Adelfo Cerame: Intermittent Carbohydrate Modulation as a Stepping Stone Towards an Anatomy Chart Physique

Adelfo's goal is to look like an anatomy chart. Now, I don't know about you, but I have seen dozens of anatomy charts that reveal less details of the human physiology than this side-shot which was taken only three days ago.

If you read the headline of today's SuppVersity article, first, you will already know that this is not day 4 of the SuppVersity Exercise Science Week, but (finally) another of Adelfo Cerame's guestposts, here at the SuppVersity. You don't have to worry, there's going to be at least some exercise science in the SuppVersity Science Round-Up, which does (business as usual) air on 1PM (EST) live! on the Super Human Radio Network. So, if you want to be among the first to hear the latest about

• the ameliorative effect of no more than 3g of glutamine on skeletal muscle damage and reductions in immune functions, when you're training like a maniac (learn more about glutamine)
• the superiority of protein blends with respect to net protein retention and why the way most protein supplementation studies are designed has brought about an overreliance on whey protein and a questionable "post-workout window of opportunity" (suggested read: "Opening the Anabolic Barndoor With the Key of Science")
• what percentage of track and field athletes would consider using performance enhancing drugs, if they had the chance and how side effects and the possibility of being busted would influence their decisions (suggested read: "The Brocebo Effect")
• gluten degrading bacteria most of us already have in heir guts and/or mouths and how they could help fight celiac and co. (learn more about gluten & co)
• the importance of doing both, cardio and weight lifting for anyone who's interested in optimal heart health (suggested read(s): "Weights or Cardio, What Comes First?")
• the fat burning effects of sildenafil and how it's combination with EGCG from green tea may turn viagra into an anti-cancer drug (read more about viagra & natural alternatives)

... the podcast, which will be part of tomorrow's Seconds is not really an option ;-) That being said, I have already taken up way too much room in Adelfo Cerame's SuppVersity guestpost - it's high time to make room at the SuppVersity's "writer's desk" ;-)

Adelfo Cerame is back in the house

Well, after a short hiatus from SuppVersity (a well excused one by the way), I’m back to continue my responsibilities of making my guest blogs every other Thursday anin order to share my experiences with the SuppVersity readers as I continue my journey through the world of fitness, nutrition and physical culture ;-)

For those of you who have not been following Adelfo's blogposts right from the beginning: You can read up on his amazing and truly inspiring story how, he got injured and turned it life around in his very first SuppVersity post.

The reason I have been a bit inconsistent with my guest blogs the past few weeks was - as some of you may rememeber - the final weeks of school before the graduation, when I had to learn, juggle two part time jobs and prepare for my upcoming bodybuilding competition in March '13. Not that I’m complaining, I love what has been put on my plate as of late and I’m definitely not going to take it for granted. Still, I am honestly happy that the storm is over now, that I'm finally done with school and have accomplished a goal that I set for myself 4 years ago, when I realized what my calling was and made the decision to go back to school and finish my degree in nutrition science. So now that school is done I can really focus on personal endeavors and other goals I have in mind. - with the first and most obvious one being the dang overall at the show in Florida, so I can finally earn my pro card to become an IFBB wheelchair pro.

I’ve been chasing this piece of paper for a while now and fell short twice last year to two worthy competitors. And as bad as I want that title, I know it’s not priority and never have and never will hold that title on a pedestal to where it becomes my main focus in life. It's my passion, yeah, but in the end it’s just bodybuilding, and not that important when I compare it to other aspects or priorities in my life…

Don't get it twisted, though! I am a competitor ...

.. and I will bring my “A+” game this March, and feel that I’ve made all the necessary adjustments and right moves to put myself in that position. This year I’ve surrounded myself with a great support system of friends, family, mentors, coaches and teammates that have motivated and pushed me physically and mentally to better myself from last year and to put me in a great position to have a shot at that thing again.

Figure 1: Comparison shot this vs. last contest prep back double biceps(img. Adelfo Cerame. 2013-13)

I’ve noticed some significant changes in my physique this year… I’ve been able to put on a tad bit more size especially in my lower back, I’ve been able to add some thickness to it and just might be able to bring out that Christmas tree that I’ve always been looking for on previous preps.

Full, pumped and yet still more defined - what more can you ask for?

In case you don't remember the full story, here is how Adelfo Cerame finally turned his 3-year love and hate relationship with carbs into a highly appreciated ergogenic & delicious friendship (read more)

The biggest difference that I notice is yet that I’m a lot fuller and that despite the fact that my conditioning is a tad better than at the same timepoint during my last prep. And If you’re wondering what adjustments I’ve made this year to make that difference? I’m guessing it’s the higher amounts of carbohydrates I’m consuming this year. That, and the higher training volume I am thus able to sustain. Combined with an increased frquency in body part specific training and the minimal amount of cardio, I've been doing throughout my prep, I was able to keep my overall carbohydrate intake at 150-200g per day, which is - according to my own previous standards, almost hillariously high. I have to thank my coach Alberto Nunez for convincing me to give this high carb moderate-to-low fat approach a try. It has worked out perfectly and according to Alberto, it's also going to help me finally bring in the conditioning and fullness, I may haave been lacking on my previous shows.

I feel that I’m way ahead of schedule from where I was at last year. And from the conversations that coach Alberto and I had; he told me that we haven’t even begun to get serious yet. Lol. So if that’s the case, then from this point on, I’m pretty curious and excited to see for myself how much further I can push my body so I can really achieve that disgusting anatomy chart look ;-)

"Bring on those homemade cheeseburgers, slow churned ice, and poptart pastries!"

Learn more about the RPE routine Adelfo used earlier in his prep

The picture Adel edited in right on top of the article was taken on Monday, when I was exactly 7 weeks out and on the last couple of days of an intermittent 3-week intensive dig at only 100g of carbs/day coach Alberto put me on. As of Wednesday (yesterday), we have started to slowly bring the carbs back  up on regular days and refeed days (WOOOO!!! Right in time for Superbowl on Sunday). Based on what I gather from the weekly evaluations that I get from Alberto, he feels that my body is lean enough to really benefit from an increase in carbohydrates, which will now after this intermittent low carb period be directed right where they belong - into the muscle! So bring on those homemade cheeseburgers, slow churned ice, and poptart pastries! It’s time to get serious!  Oh… Also bring on the fruits and vegetables! Can’t forget about those!

Well that’s all for this week folks! I’m glad to be back on a more consistent level from now on. And please feel free to leave comments below, positive or negative I will try to respond to all of them! Thanks for your on-going support :-)

Fasted Cardio & Beyond - Optimal 24h Fatty Oxidation: How It Works, Why It Works & Why It Still May Not Be Worth It

Photo of a typical disciple of the cult of the "fat burning zone".

Day 3 of the SuppVersity Exercise Science Week and for some of you maybe about time to have breakfast... hold on, breakfast? But shouldn't you work out before breakfast? I mean this whole cardio in the morning business you have taken up lately is all about doing it before, not after breakfast isn't it? You grab your WIFI-connected iPhone tune in to the Super Human Radio morning cardio mash-up and hop onto your cycle ergometer, treadmill, rowing machine, elliptical, spinning bike, stepper, or whatever else you may be using  - no breakfast no intra-workout supplement - at least no carbs, right? Ah, and of course you are going to work out at the highest intensity possible, to burn more fat later on, after all, you are no disciple of the cult of the "fat burning zone", right? Right! And still you have your doubts, hah?

Now, I can't tell you whether the above has anything to do with your morning routine. What I can tell you, however, are the long and short on 24h energy expenditure by summarizing and expanding on some of the main findings of a recent paper by Kaito Iwayama and Kumpei Tokuyama, two young scientists from the Graduate School of Comprehensive Human Science at the University of Tsukuba (Iwayama. 2013). 

Let's start with the "short", then

I guess you will be familiar with the term "metabolic chamber". That's a small room, where you, as a scientists, lock your subjects up in order to monitor their energy metabolism with your fancy electronic equipment and analytical methods for a prolonged period of time (usually 24h). As Iwayama and Tokuyama point out in their latest paper this technique has long been and in fact still is considered the gold standard as far as 24h energy expenditure measurements are concerned.

"During the last 10 years, experiments with this method have raised interesting observations such as: 1) exercise intensity has no effect on 24 h fat oxidation, 2) exercise has little, if any, effect on 24 h fat oxidation, and 3) exercise before breakfast increases 24 h fat oxidation."

Just in case you are one of those guys / gals who don't read quotations, we are going to spend the major part of today's contribution to the SuppVersity Exercise Science Week recapping what "the short" is telling us about your morning, afternoon and/or evening efforts to lose body fat and extend it into "the long" by adding references an examples, so don't worry.

I. Exercise intensity has no effect on 24 h fat oxidation

If you really want to maximize fatty acid oxidation while do a HIIT session before  a lengthy steady state aerobics.You should be aware though, that we are talking about relative increases, here (read more)

We all know that the amount of energy your body consumes during physical activity will depend on the "workload", which is defined as the mathematical product of force x way. In that, the force during a lift would be gravity g x mass of your weight. For a 10kg weight, this would yield a force of 100N[ewton], let's say you lift that weight from the ground into a hight of 1m. In that case, the workload you applied would equal 100N x 1m = 100Nm. If you move a larger weight, say 20kg, for example you would have done twice as much work... it's as easy as that, but unfortunately pretty useless when it is applied to the human human body. While it may still make sense to compare "work-matched" workouts with each other, the outcome in terms of the energetic demands a "10,000Nm bodybuilding workout" will produce, is very different from that of a "10,000Nm O-lifting workout", let alone a "10,000Nm marathon run". The relation between work and energy physicists often try to explain by stating that "(mechanical) energy is a measure of the ability to do work" is too simplistic to work (all puns intended) out in exercise physiology.

If we had a phyiscal model that described what happens in your body down to the level of the individual cell, things would be different. Currently, however, we are missing 99% of that model, so that we have to find other ways to measure the exercise induced and basal energy expenditure - and this is where the metabolic chamber comes in. It allows scientists to measure the energy expenditure independent of any workload calculations and does even allow for a quantitative estimation of where that energy is coming from, namely from fats or carbohydrates (and glyconeogensis). From previous studies, which availed themselves of this amazing piece of equipment, we know already that

• for low-intensity exercise, below 40-50% of the VO2Max the energy supplied is primarily from oxidation of plasma free fatty acids
• for intensities ranging from 50% to 95% of the VO2Max, the ratio of glucose to fatty acid oxidation, the so called respiratory rate is constantly increasing; in that, a RER of 0.8 tells us that we are fuelling 80% of our energy demands from glucose, already 
• for intensities in the 100% of VO2max range, the RER approaches 1.0 meaning that our bodies satisfy almost 100% of their energetic demands by the oxidation of carbohydrates (glycogen => glucose)

This has, as we have already seen in yesterday's 2nd post in the SuppVersity Exercise Science Week, led to the commonly held belief that low-intensity exercise would be better than high-intensity exercise for increasing fat oxidation and, thus, fat loss (Hill. 1992).

The notion that what happens after your workout is about as, if not more important than the energy, let alone fatty acid expenditure during a workout has unfortunately not reached public awareness, as of yet.

That's a pitty, right? Well at least as far as the rate of fatty oxidation is concerned, I would not be too sure about that, as previous studies suggested that the amount of fat that's oxidized in the post-exercise recovery period following isocaloric exercise performed at high (65% VO2max for 1 h) or moderate intensity (45% VO2 max for 86-89 min) is identical!

"First, consistent with the literature, fat oxidation during exercise was less for high-intensity exercise than for low-intensity exercise. Second, the increase in fat oxidation during the post-exercise period seemed to be greater after high-intensity exercise, although the difference did not reach statistical significance. Third, the sum of fat oxidation during the exercise and post-exercise periods was not significantly different between the two exercise conditions of different intensity." (Iwayama. 2013)

Aside from these fundamental insights, the studies on which this rationale is based on did also provide another intriguing, yet somewhat discriminating insight:

• While women have the edge as far as intra-workout fatty acid oxidation is concerned, their ability to burn fat during rest is low compared to their male counterparts (Hanerson. 2007). According to Iwayama and Tokuyama, this biological fact may also explain why women are typically less successful in achieving their fat loss goals in response to exercise only interventions than men (Ballor. 1991; Donnelly. 2005).

Now think about this for just a second, take a look at the data in figure 1 and now tell me: "What's the best way for women to maximize fatty acid oxidation?"

Figure 1: Fatty acid oxidation in male and female subjects in the 24h period after low /40%VO2Max) and high (70% VO2Max) intensity workouts with a matched energy expenditure of 400kcal; the data was measured in a metabolic chamber by Melanson et al. ten years ago (Melanson. 2002)

Right! That's low intensity long duration workouts. Those will allow them to burn more fat (on a relative basis) during the workout without experiencing the bump in post-exercise fatty oxidation rates Melanson et al. observed in their 2002 study. And yet, neither I nor the researchers who wrote...

“Given that time is a limiting factor for most individuals, if the goal of exercise is to maximize fat oxidation to better regulate body fat mass, then exercise should be performed at the highest intensity that can be comfortably maintained.” (Melanson: 2002)

...would recommend that our female or male readers stick to "training in the zone", only. You will learn why this is the case later in the article. For the moment, I do yet want to address the second and third assertion from the initially cited three-item list, first.

II. Whether you exercise or not has no influence on 24h fatty acid expenditure

At first sight this sounds, bullocks. I mean, it should be out of question that you burn more fat, when you work out, than when you lie around on the couch, right? And in this case you are right - at least, if you include the additional fatty acid oxidation during the workout in your calculation and discard things like standard deviations and statistical non-significance.

Table 1: Independent effects of exercise intensity (low vs high intensity) and exercise itself (control vs exercise) on 24h fat oxidation have been assessed under energy-balanced study design (except for the Lausanne
study, in which subjects were in a state of negative energy balance); "no" denotes not significantly different (Iwayama. 2013)

And still, under "macronutrient-balanced condition[s"], which are a necessary prerequisite to measure the independent effect exercise has on 24-h fat oxidation without having a negative energy balance or the ingestion of some sugary intra-workout drinks skew the results towards higher, respectively lower rates of fatty acid oxidation (cf. Bielinski. 1985; Dionne. 1999).  Exactly this is what has been done in a series of metabolic chamber experiments, Iwayama and Tokuyama reference in their paper (see table 1) to support their assertion that

"fat oxidation on days with exercise doesn’t differ from sedentary control days when the energy balance is maintained." (Iwayama. 2013)

While the results are anonymous it's clear that they do not support the notion that working out would exert an independent effect on the amount of fatty acids that are "burnt" within the same 24h period the exercise bout was conducted in.

Still, as Iwayama and Tokuyama point out, "statistically not significant" does not equate non-existent. You just have to take another look at the data from the Melanson study in figure 1 to see that there is a definitive trend towards increased fatty acid oxidation in the exercise compared to the control condition.

The difference between significant findings and "unreliable" trends reminds me of a previously not mentioned, yet potentially significant disadvantage of an otherwise highly reliable method to measure the total energy expenditure of human beings: The restricted number of participants in studies using indirect calorimetry with a room-sized respiratory chamber. The "trend" in the Melanson study, for example could well have reached statistical significance with a greater number of study participants; and the same obviously goes for the rest of the studies in table 1, as well. Still, as we are going to see in the conclusion, an over-reliance on statistics is not the only reason why "not working out" is not an option. Before we tackle that, I do yet want to address the last point on our check-list.

Exercise before breakfast increases 24h fat oxidation
 
This third and last of the initially cited assertions does not only take us back to the "breakfast problem" from the introduction, it's also the only assertion that's in accordance with the mainstream understanding of the role of exercise in the process of fatty acid oxidation. "Working out on empty", "cardio in the morning" and so on and so forth - you know the whole spiel and actually you do also know the scientific explanation of why working out like this does actually work out. No idea? Well, I did provide part of the explanation in the previous paragraph, already, when I mentioned the potential impact of fasting and feasting on the experimental results.

Gluconeogenic as most of them may be, EAAs still increase GLUT-4 and thus glucose uptake by the muscle - a true yet overlooked nutrient partitioner, so to say (read more)

Did you know that the two essential L's, i.e. leucine and lysine are the only amino acids that cannot be used for glyconeogenesis by the liver? Contrary to the rest of the pack, they are exclusively ketogenic and can only be transformed into ketone bodies.

In view of the built-in glucose repartitioning effect of essential amino acids (EAA), this is yet no reason to be worried about... well, unless you are on a ketogenic diet and make the standard mistake of each and every fitness fanatic to turn a high fat diet into a high protein diet without carbohydrates, so that you end up living on the little glucose your liver is able to produce without ever getting even close to real ketosis.

I see it dawns on you: It's the sheer necessity of burning fat for fuel, in the absence of other, more readily available nutrients like carbs, or glucose the liver would generate from proteins or aminos, for example. So, in the course of your workout you are actually burning more fat than you would if you had breakfast before hopping onto the treadmill, bike or elliptical, but what about the time thereafter?

Figure 2: 24h energy expenditure and fatty acid oxidation (both in kcal/min) on days on which cardio (60min 50% VO2max light steady state) was done before (filled circles) or after (open circles); data based on an unpublished from the same group (Shimada. unpublished)

As the data in figure 2 tells you, there is no difference in the following hours and - what's even more important - the total energy expenditure was identical - 2594kcal/day vs. 2589kcal/day in the before and after breakfast trial, respectively. In addition to that, a detailed analysis of the unpublished study by Shimada et al. the above data was taken from, does also show that

• working out before breakfast reduces the energy expenditure in the time before lunch --  over the whole period the subjects burned about 500 kcal less, when exercise was performed before breakfast
• working out before breakfast burns more glycogen and increases non-oxidative carbohydrate storage during / after breakfast -- with the carbohydrate content of the breakfast being used for glycogen repletion, this does in fact lead to another increase in fatty acid oxidation, simply because the alternative fuel, namely the carbs are not oxidized, but stored

So, 2x thumbs up for cardio before breakfast - at least in the short run and when your goal is to maximize fatty acid oxidation, but ...

Is maximal fatty acid oxidation even what you should be aiming for during a workout?

I guess you will already have read between the previous lines that my answer to this question is a definitive "no". Moreover, most of you are so clever and have been following the SuppVersity posts for so long that they could come up with their own arguments against an overemphasis of intra-, post and total 24h fatty acid oxidation, when getting lean and healthy is your goal. And probably, some of them are even identical to mine:

• Firstly, and most importantly, burning fatty acids for fuel does not equate fat loss. If you follow a real ketogenic diet (not one with tons of protein in it), you'll burn (almost) exclusively fat, but even under these "extreme" conditions most of the fat will come from the fat you eat, while the small amount that's actually taken from your hips, buttocks and whatever, will be restored unless you are in a caloric deficit, when your fatty acid oxidation will increase anyways.

• 

  The "Fat Loss Support Routine" from the Step By Step to Your own Workout Routine guide would be one example of how you can structure your weekly workout regimen to cut body fat.

  Secondly, many of the metabolic benefits of exercise are closely related to the act of glycogen depletion. This is particularly true for the increase in GLUT-4 expression and consequent improvements in muscular glucose uptake, burning only fat for fuel during a workout is thus a questionable ideal.
• Thirdly, working out "in the zone" may burn the most fat but won't have the conditioning effects high(er) intensity workouts have. While obese individuals and people who have been sitting around their whole lives will see improvements in their VO2max (and in the long run their heart-health), anyone who is not totally unconditioned misses out on the structural changes in the musculature, and as you've learned on day one of the SuppVersity Exercise Science Week adipose tissue, as well.

In short, the importance of burning fat for fuel is so overrated that exercise prescriptions that are based on the paradigm of maximal fatty acid oxidation are at least suboptimal for health, fitness and physique purposes. Some people, I guess, would probably even go so far to say that they do more harm than good. I for my part leave it up do you to decide whether you join sides with my carefully worded or the more extreme version of this conclusion, or - and this would be your good right - to wholeheartedly disagree with both of them.

References:

• Ballor DL, RE Keesey. A meta-analysis of the factors affecting exercise-induced changes in body mass, fat mass and fat-free mass in males and females. Int J Obes. 191; 15: 717-726.
• Bielinski R, Schutz Y, Jéquier E. Energy metabolism during the postexercise recovery in man. Am J Clin Nutr. 1985;42: 69-82.
• Dionne I, Van Vugt S, Tremblay A. Postexercise macro-nutrient oxidation : a factor dependent on postexercise mac-ronutrient intake. Am J Clin Nutr69: 927-930.
• Donnelly JE, Smith BK. Is exercise effective for weight loss with ad libitum diet? Energy balance, compensation and gender differences. Exerc Sport Sci Rev. 2005; 33: 169-174.
• Henderson GC, Fattor JA, Horninig MA, Faghihnia N, Johnson ML, Mau TL, Luke-Zeitoun M, Brooks GA. Lipolysis and fatty acid metabolism in men and women during the postexercise recovery period. J Physiol. 2007; 584: 963-981
• Hill JO. 1992. Physical activity and energy expenditure pro-ceedings: national task force on prevention and treatment of obesity. Physical activity and obesity conference – NIDDK, pp.60-65.
• Iwayama K, Tokuyama K. Exercise in a metabolic chamber - Effects of exercise on 24 h fat oxidation. J Phys Fitness Sports Med. 2013; 1(2): 307-316.
• Melanson EL, Sharp TE, Seagle HM, Horton TJ, Do-nahoo WT, Grunwald GK, Hamilton JT, Hill JP. Effect of exercise intensity on 24-h energy expenditure and nutrient oxidation. J Appl Physiol. 2002; 92: 1045-1052 
• Shimada K, Yamamoto Y, Iwayama K, Nakamura K, Ya-maguchi S, Hibi M, Nabekura Y, Tokuyama T (unpublished observation).

Exercise Intensity, Oxidative Damage, Glycogen Depletion and Supercompensation. Plus: Optimal 0-12h Post Workout Glycogen Repletion Protocol For Performance Athletes

Do they train at the right intensity and what is the right intensity? What's right, anyway? Lot's of questions, tons of words, a couple of answers and some interesting revelations in today's 2nd article of the SuppVersity Exercise Science Week.

This is day 2 of the SuppVersity Exercise Science Week -- another day, another news. After you've learned about the various mechanisms by which exercise will induce structural changes to your beer belly, lover handles and other problem and non-problem areas, in yesterday's first article of the SuppVersity Exercise Science Week, today's post does actually pick up on the notion of the superiority of high intensity exercise and takes a look at how low vs. high(er) intensity endurance exercise effects the antioxidant defense system of the body. This will lead us to an issue that was once considered to be a downside of high intensity workouts: their notoriousness to deplete muscle glycogen, of which we now know that it is actually one of their fundamental strengths. When we are done with that, it's about time for the sweet dessert. The latter is going to have three courses and will help you achieve maximal muscle glycogen supercompensation after a workout.

Where does the idea that you better work out at low intensities come from?

I have made it a (enervating?) habit to include a small reminder of the "dark side" the same beneficial exercise stress that elicits muscle gains, fat loss, and improvements in conditioning and overall health can have, whenever you don't allow for adequate recovery and nutrient supply, in almost every of the articles pointing to the superiority of high intensity training vs. training in the comfort zone (click here to read up on a couple of these articles).

Figure 1: A comprehensive study by Carey revealed that the increase in ratio of fat-calories to total energy ependiture, when you train in the "fat burning zone" is 3% for men, 5% for women. The total amount of fat is yet higher above the "zone" and, most importantly, the current research suggests that the glycolytic effect, which is inversely related to the relative fat oxidation, is what triggers most of the beneficial metabolic effects.

The question, how pronounced the differences actually are, on the other hand, is not just rarely addressed here at the SuppVersity, it's also something scientists are still trying to elucidate. Usually you will see creatine kinase, an accepted marker of skeletal muscle damage being accessed before and after a workout, but as I have pointed out in previous articles, my personal experience tells me that an intense strength workout is - despite its ability to increase CK levels in training noops by up to 10,000% (x100, no typo - eg. Sewright. 2008) less prone to send you down into the abyss of the Athlete's Triad, than working out for hours (worst on a daily basis) in the purported fat burning zone, i.e. the target heart rate where you'll satisfy the greatest part of your metabolic demands from body fat and of which Carey has been able to show in "relatively fit" male and female runners that it is at least 30% below the anaerobic threshold (AT: 155Hb/min; Fat Burning Zone: 105Hb/min; cf. Carey. 2009).

Aside from that, Carey's results also support the observation Wilson et al. formulate in their recent review of concurrent training, namely that "most dramatic loss in fat mass occurr[s] from moderately high to very high intensities" (Wilson. 2013). In this context, the scientists' definition of "moderately high" is already way beyond the alleged zone of maximal fat loss. "Dramatic" is by the way also an excellent attribute for the 4.5x higher fat loss effect Wilson et al. computed for the highest vs. medium exercise intensities  (91-100% vs. 61-80% HRMax) based on the data they collected for their review.

"Better fat loss, w/ high intensity, aha... but isn't that at the cost of increased oxidation?"

In view of the fact that will be coming back to the issue of "optimal fat loss" later this week, anyway, I guess it's best we get back to the topic at hand and take a look at the toll endurance workouts at different exercise intensities actually take on your antioxidant defense system. As mentioned before, it is still far from being certain which markers you would actually have to measure to get a clear picture of how much stress and damage a given exercise regimen is inflicting. Compared to the creatine kinase levels, the measurement of markers of the activity and status of the anti-oxidant defense system, which was the main outcome variable in a study by Takahasi et al. does yet appear to be more relevant - if not with respect to exercise performance than certainly with respect to overall and metabolic health.

Figure 2: Changes in myeloperoxidase, heart rate, rate of perceived exertion and trolox equivalent antioxidant capacity (TAEC) in eight healthy and untrained males aged 22.6 ± 1.4 years (mean ± SD), with 67.7 ± 4.1 kg body mass, 175.2 ± 3.7 cm height, and 15.1 ± 2.2% body fat after 20min of exercise at 70%, 100% or 130% of the anaerobic threshold.

On three separate occasions, the Japanese researchers studied the effect of different exercise intensities. The latter ranged from 70% over 100% to 130% of the anaerobic threshold and would thus represent exercising in the "fat burning zone" at moderately high intensities and high intensities.

The first thing the scientists registered was that the pre to post increase in oxidative stress at the low and medium intensities did not even reach statistical significance. The "pro-oxidative" effects of the high intensity trial, on the other hand, were statistically significant. Yet, if you look at the actual data in figure 2, I'd guess that you will - just like me - ask yourselves what all the hoopla was about: The absolute differences are mediocre, at best and their physical not statistical significance is highly questionable; and that's not just because the trolox equivalent antioxidant capacity (TEAC) actually increased from pre to post exercise (from allegedly lower pre levels in the 130% trial than before the other exercise tests.

Training at higher intensities is demanding, yeah... but not overtly demanding!

Now, all these statistical significances were calculated on a pre vs. post basis. Intensity-specific differences on the other hand were not observed. We do therefore have to be cautious not to misinterpret the scientists very own and actually non-judgmental conclusion ...

"We found that plasma concentrations of d-ROMs increased as a result of 20 min of exercise above AT. Exercise above AT also increased enzymatic and nonenzymatic antioxidant capacity. On the other hand, there was no effect after 20 min of exercise at 70–100% AT, suggesting that exercise under the AT level does not produce oxidative stress damage." (Takahashi. 2013)

... as an advice to stick to "exercise under the AT [anaerobic threshold]". There are already way too many people wasting their time on the cross-trainers of this word - don't join them, but don't overexert yourself either.

The "Iranian HIIT Solution" has already proven that a minimalist HIIT regimen in the form of 3x200m sprint sessions per week can make all the difference esp. for someone who has never participated in regular activity before (read more).

A single bout of intense exercise leads to significant improvements in glucose and lipid metabolism in obese individuals, that's the latest result of another very recent study that was conducted at the University of Glasgow (Whyte. 2013). The protocol consisted of nothing more than " four maximal 30-s sprints, with 4.5min recovery between each (HIIT), or a single maximal extended sprint (HIT) matched with HIIT for work done". With 20% higher mean power during the sprints the temporary intensity was higher, in view of the fact that the overall exercise duration was longer and there was no time for in-between sprint glycogen replenishment. Thu it's actually not surprising that the acute increase in insulin sensitivity did reach statistical significance only after the extended sprint session. The overall metabolic benefits (non-significant improvements in glucose and lipid metabolism) on the day after, of which we can assume that they were not brought about by the immediate reduction of muscle glycogen, were identical for both conditions, while the the total and relative increase in fasting fatty oxidation was more pronounced after the HIIT protocol (total: 63% and 38%; relative, based on RER: 11% and 8% ).

Figure 3: Oxidative stress and glycogen depletion are important triggers of the beneficial effects of exercise on glucose metabolism ( (based on Kawanaka. 2013).

If we go a step further and think about whether or not oxidative stress is actually something you would want to avoid at all costs, the figure from Kentaro Kawanaka's recently published alongside review of the regulation of glucose transport in skeletal muscle during and after exercise (see figure 3) can help us make up our minds. If you take a look at my mark-ups it's plain to see that ROS production and the increase in AMP (quasi "used ATP") and decreases in ATP and phosphocreatine (PCr) are major signals for the activation of a hitherto incompletely understood signaling cascade that results in increased glucose uptake by the muscle. That's the same glucose uptake, by the way that makes the most significant difference between the "normal" and, insulin-intolerant individual and makes an ideal stepping stone to full-blown diabesity (=obesity + diabetes type II).

"So, what exactly is the effect size of these improvements? Are the worth the sweating?"

To illustrate the quantity of these effects, Kawanaka uses data from a 2009 study by Koshinaka et al. who subjected rats to an acute bout of 3x20s "high-intensity sprint interal swimming" and measured muscle glycogen levels and glucose transport at different timepoints in the 16h window after the workout.

Figure 4: Insulin and non-insulin stimulated glucose transport in rat epitrochlearis muscle at rest and 4 hours after cessation of HIIT exercise (left); muscle glycogen repletion and supercompensation after a workout (from Kawanaka. 2013 based on Koshinaka. 2009)

If we take into account that 3h(!) of continuous swimming elicited the exact same improvement in glycogen uptake as those 3x20s all out "sprints", I probably don't have to say it "appears" as if the synergistic combination of brief HI(I)T training and an appropriate diet will be more productive than the endless hours on an elliptical way too many (often unfortunately female) trainees are still performing in the desperate hope to finally shed the fat from whatever problem areas they have or believe they'd have.

Glycogen supercompensation: This is how it's done

There is yet more to the Koshinika study than another confirmation of the usefulness of HI(I)T exercise for fat loss, fitness and fabulous health. The data Koshinaka et al. collected does also tell us something about post workout glycogen repletion. Most importantly (at least in my humble opinion) that the first, immediate post-exercise phase is characterized by a rapid non-insulin dependent increase in glucose uptake. The latter is actually just as high (>5µmol/g/20min; respective data is not shown in figure 4) as the maximally measured glucose uptake in phase II, in the course of which the presence of insulin has a dose-dependent beneficial effect on the total amount of glucose that's going to be shuttled into the muscle (see figure 4, left). With phase III being characterized by saturated (in fact more than saturated) glycogen stores, these observations would suggest that an "optimal" glycogen replenishment protocol would look somewhat like this:

When you increase your calorie intake on a bulk, you better go really high carb + low fat, if lean gains are what you're looking for. This is at least what a 2011 study by Mendes-Netto suggests (read more)

1. phase I: immediately post > fast absorbing carbohydrate source -- what's important during the immediate post-workout phase is exclusively the availability of glucose, insulin the presence of extra high insulin levels is more or less unnecessary
2. phase II: post workout phase (<8h) > high GI carbohydrate source -- once the glycogen levels have reached a certain level the supercompensation process requires the presence of additional insulin, therefore your post-workout meal should not be carb-free or extremely low GI
3. phase III: recovery phase (>8h) > low GI carbohydrate source -- the glycogen stores have already reached higher than baseline levels, the presence of high levels of insulin in this phase would be counterproductive as it would actually drive glucose uptake by the adipose, not the muscle tissue

Whether this maximum glycogen repletion protocol does in fact make sense for everyone is yet another question, though. For someone who trains twice a day, like Arnold, it certainly does. The same goes for endurance athletes looking for maximal performance. If Lance Armstrong, for example, would ever be allowed to compete again, he would best go for a fast absorbing carbohydrate source like Vitargo right after the race, a huge bowl of pasta and some sugary grape juice as his first meal after the race and some slow digesting carbs like a couple of bowls of oats later that day to ensure optimal glycogen levels on the next day of the Tour -- what neither Lance nor you should not forget, though, is to add some protein to the equation, even if building muscle is not your goal, the protein will speed up the replenishment of muscle glycogen (Zawadski. 1992)

"But how important is muscle glycogen, anyway?"

For the average trainee it does yet remain questionable whether or not this protocol will actually yield noticeable benefits. While it is important to replete the glycogen stores, the advantages of doing this as fast as possible are actually not really relevant for someone who trains 3-4 times per week in order to promote health, well-being and a leaner, more muscular (but not freakish) physique. Especially with respect to the latter, the majority of the more recent studies clearly suggests that muscle protein synthesis is, in the short run, not impaired by low levels of muscle glycogen (click here to learn more).

What you should never forget, though, is that your body will interpret chronically low muscle and liver glycogen levels as a clear-cut indicator that you're starving. The results are a reduced metabolic rate and the shut down of "auxilliary" and costly bodily functions such as the reproductive machinery, etc. - and we don't want that to happen, right?


References:

• Kawanaka K. Regulation of glucose transport in skeletal muscle during and after exercise. 2013. J Phys Fitness Sports Med, 1(4): 563-572.
• Koshinaka K, Kawasaki E, Hokari F, Kawanaka K. Effect of acute high intensity intermittent swimming on postexercise insulin responsiveness in epitrochlearis of fed rats. Metabolism. 2009; 58: 246-253.
• Takahashi M, Suzuki K, Matoba H, Sakamoto S, Obara S. Effects of different intensities of endurance exercise on oxidative stress and antioxidant capacity. J Phys Fitness Sports Med. 2013 1(1): 183-189.
• Sewright KA, Hubal MJ, Kearns A, Holbrook MT, Clarkson PM. Sex differences in response to maximal eccentric exercise. Med Sci Sports Exerc. 2008 Feb;40(2):242-51.
• Whyte LJ, Ferguson C, Wilson J, Scott RA, Gill JM. Effects of single bout of very high-intensity exercise on metabolic health biomarkers in overweight/obese sedentary men. Metabolism. 2013 Feb;62(2):212-9.
• Wilson JM, Marin PJ, Rhea MR, Wilson SM, Loenneke JP, Anderson JC. Concurrent training: a meta-analysis examining interference of aerobic and resistance exercises. J Strength Cond Res. 2013 Aug;26(8):2293-307. 
• Zawadzki KM, Yaspelkis BB 3rd, Ivy JL. Carbohydrate-protein complex increases the rate of muscle glycogen storage after exercise. J Appl Physiol. 1992 May;72(5):1854-9.

How Working Out Changes the Morphology of Your Body Fat and Why This Explains that Intensity and Explosiveness Hold the Key to Getting and Staying Lean, Fit and Healthy

Can the guy on the right run away from the bloated macrophage coated fat cells on the left? Today's first post in the SuppVersity Exercise Science Week does hold the answer to this existential question.

Those of you who don't just read, but also think about the headlines of these posts will probably already have theorized about the remote possibility that I could have changed my mind and discarded the original plan to do an "exercise quickie" early this week (see SuppVersity post from Saturday). Now, before you are getting mad at me, let me give you the (as I would say good) reason for doing that: Some, if not almost all of the exercise related studies, I have piled up here are actually too interesting to end up as part of a mash-up. That's particularly true in view of the fact that my time budget during the week does not allow me to discuss them in appropriate detail. So, even if wanted to end up writing >10,000 word posts, this would only work on 48h days ;-)

The solution I came up with is easy and in my humble opinion actually quite cool: The world's first SuppVersity Exercise Science Week! In the course of the next days, I will serve you one or two of the latest studies from the realms of exercise science per day - with the rest (if there is one) being "mashed up" in the Short News on Saturday. Cool? No? Well, bad luck, then ;-)

We will kick off the week with the modulatory effect of exercise on adipose tissue

We all know that exercise is a good way to support and control diet induced weight loss. Specifically for those of us who are already on the lean(er) side of a "divide", where obese is soon going to be the new normal (see "Obese is Going About to Become the New Normal"), it's probably even obligatory, if it's not being skinny fat that's our diet goal. That being said, a recent review of Izawa et al. provides a couple of intriguing insights and links between physical activity and the structural changes our white adipose tissue is undergoing (Izawa . 2013). In this first post of the SuppVersity Exercise Science Week I am going to summarize and expand on some of these points and point towards the implications these more or less recent, in parts pretty geeky and abstract findings have on the way we could, should, or might train:

• Training can increase lypolysis: Compared to subcutaneous fat (SAT), visceral fat (VAT) has a higher lipid turnover. Interestingly, the same high lypolytic rates which render people with high VAT so vulnerable to high levels of blood fats, are also responsible for the comparable ease with which you can shake those unhealthy VAT depots melt away, when you're working out and/or dieting. The fat around the organs is not just the easiest to store, it's also the easiest to access and liberate (Ross. 2000). That this is not a location-specific characteristic, has already been proven. What does yet still have to be elucidated, is when and due to which complex mechanisms the genetic differences between the subcutaneous and visceral fat cells are getting programmed and whether there may be a way to reverse them.

• Training will modulate the growth environment: The maturation of stem cells into SAT, VAT, or BAT (brown adipose tissue) cells appears to be highly dependent the specific milieu in which they are in. The latter, in turn, is characterized by the presence of  various growth factors. The best known and allegedly most important ones belong to the transforming growth  factor (TGF) family. It is their presence that will control whether a stem cell turns into a "brown" = metabollically active fat cell with thermogenic abilities or a regular white one (SAT or VAT). While BMP2- and BMP-4 are responsible for the formation of white adipocytes, BMP-7 drives brown fat cell development. Together with FGF21 another of those growth factors, these proteins determine the fate of pre-adipocytes. Unfortunately, the research on the different ways by which exercise controls these factors is yet still in its infancy. We will take a closer look at what we know already in the next paragraph.

• 

  As you know from the "CLA Destroys Body Fat" post, PPAR-γ downregulation is also the main pathway by which conjugated linolic acid strips mice of almost all their body fat (read more). The exercise induced upregulation of the so-called hypoxia-inducible factor (HIF-1α) appears to do the exact same thing: Suppress PPAR-γ and thus hit the off switch on body fat storage.

  Training reduces WAT size and number: According to a 2004 review of the literature it appears as if exercise training (aerobic) specifically in early life reduces the number and size of WAT in rodent (Stallknecht. 2004). These results have been confirmed in a 5-week study designed that was conducted to elicit the underlying molecular mechanisms only recently (Sakurai. 2010); and the results of the Sakurai study suggest that it is one of our old acquaintances that is to "blame": The peroxisome proliferator-activated receptor-γ (PPAR-γ), a central regulator of adipogenesis! It's inhibition by physical activity is what does the trick. Now, as a diligent student of the SuppVersity you will certainly remember that this is also the main pathway by which CLA, rhein (from rhubarb) and other weight loss adjuvants work their "magic" - a blockade of the PPAR-γ receptor is like hitting the "off switch" on the body fat storage control panel. And who is it who hits that switch? Well, according to the current research it appears that this is the prerogative of the hypoxia-inducible factor (HIF-1α) which is in turn controlled by exercise induced WNT and AMPK signaling.

• Training improves angiogenesis in WAT: While you hear about angiogenesis, i.e. the physiological process through which new blood vessels form from pre-existing vessels, oftentimes in the context of various endothelial pathologies, its induction within the white adipose tissue is actually highly desirable. Scientists have long been speculating that the insufficient wiring of the adipose organ with blood vessels and the subsequent hypoxia are at least partly to blame for the constant inflammation in the ever-expanding fat depots of the obese (Ye. 2009). Since HIF-1α (see previous paragraph) also promotes the expression of vascular endothelial growth factors and their receptors (VEGFRs / VEGFs), its downstream activation by preferably intense physical activity should improve the endothelial wiring of the fat tissue and thus help sooth the chronic inflammation, that's at the heart of many, if not all of the key-features of the "metabolic syndrome".

• Training increases the adipocyte size depended release of adiponectin: In the past couple of months, the adipokine adiponectin turned out to do most of the good stuff (esp. improvements in glucose and fatty acid metabolism), of which scientists previously thought it was the prerogative of leptin. It is therefore important that exercise increases the rate at which a given increase in adipocyte size (obviously in response to fat storage) will increase the release of adiponectin (Miyazaki. 2010). If we use the classic notion of the adipokine as a signal the fat cells use to tell the brain and the rest of the body how much fat remains to fuel its energetic demands, you could say: Working out allows your body to see how much fat you actually got. The physiological consequences of this revelation are increases in lypolysis and fatty oxidation, as well as overall metabolic benefits.

So far for the stuff that will make you look smart, when you parrot it in front of your gymbros. In order to not just look smart, but also be smart -- and in this case train smart -- you will yet also have to know the implications of these revelations and this is exactly what the rest of this article is going to deal with:

• 

  Making HIIT a Hit! learn how in the SuppVersity  Special (read more) and use it to get lean & healthy and, more importantly, stay lean and healthy!

  HIF-1α <> PPAR-γ <> adipocyte crosstalk - an(-other) argument for high intensity exercise: Since the HIF-1α response to a given training stimulus decreases once the body has adapted to the stressor by increasing its exercise capacity (Lundby. 2005). The crosstalk between HIF-1α, PPAR-γ, and your fat cells provide another reason to work out in the higher range of the VO2max continuum and to never neglect the imperative of constant progression (even if it's only a progression of 0.1km/h during your sprints on the treadmill - adaptation means stagnation, if you don't raise the bar appropriately)

• Wnt10B response to stretching - an argument for heavy eccentrics and/or statics to revamp your body (less fat, more muscle!): The findings of Akimoto et al. point towards the existence of another rather strength-training specific contributer to the fat loss and leanness promoting effects of exercise - the stretch-induced activation of the wingless-type (WNT) MMV integration site family member WNT10b, the quasi cousin of an upstream mediator of HIF-1α (Akimoto. 2005). The activation of the WTNs does actually get down to the root of the trouble and will not just inhibit the formation of new fat cells from pre-adipocytes, it will also divert the mesenchymal and not yet specialized stem cells to turn into osteroblasts (bone) or myoblasts (muscle). In fact, research has shown that WNT signaling is a major contributer to both the recruitment of new muscle progenitor cells from the aforementioned pool of yet unspecific stem cells and skeletal muscle hypertrophy (Polesskaya. 2005; Armstrong. 2005).

• 

  You will also benefit from integrating plyometrics into your existing routine - build the Jack of All Traits Workout
  

  The greater WNT response to power vs. strength training points towards the superiority of a plyometrics to get and stay lea: In view of the results of Leal et al., who report a 3x greater WNT gene response to power compared to strength training in their 2011 paper on the effect of different resistance-training regimens on the WNT-signaling pathway, plyometrics, which have way more in common with the power training protocol in the Leal study (40% lighter weights; faster, explosive contractions) than whatever powerlifting routine you may have been thinking of, should be a superior means to stay lean (Leal. 2011)

• Exercise restores your body's fat gauge: If you wanted to pointedly summarize the exercise induced reductions in leptin expression, the associated restoration of leptin sensitivity in the obese, and the increased adiponectin release relative to the increase in fat cell diameter, you could actually say that exercise restores your body's fat gauge. It allows your brain and the other organs to see how much body fat you still got and have them react appropriately. Funnily this is also why you body will, clever as is is, pull the emergency break, whenever your body fat levels become too low (cf. "The Athlete Triad Series").

Did you know that 10% of the fat cells have to be renewed every year? I know this is speculative and we are not talking about ZERO adipocyte maturation here, but what do you think will happen when a fat cell is due and you just hit the off-switch on adipocyte maturation?

A final word of caution: I am well aware that some of you may take this article as justification for training themselves into the ground. So please(!) keep in mind that hypoxia induced WNT10 and stretch induced WNT10b signaling, as well as most of the other fancy stuff you have learned about in the previous paragraphs are stress responses that require adequate recovery periods for the metabolic and growth responses they induce to take effect. Sleep, Eat, Train, Rest, Sleep, Eat, Train, Rest, Sleep, Eat... do you notice something? Yeah, right that's a 3/1 ratio of non-stressful occupations, namely sleeping, eating and resting to a single stressor, i.e. training. In other words, 25% of your result are "made" in the gym, 75% in bed (don't make it too stressful there ;-), in the kitchen and even, when you spend time with friends and family or simply sprawl out on the couch. Think of that, when you're designing your next training routine.

References:

• Armstrong DD, Esser KA. Wnt/beta-catenin signaling activates growth-control genes during overload-induced skeletal muscle hypertrophy. Am J Physiol Cell Physiol. 2005 Oct;289(4):C853-9. Epub 2005 May 11.
• Akimoto T, Ushida T, Miyaki S, Akaogi H, Tsuchiya K, Yan Z, Williams RS, Tateishi T. Mechanical stretch inhibits myoblast-to-adipocyte differentiation through Wnt signal-ing. Biochem Biophys Res Commun. 2005; 329: 381-385
• Izawa T, Ogasawara J, Sakurai T, Nomura S, Kizaji T, Ohno H. Recent advances in the adaptations of adipose tissue to physical activity: Morphology and adipose tissue cellularity. J Phys Fitness Sports Med. 2013:1(3): 381-387. 
• Leal ML, Lamas L, Aoki MS, Ugrinowitsch C, Ramos MS,  Tricoli V, Moriscot AS. Effect of different resistance-training regimens on the WNT-signaling pathway. Eur J Appl  Physiol. 2011; 111: 2535-2545
• Miyazaki S, Izawa T, Ogasawara JE, Sakurai T, Nomura S, Kizaki T, Ohno H, Komabayashi T.  Effect of exercise training on adipocyte-size-dependent expression of leptin and adiponectin. Life Sci. 2010; 86: 691-698.
• Lundby C, Gassmann M, Pilegaard H. Regular endurance training reduces the exercise induced HIF-1alpha and HIF-2alpha mRNA expression in human skeletal muscle in normoxic conditions. Eur J Appl Physiol. 2006 Mar;96(4):363-9. Epub 2005 Nov 12.
• Polesskaya A, Seale P, Rudnicki MA. Wnt signaling induces the myogenic specification of resident CD45+ adult stem cells during muscle regeneration. Cell. 2003 Jun 27;113(7):841-52.
• Ross R, Dagnone D, Jones PJ, Smith H, Paddags A, Hudson R, Janssen I. Reduction in obesity and related comor-bid conditions after diet-induced weight loss or exercise-induced weight loss in men. A randomized, controlled trial. Ann Intern Med. 2000; 133: 92-103.
• Sakurai T, Endo S, Hatano D, Ogasawara J, Kizaki T, Oh-ishi S, Izawa T, Ishida H, Ohno H. Effects of exercise training on adipogenesis of stromal-vascular fraction cells in rat epididymal white adipose tissue. Acta Physiol (Oxf). 2010; 200: 325-338.
• Stallknecht B. 2004. Influence of physical training on adipose tissue metabolism -- with special focus on effects of insulin and epinephrine. Dan Med Bull. 2004; 51: 1-33.
• Ye J. Emerging role of adipose tissue hypoxia in obesity and insulin resistance. Int J Obes (Lond). 2009 Jan;33(1):54-66.

Making the Right Fish Choices: Fatty Acid Contents of 33 Different Fish Species. Plus: What Are the Implications?

Pollachius virens (Photo: Tino Strauss) is king, when it comes to the n:3/n:6 ratio, but with <1% of fat you will still be hard pressed to get tons of omega-3s from eating pollock... but is more really better, let alone necessary?

I have already broached the issue of the differences in the fatty acid composition of fish - even those of the same species - in past articles such as the one(s) on fish as a potential source of mercury in your diet (read more). When I saw the recent paper by Claudia Strobel, Gerhard Jahreis and Katrin Kuhnt in Lipids in Health and Disease, I thought that it was about time to supply you with some real data on the actual n:3/n:6 ratio of different fish and its implications for the purported health benefits and anti-obesity effects of regular fish intake. Is there a "super fish" or is it as so often a matter of "mixing and matching" to achieve the right balance?

Fish? Of course, I have fish & chips or fish sticks every other day!

I guess I don't have to tell you that both the fish part of "fish and chips", as well as the "healthy" fish sticks that are pretty popular at least among German kids, should actually be sold at the bakery, right? I mean the ratio of the bread crumb coating to the pressed fish fillets inside, is hilarious and in view of the fact that these products are 'pre-fried' with cheap vegetable oil before they end up in the freezer cabinets of supermarkets all around the world, you cannot avoid the increased (partially oxidized) omega-6 intake, even if don't (as most people do) fry them at home.

So, if the fast-food version of "fish" is not an option to gear your polyunsaturated fatty acid ratio more towards the n-3 side of things, which fish shall you go for? Well, according to the data the scientists from the Friedrich Schiller University in Jena, Germany, collected Pollachius virens is the n3:n6 king among the seven most frequently consumed fish species, which are herring, tuna, pollock, alaska pollock, salmon, rainbow trout and iridescent shark (at least according to Strobel, 2013).

Figure 1: Content of EPA & DHA, other omega-3 and the sum of omega-6 fatty acids in percent of total fat of the 33 tested species in the study; ordered according to n3:n6 ratio, fish with the highest n3:n:6-ratios on the left; note: the anchovies and sardines were in a tin with oil and while they were drained before the analysis this will have decreased the n-3:n-6 ratio (data calculated based on Strobel. 2013)

On the other hand, the total fat content of pollock (<1%) is so low that you will be hard pressed eating enough of it to elicit any significant health effects. As far as the most frequently consumed fish species go, this does bring us back to our good old friend, the salmon.

Figure 2: Comparison of fatty acid content in g/100g of wild and farmed salmon (left) and respective omega-3 to omega-6 ratios (right; based on Strobel. 2013)

Unfortunately "salmon" does not equal salmon, these days. The dripping orange stuff you can buy for a few bucks (the orange color is artificially added to the feed by the way) at every supermarket, for example, is farmed salmon and contains only 2-3x more omega-3 fatty acids than omega-6s. The reddish, lean cuts of wild salmon on the other hand, have a 12-13x higher relative omega-3 content and in fact almost no omega-6 fatty acids (0.05g / 100g). With 0.53g /100g omega-3 fatty acids, wild salmon is yet just like pollock not the "bulk" source of omega-3 fatty acids you would be looking for, if you fell for the stupid idea that you could undo the damage you are doing by eating tons of (oftentimes oxidized) omega-6 fatty acids by simply throwing an even greater amount of omega-3s into the equation.

So what do we make of all that information?

The very latest on the effects of fish consumption on body weight comes from a study in the latest issue of the British Journal of Nutrition and shows that there is no effect of higher intakes of total, lean or fatty fish on 5-year risk of becoming obese in the 344,757 male and female participants of the European Prospective Investigation into Cancer and Nutrition (Jakobsen. 2013). Now, this does not exclude the existence of non-body weight related benefits, but it certainly puts the myth of the "anti-obesity" effect of fatty fish into perspective. After all, every 10g of additional high fat fish in the diets of the female study participants was associated with a 5x more pronounced increase in body weight than an equal amount of low fat fish. The general trend towards increasing BMIs was yet countered by none of the two.

In view of the fact that we are suffering from a relative deficiency in omega-3 fatty acids, only (relative to the exubarant amount of omega-6 fatty acids the average Westerner consumes on a daily basis), I see the data presented in this post not as a "shopping guide", but rather as a means to conduct a reality check of how realistic it really is that someone who follows a no fast- and convenient-food diet and keeps a non-neurotic eye on his overall n-6 intake will benefit from omega-3 intakes in the multiple gram range.

Specifically when it comes to supplementation, previous trials such as Filaire et al. did in fact find increases in oxidative stress in perfectly healthy athletes (judo) in response to 6 weeks on 600mg EPA + 400mg DHA per day (Filaire. 2010). If you also take into consideration that these negative effects on lipid oxidation were not ameliorated by higher alpha-tocopherol (vitamin E) levels, the message this and other studies are sending is clear: The putative increase in omega-3 requirements is a result of an abnormally high intake of omega-6 fatty acids.

The easiest way to escape any negative effects while still reaping the benefits therefore is to reduce (not totally avoid!) the intake of omega-6 fats (specifically from processed foods) - full stop! If you do that by incorporating a large variety of whole foods into your diet and include grass-fed beef, dairy from pastured cows and, obviously, fish on a regular basis, you won't have to increase your intake of omega-3 fatty acids by picking the orange colored, disgustingly tasting, fat dripping farmed salmon from the super market over its delicious red wild cousin, just because it has 4.5x more omega-3 fatty acids.

Bottom line: It's food quality and fatty acid ratios that make the difference; not the absolute numbers of allegedly good and bad fats, carbs and whatever else has recently fallen victim to the over-generalization that appears to be necessary to render dietary advice suitable for the masses. If there is any one thing that's to blame for the health crisis these days, it's this kind of black-and-white thinking that's behind the overgeneralized and faulty "expert advice" which is by no means propagated exclusively via supposedly unreliable sources on the Internet.

References:

• Filaire E, Massart A, Portier H, Rouveix M, Rosado F, Bage AS, Gobert M, Durand D. Effect of 6 Weeks of n-3 fatty-acid supplementation on oxidative stress in Judo athletes. Int J Sport Nutr Exerc Metab. 2010 Dec;20(6):496-506.
• Jakobsen MU, Dethlefsen C, Due KM, May AM, Romaguera D, Vergnaud AC, Norat T, Sørensen TI, Halkjær J, Tjønneland A, Boutron-Ruault MC, Clavel-Chapelon F, Fagherazzi G, Teucher B, Kühn T, Bergmann MM, Boeing H, Naska A, Orfanos P, Trichopoulou A, Palli D, Santucci De Magistris M, Sieri S, Bueno-de-Mesquita HB, van der A DL, Engeset D, Hjartåker A, Rodríguez L, Agudo A, Molina-Montes E, Huerta JM, Barricarte A, Amiano P, Manjer J, Wirfält E, Hallmans G, Johansson I, Khaw KT, Wareham NJ, Key TJ, Chajès V, Slimani N, Riboli E, Peeters PH, Overvad K. Fish consumption and subsequent change in body weight in European women and men. Br J Nutr. 2013 Jan;109(2):353-62.
• Strobel C, Jahreis G, Kuhnt K. Survey of n-3 and n-6 polyunsaturated fatty acids in fish and fish products. Lipids Health Dis. 2013 Oct 30;11:144.

Vitamin A Regrows Liver Tissue. Polydextrose Makes Dieting a Breeze. Exercise Blunts Negative Effects of High Fructose Diet. Diabetes Precipitates Female Sexual Dysfunction.

I did miss my own 1000-posts jubilee!

This week it's pretty easy to find the SuppVersity figure of the week. It's 1011 and that's the number of individual posts this "blog" currently holds. Actually, the very moment I hit the "publish" button on this one, it's going to be 1012 (see image on the right). I guess, I should have 'celebrated' that twelve posts before, but you know how I am, it's about the quality, not the quantity and though I am aware that the latter is unquestionably fluctuating, I would hope that each of you has found one or two 'pearls' - I mean, if you didn't why are you coming back regularly, then?

Apropos regularly, it's Saturday and thus about time for a couple of "On Short Notice" items. So let's not waste any time flattering and get to the science news business:

Vitamin A essential for liver regeneration. Plus: β-carotene and cancer even in non-smokers

So much for the vitamin A vs. D antagonism - in fact, one can't go without the other: Vitamin A & D synergize against liver cancer and increase survival rates by more then 75% (read more)

(Blaner 2013) -- Other than SuppVersity readers, the average slef-proclaimed health-conscious citizen probably thinks of (false) horror stories about vitamin A laden polar bear livers killing a handful of ravenous arctic explorers. The fact that the active form of vitamin A is actually one of the most important hormone-like substances in your body that's essential for the maturation process of stem cells, on the other had, got lost at least since vitamin D the supposed vitamin A antagonist became all the rage in the past decade. Scientists from the Coumbia University in New York and the Chernivtsi National University in Chernivtsi, Ukraine, are now going to publish a paper that should remind everyone (including the science community) that the contemporary black and white painting on D & A may well impair the progress we make in our understanding of our own physiology.

Missing half your liver? Not a problem if you got enough "liver building" vitamin A ;-)

In a mouse model which has been genetically modified so that the rodents weren't able to store adequate levels of retinoids  (yeah, there is a whole family of "vitamins A") in the liver, showed a delayed and incomplete regenerative response to partial hepatectomy (cutting away parts of the liver; PHE). As the scientists point out,

"[t]he requirement for proper retinoic acid signaling to allow for normal liver regeneration is underscored by studies of hepatocyte-specific RXRα-null mice [mice lacking the retinoid receptor]. When RXRα is ablated there is reduced hepatocyte lifespan, which is accompanied by premature hepatocyte death and the appearance of necrotic areas. RXRα ablation also results in delayed hepatocyte proliferation following PHE." (Blaner 2013)

At first sight this observation goes again the often cited liver-toxicity of vitamin A. In view of nature's favorite dose-response curve, which is bell-shaped and indicates that bad things (often similar or even identical ones) happen in both deficiency and toxicity states, it's only logical, though. Plus, similar effects have been observed for wound-healing decades ago (Gerber. 1982) and Ehrlich and Hunt report in a 1968 paper in the Annals of Surgery that the administration of vitamin A blunts the negative effects on cortisol on wound healing and appears to be necessary for optimal tissue regeneration (Ehrlich. 1968).

So, another good reason to pop vitamin A supplements?

Supplementation with very high doses of isolated beta-carotene could in fact induce a state of "vitamin A resistance" in response to the formation of a metabolite that blocks the RXR receptor just like a SERM like clomiphene citrate block the estrogen receptor (read more).

For a healthy person living on a paleo-esque diet supplements should not be necessary. The amount of vitamin A and its pre-cursor beta-carotene you get from a whole-foods diet is usually adequate, even if you don't consume liver or organ meat on a regular basis. The use of what you will generally get, when you go to a healthfood store and buy a "vitamin A" supplement, i.e. a high dose beta carotene, only, product is probably counter-indicated not just for smokers, where it appears to increase the risk of lung cancer development, but also in normal healthy individuals who usually get plenty of beta-carotene from the myriad of fortified foods your local supermarket has to offer - after all, one of the most recent meta-analyses showed that 20-30mg/day increase everyone's risk of lung cancer development by 16% and that of stomach cancer by 34% (Druesne-Pecollo. 2010).

Polydextrose has non-noticeable, but significant satiety effects

(Astbury. 2013) -- I know the headline sounds confusing, but basically that's the long and short of the results, Astbury, Taylor and MacDonald present in their most recent isse in the British Journal of Nutrition. The scientists fed 12 male and 9 female healthy university students (mean age 23.2y; BMI 22.3kg/m²) who had consumed identical breakfasts at 8:00am with isocaloric (210kcal) "preload" mid-morning snacks at 10:45am and 90min before they had a pasta-based test meal, of which they were supposed to eat as much as it would take to feel comfortably full.

Figure 1: Food intake (in kcal) after mid-morning snack with different amounts of polydextrose (left); caloric intake on the subsequent meals of the day (right; Astbury. 2013)

As the data in figure 1 indicates, the consumption of the liquid preload which contained either 0, 6.3, 12 or 21g of the sweet tasting polysaccharide that reaches the colon largely undigested, where 50% of the polydextrose molecules will be fermented to yield CO2 and volatile SCFA such as propionate and butyrate and the rest will be excreted intact in the feces lead to dose-dependent reductions in the amount of food that was consumed in the subsequent meal.

50% energy availability, a source of SCFA, tasty & easy to process - perfect diet 'food'?

With only 50% energy availability and 50% being fermented to short chain fatty acids (SFCA),  the 89% dextrose, 10% sorbitol & 1% percent citric acid molecule, polydextrose could actually be a better choice for dieters than WMHDP (learn more about the SCFA based fat burning effects of resistant starches and how to make fat burning pancakes)

Interestingly, the reduced energy intake was not brought about by a consciously noticeable reduction in either fullness, hunger or desire to eat in response to the test meal (the scientists assessed that by questionnaires). And despite the fact that the effect was only transient, it's actually good and important news that the men and women did not accommodate for the 12-23% (male participants) and 6-18% (female participants) reduction in energy intake on the subsequent meal.

If that worked with every meal and you could achieve a ~20% reduction in energy intake, this alone should help you shed some weight pretty effortlessly. And as if that was not enough, already the polydextrose drinks was even more palatable than the sugary original; with the highest polydextrose content being perceived as most "creamy" - bon appetit ;-)

Even shorter news - "On real short notice", so to say  ;-)

I am well aware that what began as short news has as of late turned into a bunch of regular news - well, almost. So I decided to try and cut the last two items in today's installment short, in order to have them fit into what you would actually expect from a "on short notice" ;-)

• Exercise nullifies bad effects of high fructose diet (Moraes-Silva. 2013) -- A paper by scientists from the University of Sao Paulo puts the "lack of exercise / insuficient activity" hypothesis of obesity back on the radar. Even with an otherwise highly detrimental liquid fructose overload of 100g/l in their drinking water, the rodents in the study Moraes-Silva et al. conducted, did have normal (within statistical limits) glucose tolerance, blood pressure and heart disease risk as the rodents in the sedentary and the exercised control groups.

  

  Figure 2: Regular exercise maintains insulin sensitivity, cardiovascular disease risk and blood pressure even in the presence of pathologically high liquid fructose ingestion (Moraes-Silva. 2013)

  The regular treadmill running also blunted the autonomic dysfunction that was characterized by "an approximate 50% decrease in baroreflex sensitivity and 24% in HR variability", as well as increases in sympathovagal balance (140%) and renal sympathetic nerve activity (45%). Now you tell me "it's all about diet", only. Let alone: "Exercise just makes you hungry!"

• Diabetes and female sexual dysfunction correlate (Pontiroli. 2013) -- We already know that diabetes is a, if not the #1 risk factor for male sexual dysfunction, these days. Now a recent meta-analysis that's going to be published in one of the future issues of The Journal of Sexual Medicine found a 150% increase in sexual dysfunction in type II diabetes. Whether or not this was related to the higher depression rates in diabetic women cannot be said. What is certain, though, is that the BMI was a positive predictor of the effect size. In other words, the negative impact on sexual function increased with the degree of adiposity.
  
  Additional read for those women who feel it's their husband's performance that's to blame for their anorgasmia: "Pedalium murex Linn. fruits more effective than sildenafil in the long run and increases testosterone by 125%" (read more)
   

Now that's it for today, but I am now going out on a limb and promise another serving of short news with a focus on exercise early next week - something like the previous "Health & Exercise"- or the "Get Lean & Stay Lean" quickies and for once I can even tell you about one news that's definitely going to be in there - something about working out with and without breakfast.

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The obligatory reminder: In the mean time I'd suggest you devour the latest SuppVersity Facebook News @ www.facebook.com/SuppVersity. As usual they will receive a couple of updates way before the next official SuppVersity post is going to see the light of the day. Let's see, some of the most recent news are even remotely related to the On Short Notice items of today:

• Penis pumps - Scientists believe they are going to make a revival as a means of penile rehabilitation after surgery for prostate cancer (read more)
• Stress renders cancer immortal - What has just been observed in a rodent model of prostate cancer could have important implications for other cancers, as well (read more)
• PDE5 inhibitor for him, PDE-4 inhibitor for her? Study suggests: PDE-4 inhibitors could improve female sexual function (read more)
• Goose liver for the liver - When it's high in selenium goose liver could protect your liver from the assault of excessive alcohol consumption (read more)

As promised, there will be more. So in case you have not done so already,  you best like the SuppVersity right now so that the latest news will always appear in your news-feed.... ah, and about all that geeky science reading, don't forget that there is more to life than dieting and working out ;-)

References:

• Astbury NM, Taylor MA, Macdonald IA. Polydextrose results in a dose-dependent reduction in ad libitum energy intake at a subsequent test meal. Br J Nutr. 2013 Jan 23:1-9.
• Druesne-Pecollo N, Latino-Martel P, Norat T, Barrandon E, Bertrais S, Galan P, Hercberg S. Beta-carotene supplementation and cancer risk: a systematic review and metaanalysis of randomized controlled trials. Int J Cancer. 2010 Jul 1;127(1):172-84.
• Ehrlich HP, Hunt TK. Effects of cortisone and vitamin A on wound healing. Ann Surg. 1968 Mar;167(3):324-8.
• Gerber LE, Erdman JW Jr. Effect of dietary retinyl acetate, beta-carotene and retinoic acid on wound healing in rats. J Nutr. 1982 Aug;112(8):1555-64.
• Moraes-Silva IC, Mostarda CT, Moreira ED, Silva KA, Dos Santos F, De Angelis K, Farah VD, Irigoyen MC. Preventive role of exercise training in autonomic, hemodynamic and metabolic parameters in rats under high risk of metabolic syndrome development. J Appl Physiol. 2013 Jan 17.
• Pontiroli AE, Cortelazzi D, and Morabito A. Female Sexual Dysfunction and Diabetes: A Systematic Review and Meta-Analysis. J Sex Med. 2013 [e-pub ahead of print]