Hydrogymnastics, Weight Training or Dance? What's the Best Workout to Achieve Your 2015 Physique Goals, Girls?

Do you really need a barbell or will hopping around in a group dance course or working out in the water aka hydrogymnastic suffice to build the 2015 cover model physique that's part of your new year's resolution? A recent Portuguese + Brazilian study may hold the answer to this "important" question.

It's about time to think about a good new year's resolution; and since any resolution that's aimed at losing weight and/or building a better physique, naturally involves exercise, the latest study from the University of Trás-os-Montes and Alto Douro comes right in time (Soares Costa de Mendonça. 2014).

The study that was conducted by Rosa Maria Soares Costa de Mendonça, Adenilson Targino de Araújo Júnior from the University of Trás-os-Montes and Alto Douro in Portugal, Maria do Socorro Cirilo de Sousa from the Federal Institute of Technology Education in Brazil and Helder Miguel Fernandes from the Research Centre for Sport in Portugal was designed to investigate the possible effects of 16 weeks of practicing different physical exercise programmes (strength training, dance or hydrogymnastics) on the body composition and anthropometric dimensions of adult women.

If you don't like any of the suggestions, try doing  HIIT instead!

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

HIIT Ain't For Everyone

The sample was comprised of 89 adult women aged 25–55 (41.42 ± 9.23 years), who were used to train at least three times a week and had no history of health issues that may compromise their ability to participate in the study. . Of these, 60% were married, 27% single and 12% divorced, all residing in the northeastern part of Brazil. As the scientists point out, ...

"[t]hese women were selected using a non probabilistic manner in specific locations, such as fitness clubs, hydrogymnastic gyms and a public municipal institution.

The sample was randomly divided into four groups, of which one was designed as the control group consisting of individuals that were sedentary (CG) (n = 25) and three were characterised as experimental groups:

• strength training (SG) (n = 25), in which the ladies trained three times per week under the supervision of a qualified trainer and did 3 sets of 8–12 repetitions (weights were progressively increased) with a 2–3 min rest period on each of the 50–60 workouts in which all the major muscle groups of the upper and lower limbs were exercised with the use of either machines with weights, free weights or resistance equipment,
• dance (DG) (n = 18), which the women trained three times per week at a moderate to vigorous intensity, which was defined as 60 to 85% of the maximum heart rate as identified by the calculation 220 – age for 50 to 60 minutes workouts involving activities activating all the major muscle groups in a continuous manner using basic steps and a minimum of three rhythmic variations of popular dance styles and aerobics per session with songs of a rhythmic cadence of 100 to 160 beats per minute, and
• hydrogymnastics (HG) (n = 21), in which the women trained with a frequency of three days per week at moderate to vigorous intensity, defined as 60 to 85% of the maximum heart rate using exercises that involved the major muscle groups of the upper and lower limbs with a focus on cardiorespiratory exercises, followed by muscular endurance exercises using equipment such as shin pads designed for hydrogymnastics, dumbbells, bars, plates, floating devices and pool edges with each exercise taking from 2 to 3 min to complete and the whole session lasting 45 to 55 min.

All workouts were designed according to the exercise routines from the ACSM guidelines (Garber. 2011) and the adherence to the exercise prescription was monitored by trained personnel. The workout duration and frequency were more or less identical and even the intensity was similar.

Figure 1: Changes in anthropometric parameters after 16 weeks of training (Soares Costa de Mendonça. 2014).

As you can see all training regimen lead to measurable improvements in the anthropometric parameters. Of the three different exercise regimen the "exotic", i.e. the hydrogymnastics training, was yet on overall the most effective "belly fat reducer" among the three training protocols.

Figure 2: Changes in body composition (calculated based on caliper data) after 16 weeks of hydrogymnastics, weight training, dance or idleness (Soares Costa de Mendonça. 2014).

Things look a bit different, when we take the body composition data the scientists calculated based on the skinfold measures into account: Here the strength training has a slight, but not necessarily significant edge over the hydrogymnastics (keep in mind that the efficacy of hydrogymnasticsmay partly be due to a novelty effect, i.e. new exercise = greater response | see fat mass loss after 8 vs. 16 weeks). Every ladies favorite, the group based dance exercise is yet - once again - trailing third.

Don't forget: Female Athletes' Body Composition Suffers From Chronic Energy Deficits | learn more

Bottom line: While it appears to be clear that (a) starting your next year as a couch potato is going to increase your waist line and body fat levels significantly (remember the ladies in the control group of the study at hand switched from training regularly to being sedentary for 16 weeks), it is not clear if lifting weights or doing hydrogymnastics, which involved some "weight training", as well is the better 2015 body recomposition exercise for women.

What appears to be clear, though, is that the highly popular dance courses are the least effective 2015 exercise protocol to follow, when your goal is to improve your body composition without dieting | Comment on Facebook!

References:

• Garber, Carol Ewing, et al. "American College of Sports Medicine position stand. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise." Medicine and science in sports and exercise 43.7 (2011): 1334-1359.
• Soares Costa de Mendonça, Rosa Maria, et al. "The Effects of Different Exercise Programmes on Female Body Composition." Journal of Human Kinetics 43.1 (2014): 67-78.

Fat Loss Principles That Work: 10g+ of EAAs W/ Every Meal. Do Energetic Costs of Protein Synthesis Trigger This Effect?

EAAs beyond whey: It may not necessarily look like this, but this salad (repicecorner) is an EAA power horse with cheddar cheese (25% protein, 0.49 EAA / P ratio), tuna (in oil, 29%,  0.45) and kidney beans (9%, 0.45). You see, it does not always have to be chicken breasts or whey to get beyond the 10g+ EAA threshold, I have repeatedly suggested as one of the fundamental rules of dieting for weight loss, maintenance and muscle gain.

Many people take it for granted that you become fat, when you get old. If you look at the statistics, you could even make a point that obesity has some protective effects with esp. with respect to CVD mortality. Scientists call this the "obesity paradox" (Kastorini. 2012). What's particularly paradox, at least in my humble opinion, is yet not the phenomenon itself, but rather the fact that it gets smart scientists derailed from working on useful dietary and exercise interventions to prevent the development of heart disease, cancer, metabolic syndrome etc. in early years. Instead, they argue ex-post, i.e. when the baby has already been thrown out with the bathtub by comparing sick lean (in parts even cachectic) and sick "obese" people, why their statistical shenanigan that's based on the useless BMI produces paradoxical results. And that, when studies such as the one Jacobs et al. did in 2010 clearly show that 50+ year old men and women with waist circumference >120cm and >110cm, respectively, have 2x higher all-cause mortality risk than their lean peers - irrespective of BMI (Jacobs. 2010)!

To get lean and stay lean, yet not thin and skinny fat is therefore a challenge everyone...

... from the child in the Kindergarten to the obese granny in the nursing home is facing. Against that background a previous study by Loenneke et al. comes to mind. The results of their analysis, which were published in Nutrition and Metabolism in January 2012 clearly show that the amount of times people eat meals with a 10g+ EAA content per day was inversely related to percent central abdominal fat (Loenneke. 2012). In previous studies EAAs have also been shown to improve glucose clearance without increases in insulin and in the absence of effects on the fat burnin and health promoting expresion of AMPK-alpha2 in skeletal muscle tissue (see "EAAs Stimulate Muscle Glucose Uptake by Exponentiating Insulin's Effect on GLUT4 Expression"). With the advanced publication of a study by Coker, Miller, Schutzler, Deutz and Wolfe in the online verison of the Nutrition Journal a couple of days ago, the notion that EAAs have a particularly beneficial effect on fat loss - in this case in obese elderly individuals - gets further support from a well-controlled randomized trial (Cooker. 2012).

EAA-rich protein increases fat loss to a greater extent than low EAA protein

The researchers from the Center for Translational Research in Aging and Longevity and the University of Arkansas for Medical Sciences in Little Rock, AR, USA randomized 12 elderly individuals (mean age 69 years) to an 8 week, caloric restriction diet utilizing equivalent caloric meal replacements (~850 kcal/day; the exact nutrient composition can be found in figure 1) + ~400kcal from solid foods (total intake: ~1,250kcal/day; the subjects were free to chose their solid meals but were provided with a list of examples the should pick from, if possible).

Figure 1: Macronutrient composition of the meal replacements used in the study (Cooker. 2012)

The diet was designed to induce a 7% weight loss in two months. And while both,  the rate of weight loss (~1.6lbs per week), as well as the relatively high caloric deficit are certainly appropriate for someone with a 30+ BMI and ~40% body fat, leaner people will fare better with a less pronounced kcal deficit or (alternatively) have to add some strategically planned refeeds to the equation in order to minimize the loss of lean mass and, more importantly, avoid the ensuing reduction in energy expenditure (for the obese, the latter is actually less of the problem, because the downsides of being calorically deprived are at least partly counglucose tolerance and leptin sensitivity with every gram of body can actually help the body recognize that there is still plenty of energy that has just not been available (glucose) or "visible" (fat) before).

Figure 2: Changes in lean and fat mass (kg, left) and fractional protein synthesis rates (FSR) in participants receiving iso-caloric meal replacements with identical macronutrient compositions (see figure 1), but different amounts of essential amino acids (EAAs) content (Coker. 2012)

As the data in figure 2 goes to show you even the obese individuals in the study at hand lost a non-negligible amount of lean mass - unfortunately the body composition was measure with a sophisticated, but still body impedance based device, the trends are still accurate, but it is questionable in how much we are actually talking about ~2 and 2.5kg of muscle mass (figure 2, left), because somebody's "lean body mass" does obviously include more than just skeletal muscle.

When it comes to supplements, we are often like children on Christmas eve. About all the new stuff we get we tend to forget our former favorite and often way more fun to play with toys. Don't make this mistake and ditch your PWO whey (personally, I like a ~1.5:1 whey + micellar casein mixture) for EAAs, they don't come close... read more

Be that as it may - since the before and after values were taken with the same device the changes should be correct, so that both the slightly yet not statistically significantly ameliorated loss of lean body mass and, more importantly, the significantly higher degree of body fat loss in the EAA meal replacement (EAAMR) group speak in favor of the 5 servings of a the 170 kcal, 6g EAA per day. Moreover, "the sparing influence of muscle loss might have been demonstrated with a larger sample size", so that you can take it for granted that the preservation of precious muscle mass is an advantage of being choosy with your protein sources and preferring those with higher over those with lower essential amino acid contents.

On a related note: I don't know if you noticed, but with a total energy content of 850kcal and 30g EAA these 5 meal replacements did in fact have exactly those 10g+ of essential amino acids, I have repeatedly recommended to have with each of the 3 meals most people consume in the course of the day.

In all fairness, it should also be mentioned that despite not being significantly different at baseline, the body fat percentage of the subjects in the EAA meal replacement group was ~3% higher to begin with.This may seem irrelevant, since figure 2 compares lean mass and fat mass as absolute changes and not their percentages, but in the end, the amount of fat you you can drop within a given time-frame decreases with lower body fat percentages.

Do the energetic costs of protein synthesis drive fat loss?

Another interesting observation Coker et al. made is the close association between fat loss, on the one hand, and increased protein synthesis (55%), on the other hand. The researchers take this as an incentive to do one of the of the much loved calories in vs. calories out calculation and come up with the following hypothesis:

"Acute administration of EAAMR did promote a significant increase in skeletal muscle protein FSR compared to CMR. Assuming that the energy cost of protein synthesis is 3.6 kJ/g and the baseline GAIA-derived lean tissue mass was 56.4 kg for EAAMR and 54.4 kg for the CMR, we can extrapolate that the overall energy discrepancy between the two groups was roughly equivalent to 27,170 kcal or 3.5 kg of weight loss across the entire caloric restriction-based weight loss paradigm. Based on the amount of total lean mass in each group, this value takes into account a consistent intervention structure of five servings/day across an eight week period. In short, these calculations suggest that differences in the source of intact protein/formulation of EAA may have a significant influence on diet-induced energy expenditure that coincides closely with the greater reduction of adipose tissue in EAAMR compared to CMR." (my emphasis in Coker. 2012)

I usually discard fallacious calculations like this one if they are not highlight the stupidity of trying to eat exactly as much as some funky formula + the figure on your treadmill, pedometer, heart rate monitor or whatever fancy tool you may use to "measure" your energy expenditure suggest you would have burned in the last 24h. In this case, however, I made an exception, because I feel that the notion that protein quality is one of the myriad of parameters that are missing from this foolish calculation is important, for lean and obese people from all age groups who are trying to shed body fat.

Bottom line: The take away message of the study is in the end identical to the previously mentioned study by Loenneke et al.: Make sure you hit the 10g EAA threshold with each and every of your meals, if being lean and muscular not skinny yet fat is your goal.

References:

• Coker RH, Miller S, Schutlzer S, Deutz N, Wolfe RR. Whey protein and essential amino acids promote the reduction of adipose tissue and increased muscle protein synthesis during caloric restriction-induced weight loss in elderly, obese individuals. Nutr J. 2012 Dec 11;11(1):105. [Epub ahead of print]
• Jacobs EJ, Newton CC, Wang Y, Patel AV, McCullough ML, Campbell PT, Thun MJ, Gapstur SM. Waist circumference and all-cause mortality in a large US cohort. Arch Intern Med. 2010 Aug 9;170(15):1293-301.
• Kastorini CM, Panagiotakos DB. The obesity paradox: methodological considerations based on epidemiological and clinical evidence--new insights. Maturitas. 2012 Jul;72(3):220-4.
• Loenneke JP, Wilson JM, Manninen AH, Wray ME, Barnes JT, Pujol TJ. Quality protein intake is inversely related with abdominal fat. Nutr Metab (Lond). 2012 Jan 27;9(1):5.

Yeast Hydrolysate Powered Fat Loss: 7% Reduction in Total Body Fat and 14% Reduction in Abdominal Fat - W/out Diet?

Will the fat-burning magic of 1g/day of yeast hydrolysate dissolve the fat that's still covering the last 2 packs?

It sounds like a marketing scam and I must warn you, one of the authors of a soon-to-be-published paper on the basis of which I came up with this headline is actually with a company that specializes in food additives.

This obviously warrants a heightened degree of suspicion, but it does not mean that the study results could or even must be doctored. I would thus suggest, we take a look at what the Korean scientists from Jeonju University, the University of Seoul, the Korea University and the Neo Cremar Company Ltd. actually did and found before we jump to any premature conclusions about the validity or non-validity of the data.

What exactly is yeast hydrolysate?

I guess, the first thing we have to address is what exactly it was Jung et al. administered to their 24 male and 30 female participants  with body mass indices (BMI) of at least 25 kg/m² (the obesity cut off in the Asia-Pacific region is 25 kg/m²). To this end, it's best to look at how this "supplement" was produced (if you want the short version fast forward to the first red box ;-)

1. 

   You've read about the anti-Crohn's effects of saccharomyces cerv. (bakers yeast) in the SuppVersity Facebook News, recently.

   Saccharomyces cerevisiae (IFO 2346) is incubated in a growth medium containing 2% molasses, 0.6% (NH4)2SO4, 0.1% MgSO4$7H2O, 0.2% KH2PO4, 0.03% K2HPO4,  for 3 days at 30°C.
2. After incubation, the culture is centrifuged at 10,000g for 20 minutes.
3. Immediately after the cells are removed from the centrifuge, they are suspended in 20 mM phosphate buffer (pH 7.0) and hydrolyzed with 1000 units of bromelain at 30 C for 4 h.

The result of this third step actually is already a, but not yet the hydrolysate. To achieve the "good stuff", it is then centrifuged at 10,000g for 20 min. The small molecules which are then removed from the supernatant are then passed through a 10 kDa molecular-weight cutoff membrane and eventually lyophilized - et voilà!

"Hold on! So what do I need?" Before you hit the "too complicated button" at the bottom of this page, let me briefly point out that you don't need to understand or memorize the production process. The thing you have to look for, when you are shopping for corresponding products is a yeast hydrolysate with a maximal molecular weight (that's ~ the size of the indiv. peptides) of <10kDa that was produced from Saccharomyces cerevisiae.

In the study at hand, the of this 3+1 step process was packed into 500 mg pouches before it was handed over to the subjects in the active arm of the study (the placebo contained dextrin). 

Figure 1: Inter-group baseline differences for weight + body composition for men and women (Young. 2014)

Both the placebo and yeast supplements had to be taken twice a day 30 min before breakfast and dinner. So far that all sounds like standard procedure. If you take a look at the outcome of the randomization process, you will yet see that there are non-negligible inter-group differences in body composition (see Figure 1): In conjunction with the high fat mass, the low body weight and lean mass of the ladies in the control group, could have significant effects on the change in body weight. Unfortunately, the scientists did not test the significance of this difference, but a 39% gap in lean body mass that comes hand in hand with a 13% higher fat mass can be expected to have a very relevant effect on the outcome of any dietary intervention.

Speaking of dietary interventions! there was no dietary intervention.

I know, it sounds hilarious, but there was no dietary intervention. All the participants had to do was to consume the 1g of yeast hydrolysate or the 1g of dextrin in 2x500mg servings 30 min before breakfast and dinner. That's at least what they were advised to do.

Figure 2: Changes in energy intake (% baseline) and body composition (Young. 2014)

The data in Figure 2 does yet tell you that what they actually did (voluntarily, though) was "dieting". This is particularly true for the female study participants, who reached caloric deficits of 26% by week 6-8 and 28% by week 8-10. Against that background it's not that surprising that the statistical significant changes in body comp were only observed in the female study participants.

There are no effects on resting metabolic rate! The notion that the reduced energy intake is the main, if not the only driving force of the fat loss Jung et al. observed in the study at hand is supported by observations the researchers made in a previous study from 2011 (Jung. 2011a). In the said study, the 20 obese females (body fat >28%) in the yeast group did experience a non-significantly improved fat loss compared to the control group. They did yet also suffer from a "higher" reduction in resting metabolic race (-9.69kcal/day vs. -4.35kcal/day) - similarly non-significant as the weight loss difference, obviously.

This does not mean that the yeast extract doesn't work - quite the contrary, for the average individual who is neither willing nor able to adhere to a caloric deficit without the help of tools like this, it could actually come very handy. For the average physical culturist, it would yet obviously be more interesting if yeast hydrolysates had spot reducing qualities (learn more about spot reduction). And if we take another look at the full text of the study, we could actually argue that this is basically what the authors suggest, when they refer to the results of previous studies and state:

"Yeast hydrolysate increases the reduction of body fat in obese individuals compared with placebo, which supports the hypothesized abdominal fat-lowering effects of yeast hydrolysate" (Young. 2014)

If you look at the study at hand, the question we would have to answer should thus read: Are the abdominal and total fat mass disproportionate. Or to say it differently: Did the subjects lose signifcantly more abdominal than total fat? And in view of the previously discussed problem: Did this vary between male and female participants? Unfortunately, the scientists didn't do us (or rather me) the favor of doing this for us, already. Therefore I had to do the calculations and plotting for Figure 3 myself:

Figure 3: Relative change in body fat mass and abdominal fat thickness (Jung. 2014)

As the text in the box in Figure 3 already tells you, the existing discrepancy between the reduction in total body fat and abdominal fat thickness does not necessarily "prove" the spot reducing prowess of yeast hydrolysate. We do after all know that in the chubbier folks the unhealthy fat in / on the midsection is usually the first to go.

Is the fat loss really localized? 

Furthermore, a previous study by the same researchers clearly refutes the abdominal specific fat loss effects. The corresponding paper was published in 2011 in the Journal of Food and Biochemistry (Jung. 2011a; same paper I referenced in the box above), and despite the fact that the researchers observed a trend for an increase in weight loss within only 4 weeks on the same <10kDa yeast hydrolysate, the fat loss results of the obese women who participated in the study were at best triceps (-2.15 vs. -1.05mm reduction in skinfold thickness in yeast vs. control) and not belly specific (-1.70 vs. -1.08mm reduction in skinfold thickness in yeast vs. control).

Unfortunately, I cannot tell you whether the same can be said of the 2009 paper by Suh et al., because the online archive of the Journal of Food Science and Nutrition, where it was published starts in March 2011. In view of the fact that it was not "ab-specific" in obese women, I really doubt that it will have has particularly pronounced effects on the waistline of female college students - a subject group of whom you would expect that they are at least somewhat closer to the fitness and leanness level of the average SuppVersity reader.

If you are looking for alternative, yet not necessarily more effective purported spot-reduction supp- lements / techniques, you may want to (re?)read the recent SuppVersity article about green tea, green clay & magnesium sulfate soaked "plaster body wraps" | read more

Is yeast hydrolysate an effective tool in your weight loss arsenal? A definitive answer to this question is yet still lacking. Personally, I would spend my money otherwise, because I have never had a problem with cutting back calories, when I decided that this is necessary to lose weight. If, on the other hand, you belong to those people who are constantly hungry, it may be worth trialling a once month supply of yeast hydrolysate caps (or sachets).

The only thing you should be prepared for is that it is not going to work if you don't diet. In all of the human studies I've seen so far, the weight loss went hand in hand with a reduction in calorie intake; and despite the fact that there is good evidence that the His-Pro (=Cyclo) peptides in yeast hydrolysates have additional value as potent antioxidants (Jung. 2011b), their subsequent effect on glucose metabolism will depend on a baseline increase in inflammation. In other words: The bigger your belly, gluttony and baseline inflammation, the greater the benefits.

References:

• Jung, E. Y., Kim, S. Y., Bae, S. H., Chang, U. J., Choi, J. W., & Suh, H. J. (2011a). Weight reduction effects of yeast hydrolysate below 10 kDa on obese young women. Journal of Food Biochemistry, 35(2), 337-350.
• Jung, E. Y., Lee, H. S., Choi, J. W., Ra, K. S., Kim, M. R., & Suh, H. J. (2011b). Glucose Tolerance and Antioxidant Activity of Spent Brewer's Yeast Hydrolysate with a High Content of Cyclo‐His‐Pro (CHP). Journal of food science, 76(2), C272-C278.
• Jung, E. Y., Hong, Y. H., Kim, J. H., Park, Y., Bae, S. H., Chang, U. J., & Suh, H. J. (2012). Effects of Yeast Hydrolysate on Hepatic Lipid Metabolism in High-Fat-Diet-Induced Obese Mice: Yeast Hydrolysate Suppresses Body Fat Accumulation by Attenuating Fatty Acid Synthesis. Annals of Nutrition and Metabolism, 61(2), 89-94.  
• Jung, E. Y., Cho, M. K., Hong, Y. H., Kim, J. H., Park, Y., Chang, U. J., & Suh, H. J. (2014). Yeast hydrolysate can reduce body weight and abdominal fat accumulation in obese adults. Nutrition, 30(1), 25-32.
• Suh, H. J. (2009). The weight reduction effect of yeast hydrolysate-SR101 on female college students. Journal of Food Science and Nutrition, 14(2), 123-128.

High Reps for "Spot Reduction" Works - Yet Not the Way Trainees Believe. Fat Loss Occurs in Untrained Body Parts

You could argue that people who spend money on things like this deserve to be ripped of, but then again, those people who manufacture "devices" like this are selling dreams - and who would not pay some money for a nice dream?

Be honest, I bet there was a time in your life, when you did tons of sit-ups in the mislead and stubborn believe that this practice simply had to reveal a tightly sculpted set of abs, if you just did it regularly and with all the discipline and effort the guys and girls on the TV shopping channels invest into their training... that's not you? Well what about leg raises for the lower abs, then? Not you either? How about the flabby chest that just needs some more bench pressing or the buttocks... ah, let's better not talk about those, right?

While today's SuppVersity news won't change the fundamental truth that diet will always remain the main determinant of fat loss, I would suppose that the results of a recently published study by Rodrigo Ramírez Campillo and his colleagues from Chile and Spain is going to change your perspective on reshaping your body by localized muscle endurance resistance training.

High reps for muscle shaping? Correct, but very different from what you'd probably expect

The study Campillo et al. conducted was designed to address the question of how 12 weeks of a localized muscle endurance resistance training program for the non-dominant leg, affects local and regional body tissue composition - or put simply: Can you shape your non-dominant leg by training it in the bro-scientific 'high rep shaping zone'? I guess I'm not taking away too much, if I tell you right away that the non-dominant leg of the formerly not resistance trained, but active physical education students (7 men and 4 women; average age 23y, anthropometric data see figure 1) who participated in

• 3x80 min sessions of 960-1,200 reps per week
• without scheduled rest between reps (if subjects failed, the weight was reduced) and 
• a progressively increasing intensity of 10% during weeks 1-4, 20% during weeks 5-6, and 30% during weeks 7-12

did not have striated quads and glutes in their non-dominant leg after performing the targeted 34,560-43,200 muscle contractions - and this was (as the data in figure 1) goes to show you, not simply due to a general lack of fat loss:

Figure 1. Anthropometric data of the subjects at baseline and relative changes in the course of the 12-week intervention period (Campillo .2012

In fact, the total body fat mass decreased significantly over the course of the 12-week intervention period (P≤0.05), whereas no significant changes were observed in total body mass, BMD and bone mass, while the neutral/positive nitrogen balance allowed for a relative maintenance (=statistically non-significant minus; cf. figure 2) of total lean mass.

Now that a routine as hilarious as this one does actually result in fat loss; and that it does so in the absence of any dietary interventions or significant changes in energy intake (who was it who said "Exercise just makes you hungry?" ;-) or macronutrient composition over the 12-week intervention period would already be newsworthy. What makes this study stick out, however, is the fact that it is...

"[t]o the best of the authors’ knowledge, the unique approach of the present study was to examine, with a valid anthropometric technique such as DXA, training-induced changes in lean mass, fat mass and bone mass in total body, legs, arms and trunk after a localized muscle endurance resistance training program of relatively high training volume." (Campillo. 2012)

and let's not forget about the results this "unique approach" yielded (see figure 2).

Figure 2: Relative changes in bone mass, lean mass, fat mass in trunk, control leg, trained leg and arms in response to the 12-week exercise intervention (Campillo. 2012)

The scientists explain their observation that lower body exercise does not burn lower, but rather trunk and upper body fat as follows:

I suggest you go back to my previous post "Nasty Insights into the Yo-Yo-Effect: Lower Body Fat Sticks! Plus: Why It's Easier to Get 6-Pack Abs Than Striated Glutes & Hams"

A negative energy balance, induced by regular exercise, may promote a reduction in fat mass, by means of a modified hormonal environment (i.e. increased adrenalin) and a subsequent increase in fatty acids mobilization from fat depots. However, one may take into consideration that the alteration in hormonal environment takes place all over the body, not only in the body segment that was exercised. In doing so, the increased hormonal stress environment induced by exercising the non-dominant leg, may result in fatty acids mobilization, not only of the trained segment, but also from the trunk region and arms.

The reason why the fat mass was significantly reduced in the upper body, and not in the lower body, may be related to the initial fat content of the different body parts. Thus, the fact that at baseline, subjects showed 54% of their total body fat in the trunk, 36% in their legs, and 10% in the arms, may explain, in part, the greater exercised induced-decrease in trunk fat mass." (my emphasis in Campillo. 2012)

Campillo et al. also comment on the often proposed hypothesis that fat mass change would always being at the last place where lipids accumulated stating that there has not yet been a single study that would provide experimental evidence to justify this hypothesis and that it is more likely due to the general tendency of moderate exercise to be fueled mainly from upper body fat stores, while the local adipose tissue in the lower body contributes only little to this process (see link under the image next to the quotation above for more information about how lower body fat is special).

So do you have to do "spot reduction training for your legs to burn the blubber on your abs"? If you had the choice between breathing squats and crunches, sure! And even the 34,560-43,200 one-legged leg presses in the study at hand are probably going to be more productive than doing the same amount of sit-ups... wait, let me think: 100 sit-ups a day for 12 weeks = 100 x 12 x 7 = 8,400 - hmm... maybe you just did not enough sit-ups?

If you want to learn more about the long-term benefits of HIIT or the reason why doing LISS is nice, but doing more and more LISS to burn more calories is simply stupid, go back to "Some HIIT For Life & Less LISS For More! How to Burn 27,300 Kcal Extra W/out Losing a Single Extra Pound of Fat! "

I am obviously just kidding you here. The most important message to take away from this study is that you have to create a fat-catabolic millieu if you want to lose body fat. In that it appears secondary how you achieve that and the 34,560-43,200 rep workout from the study at hand certainly is by no means the only and certainly not the best way to do that. Even Campillo et al. state in the last paragraph of their paper

"a training methodology, similar to that used in our study, may be sufficient to achieve a reduction in fat mass, but we recommend muscle endurance resistance training programs that include big muscle groups, w[h]ich may result in more time efficient energy expenditure and corporal composition modification." (my emphasis in Campillo. 2012)

So back to the basics, ladies and gentlemen. A fast paced full-body circuit training (e.g. the "Fat Loss Support Routine"), HIIT or plyometrics and a classic LISS session from time cleverly combined are still the fasted way to propel (not replace) your diet induced loss in body fat and to (re-)shape your body.

References:

• Campillo RR, Andrade DC, Campos Jara C, Olguín CH, Lepin CA, Izquierdo M. Regional Fat Changes Induced By Localized Muscle Endurance Resistance Training. Journal of Strength and Conditioning Research. 2012 [Published ahead of print]

Get Lean & Stay Lean with Emedin, Galangin & Antibiotics. Plus: Breakfast & Morning Glucose Metabolism. Diet Once, Never Eat to Satiety Again? Adipocyte Size & NAFLD

Instead of making excuses for posting yet another "short news" collection instead of the next installment of the Athlete's Triad series, I will honestly tell you that I simply wasn't in the mood. Moreover, I have the feeling that I have already outlined what is going to work, i.e. train less, eat more and don't get all psyched up about being lean and looking good. Live your life! Against that background my gut tells me that any further details would just get you off track and back into the viscous cycle of overtraining, overdieting and overthinking why things don't work out for you by evoking the impression that as long as you take supplement X you could get away with doing a little bit 'less less' and eat a little bit 'less more'.

This would be about as counter-productive as the eternal quest for the ultimate body fat blocker or fat burner of which today's Get lean and Stay Lean Quickie does actually feature three. While the temporary use of all of them as a crutch or 'afterburner' to a reasonably planned diet and workout regimen certainly makes sense, it's not like anyone of us got fat, because he or she was "fat burner deficient". A fat burner is not an essential nutrient and only an adjunct to diet and exercise! Keep that in mind not just when you read the following short news items, but also whenever you enter a supplement store (real or on the Internet) and find a new "revolutionary fat burner" on sale -- regardless of whether it has Dr. Oz or Mr. O on the packaging it won't actively, i.e. on its own and in the absence of a dialed in nutritional regimen, make you lose body fat.

• Cassia tora (Leguminosae) seed, yet another "next big thing" to get rid of the blubber?  (Tzeng. 2012 --) The results the scientists from the Department of Internal Medicine, at the Pao Chien Hospital in  Ping Tung City will be publishing in the January 2013 issue of Food Chemistry do at at least look intriguing.  Although - and this goes to show you that SuppVersity readers always (well "almost always" ;-) are the first know first - at least one of the active ingredients in Cassia tora, which is also known as Senna tora and is, besides its use in Ayurveda medicine, also used in Sri Lankan cousin, is an old friend: Emodin! The stuff that gives rhubarb the fat burning prowess you read about in not  too long ago, here at the Suppversity.
  
  

  

  CSEE  had dose dependent ameliorative effects on body weight gain and visceral body fat levels that were - ad the highest dose - identical to those of the thiazolidinedione (TZD) drug pioglitazone (Tzeng. 2012)

  After fattening them for 2 weeks with the notorious high fat diet, the Koreans assigned their now obese lab rats to groups who received either
  
  • Cassia seed ethanol extract (CSEE) by oral gavage, once per day for 8 week with CSEE doses of 100, 200, and 300 mg/kg in a volume of 2 ml/kg distilled water,
  • the diabetes drug pioglitazone dosed at 20mg/kg/day, or
  • a placebo, containing just the distilled water.
  Without any effects on the amount of food the animals consumed, the Cassia seed ethanol extract totally blunted the HFD induced weight gain (weight gain was identical to control group on normal chow, see figure to the right).
  
  In that. the highest dosage had the greatest effect on both body weight gain, as well as plasma lipid levels and epididymal WAT sizes in HFD-fed rats. These effects were probably mediated by CSEE's beneficial effect on the phosphorylation of AMP-activated protein kinase (AMPK) and its primary downstream targeting enzyme, acetyl-CoA carboxylase. In addition, the researchers found that the cassia seed extract directly increased genes that are responsible for fatty acid oxidation and down-regulated their fat synthesizing counterparts in the visceral white adipose tissue of the animals.
  
  Whether CSEE is going to be a go-to supplement of the future cannot be said, now. What is certain, however, is that it constitutes yet another example of a potentially highly effective natural alternative to the established pharmacological 'treatment' (or rather management) of the diabesity epidemic.
  
• Obese, once and forever, unless you diet for the rest of your life? (Kirchner. 2012) -- A paper that's been published in the latest issue of the Journal of the American Diabetes Association, clearly suggests that the ravenous appetite of "reduced-obese" individuals, i.e. people who have been dieting for weeks and months to shed they weight they have accumulated over years is not (solely) psychologically induced gluttony.
  
  

  

  Suggested read: "Longterm 5% Calorie Restriction & Longterm Dieting Make You Fat and Insulin Resistant." (read full article)

  When Kirchner et al. put their diet-induced obese mice were on a  food restricted for 5 weeks, they did in fact reach the same body fat levels as age-matched rodents who had never received anything but the standard chow. Their  blood glucose levels normalized and their insulin sensitivity increased, but the "reduced-obese" mice also showed markedly increased fasting-induced hyperphagia. In fact, when they given ad libitum access to their beloved high fat diet, they ate like there was no tomorrow and ended up gaining weight at a much faster pace than their never-obese peers, who were likewise allowed free access to the HFD.
  
  And it gets even worse, as the conclusion the scientists draw based on their results says that despite the fact that "caloric restriction on a HFD provides metabolic benefits", it may actually require a previously obese dieter to continue on the path of caloric restriction (i.e. never eat to 'satiety') for the rest of his/her life!
  
• Morning to evening decline in insulin response to carbs suggests breakfast is the time where your body reacts most sensitive to carbs (Saad. 2012) -- Likewise published in the latest issue of Diabetes is a study by Ahmed Saad and colleagues from the Mayo College of Medicine in Rochester and the the University of Padova in Italy, which does at first not really sound like it was revolutionary new. Two definitive advantages of the study at hand were yet that the scientists used healthy individuals as subject and gave them regular mixed meals instead of a glucose solution in order to confirm the existence and identify the characteristic features of the diurnal pattern of glucose tolerance most people take for granted.
  
  

  

  The implications of this study for intermittent fasting are not as clear as you may think and certainly don't imply that you must break your fast in the morning (read more about breaking the fast, here)

  Overall 20 healthy volunteers with normal fasting glucose (4.8 ± 0.1 mmol/L) and HbA_1c (5.2 ± 0.0%) participated in the study. They were provided with identical mixed meals during breakfast, lunch, or dinner at 0700, 1300, and 1900 h in a random order on 3 consecutive days. Physical activity was held constant so that e.g. muscle glycogen depletion and subsequent increases in AMPK induced GLUT-4 expression  would not skew the results.
  
  What Saad et al. fonud was that the postprandial glucose excursion was significantly lower (P < 0.01) at breakfast than lunch and dinner. At the same time the β-Cell responsivity to glucose was higher. This means there was more insulin released per unit of glucose, than during lunch or dinner.
  
  The time the hepatic insulin extraction was also lower at breakfast; although the difference reached statistical significance only in comparison to the dinner condition. Since the overall meal glucose appearance did not differ between meals and that the suppression of endogenous glucose production "tended to be lower (P < 0.01) and insulin sensitivity tended to be higher (P < 0.01) at breakfast than at lunch or dinner" (Saad. 2012), it is no wonder that the spike in blood glucose was largely augmented, when the subjects consumed the standardized meal for breakfast.
  
• Adipocyte size is a determinant of non-alcoholic fatty liver disease (NAFLD) risk (Petäjä. 2012) -- One thing scientists still have not really understood is how some obese people seem to be way better off than others, although their BMIs, fat and lean mass appears to be identical. In view of the latest paper by a group of researchers from Finland and Sweden on the association between the average fat cell size and the occurrence of NAFLD, it could well be that ratio of the total adipose volume to the total fat cell number, which obviously is the adipocyte size, may be providing at least another piece to the puzzle that holds the answer to this question.
  
  

  

  In a previos post on the yoyo effect, I already discussed some aspects of adipocyte morphology - read more

  The scientists have studied 119 non-diabetic subjects in a cross-sectional study. The participants had a median age of 39 (26-53) years, and a mean BMI of 30.0±5.7kg/m². Subcutaneous abdominal fat cell size, as well as the total amount of liver fat were measured by proton magnetic resonance spectroscopy, intra-abdominal (IA) and abdominal subcutaneous adipose tissue (SC) volumes by magnetic resonance imaging (MRI) and an additional gene analysis yielded information about the genotype (susceptible or not susceptble to metabolic syndrome) of the individuals.
  
  Simply based on a multiple linear regression analysis, age, gender, BMI, the intra-abdominal to subcutaneous fat ratio and the subject's PNPLA3 genotype, the results were only able to explain 42% of the variation of the liver fat. The inclusion of the adipocyte sizes increased the predictive value by 11%, so that "21% of the known variation in liver fat could be explained by adipocyte size alone" (Petäjä. 2012) This does yet also mean that once we are up to a 90% explanation  (which is unrealistic, by the way) the adipocyte size will only be able to explain "of the known variations".
  
• Antibiotic that's commonly used in animal fattening kills body fat (Szkudlarek-Mikho, 2012) -- Reserachers from the College of Medicine at the University of Toledo in Ohio have found that polyether ionophoric antibiotics including monensin, salinomycin, and narasin, which are widely used in veterinary medicine and as food additives and growth promoters in animal husbandry including poultry farming have toxic effects on adipose cells.
  
  

  

  Whether eating the chicken that ate antibiotics is going to make  you lean does still have to be established. Based on the results of the study at hand, it does however appear likely that eating antibiotics could - I do however doubt that they will achieve that without potentially serious side effects.

  Although previous studies suggest that salinomycin has anti-carcinogenic effects (Huczyński. 2012), the sharp increase in poultry consumption over the last decade(s) and the increased use of these "growth promoting" antibiotics by veterinaries and poultry farmers has often been suspected to be involved in the increase in metabolic and autoimmune diseases.
  
  At least in view of the former, i.e. metabolic diseases in general and obesity, in particular, it may therefore be surprising that the scientists from the University of Toledo discovered that the tested ionophoric antibiotics did not just inhibit the differentiation of cancer, but also that of preadipocytes into adipocytes:
  

  "The block of differentiation is not due to the induction of apoptosis nor the inhibition of cell proliferation. In addition, salinomycin also suppresses the transcriptional activity of the CCAAT/enhancer binding proteins and the peroxisome proliferator-activated receptor γ." (Szkudlarek-Mikho. 2012)

  Now, I would fully subscribe to the scientists suggestion that these "ionophoric antibiotics can be exploited as novel anti-obesity therapeutics", but until that has been done and we know which other cells' differentiation they may inhibit, as well, I'd strongly discourage anyone from 'supplementing' with the antibiotics from his or her poultry farmer next door. After all, you may well end up not just with less body fat, but with less brain tissue, as well... what? You don't care? Oh I see. The doctor must have inserted the cannula into your ears instead of your belly on your last liposuction, right?
  
• Alpinia officinarum, a plant in the ginger family, stops fat gains in its tracks (Jung. 2012) -- Jung, Jang, Ahn and the rest of the researchers from the Korea Food Research Institute in Seongnam, report in their latest paper that an ethanol extract from Alpinia officinarum, a plant in the ginger family that's cultivated in Southeast Asia and is also known as lesser galangal, is yet another mainstay of traditional medicine with significant anti-obesity effects.
  
  

  

  It looks almost like ginger and works almost like ginger, but A. officinarum contains galangin, not gingerol and works via the PPAR-gamma pathway, as well. That's something gingerol doesn't do (Huang. 2012)

  Originally used throughout Asia in curries and perfumes, A. officinarum contains a dietary flavenol called galangin, which has already been shown to exert profound anti-cancer effects (Kapoor. 2012), whether it is solely responsible for the in vitro and in vivo inhibitory effects on lipid accumulation during the differentation of 3T3-L1 adipocytes is not certain, but appears to be likely.
  
  Via its effects on the fat synthesis and breakdown and PPAR-gamma activity the A. officinarum extract (AOE) lead to dose-dependent decreases in body weight gains of mice who were fed a high fat diet. It also reduced the visceral and liver fat deposition and partially restored the abnormally elevated insulin and leptin levels of the rodents.
  

  "Collectively, these results suggest that AOE prevents obesity by suppressing adipogenic and lipogenic genes. AOE has potential for use as an antiobesity therapeutic agent that can function by regulating lipid metabolism." (Jung. 2012)

  Certainly another nice find, but let's be honest, what's the real value of all this herbs? I mean yeah they work almost as effectively (in some cases even better) than pharmacological drugs, but both share a detrimental downside, that's not mentioned under "side effects" on the package insert or supplement bottle: They will only manage a problem the root course of which is the net result of a totally messed up diet.

That's it and since you've gotten the bottom line in advance and another time, just to make sure nobody can over-read it, in the last paragraph of the last news item, I just want to remind everyone that there are a couple of other interesting science news and links, for example about ...

• the pro-carcinogenic effects of shift work and to a lesser degree constantly working at night (read),
• the connection between high GI carbs and prostate cancer (read), or
• the idiocy of battling the high GI carb induced decline in cognitive performance with even more sugar (read)

waiting for you on Facebook. Have a nice day and get lean and stay lean ;-)

References

• Huang TH, Teoh AW, Lin BL, Lin DS, Roufogalis B. The role of herbal PPAR modulators in the treatment of cardiometabolic syndrome. Pharmacol Res. 2009 Sep;60(3):195-206. Epub 2009 Apr 7.
• Huczyński A, Janczak J, Antoszczak M, Wietrzyk J, Maj E, Brzezinski B. Antiproliferative activity of salinomycin and its derivatives. Bioorg Med Chem Lett. 2012 Dec 1;22(23):7146-50.
• Jung CH, Jang SJ, Ahn J, Gwon SY, Jeon TI, Kim TW, Ha TY. Alpinia officinarum Inhibits Adipocyte Differentiation and High-Fat Diet-Induced Obesity in Mice Through Regulation of Adipogenesis and Lipogenesis. J Med Food. 2012 Nov;15(11):959-67.
• Kapoor S. Galangin and its emerging anti-neoplastic effects. Cytotechnology. 2012 Oct 25.
• Kirchner H, Hofmann SM, Fischer-Rosinsky A, Hembree J, Abplanalp W, Ottaway N, Donelan E, Krishna R, Woods SC, Müller TD, Spranger J, Perez-Tilve D, Pfluger PT, Tschöp MH, Habegger KM. Caloric restriction chronically impairs metabolic programming in mice. Diabetes. 2012 Nov;61(11):2734-42. doi: 10.2337/db11-1621.
• Petäjä EM, Sevastianova K, Hakkarainen A, Orho-Melander M, Lundbom N, Yki-Järvinen H. Adipocyte size is associated with NAFLD independent of obesity, fat distribution and PNPLA3 genotype. Obesity. 2012. Ahead of Print.
• Saad A, Dalla Man C, Nandy DK, Levine JA, Bharucha AE, Rizza RA, Basu R, Carter RE, Cobelli C, Kudva YC, Basu A. Diurnal pattern to insulin secretion and insulin action in healthy individuals. Diabetes. 2012 Nov;61(11):2691-700.
• Szkudlarek-Mikho M, Saunders RA, Yap SF, Ngeow YF, Chin KV. Salinomycin, A Polyether Ionophoric Antibiotic, Inhibits Adipogenesis. Biochem Biophys Res Commun. 2012 Oct 31.
• Tzeng TF, Lu HJ, Liou SS, Chang CJ, Liu IM. Reduction of lipid accumulation in white adipose tissues by Cassia tora (Leguminosae) seed extract is associated with AMPK activation. Food Chem. 2013 Jan 15;136(2):1086-94. doi: 10.1016/j.foodchem.2012.09.017.

No-Carb Foods, Artificial Sweeteners & The Cravings: In The End, It's The Glucose, Not The Taste Our Brains Crave

Despite the fact that candy is per definition (literally) made of sugar, you can buy "no carb candy" at every corner. The results of this study tell you why these aren't worth the money.

I have written extensively about artificial sweeteners in the past and would thus hope that it's not necessary to recount all the information about how they interact with insulin, potential toxicity risks, their (non-existent) effects on satiety... ah, well actually I do want to talk about the last point, because it is highly relevant to understand the implications of the results of recent Yale study (Tellez. 2013).

I know, it's just a rodent study, but I guess you will feel reminded of yourselves during your diet, when I tell you about the observations Luis A Tellez, Xueying Ren, Wenfei Han, Sara Medina, Jozelia Ferreira, Catherine Yeckel and Ivan E de Araujo made an experiment that is the first to demonstrate that the lack of glucose utilization in the brain makes artificial sweetener totally unattractive to mice.

Did you ever realize that sweeteners just won't cut it, when you're hungry?

Many of you may know that: You are dieting and you are craving - food in general, but pasta, candy and all the other carbohydrate-laden foods even more so. You've been training hard and feel that your blood glucose levels are right in the no-man's land between "just high enough to keep standing" and "already so low that you have to sit down". This is the time when you will begin to feel cold. You are sweating or getting shaky (these symptoms vary from person to person), get moody or feel like you had to run even more just to abstain from doing the one thing of which you know that it would solve all your problems (temporarily): Heading over to the kiosk next door and buying the next best Snickers or Mars bar.

Yes, Adelfo Cerame is a professed, but reformed carbophobic. Learn more about how reintroducing carbs into his diet finally got him his pro-card in this and his other guest posts

The poor critters in the study Tellez et al. conducted did not have a kiosk available. What they did have, though, was glucose and artificially sweetened water. Now, the scientists conducted the same experiment in two conditions.

• During condition one, the rodents were fed, satiated and happy (fed). 
• During condition two, however, they had been glucose deprived and were in a similar state as you may have been after the previously described workout. 

What's quite telling (and by the way new) is that the glucose availability had a major impact on their sweetener preferences. When fed and happy, the mice went for the super-sweet sugar- and calorie-free artificially sweetened water.

The disgustingly sweet but glucose-free water did however lose all its appeal once the mouse brains realized that the glucose supply was becoming tight:

"Consistently, hungry mice shifted their preferences away from artificial sweeteners and in favour of glucose after experiencing glucose in a hungry state." (Tellez. 2013)

And what's more, this deliberate(?), or probably instinctive, decision to turn their back on the fake sugars and avail themselves of the "real sweet deal" of which they new it would deliver what the mice needed was immediately rewarded. Rewarded in the most physiological sense of the word: with a whopping dose of dopamine, the very hormone that entrains stimulus < > response relationships like these.

Sugar will increase dopamine, sweeteners won't

You can tell how real this "conditioning" effect was from another observation the researchers made, when they analyzed the brain activity of their lab animals and found that a big gulp from the sugar water did not just bring the blood glucose of the sugar-deprived animals back up, it

"was [also] found to produce significantly greater levels of dopamine efflux compared to artificial sweetener in dorsal striatum" (Tellez. 2013)

When the scientists artificially disrupted the oxidation of glucose directly at the level of the dorsal striatum, which is also known as the neostriatum or striate nucleus that is activated by stimuli associated with reward and aversive, novel, unexpected, or intense stimuli, the sweetness preferences of the mice remained the same. This observation directly supports the conclusion that we are in fact dealing with a fundamental food-reward effect here; and effect, of which you can be certain that is is also involves in "past addiction" ;-)

So what does this tell you about fake foods?

Suppversity highly suggested read: "Science Round-Up Seconds: The Pro-Insulinogenic Effect of Artificial Sweeteners + Mechanisms & Consequences" | read more

As the researchers themselves point out, their results demonstrate that glucose oxidation controls the intake levels of "sweet tastants"  (=umbrella term for everything that stimulates the sweet taste receptors) by modulating the extracellular dopamine levels in dorsal striatum.

For you, this means that you know better than believe that you could get away with that low carb, sugar free candy bar, chewing gum or whatever else it may be that you are using to soothe your sweet tooth you are effectively cheating yourself. It works only in conjunction with your free will to avoid the carbs and usually only for so long as you allow yourself planned and controlled refeeds.

Note: When you are in full ketosis, things may be different; although the effects of ketones on dopamine levels are - afaik - not well researched, yet.

Let's finally try to draw some more general conclusions about carbohydrate intake in general - I mean beside the real sweet stuff, like candy, etc. Let's take the no-carb noodles you or hopefully not you, but your obese neighbor just bought, for example. They may taste just like the real deal. In the absences of the (expected) subsequent influx of glucose and its oxidation in the brain, they will yet never provide the hedonic response you are looking for. They are fake, a good one that may fool the first line of nutrient sensors, but a fake that's not good enough to reproduce the expected downstream effects on neurotransmitters.

Now, the good news is: No-carb noodles are probably non-addictive. The bad news, however, is: No-carb noodles are also highly, or I should say utterly unsatisfying replacement for real pasta, because the lack of carbohydrates, or rather the glucose that would get oxidized right in your brain, when you consume a bowl of real pasta is the critical physiological signal that makes pasta what it is: A highly addictive comfort food. For the average pasta junky, a "no-carb noodle" is thus never going to cut it, unless he or she is willing to cure him- or herself of her sugar addiction first.

---

SuppVersity suggested read: "Coke vs. Diet Coke vs. Milk - The "Unhealthy Beverage Shoot-Out": Milk Reduces, Coke Increases Visceral Fat. Dreaded Diet Coke on Par With Plain Water" | read the complete article

Bottom line: Unlike "zero carb candy" or "no-carb noodles" an effective "diet aid", or let's rather say, one of the foods you should select, whenever you are trying to rid yourself of body fat (low GI starches, fruits and even vegetables (*I write "even" because the amount of carbs in some veggies borders zero)) can offer this "second line" effects in your brain; effects, none of the fake foods you buy at the supplement store, the super market and as of late even some kiosks will ever be able to produce. These real foods are the ones that will have you feel satisfied and they are the ones that should make up more than just the figurative lion's share of your diet - not the calorie, carbohydrate and nutrient free no-carb noodles and their low-carb brethren that will just have you crave the "real deal" even more.

194 Bananas in 3 Weeks, Same Liver Fat & Lower Body Fat 6 Months After; Nigella Sativa Boosts Testosterone & Fertility; Sugar Dampens Caffeine Rush + Thyroid & Body Comp.

Three weeks of +1,000 kcal carb overfeeding (approx. 194 bananas!): Does it supersize your liver fat? This and more in today's installment of On Short Notice

As promised in yesterday's first part of the weekly written news-round up aka On Short Notice, we won't waste any time on lengthy introductions (the "short" items themselves are already long enough ;-) and get right down to business! For today this means that we are going to take a peak at the latest studies on

• the reality of thyroid hormone metabolism
• the dampening effects of sugar on high dose caffeine
• the sugary truth about the reversibility of early NAFLD
• the pro-testosterone, pro-fertility effect of black cumin

as well as the latest data on US drug sales and an upcoming blogpost discussing "training for anabolism" - enjoy!

Just in case you feel that's not enough, I suggest you listen to this week's installment of the SuppVersity Science News Roundup (click here to download) on Super Human Radio, as well!

• 

  Figure 1: The more energy reserves a metabolically healthy and euthyroid person has and the more he or she eats (though this was not quantified we can probably assume that the heavier participant also consumed more energy on a daily basis), the less energy efficient is his metabolism going to be - the margin is yet not unlimited, eat 40% more and get fat regardless of what type of food those calories come from (generated based on Roef. 2012)

  Levels of thyroid hormone associated with greater body weight and body fatness I know this sounds surprising, but int he end the latest results from the Department of Endocrinology at the Ghent University Hospital in Belgium only confirm what I keep preaching here at the SuppVersity over and over again: The main reason that the calories in vs. calories out calculations don't work is that the "calories out" part of the equation depends on both the "calories in" and the "calories stored", as well as the "accessibility of the calories stored" parameters, and [...].
  Put differently, the reason that the 941 generally healthy and euthyroid (=normal thyroid function) male siblings (25-45 yrs, median BMI 24.6) with the highest body weights and the greatest body fat mass also had the highest levels of leptin, free and total T3 & T4, as well as thyroid binding globulin is simple: In the presence of ample energy supply their bodies will treat their resources more wasteful, than those of the skinny or wanna-be-skinny, ah... I mean "ripped" guys who undereat and overtrain.
  The opposite is the case for the more muscular study participants, whose greater lean mass and muscle cross-sectional area were associated with lower (F)T3, (F)T4 and TBG levels (p ≤0.0003). They simply cannot afford (you could also say that they don't need) to ramp up their already higher fatty acid oxidation and overall energy expenditure, even further. Lastly, there was a clear-cut association with higher free T3 levels and lower insulin sensitivity, and - I had almost forgotten to mention that - "[n]o associations between TSH and body composition or metabolic parameters were seen."
  I suggest you print the finding about TSH levels and ask your doctor if he judges the speed of his car by looking at the gaspedal (TSH is more or less the gas-pedal that will tell your thyroid how hard it's got to work, but won't tell you how much of active thyroid hormone it is capable of producing) rather than the speedometer, when he is too cheap to order a full thyroid panel the next time you ask him to do so ;-)

• 

  Figure 2: While the initial caffeine spike is blunted by the ingestion of a sugar-laden breakfast, the area under the curve (bottom, right) a similar, yet less pronounced effect and both, the reduction of the initial spike in serum caffeine, as well as difference of the total influx over time are dose dependent (Skinner. 2012)

  Sugary breakfast reduces early rise in serum caffeine levels by up to 90% That's at least the result of a recent study by Tina Skinner and her colleagues from the University of Queensland in Down-Under. The high carbohydrate meal, in this case a toast with jam, cordial, and an energy bar ("Vanilla Crisp" PowerBar Performance Bar), the scientists served their 14 healthy active male participants (age 24.8 ± 3.7 yrs, body mass 74.6 ± 8.5 kg, height 184.0 ± 8.5 cm; mean ± SD) who had reported fasted, well hydrated and 48h after they had consumed their last caffeinated beverage at the lab (Skinner. 2012). It does not really take a rocket scientist to see that the absence of the initial onslaught of caffeine as a result of the pre-ingestion of the sugary "breakfast" will probably diminish, if not totally blunt the stimulating effects of coffee.
  In view of the fact that this effect was particularly pronounced during the "high dose" (=9mg/kg body weight; ~540-900mg; equiv. to 3-4.5 large cups of strong coffee), it is yet probably of greater importance for stim junkies and athletes looking for the pre-workout edge before they hit the gym, than for the average white color worker who needs to get his daily buzz, if he does not want to miss his bus (or train ;-)
• Liver-fattening effects of carbohydrate overfeeding are genetically dispositioned, but the recently published data from a study that was conducted by scientists from the Minerva Foundation Institute for Medical Research, the University of Helsinki and other Finnish research facilities shows that an appropriate diet can reduce increased liver and body fat levels, reduce body fat levels and improve lipid and glucose metabolism, regardless of the genotype (PNPLA3-148II = disadvantaged vs. PNPLA3-148MM) of the subjects.
  But let's take on thing after the other. After some standard baseline tests, the 16 subjects (mean age 54 year; BMI at baseline 30.6kg/m²; 5 men, 11 women) were "overfed" with a high carbohydrate diet from the "every low-carbers worst nightmare" category:
  

  

  Figure 3: Change in body composition from due to 3-week overfeeding (blue), 6 months dieting (compared to post overfeeding - red; Sevastianova. 2012)

  "The subjects were instructed to continue their normal diet and in addition to consume an extra 1000 kcal/d with 98% of energy from carbohydrates. The extra diet consisted of candy (Oy Karl Fazer Ab), pineapple juice (Tuko Logistics Oy), sugar-sweetened soft drinks (Oy Hartwall Ab), and/or carbohydrate-loading drink (Squeezy Sports Nutrition GmbH) and was provided free of charge from the research unit to the study participants." (Sevastianova. 2012)

  As you will probably have expected the highly insulinogenic, additional 21,000kcal from glucose and fructose (~5250g or 194 bananas, medium size to be precise ;-) did leave "their marks" on the waist and hips of the subjects, but probably not to the extend you may have anticipated (see figure 1). Even more suprisingly, the short term overfeeding did not deteriorate any of the blood glucose parameters (all changes had p-values way beyond what would be statistcally significant, the glucose clearance over 2h did even improve! - statistically likewise non-significant, though).
  Most importantly, however, the body composition, triglyceride levels (-6%), HDL (+11%) and all the important body composition measures (see figure 3) improved and the liver fat returned to baseline in the course of the 6-months "diet period", which consisted of - mark my words - nothing but making a switch to a diet with more vegetables, less simple sugars, white flour, and alcoholic drinks and dietary counseling wrt to food types and appropriate (=moderate) portion sizes. No extreme low carbing, no drastic calorie reductions, just healthy whole foods - regardless of "your bad genes"!
• Nigella sativa, aka black cumin, jacks up testosterone and makes tired sperm get a move on Being well aware that you cannot go without a weekly post about at least one natural testbooster,  you will probably be relieved to hear that Rahmatollah Parandin, Namdar Yousofvand and Rostam Ghorbani have published a paper in the latest issue of the Iranian Journal of Reproductive Medicine in which they describe the fertility and testosterone boosting effects of 200 and 400mg/kg of an alcoholic extract from Nigella sativa seeds (Parandin. 2012).
  *Reminder: Regardless of whether we are dealing with rodents or humans, a "testosterone booster" that works in sick animals or humans does not necessarily work in healthy ones, as well. It is much more likely, that the effects on testosterone are secondary to the effect of the effect the herb or whatever else has on the overall health of the lab animals / participants, so that someone who is not sick in the first place won't see any (or at best minimal) improvements.
  The seed extract that was administered to healthy*  male Wistar rats 60 days contained a mix of various active ingredients
  
  • 30-48% Thymoquinone,
  • 7-15% P-cymene, 
  • 6-12% Carvacrol, 
  • 2-7% 4-terpineol, 
  • 1-4% T-anethole, and 
  • 1-8% Sesquiterpene,
  of which Prandin et al. state that Thymogquinone is currently considered to be be the pharmacologically active constituent of N. sativa (cf. Padhye. 2008) - keep that in mind, when you cannot resist giving this stuff a try ;-)
  Now, the ~23% increase in testosterone is certainly nothing like the "140% increase in testosterone" certain supplement companies state one of the testers had (without any peer-reviewed data whatsoever, by the way), but as mediocre as it may seem, it was achieved from a healthy baseline level and it went hand in hand with improvements in all sperm parameters, of which I picked the sperm count and plotted it together with the latest human data from the University Department of Growth and Reproduction at the Rigshospitalet of the University of Copenhagen in Denmark in the second graph in figure 3 (Jørgensen. 2012).

  

  Figure 4: Yeah, Nigella boosts testosterone by 20% (left), but there are other things in life... what about it's effect on sperm count (right) for example? The increase the rodents in the high-dose group experients would catapult the infertile Danish men almost into the normal zone (based on Jørgensen. 2012 & Parandin. 2012)

  Now this is certainly by no means scientific evidence and I am not suggesting that it will help solve potential fertility problems (not just because sperm count is only one out of a dozen parameters, but also because we don't know whether what works in healthy rodents will work in sick people; see red box above for the other side of the coin). What I found quite important though, is to give you an idea of what those abstract numbers could eventually mean. Contrary to the 20% increase in testosterone which will hardly help you to build significantly more muscle mass, a similar bump in sperm count (and other fertility parameters) could very well make the difference between fertile and infertile!
  So, at whichever Internet source you may be able to dig up a respective extract and regardless of whether you want it for fertility or futility, ah... I mean "testosterone boosting" issues, make sure that it has a high Thymoquinone content and that you have enough of it to hit the human dose equivalent (click here to learn how to calculate HEDs) of 65mg/kg or 4-5g per day!
  

Figure 6: US Drug sales 2010 & 2011 as posted on the SuppVersity Facebook wall earlier today (based on Lindsay. 2012).

The End - for today, at least. I guess I won't take too much away, if I tell you that there was actually another item scheduled for today... a post about "High or Low, Long or Short, Heavy or Light what are the Best Set Numbers and Rest Times,Weights and Rep Schemes, When You're Training for Anabolism" - and while this is "anabolism" in the old and actually sort of outdated sense of more testosterone and less cortisol, I'm pretty confident that the muscle-heads among you would have liked it, if it did not get longer and longer, so that I decided to polish it up a little and put you on the rack for another two days or so ;-)

So, in case that's driving you crazy, you may want to consider asking your Dr. for a script for an antipsychotic, currently the #5 on the 2011 (=the latest) US drug sale ranking (see figure 6; remember the data is $-based not script-based), I posted along with a handful of other interesting news-items earlier today on the SuppVersity Facebook wall.

References:

• Jørgensen N, Joensen UN, Jensen TK, Jensen MB, Almstrup K, Olesen IA, Juul A, Andersson AM, Carlsen E, Petersen JH, Toppari J, Skakkebæk NE. Human semen quality in the new millennium: a prospective cross-sectional population-based study of 4867 men. BMJ Open. 2012 Jul 2;2(4).
• Lindsley CW. The top prescription drugs of 2011 in the United States: antipsychotics and antidepressants once again lead CNS therapeutics. ACS Chem Neurosci. 2012 Aug 15;3(8):630-1.
• Roef G, Lapauw BM, Goemaere S, Zmierczak HG, Toye K, Kaufman JM, Taes Y. Body composition and metabolic parameters are associated with variation in thyroid hormone levels among euthyroid young men. Eur J Endocrinol. 2012 Sep 6.
• Padhye S, Banerjee S, Ahmad A. Mohammad R. Sarkar FH. From here to eternity- the secret of Pharaohs: Therapeutic potential of black cumin seeds and beyond. Cancer Ther 2008; 6: 495-510
• Parandin R, Yousofvand N, Ghorbani R. The enhancing effects of alcoholic extract of Nigella sativa seed on fertility potential, plasma gonadotropins and testosterone in male rats. Iran J Reprod Med. July 2012; 10(4): 355-362.
• Sevastianova K, Santos A, Kotronen A, Hakkarainen A, Makkonen J, Silander K, Peltonen M, Romeo S, Lundbom J, Lundbom N, Olkkonen VM, Gylling H, Fielding BA, Rissanen A, Yki-Järvinen H. Effect of short-term carbohydrate overfeeding and long-term weight loss on liver fat in overweight humans. Am J Clin Nutr. 2012 Sep 5.
• Skinner TL, Jenkins DG, Folling J, Leveritt MD, Coombes JS, Taaffe DR. Influence of carbohydrate on serum caffeine concentrations following caffeine ingestion. J Sci Med Sport. 2012 Sep 7.