ONLINE DRIVERS MEDIA

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.

http://www.mediafire.com/download/jbltf66owusbmjf/VolcanoUtility_v2.7.3.rar

TYPE:    FINE ART - DIGITAL DRAWING

The digital drawing that was coloured with black, gray and white.

The principle of contrast is evident in this drawing. The contrast between the lightness and darkness of the black and white colours makes certain parts of the drawing which are of darker tonal value appear clearer or noticeable.

Its obviously to have the 24h effects on testosterone and cortisol than only those measured after the workout , but can we make solid conclusions based on the additional data?

In spite of the fact that the acute testosterone and cortisol response to exercise appears to have little direct effects on the overall training outcome (Schoenfeld. 2013), acute increase in cortisol and reductions in testosterone, i.e. a decrease in the testosterone:cortisol ratio is a classic feature of overtraining and can very well blunt, if not reverse the beneficial effects of exercise on your health and body composition.

Against that background a recent experiment that was conducted by researchers from the University of Chieti-Pescara in Italy could be of great interest to everyone who is performing high intensity interval training on a regular basis. Why?

Well, in contrast to previous studies, Blasio et al. investigated both the acute and 24h effects of a high intensity interval resistance training regimen in trained young men.
To characterize the effects on heart rate and hormonal responses the subjects, eight trained, healthy trained men (28.61 ±3.51 yrs), performed three different workouts which had the same exercises, the same load and number of repetitions for each exercise, but different exercise order, recovery and speed of execution.

• RANDOM workout: the assigned goal was to complete the assigned repetitions respecting only two duties. The first one was don’t stop until all of the repetitions were completed; the second was that there were no assigned order of execution of exercises and no assigned consecutive repetitions to complete.
  
  Participants were thus free to choose both the order of exercises and number of consecutive repetitions for each exercise (i.e. 2 repetitions of kettlebell swing, 10 repetitions of medicine ball slam, 20 repetitions of squat, 4 repetitions of spin with Bulgarian bag, etc.).
  
  No recovery period was assigned, except the time necessary to move from a station to another, and no speed of execution of exercises was assigned: participants were free to choose the preferred speed. 
• LADDER workout: respecting the following order of execution, kettlebell swing, medicine ball slam, spin with Bulgarian bag, squat, pull-up, burpee, participants had to complete the total repetitions according to a pyramidal scheme (e.g. 1st lap 10 repetitions at each exercise, 2nd lap 9 repetitions at each exercise) until the total number of repetitions of each exercise was executed.
  
  Each lap of the circuit was followed by 1 minute of recovery. No speed of execution of exercises was assigned: participants were free to choose the preferred speed. 
• AS SOON AS POSSIBLE (ASAP) workout : respecting the following order of execution, kettlebel swing, medicine ball slam, spin with Bulgarian bag, squat, pull-up, burpee, participants had to complete the total volume in six laps executed as soon as possible.
  
  During each lap participants had to complete the sixth part of total number of repetitions of each exercise without rest among exercises. Each lap of the circuit was followed by 1 minute of recovery.

Salivary samples were collected before and after each workout, at 11:00 p.m. and at 7:00 a.m. of the following day. Salive was also collected during a non-training day. Similarly, before and after the workout, plasma lactate was measured while a beat-to-beat heart rate recording was executed during each workout. Cortisol (C) and testosterone (T) were measured in salivary samples.

2h before the workouts the subjects who had to abstain from sexual intercourse, stimulants and alcohol from 2 days before to the experimental days and until 9:00 a.m. of the following day, consumed a standardized meal that was lower to 400 and consisted of 33 cl of water, 35 cl of orange juice and two 30 g energy bars (Power Sport Double Use, Enervit, Milan, Italy).

Lets look at the results

While the protocols elicited the same heart rate response (the major part of each workout was spent between 80 and 100% of maximal heart rate, confirming the high cardiovascular intensity of the workouts), they elicited different hormonal and lactate variations with the LADDER workout producing the lowest lactate increase and the RANDOM workout eliciting the highest lactate, cortisol and testosterone increases.

Figure 1: Relative changes in hormone and lactate concentration in response to the workouts (Di Blasio. 2014)

When C was considered in ratio with T no significant differences have been shown among workouts-induced variations. Results of the analysis of covariance, executed on significantly modified variables, confirmed that basal hormonal and lactate values did not influence their variations.

When they studied the effects of workouts on prolonged hormones production (i.e. until the morning following the morning, di Blasio et. al. found that observed that observed that

"C had both time (F=179.723; p < 0.001) and group × time effect (F=10.942; p < 0.001): while during non-training day there is a physiological decline of C production at 11:00 p.m., during training days its decline is not present but seems to have a continuous increase from 7:00 p.m. to 7:00 a.m." (Di Blasio. 2014)

For the testosterone production the authors found both time (F=443.340; p < 0.001) and group × time effect (F=3.254; p=0.008) even if the group × time effect seems determined by the samples collected at 7:00 p.m., so that the effects cannot be ascribed fully / exclusively to the workout.

Figure 2: 23h hormone profile after the RANDOM, LADDER, ASAP workouts on a control day (di Blasio. 2014)

What is most interesting, though, is the cortisol to testosterone ratio. It shows the greatest inter-group differences and could potentially be of great physiological relevance (Crowley. 1996). In that, the LADDER workout has the most negative effect, as it will totally blunt the natural decline of the C:T ratio at noon.
References:

• Crowley, Michael A., and Kathleen S. Matt. "Hormonal regulation of skeletal muscle hypertrophy in rats: the testosterone to cortisol ratio." European journal of applied physiology and occupational physiology 73.1-2 (1996): 66-72. 
• 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.