirmed that both groups allegedly burned the same amount of energy, (only 213.7 and 226.5 kJ in the HIIT60s and HIIT10s group, respectively), it seems a bit odd that the 60s sprints were supposed to be done as intensely as the 10s sprints. The same goes for the (likewise measured) power during the sprints on the cycle ergometer, i.e. 232 ± 37 W and 249 ± 39 W for 85% VO2max and 90% VO2max, respectively, for HIIT 60s and 237 ± 45 W and 255 ± 47 W for 85% VO2max and 90% VO2max, respectively, for the HIIT10s group, where we likewise do not see a statistical significant difference, even though one may expect an advantage for the shorter intervals, too.

• HIIT10s - consisted of 48 × 10-s sprint intervals with 20-s recovery and 
• HIIT60s - consisted of 8 × 60-s intervals with 120-s recovery
• CON - just maintained their regular workout routines

Two things that were undoubtedly identical, though, were (a) the work-to-rest ratio of 1:2, and (b) the heart rate during the sprints (HIIT60s 182 ± 12 bpm and HIIT10s 184 ± 9 bpm). Similarly, all subjects trained three times a week (on Mondays/Wednesdays/Fridays or on Tuesdays / Thursdays / Saturdays) for four weeks. All workouts were done under supervision and at workloads equal to the subjects' predetermined 85%(week 1-2)–90%(week 3-4) VO2max after a 5-min warm-up and before 3-min cool-down period at 30% VO2max.

Figure 1: Relative changes in interesting markers of conditioning, hormone levels and skinfold (body fat); * indicates sign. pre- / post-difference; # indicates sign. difference to control group (Chiah-Lun. 2016).

Pre- and post-testing, which also included blood draws to analyse the concentration of lactate, blood glucose, lipids and testosterone and cortisol levels (body composition was determined by employing the sum of three skinfolds; the performance tests were identical for both groups and designed in a way that would allow for an unbiased (by training) comparison of the two regimens) yielded the following results:

• Cardiorespiratory Parameters and Performance - compared with CON, the HIIT60s and HIIT10s interventions resulted in 18.4% (d = 0.5) and 17.9% (d = 0.5) increases in VO2max, and non-significant increases in an endurance test, namely 7.7% (P = 0.01, d = 0.3) and 8.5% (P < 0.01, d = 0.3) in the HIIT60s and HIIT10s group, respectively.
  
  Similar increases were observed for performance markers at the aerobic threshold (AT), namely the O2 pulse (P < 0.01), the absolute VO2 at AT (P < 0.01), and the relative VO2 at AT (P < 0.01), as well as the AT as percentage of VO2max (indicating a sign. increase in the ability to use fat as fuel at high(er) intensities).
  
  As far as the question in the headline is concerned, the study did yet produce NULL results - a significant inter-group difference between the workload-equated HIIT protocols was not observed.
• Body composition - While there were no sign. group x time interactions, in the case of skinfold thicknesses in the chest (P = 0.86) or thigh (P = 0.31), the effect measured for time was significant: skinfold thickness decreased at posttraining (relative to baseline) in both the chest (P = 0.04, d at HIIT60s and HIIT10s were 0.3 and 0.2) and the thigh (P < 0.01, d at HIIT60s and HIIT10s was 0.9).
  
  What many of you will consider most interesting, though, is that skinfold thickness of the abdomen showed a significant interaction (P = 0.04), too. (Un-)fortunately (?) again without significant inter-group difference, just like the total percent body fat was significantly lower at posttraining, which decreased in both HIIT groups similarly, yet, again, without inter-group difference (P = 0.63, d = 0.2).
• Glucose and insulin management: In contrast to studies in untrained and/or obese individuals, significant improvements in markers of glucose or lipid management (even compared to control) were not observed - the levels of  insulin (d = 0.3), HbAlc (d = 0.4), HOMA-IR (d = 0.2), blood glucose (d = 0.2), TG (d = 0.3), total Chol (d = 0.2), HDL-C (d = 0.2), and LCL-C (d = 0.2), simply didn't change significantly from pre- to post in any group.

• 

  Recent Study: HIIT training sheds significantly more belly fat over (-10% vs. 0%) and under (-25% vs. +10%) female abs than isocaloric medium intensity steady state exercise aka MICT | read more.

  Testosterone and cortisol: What did change, though, were the levels of testosterone and cortisol in the subjects' blood, where the authors detected (a) significant main effects of training for both testosterone (P = 0.01, d = 0.5) and cortisol (P = 0.04, d = 0.6), and (b) a significant T-increase only in the HIIT10s group.
  
  As you know from previous articles, though, we have to be careful not to overestimate the purported benefits of the 13.6% increase in testosterone the scientists recorded (even if it's not measured directly after the workout) - and that's not just because the cortisol levels in that group likewise increased (by 16%), but rather because that's too little of a temporary increase (levels in the control group increased by 9.7% as well) to have any physiological effect, even if the testosterone increases did matter (learn why they probably don't)

For the sake of completeness, it should also be mentioned that there were no differences in blood lactate levels, and blood pressure RPE in either of the group (pre-/post-testing and inter-group comparison yielded no differences that were worth mentioning, let alone statistically significant).

In view of the fact that studies indicate that  push-ups and pull-ups burn 50% and 62% more energy than we thought (learn more), a body-weight HIIT workout makes absolute sense.

Bottom line: As previously stated, I doubt that that the total work done included the work during the rest periods, the latter, however, is important, because it would probably imply that the subjects in the HIIT60s group burned significantly more energy than the HIIT10s group.

Furthermore, the total energy expenditure during the workouts seems to be relatively low, after all, even the rest periods were "active rest"; and burning only ~220-250kJ or 52-60 kcal during a training session that lasted 24 minutes appears hilariously little (Tabata HIIT burns 6.5x more per min.). Still, I am certainly not in the position to criticize Chia-Lun for doing a study many of us have been waiting for.

The latter, by the way, is particularly true in view of the fact that the study has another huge strength: it is a long-term study and the results are thus practically relevant to the initially raised question "What's the Optimal HIIT Protocol for Trained Individuals? 48x10s or 8x60s for Aerobic & Sprint Perf. & Body Comp.?" And, regardless of whether you consider the two protocols work-equated or not, the answer is clear: both are equally effective. So your choice should be guided by individual preference (not by the testosterone increase in HIIT10s - don't be ridiculous). After all, what is "optimal" is always an individual thing | Comment on Facebook!

References:

• Chia-Lun, Lee, Hsu Wei-Chieh, and Cheng Ching-Feng. "Physiological Adaptations to Sprint Interval Training with Matched Exercise Volume." Medicine and science in sports and exercise (2016).

Double Your Muscle, Maximize Your Endurance Gains: Train in the PM, not the AM, and Do Your Cardio Before Weights

Both, time and exercise order matter - at least when untrained subjects have trained for at least 12 weeks.

The debate about whether you should (a) do cardio and weights together and (b) whether you shall do either or both in the AM or PM for maximal muscle anabolism is older than the SuppVersity and has thus been addressed in many of the hitherto published approx. 2300 articles on suppversity.com.

The reason you should still read today's article, however, is that the approach to the topic is a bit different than usual, so that the study, which certainly leaves much to be desired (more on that in the bottom line), adds more practically relevant (which you cannot say about studies measuring the testosterone : cortisol ratio, for example) data.

AM or PM, you got to make sure you slept / sleep enough & well before or after workouts

Sunlight, Bluelight, Backlight and Your Clock

Sunlight a La Carte: "Hack" Your Rhythm

Breaking the Fast to Synchronize the Clock

Fasting (Re-)Sets the Peripheral Clock

Vitamin A & Caffeine Set the Clock

Pre-Workout Supps Could Ruin Your Sleep

Said data has been gathered over 24 weeks during which previously untrained, but healthy participants none of which belonged to either an extreme morning or evening chronotype or worked night shifts followed identical strength (S) and endurance (E) training regimen. The interesting and uncommon thing was was, that these workouts took place either in the AM (m, as in morning) or in the PM (e, as in evening) and were, on top of that, differently ordered (i.e. endurance (E) before strength (S) = E+S or strength (S) before endurance (E) = S+E) - according to cocker we should thus have 2x2 = four groups... and indeed, here they are:

• mE+S n=9, training in the morning, endurance before strength
• mS+E n=9, training in the morning, strength before endurance
• eE+S n=12, training in the evening, endurance before strength
• eS+E n=12, training in the evening, strength before endurance

In that, the workouts were identical with two workouts per week in the first and two-to-three workouts per week in the second 12-week-period (an additional session was added every two weeks so that all participants performed 5 training sessions in a 2-week period, the reasoning behind this was to "allow further progression in training adaptations" | Küüsmaa. 2016). Here are some details:

"The morning training groups (mE+S and mS+E) performed all training sessions between 6:30-10:00h, while the evening training groups (eE+S and eS+E) performed their training sessions between 16:30-20:00h. The training programs were identical for the E+S and S+E group independent of the training time, only the sequence of strength and endurance training was reversed. Endurance and strength training were combined into the one training session so that no more than a 5-10 minute break was allowed during the two training sections. The duration of the combined endurance and strength training sessions progressively increased from 60 to 120 minutes. All the training sessions were supervised.

Strength training consisted of exercises aimed at improving both maximal strength and muscle hypertrophy and was planned as a whole body periodized program with the main focus on knee extensors and flexors as well as hip extensors. Each training session consisted of three lowerbody exercises: bilateral dynamic leg press, seated dynamic knee extension and flexion. Four to five exercises were performed for other main muscle groups (lateral pull down, standing bilateral triceps push down, bilateral biceps curl, seated military press, or bilateral dumbbell fly, trunk flexors and extensors). Strength training was designed to improve muscular endurance in the first 4 weeks, which was performed as circuit training (intensity 40-70% of 1 RM). The subsequent 4 weeks (weeks 5-8) were designed to produce muscle hypertrophy (intensity 70-85% of 1 RM) and followed by 4 weeks (weeks 9-12) of mixed hypertrophic and maximal strength training (intensity 75-95% of 1 RM). A similar strength training program with slightly higher intensities was carried out also during the second 12 weeks of training" (Küüsmaa. 2016).

The cardio workouts were a mix of interval and continuous cycling on an ergometer. The sessions averaged from 30-50 minutes. Interval (85-100% of HRmax for 4x4 min, 4 min active rest in between) and continuous (65-80% of HRmax) training protocols were performed weekly.

Yes, this study really had it all, HIIT, steady state, weights... and no, that does make it more reliable. Rather than that, it makes it more difficult to identify cause and effect and thus to interpret the results. This is why I would like to warn you: do not to assume that either of the initially raised questions for the optimal workout time and order would be answered by this single study once and for all. Needless to say that this doesn't mean the study results are worthless, but if you feel what worked for the subjects in the study at hand doesn't work for you, don't be a lemming and stick to a protocol of which you feel and see after giving it a fair chance (3-4 weeks) that it's bad for you.

As you'd expect it from a study like this, participants were tested for dynamic leg press 1 repetition maximum (1RM) and time to exhaustion (Texh) during an incremental cycle ergometer test both in the morning and evening before, during (12-week, see Figure 1) and after the 24-week intervention. all relevant information to address the practical value of training in the AM vs. PM and doing endurance before or after weights - a fact I would like to highlight (and applaud to), because that is unfortunately not the case in many other studies that lack practically relevant study outcomes, such as performance increases (here 1RM and Texh) and gains (here CSA values).

Figure 1: Study design and measurements. 1 RM = one repetition maximum in the dynamic leg press; Texh = time to exhaustion during the incremental cycling test; CSA = cross-sectional area; m = morning; e = evening (Küüsmaa. 2016)

I mean, who cares about acute (post workout) levels of exhaustion, 2-6h max protein synthesis or the testosterone to cortisol ratio and its diurnal rhythm if neither of these values can answer the question we are actually asking: Does it help you make extra strength, endurance or muscle gains? Not me (if you care, here's another of these studies, just out, speculating based on questionable markers of a "differential hormonal milieu" and free to read | Burley. 2016), because all these values are as reliable predictors of muscle gains as yesterday's weather forecast for Christmas... well, ok, maybe a bit better, but eventually it's results like those, Küüsmaa et al. present in their recent paper in Applied Physiology Nutrition and Metabolism, that matter:

• 

  It's the Same (!) Time of the Day That Matters If You Want to Excel | Learn more about the effects of habitual training times on performance!

  1RM gains were similar in the morning (14-19%; p<0.001) and evening (18-24%; p<0.001); no sign time-of-day-effect
• CSA increased in all groups by week 24 (12-20%, p<0.01), however, during the training weeks 13-24 the evening groups gained more muscle mass; time-of-day main effect; p<0.05)
• Texh increased in all groups in the morning (16-28%; p<0.01) and evening (18-27%; p<0.001), just as the 1RM gains without effect of the exercise order, but with the data suggesting an advantage of doing cardio first (E+S) at 12 and 24 weeks

The overrated testosterone to cortisol ratio, the scientists assessed as well and even its diurnal rhythms, on the other hand, remained statistically unaltered by the training order or time at any point in the study. So that the study only confirms what I have said before to use the Bro's "holy yardstick of anabolism", i.e. the testosterone to cortisol ratio (T/C) after or in the vicinity of your workouts as an "anabolic guide" won't work, because it's simply not an acceptable predictor of any of the previously mentioned relevant training outcomes (strength, muscle size, and endurance).

Figure 2: Change (%) of the CSA of vastus lateralis (left), endurance performance in the AM (right, top) and PM (right, bottom) in the different training groups - left figure: *sign. (p < 0.05) within-group increase; # sign. different from controls; & sign. time-of-day main (TOD) effect | right figures: ¤ sign. between group differences as indicated; # sign. different from controls; $ sign. order main effect; sign. time-of-day (TOD) main effect (Küüsmaa. 2016).

The actual relevant messages of the study at hand have thus nothing to do with the T or C values or the T/C ratio. Rather than that, the present study "indicate[s] that combined strength and endurance training in the evening may lead to larger gains in muscle mass [in the 2nd part of the study, the PM training groups gained twice the amount of muscle the AM group did], while the E+S training order might be more beneficial for endurance performance development" (Küüsmaa. 2016). What is interesting, however, is that "training order and time seem to influence the magnitude of adaptations only when the training period exceeded 12 weeks (Küüsmaa. 2016; my emphasis) - that's an important observation from which I would like to segue right into the previously announced bottom line discussion of the few potential shortcomings of the study at hand.

Maybe, you don't have to choose between endurance and muscle gains! I am not sure if you looked close enough at Figure 2 to realize that, but the data from the study at hand shows that the PM cardio before weights group (eE+S) made both, the greatest CSA (muscle size) and Texh (exercise till you drop) gains of all groups... yes, I know the difference to the other PM group for CSA was as nonsignificant as the difference between the endurance gains in the AM vs. PM group, but overall that doesn't change the fact that the study at hand suggests that cardio before weights is the better way to go.

Does the study prove that everyone should do cardio first? Wtf!? Obviously not. Why do I even tell you about individuality and the influence of habits and training experience in the bottom line if you still think one study could prove everything you've been successfully for years wrong? Ah, and no, you don't have to start doing cardio and weights on the same day, if doing it on separate days works for you ;-)

Bottom line: I've already hinted at it at the top and in the the last line(s) of the main part of this article: compared to your average "Cardio or weights first?" and / or "AM or PM what's the best time to train?" experiments, the Küüsmaa study provides practically relevant outcome measures, unfortunately, it also provides evidence that its results may be subject specific and may not translate one-to-one from untrained beginners, as they were used in the study at hand to trained (semi-)professionals.

What does that mean? Well, if the influence of the time of the day (AM vs. PM) became significant only in the latter 12 weeks. That would suggest that (a) one's training experience and/or (b) the marginally increased training load determine the importance of AM vs. PM training - whether this relationship is linear, as in "the more training experience you have and / or  the higher your training volume, the more you will benefit from doing your workouts in the PM", however, requires future studies in better-trained individuals and with differences in training volume that go beyond the planned addition of one workout every other week that was used in the study at hand.

With that being said, the take-home messages of the study are still: (1) Do cardio first, if you want to increase your endurance performance, too; (2) Train in the PM (if you can choose freely and are not an extreme morning type) and benefit from a likely increase in size and a non-significant increase in 1RM gains; but (3) don't forget that our response to training may depend on (a) training experience (see previous elaborations), (b) habits and (c) individuality. If you find that doing (1)-(2) sucks for you, just return to what you've previously done | Comment on Facebook!

References:

• Burley, Simon D., et al. "The Differential Hormonal Milieu of Morning versus Evening May Have an Impact on Muscle Hypertrophic Potential." PLOS ONE 11.9 (2016): e0161500.
• Küüsmaa, Maria, et al. "Effects of morning vs. evening combined strength and endurance training on physical performance, muscle hypertrophy and serum hormone concentrations." Applied Physiology, Nutrition, and Metabolism ja (2016).