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Eggs or Flakes? Not 30% vs. 25% protein! A brief reminder of the fact that the stuff you eat is still food.

I am not quite sure when or why this happened, but I know that more and more people are thinking in terms of "macros" instead of foods. What I do know, though, is that the recent publication of studies from the Pennington Biomedical Research Center at the Louisiana State University System (Bayham. 2014) and an ostensibly unrelated study that was conducted by researchers from the Alimentary Pharmabiotic Centre, Biosciences Institute in Cork and scientists working at the local university and the University of Pittsburgh School of Medicine (Patterson. 2014) confirms - once again (!) - how futile this ignorant approach to nutrition actually is.

Eggs vs. cereals - not the best example, but...

In that, I am well aware that the "battle" between an egg- and a cereal-based breakfast in the Patterson study is not exactly a good model of whats currently going on in the health and fitness community. With cereals being labeled as "the devil" (its always nice to be "anti", isnt it?), no one would after all consider having ...

• One-and-a-half cup of Special K® RTE cereal, 200 ml Silk® original soymilk, one slice of Natural Grain “Wheat n’ Fiber”® bread, 13 g of butter, and 10 g of sugar-free strawberry jam (CG)

... for breakfast. In view of the fact that the same can be said for the calorie- and mocronutrient matched "high quality protein" breakfast, i.e.

• Two scrambled eggs, 120 mL skim milk, two slices of Holsum® thin white  bread, 5 g of butter, and 18 g of Smuckers® strawberry jam

... I still believe that the consequences of "breaking the fast" (learn why I am calling breakfast thus in "Breakfast or Breaking the Fast" | read more) with eggs vs. Special K are still relevant to the previously introduced context. And if you know that the acetylated form of ghrelin and PYY are "satiety hormones", it does not take a rocket scientists to interpret the data in Figure 1.

Figure 1: Level(s) of "satiety hormones" after the different breakfasts (Bayham. 2014)

What is difficult to tell, though, is whether the increased satiety after the egg breakfast would actually lead to a reduced intake at the subsequent meal.

• On an individual basis, i.e. on just one of the two eating occasions, the higher levels of acetylated ghrelin and PYY did not suppress the 20 healthy overweight or obese subjects energy intake during the subsequent lunch
• For day 1 and day 7, together, on the other hand, the 64kcal the egg eaters consumed less than the cereal eaters did reach statistical significance.

If we throw overboard all the things we (believe) we know about the fallacy of calorie counting, this would translate into a ~448kcal difference for one week and a whopping difference of 23,360kcal for a year, which should shed ~3.3kg of body fat a year.
Whether or not similar concrete weight loss vs. gain effects can be achieved with different types of fat is nothing study #2 in todays science mash-up here at the SuppVersity could answer. What it can tell you though, is that protein and obviously carbohydrates, where even Mr. Average Joe thinks in terms of "low GI" = good and "high GI" = bad carbs, these days, is by no means the only food component, where unspecifically counting macros is not going to cut it (or get you cut, if thats what you want to achieve).

This is not just about fish oil

"Of course, the bad omega-6s" ... I know that this is what youre thinking right now, but lets be honest, isnt that a bit narrow-minded?  It sure is and still, the results Ellaine Petterson and her Irish and American colleagues present in their most recent paper demonstrate quite clearly that the ingestion of fish and flax seed oil has pretty unique effects that go beyond its ability to increase the tissue concentrations of DHA to levels way beyond what youd see in low fat or high fat diets with palm, olive or safflower oil powered high fat diets.
In addition it lead to an increase in the relative abundance of bifidobacteria, a gut tenant that has been linked to all sorts of beneficial health effects, but has recently been outshadowed by various strains of lactobacilli (0.95% vs. more than 2% in all other groups), which - and this is an important information - were the lowest in the rodents who were kept on diets with 45% of the energy from fish and flaxseed oils.

Whether or not, the negative effects of fish oil on the lactobacillacea count in the guts of the lab animals is also partly responsible for the more or less disappointing effects the fish and flax seed diet had on the body composition (Figure 2) of the wild-type C57BL/6J male mice (21 d old) in the study at hand is questionable.

Figure 2: Body composition analysis at the end of the study (Patterson. 2014)

Its not impossible, though. A brief glance at the insulin levels and leptin levels in Figure 3 reveals that neither of them looks anyway close to what someone whos religiously taking his fish oil caps on a daily basis would be expecting. In the end, it is thus not really that surprising that only the palm oil diet group ended up with an inferior lean-to-fat mass ratio of 1.17 (vs. 1.33 in the omega-3 group).

Figure 3: Changes (%) in relevant metabolic markers in response to the different diets (Patterson. 2014)

The results of the study at hand, i.e. the effects on body composition (Figure 2), as well as blood glucose and lipid metabolism (Figure 3) are thus clearly not in line with the ubiquitously placated message that "fish oil is good for you" - a message, the indoctrinated average supplement junkie will still discern from the abstract of the study:

"[...] Ingestion of the HF-flaxseed/fish oil diet for 16 weeks led to significantly increased tissue concentrations of EPA, docosapentaenoic acid and DHA compared with ingestion of all the other diets (P< 0·05); furthermore, the diet significantly increased the intestinal population of Bifidobacterium at the genus level compared with the LF-high-maize starch diet (P< 0·05). These data indicate that both the quantity and quality of fat have an impact on host physiology with further downstream alterations to the intestinal microbiota population, with a HF diet supplemented with flaxseed/fish oil positively shaping the host microbial ecosystem." (Petterson. 2014).

Neither the "loss" of lactobacilli, nor the - if anything - negative effects of the high omega-3 diet on the lean-to-fat-mass ratio and the amount of insulin thats floating around in the rodents blood are mentioned in said abstract.

Fat = Diabetes - A FAT Mistake?

If you go take a look at the actual study data, we are thus left with the question, whether the purported benefits of having high amounts of omega-3 fatty acids in our cells (see red info box a couple of paragraphs above) are real enough (or really enough - whatever you prefer) to discard the fact that the study at hand would actually suggest that olive and not fish + flaxseed oil should be your go-to source of dietary fat on a high fat diet.

Moreover, if we abandon any paradigmatic believes, we would even have to concede that - within the current context, i.e. a rodent study and a diet with protein contents of only 19.2% (low fat) and 23% (high fat), the low fat mix of 1.25% of palm, 1.25% olive, 1.25% safflower oil, 0.625% fish and 0.625% flaxseed oil the rodents in the starch and sucrose groups received is superior to any of the high fat variants.

You may say that this is "rodent shit" (and it is, because this is what the scientists analyzed to access the SFCA metabolism of the mice) and a mere coincidence, but wouldnt you agree that this oil mix looks a little too much like the mixture youd get on a low-to-moderate fat diet with olive oil as a staple for everything, where you add oils, palm and safflower oil from processed foods on your cheat days and fish oil / omega-3s from your once or twice a week serving of salmon... ?
References: 

• Bayham, Brooke E., et al. "A Randomized Trial to Manipulate the Quality Instead of Quantity of Dietary Proteins to Influence the Markers of Satiety." Journal of Diabetes and its Complications (2014).
• Filaire, Edith, et al. "Effect of 6 Weeks of n-3 fatty-acid supplementation on oxidative stress in Judo athletes." International journal of sport nutrition 20.6 (2010): 496.
• Danthiir, Vanessa, et al. "Cognitive Performance in Older Adults Is Inversely Associated with Fish Consumption but Not Erythrocyte Membrane n–3 Fatty Acids." The Journal of nutrition (2014): jn-113.
• Patterson, E., et al. "Impact of dietary fatty acids on metabolic activity and host intestinal microbiota composition in C57BL/6J mice." The British journal of nutrition (2014): 1-13.

In general, you have to count and limit your weekly HIIT sessions. Doing as much as humanly possible, could yet make sense, when youre preparing for Olympia 2016 and realize 5 weeks before the event that you have been lingering for too long ;-)

I think as a SuppVersity reader you know by now that "more wont yield more" - no matter if we are talking about supplements or exercise. Now, while weve had countless examples of the "more aint more" principle thats also at the heart of the "Three Simple Rules of Supplementation" (read article) for supplements (e.g. zinc, chromium, etc.) and the simple notion that eating less wont always result in greater weight loss, evidence for the pro-anabolic / adaptive effects of exercise in general, and non-steady state cardio, in particular is scarce. Against that background its all the more important for us to cherish the publication of a paper from the Norwegian University of Science and Technology and the St Olav University Hospital in Trondheim Norway, Roy told me about by messaging me via the SuppVersity Facebook Page.

"More HIIT doesnt help more, either"

I guess the above would be the elevator pitch for the mythical "turbo lift" in Star Trek. For someone like yourself who has learned never to swallow "expert" wisdom just like that, the statement "more HIIT doesnt hep more, either" obviously wont be satisfying.

Figure 2: Illustration of the training in the low frequency (LF) and high frequency (HF) group.

If you look at the illustration above, you will already know somewhat more about the "more" in the previous sentence. As you can see, the parameter that has been modified is not the volume, its the frequency!  - and thus one of the parameters of which many gymrats think that it could hardly be high enough (AM + PM training, 7 days a week - does that ring a bell?). What this people ignore is the simple truth that ...

... adapatation takes time and training more often does not accelerate this process!

In the end, I am actually quite surprised to see that the net VO2 "gain" the scientists measured in the subsequent detraining phase (see Figure 2) was identical. Or, more explicitly, that packing 24 training sessions into three weeks did not blunt the mitochondrial adaptation processes that are responsible for the increase in VO2max, altogether.

Figure 2: VO2max and heart rate values of the 16 healthy subjects before / after high vs. low frequency HIIT (Hatle. 2014)

If we are brutally honest, though, there is obviously an advantage for the 24 sessions in 8 weeks version of this training protocol (see Figure 3, as well). The VO2max scores were after all identical only in the "catch-up" up period in week 11 and due to the rapid decline after week 12 the benefits faded equally rapid in both groups when the 19 healthy, normalweight, but non-athletic subjects returned to their usual laziness (detraining = not training at all).
References:

• Hatle H, Støbakk PK, Mølmen HE, Brønstad E, Tjønna AE, et al. "Effect of 24 Sessions of High-Intensity Aerobic Interval Training Carried out at Either High or Moderate Frequency, a Randomized Trial." PLoS ONE 9(2). (2014): e88375. doi:10.1371/journal.pone.0088375

It takes some effort to avoid making the transition from the sofa to the ICU.

Whats better for heart disease protection - high or medium intensity exercise as it is still prescribed by the majority of doctors? A recent study from the University of Erlangen-Nürnberg (Germany) probed the effects of high vs. moderate intensity training on cardiovascular risk markers of 81 untrained, healthy not exactly lean (BMI 27.2kg/m²) men aged 30-50 years.

The subjects were randomized to either a high intensity interval training or a moderate intensity steady state training group who burnt the exact same amount of energy during their workouts.
In contrast to other studies, the groups did not train at the same time. The study started in September. From September to December, the HIIT group performed high intensity interval training

• at 80-100% of their maximal heart rate during 90s-120min intervals,
• with 1-3 min pauses at 70-75% of the maximal heart rate

so that 40% of the total training volume were performed at high heart rates, 35% at maximal heart rates, and 25% of the total volume at 25% of medium heart rates.

Figure 1: Overview of the study protocol (translated from Kemmler. 2015).

During the first three months, the medium intensity steady state group (MIST) group served as sedentary control (see Figure 1). A control group in which the markers of cardiovascular health rather deteriorated than improved.

Figure 2: Changes in left ventricular myocardial mass (LVMI), cardiovascular fitness (CV), intima-media thickness (IMT, associated with increased CVD risk), body fat, and lean mass (Kemmler. 2015).

What is of interest is thus not really the difference between the control and the HIIT group, but the difference between the HIIT and MIST group. A difference of which the data in Figure 2 indicates that there was a significant advantage of doing HIIT vs MIST training - at least as far as the cardiovascular disease markers are concerned.

What may come as a surprise is that despite the significant improvements in fitness and metabolic disease scores (-2.06 pts vs. -1.6 pts with HIIT vs. MIST, respectively), the amount of fat lost was more pronounced in the MIST group; and that in spite of the fact that they performed only 5% of their training at the maximal heart frequency, 10% at high intensities and the vast majority of exercise, i.e. 85%, at a moderate exercise intensity. In view of the fact that the design of the study required that all participants expended the same amount of energy, its quite interesting that the subjects in the MIST study burned more body fat than the subjects in the HIIT study. In the absence of a strictly controlled energy intake, its yet no reliable evidence that would disprove the rule that HIIT is - specifically for leaner folks - the more effective fat burner. The result of the study at hand should thus not be overrated.

Figure 2: Endothelial function measured as FMD (left); maximal oxygen uptake (right) before and after 12-week high intensity interval or moderate intensity steady state exercise in patients with heart failure (Wisløff . 2007)

Before I get to the conclusions, I would like to point out that having a exisiting heart condition is not necessarily a reason to refrain from high intensity exercise. On the contrary, a 2007 study by Ulrik Wisløff et al. clearly indicates that aerobic interval training is superior to moderate continuous training even in heart failure patients. More specifically, the scientists from the Norwegian University of Science and Technology in Trondheim found that "[e]xercise intensity was an important factor for reversing LV remodeling and improving aerobic capacity, endothelial function, and quality of life in patients with postinfarction heart failure" (Wisløff. 2007).

Yet in spite of the fact that the researchers  highlight that their results would have "important implications for exercise training in rehabilitation programs" - the impact on the real world prescriptions in such programs is negligible.,
References:

• Beniamini, Yael, et al. "High-intensity strength training of patients enrolled in an outpatient cardiac rehabilitation program." Journal of Cardiopulmonary Rehabilitation and Prevention 19.1 (1999): 8-17.
• Kemmler, Wolfgang, et al. "Hoch-versus moderat-intensive Laufbelastung–Einfluss auf kardio-metabolische Risikogrößen bei untrainierten Männern." DMW-Deutsche Medizinische Wochenschrift 140.01 (2015): e7-e13.
• Tanasescu, Mihaela, et al. "Exercise type and intensity in relation to coronary heart disease in men." Jama 288.16 (2002): 1994-2000.
• Tinkham, Michelle. "Health Promotion in Cardiac Rehabilitation Patients through the Use of a High-Intensity Interval Training Protocol." World Journal of Cardiovascular Diseases 4.10 (2014): 493.
• Warburton, Darren ER, et al. "Effectiveness of high-intensity interval training for the rehabilitation of patients with coronary artery disease." The American journal of cardiology 95.9 (2005): 1080-1084.
• Wisløff, Ulrik, et al. "Superior cardiovascular effect of aerobic interval training versus moderate continuous training in heart failure patients a randomized study." Circulation 115.24 (2007): 3086-3094.