Is Air Frying Healthier Than Deep Frying? Which Oil's Best for Each Method and How Do They Compare to Cooking?

Air- or deep-frying, what's healthier? For most people that's not even a real question... rightly so? 

"That's even a question?" I know, I know... With the health aura surrounding air frying it appears to be hilarious to even base a complete episode of SuppVersity | True or False on the question whether air frying is in fact so much healthier than deep frying, but listen up: a recent study from the University of Porto says that "most chemical parameters were similar on both frying processes, including [pro-carcinogenic] acrylamide content" (Santos 2017).

Can it really be that the air frying devices are another overhyped kitchen device you don't really need?

Lean more about frying & co at the SuppVersity

The Quest for the Optimal Frying Oil

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GMO Soybean Oil Proven to Be Pro-Inflammatory

"Pimp My Olive Oil" - W/ Extra Antioxidants

Frying Does not Just Oxidize Oils, It Does Fat More!

If you bought one of these devices and use it regularly, you will be happy to hear that the answer to this question is a categorical "no". There's little, or I should say "no" doubt that air frying will produce healthier (not healthy) fried foods than deep frying and the example of everyone's favorite fried food, Pommes Frites or as my American friends say "fries", exemplifies why:

• 

  Figure 1: The 70% reduced fat content in air-fried potatoes is not just an advertisement claim (Santos 2017)

  Air frying will reduce the amount of fat and thus the caloric content of the fried foods: For classic fries Santos et al calculated a 70% reduction in fat and thus 45 kcal less per 100 g 
• Air frying will do less harm to antioxidants like vitamin C: Even though the fries in Santos study showed only "slightly better results" for the amount of ascorbic acid in the final product, it's the trend that counts - especially, in view of the fact that you may expect to see similar effects with other foods and/or antioxidants.

But air fried fries don't taste well, do they? Well, in the study at hand, the 10 assessors, including professors, investigators and students (8 females, 2 males with age range of 23 to 55) of the Faculty of Pharmacy of University of Porto, the air fried fries did quite well:

Figure 2: Boxplot of quantitative descriptive sensory analysis of potatoes in different frying process: deep-frying, Actifry and Airfryer; commercial soybean oil (SO), sunflower oil (SFO), canola oil (CO) and olive oil (OO) all from the supermarket (Santos 2017)

• the adhesiveness was only significantly different for potatoes that were fried in soybean oil, and slightly elevated in the air-frying vs. deep-fried products (p < 0.05),
• the crispiness of air-fried fries and deep-fried fries was likewise impaired with canola oil; in that, there was a trend for increased crispiness w/ deep frying.
• the color attributes and odor intensity presented higher scores in deep-frying than air-frying (p < 0.05); and again, canola oil was the odd one out with potatoes fried in CO (deep-frying and Airfryer) showing inferior odor attributes than other vegetable oils (p < 0.05), probably due to increased fatty acid oxidation, consistent with its increased PUFA content.
• a bad aftertaste was observed mostly with deep-fried products and may be attributed to the formation of unwanted fatty acid oxides, especially when high omega-6 oils like soybean or olive oil were used

With respect to the overall acceptability, the subjects who are used to consuming fries that are fried in sunflower oil (that's the way people do it in Spain) awarded the SFO-deep-fried fries the highest, the ones that were fried in canola oil the worst score.

Figure 3: Health and taste may often deviate, but the fact that olive oil was the best compromise for both (even though individual subjects didn't like the taste), taste and predictable health effects based on oxide-formation (Saontos 2017).

A completely different image emerges for air-frying, where using sunflower oil produced the lowest and using soybean oil the highest score. That's bad news? Well, not really, because olive oil came to the rescue and achieved, albeit with a high variability within the panel, ratings similar to the best potatoes for both frying processes.

Photos of the devices that were used in the study. No sign. differences were observed between the Tefal and Phillips devices, which makes it unlikely that you'd seen different results w/ your air frying device at home.

Methodology: Deep-frying was carried out in a domestic electric fryer (TRISTAR, FR-6929) with adjustable temperature up to 190 °C, 1.75 L capacity, and maximum load of 200 g per L. A portion of potatoes cubes (200 g) was fried in 1.5 L of vegetable oil, at 175 °C, during 6 min. The temperature was periodically controlled with a calibrated digital thermometer. Air-frying was tested in two different equipment’s: Actifry (Tefal, SERIE001) with a nominal power of 1400 W, and Airfryer (Philips, HD9220) with a nominal power of 1425 W. A portion of potatoes cubes (300 g) was involved in 3.6 g of vegetable oil, and fried during 20-25 min (Actifry) or 15-20 min (Airfryer; manual agitation at 10 and 15 min), adjusted to the equipment’s specifications.

Olive oil will also have no (sign.) effect on the amount of pro-carcinogenic acrylamide, of which I've previously pointed out that it was not affected by the device in which the scientists fried their potato sticks.

Figure 4: Levels of acrylamide according to frying method and oil used to fry/involve the fries before frying; commercial soybean oil (SO), sunflower oil (SFO), canola oil (CO) and olive oil (OO) all from the supermarket (Santos 2017).

What did affect the levels of acrylamide, at least in the Tefal Actifry device, was the type of oil that was used; with the highly popular sunflower oil (SFO) triggering a significant increase in the formation of acrylamide, it should be quite obvious that this shouldn't be your #1 choice for air-frying even if you don't own a Tefal device, in which the increased acrylamide formation may be explained by the direct contact with the chamber surface.

What's the latest on frying and your health, anyway? In one of the most recent reviews of the health effects of fried foods, Luke Forney highlights that "[n]ot all fried oil[/food] is equal" - or, as I would like to say: not all fried food is evil ;-) As a SuppVersity reader you will be aware of the so-called "French Paradox", i.e. the observation that the French eat all the good foods, the Americans deem unhealthy (high-fat cheese, absolutely non-whole grain baguette, etc.) and wash it down with liters of red wine and still have a significantly better heart health and smaller waists than their low-fat munching Amerian friends.

The "Spanish Paradox" shows no significant increase in heart disease risk (not shown in this figure) and, if anything, a non-significant reduction in all-cause mortality with increasing amounts of fried foods in the diet (Guallar-Castillón 2012).

For fried foods, however, it's the "Spanish Paradox" (Guallar-Castillón 2012; Gadiraju 2015), as frying is much more important in the Spanish than it is in the French cuisine. On the other hand, the Spaniards eat fried foods no more than three times per week and, probably, more importantly, (a) make the right oil choice(s) by choosing refined olive oil (not extra-virgin) over higher omega-6 or less stable oils and (b) avoid using oils repeatedly (that's a common practice in every fast-food restaurant). Thus they prevent the formation of both harmful phytosterol oxidation products (from using extra-virgin vs. regular olive oil | Ryan 2009) and polycyclic aromatic hydrocarbons (from (re-)using oils or using oils with a low heat stability, e.g. soybean oil, walnut oil, etc.).

Addendum: The topic of reusing oils is important enough for an addendum based on a study that has been published one day after I published this article.

Figure*: Changes in key-markers of oxidation (total polar material, TPM, and acid value) in french fries and breaded chicken, (Sung 2017).

In their experimental analysis of the oxidative properties of a commercial standard frying oil mix of soybean oil and palm olein (6:4 ratio with 650 ppm added tocopherols) as it is used in many fast food restaurants, Song et al. (2017) show that the key-markers of oxidation increase by more than two- and tenfold within less than 20 and less than 10 frying cycles (both happens even in the best fast food restaurants) in potatoes = french fries (Figure*, left) and breaded chicken (Figure*, right), respectively.

With that being said, Forney's review also reminds us that it's not necessarily the often overestimated amount of oxidized fat in fried foods that's making fried food lovers fat and sick. Rather than that, it is their high calorie-density and thus their significant contribution to "weight gain and obesity, which then increase diabetes, hypertension, and hyperlipidemia, which in turn are the most important factors leading to cardiovascular disease such as heart attack and stroke" (Forney 2016) - so, never forget: calories count, it's just more complex than CICO.

Next to acrylamide, the total antioxidant content and the degree of fatty acid degradation were two additional health-relevant characteristics of the test products the scientists evaluated. If we scrutinize this data, two important take-home messages emerge:

1. There's no question that you'd be better off not frying your potatoes, at all.
2. If you insist on frying, air-frying is the sign. healthier method when all's said and done.

Ok, I guess that most of you have been suspecting just that before they had read the SuppVersity article at hand. What I doubt, however, is that you also knew that... 

• air-fried potatoes contain significantly lower amounts of trans fats (TFAs); the level is in fact so low that there was no significant difference between the transfat content of boiled and air-fried potatoes
• if you insist on deep-frying your potatoes, using olive oil will sign. reduce the exuberant amount of transfats in comparison with other vegetable oils (p < 0.05), using (regular) canola oil, on the other hand, will yield sign. higher TFA levels (the scientists do yet remark that this may be an artifice due to methodological problems)

Moreover, common sense will not tell you that deep frying will leave your potatoes with significantly higher amounts of tocopherols (vitamins E) than air-frying, which, in turn, has the advantage of lowering the vitamin C content to a similar extent as cooking and thus sign. less than deep-frying.

Figure 5: Changes in total phenolic content and antioxidant activity in the DPPH assay (left), as well as increase in secondary lipid oxidation products during frying (right); all values expressed as rel. differences to cooked control,

Unlike deep-frying, which will reduce the total phenolic content of the content sign. (with olive oil reducing the loss to 3% and sunflower oil increasing it to 18%), air-frying will actually increase the number of phenolic compounds compared to boiling. In that, it is important to note that it would be stupid to use this observation to say that air-fried potatoes are healthier than cooked potatoes; after all, there's an apparent decrease in DPPH radical scavenging activity for both air-frying devices (p < 0.05 | see Figure 4, right).

And for those who are still not convinced, the scientists' analysis of the amount of unwanted and unhealthy secondary oxidation products, namely unsaturated aldehydes, that were estimated by the anisidine value (p-AV), likewise adds to the evidence that if you want to eat fries, you'd choose the ones from the air-fryer over deep-fried fries, which presented consistently a higher fat degradation state in comparison with all other processes (p < 0.05). Air-frying, on the other hand, left most if not all of the fats intact and showed no significant difference to the control (=boiling) condition. Similarly encouraging results were found for the total content of polar compounds (TPC), which increased only with deep- not with air-frying.

In my 2014 article about the "Quest or the Optimal Cooking Oil", canola oil fares much better than in the study at hand. Why is that? The reason is quite simple: it's not the same oil. Unlike the study at hand, the studies, I cite to verify the usefulness of canola oil for frying, all used high-oleic acid canola oil, which is high in MUFA and low PUFA - similar to olive oil | more.

Bottom line: You won't be surprised to hear that air-frying is indeed healthier than deep-frying potatoes. I am pretty sure, though, that you would not necessarily have expected the good old (non-virgin) olive oil to rank so high for both the sensory and the chemical qualities of fries.

I have to warn you, though, while I see no problem with using olive oil to involve your potato sticks before you turn them into Pommes Frites in an air-fryer, Frying in olive oil for more than 6 minutes, at temperatures >190°C or re-using the oil as it is done in 99.9% of the restaurants and commercial kitchen (who would throw away the oil after using it to fry a single serving of potatoes) will affect olive oil to a significantly greater degree than the low PUFA oils I suggested for frying in my 2014 article about "The Quest for the Best Cooking Oil" | Comment on Facebook!

References

• Fortney, Luke. "Fried Foods: Friend or Foe?." Integrative Medicine Alert 19.3 (2016): 25-28.
• Gadiraju, Taraka V., et al. "Fried food consumption and cardiovascular health: A review of current evidence." Nutrients 7.10 (2015): 8424-8430.
• Guallar-Castillón, Pilar, et al. "Consumption of fried foods and risk of coronary heart disease: Spanish cohort of the European Prospective Investigation into Cancer and Nutrition study." BMJ 344 (2012): e363.
• Ryan, Eileen, et al. "Phytosterol oxidation products: their formation, occurrence, and biological effects." Food Reviews International 25.2 (2009): 157-174.
• Santos, CSP, et al. "Deep or Air frying? A comparative study with different vegetable oils. Eur. J. Lipid Sci. Technol. (2017). Accepted Author Manuscript. doi:10.1002/ejlt.201600375
• Song, J., Kim, S., Kim, J., Kim, M.-J., Lee, S.-M., Jang, M.-I. and Lee, J. "Oxidative properties and moisture content in repeatedly used oils for French fries and breaded chickens during frying." Eur. J. Lipid Sci. Technol. (2017). Accepted Author Manuscript. doi:10.1002/ejlt.201600279

Western vs. Ketogenic Diet - Greater 'Gains' Materialize Only After Glycogen-Loading in 12-Wk Study in Trained Subjects

Unfortunately, I cannot tell you if the "Western" diet was also full of junk food. I just know that its 20/55/20 ratio of PRO/CHO/FAT is everything but ideal for one's body composition.

While it has not officially been published, yet, I am pretty sure that Jacob M. Wilson's latest paper is going to be one of the most-downloaded articles in the upcoming issue of the Journal of Strength and Conditioning Research it's about to be published in. You're asking yourself why I am so sure about that? Well, it's already the most-discussed ahead-of-print article in months (see any Facebook Fitness / Exercise Research group or bulletin board), because it claims to confirm that ketogenic diets "can be used in combination with resistance training to cause favorable changes in body composition, performance and hormonal profiles in resistance-trained males" (Wilson 2017) - a claim that gets both ketophiles and keto-haters absolutely fired up.

Would be interesting to compare keto to high-protein, not western diets, right?

Practical Protein Oxidation 101

5x More Than the FDA Allows!

Low Carb Unfit for Crossfit(ters)

Protein Oxidation = Health Threat

Keto Diet ⇒ Perform. ↓

Keto for Superior Weight Loss?

Before I will delve into a brief discussion of what the study is actually about, I would like to point outu that I have revised the original draft several times - both, to incorporate/answer questions that I've found online and in response to a brief conversation with the authors, who were by no means the first to "examine resistance training adaptations using a human model" (Wilson 2017). What Wilson et al. can boast of, though, is that their paper is the first to address the issue using a decently realistic resistance training program in healthy, previously trained young men. A scenario in which the authors hypothesized a priori that ...

"the KD [ketogenic diet group] would decrease body fat to a greater extent than a WD [western diet] group, while maintaining skeletal muscle hypertrophy, strength, and power" (Wilson 2017).  

In that, the effects of the heavily criticized glycogen load you may have read about elsewhere, was not a means to make this hypothesis come true, but an effort to generate a level playing field of which the authors write that it also constitutes a "tertiary purpose" of the study, which was thus also intended as a means to investigate "the effects of carbohydrate refeeding following KD adaptation on body composition and performance" (ibid.)

The glycogen loading was not meant to skew, but to create a level playing field.

Unfortunately, this strategy backfired in a way that's currently getting people all over the interwebs so "excited" (to say the least) that they focus exclusively on this failed attempt to compensate for the glycogen advantage and do not acknowledge the strengths of the study.

Update from April 21, 2017: You can read more about the study from the authors themselves if you want to. Ryan Lowery also addresses the "glycogen loading" making practically the same point I did: anybody who would have invested time and effort to read the whole paper, would have read that they never claimed the aprupt increase in lean mass in the final week was anything but water.

Strengths such as (1) the selection of trained subjects and exclusion of those with a squat performance that was significantly below 1.5 times the subjects' own body weight (here we have one of the criticized issues with the reporting, though, because the value Wilson et al. provide is 1.56 ± 0.14 and thus below 1.5 if you subtract the standard deviation from the arithmetic mean), as well as the prescription of (2) a realistic resistance training routine with a hypertrophy focus (see Table 1).

Table 1: Training protocol; *rest was 60-90 seconds on hypertrophy days and 3-5 minutes on strength days (Wilson 2017).

Extra cardio or other endurance training and/or other athletic activity outside of the three weekly workouts was strictly prohibited. All exercises were either performed for the given number of reps or to failure. The load utilized for weeks 3-6 ranged from 65 to 95 % of subjects’ initial 1RM. However, these loads were increased by 2-5 % for the final 7-9 weeks of training depending on subject’s ability to perform the prescribed repetitions during weeks 3-6.

Figure 1: Visualization of the macronutrient composition of the diets (Wilson 2017).

As the authors explain, the "subjects tapered by decreasing volume by 40-50 % through decreasing sets on auxiliary lifts on Monday and Wednesdays and only performing 1RM testing on Fridays" (Wilson 2017) in the final two weeks of the study period, of which it may be worth mentioning that it lasted 12 weeks: a two-week lead-in, 9 weeks until the highly debated glycogen repletion protocol began and another week until the final measurements of exercise performance and body composition.

How different were the diets in reality? Unfortunately, the researchers don't elaborate (and probably didn't even review) which foods their subjects actually eat. Accordingly, we're left with the macros and some extra information on the saturated, poly-, and monounsaturated fat and fiber content of the diet. What I can tell you is this: the average protein intake in both groups was identical, amounting to ~130g/day; the fiber intake was 2-fold higher in the WD group; and the percentage of saturated, monounsaturated and polyunsaturated fat in the diet were similar (47%, 30% and 23% in the KD and 48%, 34% and 18% in the WD group, respectively) - if that's relevant for the results is questionable, though. Unless, obviously, you believe in the myth of the tooth fairy... ah, I mean, the "anabolic prowess of saturated fats" that was born out of a single study showing increased testosterone levels on higher SFA-diets.

Dietwise, the subjects, N=25 resistance-trained males who had an average max squat performance of 1.56 ± 0.14 times their body weight and an average of 5.5 ± 3.8 years of training experience, were randomly assigned to...

• 

  Only recently scientists have been able to show that coffee can kickstart ketosis, even if you eat a sign. number of carbs for breakfast | learn more.

  the WD = western diet - 20% calories from protein, 55% from total carbohydrate, and 25% from fat
• the KD = ketogenic diet - 20% calories from protein, 5% from carbohydrate including fiber, and 75% from fat 
• in both groups, subjects were instructed to consume food immediately following training that contained a minimum of 20-30g of protein, with the remainder of the meal reflecting the accurate ratios prescribed throughout the day

The individual energy content was calculated based on maintenance calories determined by the Mifflin St. Jeor equation. Now, while this is standard procedure in metabolic research it is still problematic, as the equation can be 15% off the actual requirements. Accordingly, it is not clear, whether the subjects were in a caloric deficit. Since this holds true for both groups and the overall energy intake was identical in both groups, though, this is not relevant to the study's original research goal, which is to determine differences between a ketogenic and a western diet.

Excellent dietary adherence and full ketosis in the main part of the study

What we can tell, though, is that the subjects' adherence to the diets was excellent (2608.6 ± 157.5kcal/day vs.  2549.5 ± 212.5 kcal/day,  217.02 ± 15.5 g fat per day vs.  83.4 ± 13.3 g fat/day, 133.6 ± 10.8 g protein per day vs. 132.2 ± 13.3 g protein per day, 30.9 ± 5.9 g carbohydrates per day vs. 317.6 ± 31.1 g carbohydrates per day in the KD vs. WD group, respectively) and confirmed by both both food logs and weekly urinary ketone measurements.

Does the study "fly in the face of all other research" and present "totally unrealistic results"? That's at least what I read on Facebook several times - alongside accusations of scientific fraud that have no basis in facts, by the way.

Let's take a look at the little research there is: There's the recent revelation that low carbohydrate dieting impairs the adaptive response to aerobic training in Louise Burke's excellent paper in the Journal of Physiology (Burke 2017); a paper, of which not even its authors would claim, though, that it settles the debate once and for all - neither for endurance athletes, of whom Cox et al. write that "five separate studies of 39 high-performance athletes" show that "this unique metabolic state [ketosis] improves physical endurance by altering fuel competition for oxidative respiration" (Cox 2016; further evidence e.g. Ball 1995; Gore 2001), nor for athletes competing in anaerobic sports, where studies studies in gymnasts (Paoli 2012), or dieting martial artists (Rhyu 2014) report favorable results with ketogenic diets.

Comparison of the body composition changes in Jabekk 2010, a study in untrained overweight women w/out dietary restriction and the results Wilson et al.. report before the glycogen reload in week 11 that's obviously absent in the Jabekk study.

Let's get more specific, though: If we exclude the effects of the glycogen reload (i.e. stick to the body composition changes from week 1-10) and compare these to the observations of a 2010 study by Jabekk et al., it also becomes obvious that the changes in body composition are not as "unrealistic", as some critics have claimed: With almost identical macronutrient compositions, i.e. 6%, 66%, and 22% in the "low carbohydrate" (de facto ketogenic) diet and 41%, 34%, 17% of the energy from carbs, fats and protein in the "normal" (de facto western) diet, Jabekk's study has a very similar dietary composition as the study at hand.

Due to fundamental differences in the subject selection (untrained, overweight women vs. trained, lean men) and other aspects of the study design, including a non-restricted energy intake and non-hypertrophy-specific workouts, it should be obvious that the results of the studies cannot be 'identical'. Within the statistical margins of error (which are unfortunately not provided in Wilson 2017; that's also why the error bars are missing in the figure on the left) and in view of the previously mentioned design differences, Jabekk's results are yet similar enough to refute the claim that Wilson's study results were "totally unrealistic" or had to be discarded, altogether, because they would "fly in the face of all previous research" (my emphasis).

The last-mentioned ketone tests confirmed that all subjects in the ketogenic dieting group (KD) had reached full ketosis at the beginning of the 2nd week of the two-week lead-in - an important observation that was not made (either because it was not tested or because the high protein content of the diet allow the subjects to reach full ketosis) in some previous "low carbohydrate diet"-studies.

Figure 2: Changes in body composition (in the given timeframe in kg) according to DXA scans (Wilson 2017).

So far, so good... I guess, it's about time to address the catch, then: Before the final DXA scans (results see Figure 2), muscle circumference and strength tests were done, the subjects in the KD group were subjected to a classic glycogen loading protocol consisting of two days on 1g/kg carbohydrates, followed by two days on 2g/kg carbohydrates and 3g/kg carbohydrates in the last 2 days before the DXA scan - obviously, with an isocaloric decrease in dietary fat that maintained the caloric intake at the previously described calculated maximum.

Hindsight is easier than foresight: If you glycogen-load, it'd be logical to do so in both groups

In general, there's nothing wrong about this. To create a truly equal playing field, however, it would yet have been smarter to either glycogen-load (or, alternatively, -deplete) both groups. With only one group getting the extra boost in muscle fullness, however, the DXA data from week 11 is as skewed (albeit into the other direction) as the measures that were taken in week 10, when the emptied glycogen stores in the KD group gave the similarly elusive impression that the consumption of a ketogenic diet had impaired the subjects' lean mass gains while extremely augmenting their fat loss.

Percent changes in leg lean and fat mass vs. baseline following glycogen depletion and creatine and glycogen loading with and without creatine (Bone. 2016) | learn more in my previous article about the study.

Glycogen or real muscle gains? If you scrutinize the data in Figure 2, you will realize that the keto group was trailing 50% behind in weeks 1-10, i.e. while the subjects were actually consuming a ketogenic diet. Only after the increase in carbohydrate intake in week 11 that was not all-too-different from the glycogen loading protocol in a recent study by Bone et al. (2016), they caught up and overtook the western diet group. The ~2kg (~3% of baseline lean mass) extra lean mass in the ketogenic vs. western diet group, however, is pretty much identical to the 2.0 ± 0.9 % increase in DXA-measured lean mass Bone et al. observed in response to a similar glycogen loading protocol in their study.

If we assume that the effects of the loading protocol were similar to those Bone et al. (2016) observed with an almost identical protocol in their recent study (see discussion in the red box, above), the extra glycogen would appear as a ~3% increase in lean mass on the DXA scans - and that's pretty much what we see in the study at hand. Accordingly, the "real" muscle gains in the KD group are probably somewhere in-between what we see in Figure 2 (left) for the 1-10 wk and 1-11 wk period. This, however, would imply that the "real" lean mass gains (and the increase in muscle thickness, see Figure 3) over the course of the study would - within the usual statistical margins of error - be identical for both diets.

It's not true that Wilson et al. do not address the issue of glycogen-driven 'extra gains'

In view of the harsh criticism Wilson et al. have received over the Easter weekend, it should be mentioned that the authors come to a very similar conclusion (without, however, citing the study Bone et al.), when they write in the discussion of their results that "the abrupt, yet not unexpected, changes in LBM were primarily driven by drastic changes in water flux during the last week of the study" (Wilson 2017) - and conclude, just as I did, that both "groups gained similar amounts of muscle mass throughout the entire study" (ibid.).

Figure 3: Rel. changes (%) in muscle thickness and performance data from week 1-10 and 1-11 (left) and absolute DXA data with lean mass at the top and fat mass at the bottom (full bars = KD, open bars = WD | Wilson 2017).

The fact that the authors do not make this more explicit in the abstract and, even more importantly, speak of a body composition "advantage" for the KD diet in the "practical implications" section of the paper, is in fact reason for warranted criticism. After all, the alleged improvements in fat loss vanish just as the increases in lean body mass did, if we subtract the ~6% "virtual" loss of body fat Bone et al. observed as a result of glycogen depletion, alone, and/or estimate the "real" body fat loss by averaging over the fat mass Wilson et al. measured in week 10 and 11, respectively.

If there's no inter-group difference, the study at hand still shows just what the first part of the conclusion of the abstract says: "The KD can be used in combination with resistance training to cause favorable changes in body composition, [and] performance" (Wilson 2017).

So, even if we assume that the extra gains were an experimental artifice and assume that a potential fat loss advantage did not exist, we should at least be able to agree that the study at hand confirms, irrespective of its methodological problems and 'suboptimal' reporting of the results, that ketogenic diets can build the same amount of lean mass and strip the same amount of fat off the bodies of trained young men, when all other parameters are kept equal. Whether the "western diet", a high carb, lowish protein, medium fat diet, is an adequate yardstick when it comes to the question "What's the best diet for gymrats, physique athletes and/or bodybuilders?", however, is yet another story.

Figure 4: Despite all the criticism: There's one major problem with the study that has gone largely unnoticed: In the absence of data from the last week the subjects were actually consuming a ketogenic diet it is IMHO unwarranted to conclude that a KD "cause[s] favorable changes [...] in hormonal profiles" (Wilson 2017).

So, keto-dieting rules, right? If we try to average the effects of the glycogen load out, the study at hand still yields an important result: it confirms that there is no body composition and muscle size disadvantage to consuming a ketogenic diet compared to an isocaloric "western" high carbohydrate, lowish protein diet.

How's that? Well, due to the fact that the scientists' well-meant effort to level the playing field by restoring their subjects glycogen stores in week 11 backfired, it is impossible to say, whether the "favorable changes", Wilson et al. point out in the conclusion of the abstract were more or less pronounced in the ketogenic compared to the western diet group.

What is possible, however, is to speculate based on data from before and after the glycogen-load. If we thus try to 'fix' the data by (a) averaging over the data from weeks 10 and 11, respectively, or by the means of (b) logical inference based on the results of Bone's previously discussed study that used an almost identical protocol to determine the effects of glycogen loading on DXA scans (Bone 2016), we will arrive at a conclusion that mirrors the one Wilson et al. phrase in the discussion of their results - that both "groups gained similar amounts of muscle mass throughout the entire study" (Wilson 2017); and that's, if we are honest, exactly what the first part of the heavily criticized and, as I believe, largely misunderstood conclusion of the study's abstract says: "The KD can be used in combination with resistance training to cause favorable changes in body composition" (Wilson 2017; my emphasis).

Unfortunately, the person who wrote the "practical applications" section of the paper seems to have 'forgotten' about that when he wrote that the KD was overall "advantageous for body composition [...] as compared to a WD" (ibid; my emphasis). That's clearly not in line with the message that emerges in the authors' previously cited discussion of the results.

What is likewise questionable is whether the study outcome would have been similar for the practically more relevant comparison of a ketogenic diet to a classic bodybuilding-style high protein, medium carbohydrate control diet - a diet with lower amounts of carbs and fats and significantly more protein than the unquestionably suboptimal "western" diet in the study at hand. Ah... and one last thing: It is not just questionable, but, in my humble opinion, simply unwarranted to claim that the ketogenic diet had beneficial effects on the subjects' testosterone levels when the latter were assessed after one week of glycogen loading (cf. Figure 4) | Comment!

References:

• Ball, Thomas C., et al. "Periodic carbohydrate replacement during 50 min of high-intensity cycling improves subsequent sprint performance." International Journal of Sport Nutrition 5.2 (1995): 151-158.
• Bartlett, Jonathan D., John A. Hawley, and James P. Morton. "Carbohydrate availability and exercise training adaptation: too much of a good thing?." European journal of sport science 15.1 (2015): 3-12.
• Bone, Julia L., et al. "Manipulation of Muscle Creatine and Glycogen Changes DXA Estimates of Body Composition." Medicine and science in sports and exercise (2016).
• Burke, Louise M., et al. "Low Carbohydrate, High Fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers." The Journal of Physiology (2017).
• Cox, Pete J., et al. "Nutritional ketosis alters fuel preference and thereby endurance performance in athletes." Cell Metabolism 24.2 (2016): 256-268.
• Gore, Christopher J., et al. "Live high: train low increases muscle buffer capacity and submaximal cycling efficiency." Acta physiologica scandinavica 173.3 (2001): 275-286.
• Jabekk, Pal T., et al. "Resistance training in overweight women on a ketogenic diet conserved lean body mass while reducing body fat." Nutrition & metabolism 7.1 (2010): 17.
• Paoli, Antonio, et al. "Ketogenic diet does not affect strength performance in elite artistic gymnasts." Journal of the International Society of Sports Nutrition 9.1 (2012): 34.
• Roberts, Michael D., et al. "A putative low-carbohydrate ketogenic diet elicits mild nutritional ketosis but does not impair the acute or chronic hypertrophic responses to resistance exercise in rodents." Journal of Applied Physiology 120.10 (2016): 1173-1185.
• Wilson et al. "The Effects of Ketogenic Dieting on Body Composition, Strength, Power, and Hormonal Profiles in Resistance Training Males." J Strength Cond Res. 2017 Apr 7. doi: 10.1519/JSC.0000000000001935. [Epub ahead of print]

Eccentric Training Keeps You Gainin' and T & GH Up When, in Weeks 5-10, Traditional Training Stops Yielding Results

Extra gains, testosterone, and GH in one scientific paper?  That will catch every gymrats interest, right?

I know, the name SuppVersity implies that gains were all, or at least to a significant degree about supplements. In fact, though, they are about busting your ass out in the gym and eating like a freak. And with respect to the former, a new study from the University of Jyväskylä in Finland suggests that there is a deeper truth to the former part of this often-heard claim: busting your a** in form of eccentric training, i.e. using the maximal weight you can lift on the concentric and a supra-maximal weight on the eccentric phase of a more will indeed produce significantly greater increases in maximal voluntary contraction torque (MVC) and (almost) significant increases in muscle gains.

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What is particularly interesting about the study that has just been published in "Physical Reports" is the fact that Walker et al measured both, the hormonal response that is usually evaluated only acutely, i.e. in studies where the subjects train only once, and the corresponding strength and size gains... and guess what: (1) The hormonal response to the allegedly slightly artificial "leg-extension only"-training program diminishes with time, unless (2) the workouts are kept challenging by increasing the weight on the eccentric portion of the exercise and thus maximizing the stimulus on the leg extensors.

This study only looks as if it was your ordinary "legs only, that's not the real world" trial

Before we jump to any unwarranted conclusions that are probably totally unwarranted, anyway, I'd suggest that we take a closer look at what exactly the Finish-Australian-Chinese co-production (talking about the home Universities of the authors, here) did to their N=18 healthy, young, male subjects who had a strength training background of 2.7 ± 2.3 years and an initial 10‐RM inclined leg press load of roughly 2kg per kilo body weight. While both groups performed the same three sets of bilateral leg press, three sets of unilateral knee extension and three sets of bilateral knee flexion twice a week (at least 48 h recovery between training sessions) and with a weight equal to their individual 6 rep max (RM) for 8 weeks (week 1 and 10 were testing weeks), ...

• the isoinertial (ISO) group performed the exercises with the same load for both concentric and eccentric phases, while 
• the accentuated eccentric (AEL) group performed the exercises with 40% greater load during the eccentric phase compared to the concentric phase (i.e., eccentric load = concentric load + 40%)

To rapidly change the weight, the scientists used "custom weight‐releasers" for the leg press and a "custom‐built pin" for the knee extension exercise. This makes it difficult to copy the protocol in the real-world, but if you don't train on your own, you can ask your training partner to assist you on the concentric portion of the lifts and hope that the results are going to be similar.

Figure 1: Relative improvements (mean ± SD) in maximum isometric knee extension torque (A) and lower limb lean mass (B) from pre‐ to mid‐training and mid‐ to post‐training. *P < 0.05 within group, #P < 0.05 between groups (Walker 2017).

Speaking of results: As I pointed out earlier, the maximal strength (MVC) and lean mass, both, increased to a greater extent in the AEL group (see Figure 1).

This is not a leg-training only study: If you're now mad that this is not exactly a realistic workout, you will be happy to hear that the subjects were instructed to continue with their normal upper body strength training program (albeit at least 24h away from the leg training sessions). The results should thus be representative of what you could see if you applied the same training principles to your workouts, even if you're training your upper body, as well. Moreover, the subjects' training logs show that they had a lot of other exercises going on... now that's realistic, but it's impossible to exclude that their non-competitive recreational activities (1‒3 times per week) didn't affect the study outcomes in one way or another.

Figure 2: If you compare the hormonal response early (solid) and late (dashed) line you will see the attenuation of T, cortisol, and GH that occurred in the ISO group (left) over time (Walker 2017).

What may seem - at least at first sight - even more intriguing than the "gains" is that the acute testosterone, growth hormone, and cortisol responses were reduced in the traditional = isoinertial training group, while they remained elevated in the subjects training with an accentuated eccentric load (P < 0.05‒0.1 between‐groups).

As the authors rightly point out, "the maintenance of acute hormonal responses and continued strength gain in AEL but not ISO are consistent with the hypothesis that maintained acute responses indicate an efficacy of a training stimulus to evoke ongoing adaptation" (Walker 2017). What this does not mean, however, is that the hormonal response is not in as much a result of this stimulus as the gains you see in Figure 1.

You want to dig deeper into the hormonal response seen in this study? I'd suggest you read the excellent discussion Walker et al provide in their open access paper - simply click here!

We thus have to be careful: Correlation, i.e. the stimulus triggers both the gains and the increase in GH and testosterone, doesn't necessarily equal causation, i.e. the increase in GH and testosterone trigger the gains. But how de we know which of the two hypothesis is accurate? Well if the latter was the case, the scientists should at least have found a statistically significant relationship between the hormonal response and the gains of their subjects. Such a relationship, however, did not exist - and that's in line w/ previous research (West 2012; Schoenfeld 2013; Egerman 2014), where correlations were - if at all - only found on a group level.

Figure 3: West's and Philipps' 2012 paper showed that the post-workout cortisol- (right), not testosterone- (middle) or GH- (left) response predicts the total lean mass gains in response to weight training in a large cohort trained men (West 2012).

And, as you can see in my favorite figure from West 2012, these correlations point to cortisol and growth hormone, not testosterone as a potential indicator or mediator of training-induced muscle growth, of which Walker et al. argue in the discussion of their results that they may facilitate the energy-demanding process of muscle remodeling (as GH and C are both "lead to metabolism of fatty and amino acids, respectively, to be used as sources of energy" (Walker 2017)). Personally, I would rather point towards the intracrine and anti-inflammatory effects of GH and cortisol I discussed in the "Intermittent Thoughts About Muscle Growth"-Series.

Don't (ab-)use these results to argue in favor of a causal involvement of the PWO increase in growth hormone and testosterone in muscle gains!

Accordingly, their "data suggest that tracking of acute hormonal responses on an individual level may not provide a sensitive enough guide for decisions regarding program design and periodization" (Walker 2017) - or, in other words, we're back to square one, i.e. the realization that PWO cortisol, GH, and testosterone levels are probably not worth bothering with.

Figure 4: Volume load (mean ± SD) during pre- (week 2) and post-training (week 9) test in the isoinertial training group (A) and accentuated eccentric load group (B) in week 2 ("Pre‐") and week 9 ("Post‐training") loadings. *P < 0.05 versus pre‐training, **P < 0.01 versus pre‐training. con = concentric, ecc = eccentric phase (Walker 2017).

Now the question that remains is: If it's not the hormonal response, what is it that makes the difference? Well, I have to admit that I don't have the answer to this question. What I do know, however, is that it is very unlikely - and that's much in contrast to many previous studies - that it's the total training volume (as defined as total weight x total reps); and that's not because the latter was, as it is the case in many other studies, standardized, but rather because it didn't differ that much between the ISO and AEL groups (see Figure 4).

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So, eccentric training provides an extra stimulus... do you really need to know why eccentric training works? Well, ok... I know I want to know that, too, but I guess we will have to stick to "it provides an extra growth stimulus" when it comes to the mechanism of action.

With that being said, the study at hand may not be able to answer why it's working. What it does add to our knowledge about eccentric training is that its advantages start to kick in only after 4-5 weeks and thus at the very point when the body appears to adapt to isoinertial (=classic) resistance training. I mean, look at the mid-post-gains in Figure 1 - ZERO strength and size increases are not what you want to see as a reward for your hard work on the grind, is it?

I know it isn't, but that's actually a problem because only "busting" and no "resting" isn't going to yield results, either. Further studies are thus IMHO necessary to investigate (a) the long-term benefits of eccentric training (I think it's unlikely that it will work forever), whether (b) similar benefits couldn't be achieved by plain-old periodization (e.g. switching exercises, rep schemes etc. periodically) and (c) if the same results could be achieved if this intensity technique was also applied in the upper body workouts the subjects fitted in on their off days | Comment!

References:

• Egerman, Marc A., and David J. Glass. "Signaling pathways controlling skeletal muscle mass." Critical reviews in biochemistry and molecular biology 49.1 (2014): 59-68.
• Schoenfeld, Brad J. "Postexercise hypertrophic adaptations: a reexamination of the hormone hypothesis and its applicability to resistance training program design." The Journal of Strength & Conditioning Research 27.6 (2013): 1720-1730.
• Walker, Simon, et al. "Acute elevations in serum hormones are attenuated after chronic training with traditional isoinertial but not accentuated eccentric loads in strength‐trained men." Physiological Reports 5.e13241 (2017) DOI: 10.14814/phy2.13241
• West, Daniel WD, and Stuart M. Phillips. "Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training." European journal of applied physiology 112.7 (2012): 2693-2702.

'Bizzy Diet' Sheds 2% Body Fat (2kg) in Only 3 Weeks, Study in 51 Women (BF 25%) Shows - W/ and W/Out 'FitMiss Burn'

The "Bizzy Diet" works, the supplements that are suggested in the program at BB.com are useless, though.

You know that I am a fan of supplement companies that try to support the often hilarious claims on their product labels with science. Against that background, I feel there's nothing wrong with MusclePharm sponsoring, ah... I mean "funding" a recent study by researchers from the University of... ah, I mean, from Bodybuilding.com and the Ohio State University (Kendall 2017) - and that's not just in those (not exactly rare cases) when said research proves that their "thermogenic" powerhouse is actually a hilariously underdosed barrel burst.

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In the study at hand, the corresponding supplement is MusclePharm's FitMiss Burn "thermogenic fat burner" for women. A product that contains an undisclosed amount of Guarana Seed Extract (Paullinia Cupana), (22% Caffeine) Caffeine Anhydrous (100mg), Pyroglutamic Acid, Green Tea Extract (40% EGCG) (Camellia Sinensis)(Leaf), Papain, Yerba Mate (Llexparaguariensis)(Leaf), Yohimbine HCl, of which all have some scientific back-up as fat-burners alongside the other ingredients you can see in the graphical summary of the study results I created in Figure 1:

Figure 1: Graphical summary of the results; no sign. inter-group differences for Bizzy Diet (alone) vs. BD + FitMiss Burn.

In view of the fact that there's research backing almost all of the other ingredients, as well, it may seem surprising that the those of the fifty-one apparently healthy women between the ages of 18 and 35 years volunteered to participate in this randomized, double-blind, placebo-controlled study, who have been randomized to receive the product didn't see any benefit from their two capsules of FitMiss Burn, right?

Exercise characteristics in the three groups of young women during the 3-week study period (Kendall 2017)

Why did the control group see almost identical improvements in body composition? That's a good question. After all, the 14 women in the control group were "instructed to maintain their normal dietary habits" (Kendall 2017) and trained significantly less (see Figure on the left), ate more food and less protein over the course of the three-week study. Well, the explanation for this "phenomenon" lies within our naive trust in the accuracy of DXA scans and studies with small group sizes. With standard deviations that are two-times larger than the relative pre-/post-changes in body composition, we simply have to rely on the scientists' statistical analyses and those reveal that: (a) the diet groups lost sign. more body fat and (b) had a sign. different lean mass trajectory (lost or maintained vs. gained) compared to the control group... let's be honest, that's not a phenomenon.

Well, that's true, but if you scrutinize the label you'll realize that the total amount of active ingredients, i.e. 1,450 mg per serving (2 capsules per day) simply cannot contain caffeine, green tea, yerba mate, yohimbine, glucomannan, white kidney bean extract... to allow for all of them to have measurable effects. After all, the studies I previously alluded to used...

• at least 200mg of caffeine (usually alongside other ingredients),
• more than 500 mg green tea extract (e.g. Nagao 2007), and
• the human equivalent of 7g of yerba mate (e.g. Arçari 2009)

which would already exceed the total weight of the proprietary ""Energy & Focus Complex" in the product... and we haven't even talked about the "Appetite Reduction & Fat Metaboliser" blend from which we'd need 2x1g per day of glucomannan (e.g. Salas-Salvadó 2008), 7.5-30g of guar gum (Pittler 2004), and much more of all other key ingredients.

Figure 2: Original grocery list for the "Bizzy Diet 21-Day Fitness Plan" (Bodybuilding.com | download PDF)

Well, now that it's clear that the supplement didn't work and couldn't work, let's take a closer look at the "Bizzy Diet" (you can learn more about the diet at bodybuilding.com): Basically, we're looking at a high calorie (1,000kcal/d) version of a low-carbohydrate protein-modified fast.

Over the course of the three-week study period the women had to cut their habitual food intake to 1,000kcal, cut out almost all carbs, eat every 3h (this is probably an irrelevant rule of the diet, but will certainly keep you "bizzy" ;-) and 'gorge' on eggs, bacon, tuna, broccoli and the other foods the meal plan on bodybuilding.com suggests - is it any wonder that the (almost overweight) ladies went from ~27% to ~25% DXA-assessed body fat on that diet? Not really.

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Why did you even discuss the study at hand? I know that some of you may now ask yourselves just that: Why? Well, the answer is simple: Firstly, I want you to scrutinize the labels of the supplements you buy and not be fooled by "proprietary blends" - in cases like the one at hand, it doesn't matter if the amount of the individual ingredients is undisclosed: even a first-grader will be able to see that they're underdosed if the label lists 20+ ingredients and the total weight of active ingredients is below 2000 mg (or less).

And secondly, I want you to understand how powerful dieting is: I mean, the 2% reduction in body fat the ladies in the study at hand achieved with their 1,000kcal protein- and nutrient-rich low-carbohydrate diet is worth reporting, isn't it?

References:

• Arçari, Demétrius P., et al. "Antiobesity Effects of yerba maté Extract (Ilex paraguariensis) in High‐fat Diet–induced Obese Mice." Obesity 17.12 (2009): 2127-2133.
• Kendall, Kristina L., et al. "A Randomized, Double-Blind, Placebo-Controlled Trial to Determine the Effectiveness and Safety of a Thermogenic Supplement in Addition to an Energy-Restricted Diet in Apparently Healthy Females" Journal Of Dietary Supplements (2017) - Ahead of print.
• Nagao, Tomonori, Tadashi Hase, and Ichiro Tokimitsu. "A green tea extract high in catechins reduces body fat and cardiovascular risks in humans." Obesity 15.6 (2007): 1473-1483.
• Pittler, Max H., and Edzard Ernst. "Dietary supplements for body-weight reduction: a systematic review." The American journal of clinical nutrition 79.4 (2004): 529-536.
• Salas-Salvadó, Jordi, et al. "Effect of two doses of a mixture of soluble fibres on body weight and metabolic variables in overweight or obese patients: a randomised trial." British Journal of Nutrition 99.06 (2008): 1380-1387.