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Wednesday, November 4, 2015

Resting 3 vs. 1 Min. Between Sets Pays Off: Greater Size + Strength Gains - Probably Mediated by 15% Higher Volume

Resting long enough to maximize your training volume could be the key to success, i.e. strength and size gains.

If you have been following the various affords to ascribe differences in strength and, even more so, size-increases to a specific training variable, you will remember that the only promising parameters that appear to be supported by more than the literal "outlier study" are training load and volume.

Of these, the former is pretty much uncontested. The latter, however, is still questioned by a camp of inconvincible skep- tics, who simply ignore the fact that there's ample evidence that "[h]igher-volume, multiple-set protocols have consistent- ly proven superior over single set protocols with respect to increased muscle hypertrophy" (Schoenfeld. 2010).

It would be interesting to see if rest periods should also be periodized!

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What still isn't clear, though, is the role of other training parameters, such as the time you take to recover between multiple sets and exercises aka the "rest intervals". As Schoenfeld et al. point out in the introduction to their most recent study, "several studies have investigated the effects of varying rest interval length on muscular adaptations," (Schoenfeld. 2015) albeit with contradictory results: While Ahtiainen et al (2005) were unable to find a significant inter-group size or strength difference in well-trained subjects (6.6 +/- 2.8 years of continuous strength training) who rested 2 minutes compared to those who rested only 5 minute in response to their 21-week training intervention, Buresh et al (2005) reported more recently that significantly greater size increases of the arms and a trend for greater muscle hypertrophy in the legs in young, albeit untrained subjects who rested for 2.5 minutes instead of just one.

Figure 1: Previous studies found "conflicting" evidence. While Ahtiainen et al. found no effects of 2 vs. 5 minutes in trained, Buresh et al. found effects of 2 vs. 1 minutes rest in untrained subjects. With different subjects, different workouts and most importantly different rest times that were compared it is yet not exactly right to say that the studies contradict each other.

Now, obviously, the ostensible "contradiction" I alluded to in the previous paragraph does eventually not exist. With trained vs. untrained subjects, different workout protocols and most importantly different rest intervals (1 vs. 2 minutes and 2 vs. 5 minutes) the studies by Ahtiainen and Buresh cannot really contradict each other. The same must be said of an even more recent study by Villanueva et al. (2014) the surprising findings of which, i.e. "longer rest periods compromise the gains of older trainees", I've discussed last year, already.

What about the lack of different increases in strength endurance? I have to admit that I do not discuss this finding of the study in detail. While one would expect that shorter rest intervals would produce greater strength endurance adaptations, the researchers observed the opposite, an - albeit non-significantly larger increase in strength endurance in the 3-minute-rest group that correlated with the increase in 1RM strength. Further studies will have to show what the underlying mechanism of this counter-intuitive observation is and whether it may be muscle specific, i.e. occur only in the upper, but not in the lower body.

Eventually, however, this does not change that there is, as Schoenfeld et al. write that "a need for more research to provide greater clarity on the topic" (Schoenfeld. 2015). A "clarity" Schoenfeld et al. sought to find with a study that "used current rest interval recommendations for hypertrophy and strength of 1 versus 3 minutes, respectively, and employed validated measures to directly assess site-specific changes in muscle thickness" (ibid). In that, the researchers speculated that ...

"[c]onsistent with generally accepted guidelines on the topic (Willardson. 2006), we hypothesized that short rest intervals would produce greater increases in muscle growth and local muscle endurance while long rest intervals would result in superior strength increases" (Schoenfeld. 2015).

As you will know if you didn't miss the headline of this waredownloadsoft article, this hypothesis was only partly validated. The data in Figure 2 confirms that the subjects, "experienced lifters (defined as consistently lifting weights for a minimum of 6 months and a back squat / body weight ratio ≥ 1.0)" (Schoenfeld. 2015), gained significantly more strength, when they rested 3 versus just 1 minute between the 3 sets of their three weekly workouts (Figure 2 does also tell you that the strength endurance increases were identical in both groups).

Figure 2: Changes in markers of strength and strength endurance; * denotes significant pre- vs. post difference, # denotes significant inter-group difference (here in favor of long(er) rest periods | Schoenfeld. 2015).

What was Schoenfeld et al. did not find, however, were increased size gains in the short-rest period group whose 24 workouts that were performed on non-consecutive days over the course of the 8-week study period, were otherwise identical with those of the long-rest period group and comprised a total of 7 exercises for all major body parts, namely...

three leg exercises, i.e. barbell back squats, plate-loaded leg presses, and plate-loaded leg extensions),
two exercises for the anterior torso muscles, i.e. flat barbell presses and seated barbell military presses, and
two exercises for the posterior torso muscles, i.e. wide-grip plate-loaded lateral pulldowns, and plate-loaded seated cable rows

This is a highly significant result even for you who is - according to an older waredownloadsoft Poll - probably training according to a split regimen, albeit most likely with very similar exercises. What may be different from the some, but obviously *smile* not your workout though, is that the supervision by members of the research team ensured that the subjects stuck to the prescribed cadence of 1 second for the concentric and "approximately 2 seconds" (ibid.) for the eccentric part of every the exercise. This as well as the imperative progression to higher weights, whence the prescribed number of 8-12 reps per set could be performed is unfortunately overlooked by many recreational trainees - with disappointing consequences in the form of inferior or even no size and strength gains, by the way... but I am digressing, let's rather take a look at the already mentioned, unexpectedly superior strength size gains in the long(er) rest interval group (Figure 3).

Figure 3: Changes in muscle thickness and corresponding effect sizes; * denotes significant pre- vs. post-changes, # denotes significant inter-group differences; overall it is obvious that there's a long(er) rest advantage (Schoenfeld. 2015).

As the single "#" in Figure 3 tells you, the inter-group differences and thus the advantage of the long(er) rest intervals was statistically significant only for the quads, though. If we also take into account the lack of statistically significant effects on the sleeve sizes (biceps and triceps) in the short rest interval group, as well as the obvious differences in effect sizes (Figure 3, right), there's yet little doubt that the hypothesis that shorter rest intervals yield greater size increases must be considered falsified - at least under the given experimental conditions (trained subjects, three full-body workouts per week, standard hypertrophy set and rep-ranges, etc.).

So what's the verdict, then? At first sight it would appear as if the study at hand would totally refute the idea that shorter rest intervals, or I should clarify, rest intervals that are as short as 60s (*) should have a place in your training regimen altogether (*Schoenfeld, et al. rightly point out that Ahtiainen's result suggest that even 120s could have been enough time to rest - it is thus important to give precise recommendations for rest intervals, not something as arbitrary "short" vs. "long"). We should not forget, though, that even a thoroughly conducted study like the one at hand has its limits and definite conclusions should not be drawn hastily based on a single study result - even if it is, as in this case, corroborated by the results of Buresh et al (2009).

Figure 4: The total training volume in the long(er) rest period group (3 vs. 1 minutes of rest) was on average 15% higher. Due to the relatively high inter-individual differences and the relatively low number of participants (N=21) a statistically significant correlation between the weight lifted per week (total volume in kg as in the figure) and the surprisingly superior gains in the 3-min-rest group could not be established (based on Schoenfeld. 2015).

With that being said, a secondary outcome of the study provides a reasonable explanation for why both, the strength and the size gains benefited from long(er) rest intervals: The total training volume I've plotted in Figure 4. As Schoenfeld et al. point out, the latter has previously been suspected to mediate the effects of inter-set rest on strength and hypertrophy on total training volume and strength (Henselmans. 2014). A correlation between the visible differences in training load (see Figure 4) and the magnitude of training adaptations, however, could not be found in the study at hand. As the authors highlight, the reason for this lack of statistical significant correlations may yet be a simple lack of statistical power, so that one "cannot rule out the possibility that the greater training load achieved by the longer rest period group was responsible for the greater training adaptations" (Schoenfeld. 2015 | Buresh et al. found such an effect for the upper, yet not for the lower body).

Personally, I tend to believe that, with a higher number of subjects, a correlation between the total training volume that was on average 15% higher in the 3 vs. 1 minute rest group could have been established. This, in turn, would support the notion that long(er) rest periods - maybe, as Schoenfeld et al. suggest based on the data from Ahtiainen's study, at least 120s - are necessary to maximize the total training volume and thus the overall = strength and hypertrophy response to workouts. Whether that is true for all types of workouts (e.g. split- vs. full-body), all subject groups (e.g. people who are used to short rest periods vs. those who are not) as well as special athletic requirements (e.g. power vs. strength & hypertrophy) will have to be determined in future studies, however | Comment on Facebook!

References:

Ahtiainen, Juha P., et al. "Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men." The Journal of Strength & Conditioning Research 19.3 (2005): 572-582.
Buresh, Robert, Kris Berg, and Jeffrey French. "The effect of resistive exercise rest interval on hormonal response, strength, and hypertrophy with training." The Journal of Strength & Conditioning Research 23.1 (2009): 62-71.
Henselmans, Menno, and Brad J. Schoenfeld. "The Effect of Inter-Set Rest Intervals on Resistance Exercise-Induced Muscle Hypertrophy." Sports Medicine 44.12 (2014): 1635-1643.
Schoenfeld, Brad J. "The mechanisms of muscle hypertrophy and their application to resistance training." The Journal of Strength & Conditioning Research 24.10 (2010): 2857-2872.
Schoenfeld, et al. "Longer inter-set rest periods enhance muscle strength and hypertrophy in resistance trained men." Journal of Strength and Conditioning Research (2015): Publish Ahead of Print.
Villanueva, Matthew G., Christianne Joy Lane, and E. Todd Schroeder. "Short rest interval lengths between sets optimally enhance body composition and performance with 8 weeks of strength resistance training in older men." European journal of applied physiology (2014): 1-14.
Willardson, Jeffrey M. "A brief review: factors affecting the length of the rest interval between resistance exercise sets." The Journal of Strength & Conditioning Research 20.4 (2006): 978-984.

You can't expect wonders from protein supplements... no matter, when you take them, by the way. But I wouldn't mark them down as useless - even for rookies - based on the study at hand.

When I look at the 14 year old kids who need an written permission from their mum to train at the gym buying protein tons o powders and dozens of bars from the vending machines at the gym, even I have to shake my head. Not necessarily, because they're buying those products, but rather about what they tell each other about the effects: "Yo,... recently I ate this protein bar right after my workout and I felt swole for day..."

Now, you know that I am into supplement psychology and have no doubt about the fact that said kiddo felt swole all day, but we all know that protein is in no way a supplement the muscle-building and strength advantages of which will show within hours. And with that, I have a perfect transition to today's topic: The recent study from University of Central Florida in Orlando (Boone. 2015).

You can learn more about protein intake at the waredownloadsoft

Are You Protein Wheysting?

5x More Than the FDA Allows!

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Protein Timing DOES Matter!

Less Fat, More Muscle!

You will probably remember the most striking result of this study in which Carleigh H. Boone and colleagues "examine[d] the short-term effect of resistance training with and without protein supplementation on changes in muscle morphology and strength in untrained young men" (Boone. 2015).

Some of you may now be wondering: Why on earth do they even test that? We have ample evidence that protein supplements are powerful muscle builders! And you are right, but as it is the case for (almost) every research question in exercise science, even the highly acclaimed benefits of pre- or post-workout protein supplementation are somewhat contested. There's the evidence that supports the benefits of peri-workout protein supplementation on exercise induced muscle gains. Unfortunately, many of these studies may have been over-interpreted. Why?

FSR ≠ more muscle. Just because the post-exercise fractional protein synthesis increases this does not mean that you will gain more muscle in the long term. Check out this SV Classic to learn why!

Well, many of the often-cited studies in rookies, like Biolo et al. (1995), Phillips et al. (1997), or Tipton et al. (1999), measured increases in acute muscle protein synthesis and markers of anabolism. Due to their short design, however, increased long-term gains could only be predict, but not detect. In my 2014 article "Study Confirms: Acute Post-Exercise Myofibrillar Protein Synthesis Is Not Correlated with Resistance Training-Induced Muscle Hypertrophy in Young Men" (read more) you have learned, though, that the assumption that significant increases in post-workout muscle protein synthesis will necessary lead to significant augmented increases in muscle size in the long run is logical. but futile.

There are studies where this is the case, e.g. Coburn et al. (2006); Hulmi et al. (2010); Walker et al. (2009); Willoughby et al. (2007) - in both, trained and untrained individuals, but as Boone et al. rightly point out, there are also studies by Antonio et al. (2000) or Hoffman et al. (2009) in which protein or amino acid supplements had no beneficial effects on muscle or strength gains in either or trained and untrained individuals. The randomized, double-blinded study Boone et al. (2015) conducted is thus by no means superfluous. It is yet no perfect either, because with a length of only our week, the scientists picked exactly the time-frame in which things, or I should say "gains" happen faster than you can measure them. Furthermore, the use o a lower body unilateral resistance training makes it very difficult to infer the effects of protein supplementation on (a) muscle morphology [cross-sectional area, muscle thickness, pennation angle], (b) lower body power output, (c) maximal dynamic strength, and (d) maximal isometric strength in other muscle groups and in response to an overall metabolically more demanding workout.

Protein Timing Does Matter! Yet Only in Trained Men. More Than 2x Higher Relative Protein Retention W/ Immedi-ate vs. 6h Post Whey Consumption in Bodybuilders vs. Rookies | read more

Why does trained vs. untrained matter? We know that the growth stimulus in response to exercise and the unused growth potential are both maximal in untrained individuals. As far as strength is concerned, they have the additional advantage of making rapid gains by learning to master the exercises properly and neurological adaptations which are for the most part responsible for the rapid strength increases in the first months of resistance training. It is thus only logical that there's evidence that rookies do in fact gain "no matter what", while advanced trainees will have to up their game by advanced training techniques, protein supplementation and as I pointed out in a 2014 article, here at the waredownloadsoft even protein timing, which appear to be pretty useless for the people who have just been picking up the bar- and dumbbells.

Since the scientists have concise dietary records (Figure 1) and used a supplementation regimen that included not just 17g of whey protein concentrate, but also 3g of cholostrum and an extra 2g of leucine (PLA was an iso-caloric amount of resistant maltodextrin) to trigger a maximal increase in protein synthesis when the shake was consumed ad-libitum (in this case whenever the subjects wanted) on non-training days and immediately after the training sessions on training days, the data is still worth discussing (also because I already mentioned it on Facebook and I don't want you to over-estimate the overall significance of the study).

Figure 1: Overview of the macronutrient (in g) composition of the subjects' diets at baseline and during the study (the value for protein include the amount of protein from the protein shake in the PRO group | Boone. 2015).

As you can see in Figure 1 the protein intake of the twenty untrained young men who were randomly assigned to either a resistance training + protein (PRO; 21.4 ± 1.9y, 75.3 ± 15.7kg) or resistance training + placebo (PLA; 22.9 ± 3.1y, 76.8 ± 14.4kg) group was almost identical at baseline (1.2g/kg) and increased from 1.2 to 1.3g/kg in the protein group (+18.2%) while it dropped to 1.0g/kg body weight in the placebo group (-17.1%).

No such differences existed with respect to the supervised resistance training programs which started with five minutes of non-fatiguing aerobic activity on a cycle ergometer at a self-selected resistance and cadence. This was followed by a specific warm-up consisting of body weight squats, alternating lunges, walking knee hugs, and glute kicks (10 each). The subsequent, actual training sessions is described as follows.

"Each training session consisted of unilateral countermovement jumps (CMJ), leg press (LP), and leg extension (LE) using the dominant leg. CMJ were performed for a total of three sets of 8 repetitions with maximal effort. The LP and LE exercises were performed for a total of three sets of 8-10 repetitions at 80% of the participant’s previously determined 1RM with 90 seconds allotted between sets and exercises. If a participant was unable to perform the minimum amount of repetitions during the first or second sets of LP or LE, weight was decreased to an intensity deemed appropriate by a certified trainer. Consequently, if the participant was able to perform all repetitions with proper form and minimal strain, weights were progressively increased during the subsequent training session at the certified trainer’s discretion" (Boone. 2015).

After twelve of these training sessions, which took place at the university’s Strength and Conditioning Lab, on three nonconsecutive days per week.

Why would it have been nice to know when the size and power gains were measured? The answer is "the pump", ... well, not exactly. It's rather the cell swelling that occurs in the hours and days after a workout. The latter may have increased the overall impression of size gains and thus reduced the significance of potential differences if there was not a interval of at least 5 better 7 days between the last workout and the measurement of the muscle sizes. Bullocks?

Working out leads to increases in water content (left) corresponding increases in muscle "size" (right) at the 10 & 20 cm measuring points of the the quads; all values expressed as relative changes (%) vs. baseline | more

No, reread my 2014 article "Cell Swelling Keeps Muscles "Pumped" For More Than 52h. Size Increases of Up to 16% After a Single Leg Workout! Plus: Changes in Tendon Water & Collagen Content" (read the full SV-Classic article)- that the data will be distorted is a proven fact, with just one study investigating the extent, though, we cannot tell if the data will always be 16% off and the difference thus practically relevant.

Another reason why I was specifically looking for information on the interval between the last training and testing sessions was the lack of increases in peak and mean power (the changes in Figure 2 are all non-significant). If we know when the testing was done, one may be able to tell if this was a result of residual fatigue or if there were in fact no power gains in any of the two groups.

I've plotted the size, strength and power gains, which were assessed on an unfortunately non-disclosed time (see box above for elaborations) in Figure 2:

Figure 2: While even the small size gain in the rect. femoris in the PRO group was stat. sign. compared to the pre-value, none of the visible differences between PRO and PLA reached stat. significance and the mean and peak power did not even change at all... well, statistically speaking (see box above for a discussion why this may be the case | Boon. 2015)

Now, it's not like there were no gains, the cross-sectional area and muscle thickness increased significantly, but the scientists observed neither statistically nor practically significant (mostly due to the large inter-individual differences, e.g. a standard deviation of +/-12% for the CSA increase of the Rectus Femoris in the PRO group).

Table 1: Changes in maximal dynamic, isometric, and specific strength following training - Values are means ± SD. * Significant change from Pre to Post (p < 0.05 | Boone. 2015).

Since the strength data in Table 1 is similarly inconclusive, there is little doubt that is - for the study at hand - 100% warranted to say that while "the current findings suggest that short-term resistance training resulted in significant increases in muscle strength and size in untrained young men", they also suggest that "[t]he addition of a post-exercise protein supplement used in the current investigation was not sufficient to enhance the effect of resistance training" (Boone. 2015).

Polydextrose and Resistant Malto-dextrin May be Useful Dieting Aids, But are They good Placebos?

So what? Don't dumb your protein supplements, yet ;-) Aside from the previously mentioned study duration and the unrealistic training regimen, there is another thing I would like to highlight to substantiate my previously voiced warning that you should not overestimate the practical significance of the study at hand: The "placebo" supplement. Usually you'll see that protein is tested against regular maltodextrin. In the study at hand, however, it was tested against resistant maltodextrin of which you, as a waredownloadsoft reader know that it has been shown to significantly curb the appetite in humans and rodents. More recently, Hira et al. (2015) calculated that only 10g of these resistant starches per day may be able to reduce the energy intake by a whopping 7%.

This puts the -9.4% reduction in energy intake in the placebo group into an altogether different light and makes me question whether the placebo was as inactive as it should be. I have to admit, though, that eventually a lower total protein intake and a lower total energy intake as it was observed in the PLA group at identical study outcomes would even substantiate the claim that additional protein is useless in rookies, but who knows which other unknown effects the 20g of the resistant maltodextrin "placebo" had ;-)

Enough of the speculations, though. Let's stick to the facts: (1) Very few of you will be in the first four weeks of their resistance training "career", (2) even fewer of you will train only one leg, and I'd hope that (3) none of you plan to train for only the next for weeks only. So, that alone would make me want to repeat the scientists' own suggestion that "more research needs to be done" while telling you to (a) keep the results of this study in mind and file them under "protein is no wonder drug", while (b) keep taking your protein supplements. There's good enough evidence to say that >90% of you are going to benefit in one area or another - and always remember whey is more than a muscle builder (learn more) | Comment on Facebook!

References:

Antonio, Jose, et al. "Effects of exercise training and amino-acid supplementation on body composition and physical performance in untrained women." Nutrition 16.11 (2000): 1043-1046.
Biolo, Gianni, et al. "Increased rates of muscle protein turnover and amino acid transport after resistance exercise in humans." American Journal of Physiology-Endocrinology And Metabolism 268.3 (1995): E514-E520.
Coburn, Jared W., et al. "Effects of leucine and whey protein supplementation during eight weeks of unilateral resistance training." The Journal of Strength & Conditioning Research 20.2 (2006): 284-291.
Boone, Carleigh H., et al. "Muscle strength and hypertrophy occur independently of protein supplementation during short-term resistance training in untrained men." Applied Physiology, Nutrition, and Metabolism ja.
Hira, Tohru, et al. "Resistant maltodextrin promotes fasting glucagon-like peptide-1 secretion and production together with glucose tolerance in rats." British Journal of Nutrition (2015): 1-9.
Hoffman, Jay R., et al. "Effect of protein-supplement timing on strength, power, and body-composition changes in resistance-trained men." International journal of sport nutrition 19.2 (2009): 172.
Hulmi, Juha J., Christopher M. Lockwood, and Jeffrey R. Stout. "Review Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein." Nutrition & metabolism 7 (2010): 51.
Phillips, Stuart M., et al. "Mixed muscle protein synthesis and breakdown after resistance exercise in humans." American Journal of Physiology-Endocrinology And Metabolism 273.1 (1997): E99-E107.
Walker, Thomas B., Et Al. The Influence Of 8-Weeks Of Whey Protein And Leucine Supplementation On Physical And Cognitive Performance. Air Force Research Lab Brooks Afb Tx Human Effectiveness Directorate, 2009.
Willoughby, D. S., J. R. Stout, and C. D. Wilborn. "Effects of resistance training and protein plus amino acid supplementation on muscle anabolism, mass, and strength." Amino acids 32.4 (2007): 467-477.

Yes, drastic measures will make the weight melt faster, but even if you tube-feed yourself lean, you will not stay this way without lifestyle changes like an increase in fiber intake.

There are a billion different ways to lose weight, but if you aligned all these ways along in a diagram with two axes: One that describes the degree of invasion in your regular dietary habits and the other indicating the time that's necessary to see results, the two "tricks" discussed in today's waredownloadsoft post would be placed somewhere in the edges of the 2nd and third quadrant.

You don't get that? Well, I guess that's a science guy's way of saying we are dealing with totally different ways of losing weight, of which one, i.e. the use of guar gum to increase the satiety effects of your meals, suitable for long-term weight loss, while the other, i.e. the use of a very low-calorie

You can learn more about the fiber at the waredownloadsoft

Polydextrose & Res. Malto 4You

Most people don't get enough fiber

Foods, Not Ma- cros for the Gut

Fiber and Mortality Risk

Appetite Short News /Fiber

Xanthan GI Reducer?

protein-based that is enterally fed to obese individuals, being geared towards maximal fat loss in a minimal amount of time - no matter how severe this may mess with your regular eating habits.
In spite of the fact that I hope that few of you are in a situation similar to the one the 364 severely overweight patients (59% women; all with a mean BMI of whopping 46.6 ± 7.2 kg/m²) who participated in a recent study from Italy, I believe that you may be interested to hear how these guys and gals lost 5.4cm of their waists and improved their insulin levels by 11 pts and their glucose levels by 16 pts within only 14 days.

Figure 1: Changes in relevant markers of body comp. glucose and lipid metabolism (Castalado. 2015).

Yeah, the results are impressive, but I doubt that many people like to be fed through a nasogastric tube 24/7, right? Well, that's unfortunately what may be required to ensure that the homemade very
low-calorie (~6 kcal/kg of ideal body weight/day) protein-based formula (2000 mL per day) the scientists used can actually work its full weight loss magic.

Table 1: Ingredients (Castalado. 2015).

I am deliberately writing that enteral feeding may be required! Without scientific evidence you wouldn't see the exact same results if you feed your subjects the whey-based formula that was infused with arginine, ornithine, taurine, cysteine, tryptophan, proline and citrulline, as well as omega-3s, carnitine, policosanol and prebiotics (see Table 1) orally, there's still hope that the nasogastric tube is not necessary, even if the constant nutrient influx the researchers achieved by administered the "drink" continuously (24 hours a day) by means of a small, light, and rechargeable peristaltic feeding pump may figure.

Eventually, it should be obvious, though, that a weight-loss strategy like that is not appropriate for someone with only a few extra-kilograms. For people like that "trick" #2 may be of significantly greater interests.

Fiber increases satiety, but more importantly, it also reduces food intake

In the end, it's not actually new that fiber can make you feel more satiated. What is yet by no means clear, however, is (a) whether this is a "one-time thing", i.e. whether the effect will still be there, when you got accustomed to high fiber foods, and (b) whether an acute feeling of increased satiety after a "fiber-upped" food (= foods that are artificially supplemented with fiber) will also make you eat less on subsequent meals.

Soluble or insoluble, what's "better"? Soluble fiber is the fiber that will be fermented by the bacteria in your gut, insoluble fiber will pass "right through" (that's an over-generalization obviously). These bacteria turn the fiber into short-chain fatty acids (SCFA) which have two important functions (1) they serve as an energy source and (2) they interact with certain receptors in your gut and trigger the production of "satiety hormones" like the "fat-burning-insulin-sensitizing hormone" GLP-1. Effect (1) has mislead scientists to believe that the energy from the SCFAs may hamper the beneficial effects of fiber (and in certain cases does actually happen | Isken. 2010), but the overwhelming evidence shows that both have beneficial effects on your metabolic, intestinal and overall health (Weickert. 2008; Howarth. 2001; Papathanasopoulos. 2012).

Both has recently been studied by scientists from Taiyo Kagaku R&D. In three separate studies, Rao et al. determined the whether small doses of partially hydrolysed guar gum (PHGG), a soluble dietary fibre would effect post-meal satiation and subsequent energy intake with acute and long term administration.

"The following three separate studies were conducted: in study 1, healthy subjects (n 12) consumed 2g of PHGG along with breakfast, lunch and an evening snack; in study 2, healthy subjects (n = 24) consumed 2 g of PHGG or dextrin along with yogurt as breakfast for 2 weeks; in study 3, healthy subjects (n = 6) took 6 g each of either PHGG or indigestible dextrin or inulin along with lunch" (Rao. 2015)

The results of the studies confirmed that (1) the acute satiety effect of soluble fiber (in this case guar gum) persists (at least for two weeks) and that (2) slightly larger amounts of soluble fiber will have beneficial effects on energy intake.

Figure 2: Two important findings (1) the appetite suppressive effects actually increase from day 1 to day 7 and (2) the energy intake is reduced even if you take into accout that soluble fiber has calories, too (Rao. 2015).

What's specifically interesting about the last result is that most of the reduction in energy intake occurred in the form of snacks; and in view of the fact that snacking is one of the motors of the obesity epidemic, this is one of the few results from a medium-term study that may actually translate into long-term results.

waredownloadsoft Suggested Previous Article: "Polydextrose and Resistant Maltodextrin as Dieting Aids W/ GLP-1 Boosting & Appetite Reducing Effects: 7% Reduced Energy Intake per 10g/day of Polydextrose in Clinical Trials" | read the full article

Bottom line: In spite of the fact that the side-effects of the "hard-core" diet regimen (tube feeding) were astonishingly mild (initial side effects like headaches and even the hunger disappeared or were sign. reduced in week two), I cannot really recommend a nasogastric tube to anyone but the extremely obese.

What I do recommend, though, is a high-fiber diet. In that I am not entirely sure, however, if supplementing your diet with extra fiber (for example as guar gum) is the ideal solution for those of you who want to lose weight. Why? Well, if you try to achieve your daily fiber goals (like 25g+ as it is suggested by AHA reasearchers, for example | Howarth. 2001) solely via natural sources, this will make you gravitate towards healthier food items and you all know: It's the food you eat, not its macros that determines whether it'll make you fat or help you to lean out | Comment on Facebook!

References:

Castaldo, Giuseppe, et al. "A 2-Week Course of Enteral Treatment with a Very Low-Calorie Protein-Based Formula for the Management of Severe Obesity." International Journal of Endocrinology 2015 (2015).
Isken, Frank, et al. "Effects of long-term soluble vs. insoluble dietary fiber intake on high-fat diet-induced obesity in C57BL/6J mice." The Journal of nutritional biochemistry 21.4 (2010): 278-284.
Howarth, Nancy C., Edward Saltzman, and Susan B. Roberts. "Dietary fiber and weight regulation." Nutrition reviews 59.5 (2001): 129-139.
Papathanasopoulos, Athanasios, and Michael Camilleri. "Dietary fiber supplements: effects in obesity and metabolic syndrome and relationship to gastrointestinal functions." Gastroenterology 138.1 (2010): 65-72.
Rao, Theertham Pradyumna, et al. "Post-meal perceivable satiety and subsequent energy intake with intake of partially hydrolysed guar gum." British Journal of Nutrition 113.09 (2015): 1489-1498.
Weickert, Martin O., and Andreas FH Pfeiffer. "Metabolic effects of dietary fiber consumption and prevention of diabetes." The Journal of nutrition 138.3 (2008): 439-442.

No, even the reanalysis doesn't say that a bit more protein, alone, will make you look like this ;-)

I've written about both observational and experimental studies that show how increased protein intakes can improve your body composition. So why mention another one?

Well, the study at hand which has been conducted by scientists from the Purdue University is interesting, because (a) it's not as extreme as Jose Antonios 2014 study in which the subjects consumed "Fivefold More Than the FDA Allows" (learn more), (b) it is not a simple short-term diet intervention where the high protein diet comes - as usual - out victorious and it is (c) actually a re-analysis of one of those studies that is often cited to "prove" that increased protein intakes, let alone the use of whey protein, wouldn't be advantageous for overweight and obese individuals trying to shed body fat.

But let's tackle one thing after the other. The original goal of the study at hand was to re-assess the data from Weinheimer's 2012 study which concluded that "whey protein supplementation [10, 20, 30, or 30 g of whey protein twice daily] does not affect exercise [2x resistance training 1x cardio per week] training-induced changes in body composition and indices of metabolic syndrome in middle-aged overweight and obese adults" (Weinheimer. 2012 | just to make sure you're not confused: While the lead authors changed Weinheimer <> Campbell, it's still the same team).

You can learn more about protein intake at the waredownloadsoft

Are You Protein Wheysting?

5x More Than the FDA Allows!

More Protein ≠ More Satiety

Protein: Food or Supplement?

Protein Timing DOES Matter!

Too Much Whey Pro-Diabetic?

Instead of dealing with absolutes and overall averages, only, Campbell et al. reanalyzed their data to elucidate the influence of total protein intake (TPro) and changes in protein inatke (CTPro) on exercise-induced changes in body composition and metabolic syndrome indexes. As the scientists point out in the introduction to their soon-to-be-published paper, they conducted this assessment from 3 perspectives for protein intake as follows (Campbell. 2015):

TPro as a continuous variable with the use of a multiple linear regression model;
CTPro during the intervention vs. each subject s usual protein intake (post-intervention value minus pre-intervention value) with the use of multiple linear regression; and
TPro as a categorical variable, <1.0, ≥1.0 to <1.2, and ≥1.2 g per kg bodyweight, using a stratified analysis approach.

In that, Campbell et al. (2015) already expected that they would be able to correct their original findings. More specifically, they hypothesized that they'd find that a higher total protein intake, expressed as a continuous or categorical variable, would enhance the training-induced reduction of fat mass (FM) and gain of lean mass (LM), but not influence responses of MetS indexes (these were waist circumference, glucose, TGs, HDL cholesterol, and blood pressure).

Table 1: Overview of the results of the multiple linear regression analysis the beta² are quantitative indicators of the link between total protein intake (TPro) and change in protein intake (CTPro) (Campbell. 2015).

In addition, the scientists were quite convinced that they'd be able to show that the changes in body composition had been the most pronounced in those subjects with the highest increase in total protein intake over the course of the 36 week study period. And guess what!? Campbell et al. were able to confirm both hypotheses in their ahead-of-print paper:

In conjunction with exercise training, higher total protein intakes promoted positive changes in body composition. What the higher protein intakes did not do, however, was to promote further improvements in critical markers of metabolic syndrome in the 117 overweight and obese middle-aged adults who participated in the 2012 original 36-week intervention.
In addition, the changes in body composition, Weinheimer et al. observed when they conducted the study three years ago were the most pronounced in those subjects who recorded the largest changes in total protein intake via diet or supplements.

Now, this was to be expected, right? So why is it important? Well, it is important because Campbell's results falsify the assumption that protein supplements or increases in protein intake do "not affect exercise training-induced changes in body composition and indices of metabolic syndrome in middle-aged overweight and obese adults" (Weinheimer. 2012).

This is why I like the study: You rarely see the same group of scientists go back to their own dataset doing a re-analyses with that far-reaching effects on the original conclusions that were drawn three years ago. Without this kind of thorough research, we'd have even more "irrevocable scientific evidence" pointing us in the wrong direction, only because the analytical methods were not specific enough to give us an idea of the true complexity of the results.

Does this quote sound familiar? It should, it was after all the conclusion of the original study I have seen being cited several times byby various people to argue that increases in protein intake or the use of protein supplements (and specifically whey, which was used in Weinheimer's original study) would be a waste of time and money.

Figure 1. Temporal changes in the most important markers of body composition according to total protein intake of the subjects during Weinheimer's 2012 36-week intervention study (Campbell. 2015).

Now that Campbell et al. have published the re-analysis of their own data the correlation coefficients in Table 1 and the data in Figure 1 clearly show that a high and even more so a higher total protein intake can make a highly significant and practically relevant difference when it comes to the long-term effects of exercise on both lean body mass and fat mass. If we take more than just a cursory look we can also make the following statements about the effects of generally high protein intakes and significant increases in protein intake on the basis of the regression coefficients in Table 1:

"Will "Muscle Building Supplements" Give You Testicular Germ Cell Cancer?" - Find out why the myth about "pro-carcinogenic" protein powders is bogus here!
For all subjects, higher total protein intakes and higher changes in protein intake were associated with significantly more favorable changes in body composition, fat mass and BMI; only the association with lean mass increases did not reach statistical significance in all subjects.
The latter is in contrast to increases in protein intake. In subjects who didn't just have a high baseline protein intake, but who actually ate more protein (from the diet or the whey supplement they received in the original study from 2012), the increase in protein intake was associated with increases in lean mass and decreases in fat mass.
Comparable results were observed for regional (arms, legs, trunk, android, and gynoid) BM, FM, %FM, LM, and %LM changes (not shown in Table 1).

That's all great and certainly supports the physique improving benefits of high protein diets. What's a bit disappointing, though, is that similar correlations between higher or increased total protein intakes were not observed for any of the markers of metabolic syndrome (waist circumference, glucose, TGs, HDL cholesterol, and blood pressure).

"Fivefold More Than the FDA Allows: Extreme High Protein Diet (4.4g/kg | 307g/day) Benign & Non-Obesogenic. Plus: Macronutrient Prescription & Changes in Food Quality" - Read my article about the repeatedly referenced study by Antonio et al. | read it!

So, is eating high(er) protein worth it? Yes, it is. And it's actually quite important to highlight that sometimes it's the lack of detailed analyses of the data that may skew the results in ways that conceal health relevant findings. I know, for most doctors "health relevant" improvements would necessarily include the previously mentioned markers of metabolic syndrome, but one thing you must not forget is that those improvements occurred in all subjects in response to the exercise regimen. They were just not statistically significantly augmented in the subjects who consumed the most protein.

Speaking of consuming "the most" protein. If you compare the "high" protein intake in the original study by Weinheimer et al (2012) to the protein intake in the previously cited study by Antonio et al. 1.2g/kg+ is at best a moderate, but by no means a "high" protein intake.

This difference between "really high" (2.5-3.0 g/kg and more) and "RDA-definition high" (more than the RDA of 0.8g/kg) could well be a difference we must not ignore. After all, Campbell's stratified 2015 analyses of the data showed that the appetite ratings were significantly reduced only in those subjects in the higher, i.e. >1.2g/kg, tertile of protein intakes. If we also take into account what Antonio et al. (2014) observed in an allegedly different scenario with "really high" protein intakes, we may speculate that even higher protein intakes might (a) have yielded more "spectacular" changes in body composition and (b) have turned non-significant metabolic health advantages in the high protein eaters to significant ones | Comment on Facebook!

References:

Antonio, Jose, et al. "The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals." Journal of the International Society of Sports Nutrition 11.1 (2014): 19.
Campbell, et al. "Higher Total Protein Intake and Change in Total Protein Intake Affect Body Composition but Not Metabolic Syndrome Indexes in Middle-Aged Overweight and Obese Adults Who Performed Resistance and Aerobic Exercise for 36 Weeks." J. Nutr. jn213595 (2015): Ahead of print.
Weinheimer, Eileen M., et al. "Whey protein supplementation does not affect exercise training-induced changes in body composition and indices of metabolic syndrome in middle-aged overweight and obese adults." The Journal of nutrition 142.8 (2012): 1532-1539.

How large is the impact of not being active on childhood, adolescent and adult obesity. Plus: Are there critical time periods in gestation, infancy childhood and adolescence?

You may have heard the claim that "fat cells form during childhood and puberty and stay forever" before, right? Well, if that's the case it would be logical to assume that our childhood may be a critical developmental windows in which we have the time-limited opportunity to shape or help shape our own or our kids body composition for the rest of our or their lives.

Scientists from Mater Health Services South Brisbane, the University College of London, and the Griffith University have now reviewed the relatively scarce experimental and abundant observational pertinent research in order to examine "the role of physical activity during periods of risk to reduce the probability of obesity onset and maintenance in adulthood" (Street. 2015).

Reduced obese individuals and other things related to "metabolic damage"

Chronic Dieting Can Make You Skinny Fat

Nasty insights into the YoYo-Effect

Is There Diet-Induced Metabolic Damage?

Energy Deficits Can Make Athletes Fat

Fat Cell Size, NAFLD & Reduced Obesity

Metabolic Damage - What's the Evidence?

Unfortunately, but not surprisingly, most of the experimental evidence comes from rodent studies. If we tried to summarize the results of these studies in a half-sentence it would say that they demonstrate general positive effects of early exercise on the outcomes for all animals irrespective of maternal obesity status or post-weaning diet.

"Although high-fat post-weaning diets resulted in generally fatter animals, the body composition, endocrine and immune system profiles of these animals were healthier than non-exercising high-fat diet animals and comparable to standard chow non-exercising animals" (Street. 2015).

Interestingly, these effects do not disappear when the animals stop exercising. Rather than that studies indicate that exercise at an early age can protect animals against obesity onset for 5 weeks following exercise cessation (Caruso. 2013) - that's quite impressive if we take into account that rodents have a much shorter lifespan and a rapid early development period compared to humans (five rodent weeks in the early life are similar to several human years).

In spite of the fact that we don't know for sure for how long these protective effects will last in humans, there's little doubt that the same up-regulation of markers associated with increases in the skeletal muscle mitochondrial function, of which scientists believe that they protect the young rodents from obesity, will occur in humans as well (Shindo. 2014). Luckily, this is not the only thing we already know about rodents and assume for humans. Here's more:

Figure 1: If rodents are exercise in "childhood" (3WK), already, they will be significantly leaner - irrespective of whether they are fed an obesogenic HFD or the regular SMD diet (Wagener. 2012).
the earlier, the better - the earlier young rodents are exercised (e.g. in the rodent equivalent of childhood), the more pronounced the protective effect against adult obesity (Wagener. 2012) - as you can see in Figure 1 earlier exercise will also yield significantly reduced body fat levels on standard rodent chow (SMD - 3WK);
muscle & brain are involved - next to changes in the mitochondria, the "stay lean" effect is also mediated by changes in structure and/or function of brain regions involved in appetite regulation in mouse & man (Street. 2015);
males benefit more than females - the benefits of early exercise appear to be more pronounced for male vs. female animals (Schroeder. 2010); whether that's due to the higher muscle mass remains to be elucidated

In view of the fact that corresponding studies in human beings are not just time-consuming and expensive, but could also be unethical (think of kids being randomly assigned to non-exercise groups getting fat and sick as adults), it is not surprising that most of the evidence from human studies is of observational nature. Much in line with the findings from rodent studies, it has been suggested that three critical periods are important for obesity onset before adulthood: gestation and early infancy, the adiposity rebound and adolescence.

"Each period is characterized by substantial yet qualitatively different changes in growth and maturation. The culmination of each period represents a milestone in development and a subsequent reduction in the developmental plasticity of the maturing system. Given the inherently greater plasticity of earlier periods, obesity risk later in the life course is greater if the pre-conditions for obesity are established and maintained early. Disrupting the trajectory of obesity during development is likely to pay dividends in adulthood with a healthier body composition and metabolic profile. The disrupting effect of physical activity is less well understood in relation to obesity risk during and following critical periods" (Street. 2015).

Let's briefly recap what we know about these periods and how exercise during gestation (obviously in this case the mother would exercise), early infancy and adolescence influence our obesity risk as adults:

Figure 2: Body fat levels according to quartiles of physical activity in late pregnancy (Harrod. 2014).
Gestation - Physical activity during pregnancy has been associated with reduced odds of a large-for-gestational age (LGA) infant, as well as reduced risk of small-for-gestational age, which are both linked to increased obesity risks later in life. In addition, there is evidence of reduced body fat levels, but identical lean mass and a significantly reduced risk of macrosomia (=excessive body weight) in babies born to mothers with higher levels of physical activity during pregnancy.

Overall, however, the existing evidence - specifically for strength training - is conflicting and we are far from fully understanding the complex interactions between physical exercise, nutrition during gestation and the weight and body composition of the newborn baby (a usual more does not necessarily help mor). What appears to be certain though is that if beneficial effects occur, those will last for at least 12-24 months (Mattran. 2011; Chu. 2013). In one study scientists even found significantly reduced obesity risks up to age 5 even if the physical activity of the mother was the only significant difference between the kids (Clapp. 1996)
Figure 3: Observational data shows that there is an inverse linear association between infant activity scores and body fat percentages as early as in year 1 (Li. 1995).
Infancy - Although it is correct that our body composition in infancy is still largely influenced by our mother's physical activity during gestation, there's good evidence that an earlier achievement of gross motor milestones (sitting, crawling, etc.) gives us the activity headstart we need to stay lean. Based on the correlation between earlier motor milestones and lower subscapular and triceps skin-folds measurements of 12 month-old kids Street et al. conclude that "more active infants depose less fat over the first year [...] because active energy expenditure has resulted in increased metabolic capacity".

In contrast to rodents, the "early activity bonus" does not last long in humans. With 5 years "early active" children are no longer significantly leaner than their peers, unless they were continuously more active and/or were fed different diets.

In spite of the fact that early life activity does not provide life-long protection against obesity, though, the experimental and observational evidence of an inverse relationship between physical activity and body fat levels in infancy (Li. 1995) highlights the importance of leading an "active life" - in the most general sense - as early as possible. This is also relevant, because activity builds, while inactivity "kills" muscle, which is in turn associated with a further reduction in physical activity: Overweight infants, for example, have been shown to reach motor milestones later than leaner counterparts (Slining. 2010). Now you've just learned about the link between these milestones and staying lean in a previous paragraph. Accordingly, you will know that this means that the "sweet", chubby babies and toddlers may be caught in a vicious cycle of "obesity > low activity > lower muscle > lower activity > more obesity > lower activity ... "even before the know what the word "activity" means.
Figure 4: Normal body fat development during infancy (Street. 2015).
This does not mean that babies have to be "ripped", but I guess we all have seen kids with body fat levels way beyond the normal ~30% at 6 months (see Figure 4). The real problem, however, occurs thereafter, when the slow and steady decline in body fat should be driven by increases in a kid's activity energy expenditure (AEE). The latter takes the role of the energetic needs of growing which have previously been every toddler's #1 energy consumer. If the growth process slows and "activity", which does by the way include "vocalization primarily in the form of crying [which] is the next greatest pre-ambulatory energy cost after the energy cost of growth" (Street. 2015), does not take it's place, obesity ensues.

Obviously, you could counter that by calorically restricting your toddler, but this is (a) unhealthy and (b) the exact opposite of what the mums and dads do. In fact, way too many of them are priming their kids to become obese sugar addicts by giving their kids a sugar-sweetened beverage (a "healthy baby tea" *rofl*), whenever the kids utter a sound just to make them shut up do. It is thus no wonder that studies have linked infant temperaments that are characterized by negative affectivity/emotionality and a more frequent use of vocal signals such as crying and thus more frequent maternal feeding responses to increased fat gain (Baughcum. 1998; Darlington. 2006). That's alarming, even if it has not yet been conclusively shown that the two are causally and not just corollary related.

Does the Optimal Meal Frequency Depend on Age? Study Suggests: Kids Better Eat Often, Adolescents Rather Step Away From Their Sugary Sins - Quality Counts! Read more!

Childhood - An important feature of childhood development, particularly in terms of its association with increased obesity risk, is a fall in body mass index (BMI) until about 5–7 years of age, which is followed by the so-called "adiposity rebound" (AR).

The earlier this rebound occurs, i.e. the earlier kids start to become fat again, the higher their risk of obesity as late as adulthood (Whitaker. 1998; Taylor. 2004). More specifically, studies like Whitaker et al. (1998) show that "early gainers" have a 20% higher obesity risk later in life and an extra 20% risk if they were already overweight - or I should say "over-fat" - at the age of 5-7 years.

It is thus only logical that studies show that obese pre-schoolers often become obese adults (Nader. 2012). Next to the Western junk-food diet, research findings in the recent decades support a relationship between increased obesity risk, low physical activity and high sedentary pursuits during childhood (Reilly. 2010).

Figure 5: Risk increase / decrease of becoming an obese teenager for weight status at AR, maternal and paternal BMI during; I think it's quite telling that even the "medium" weight (=average kids) already have increased obesity risks, these days (data from Whitaker. 1998).

A recent study by Schuster et al., for example, shows that "overweight fifth-graders were more likely to become obese if they had an obese parent (P < .001) or watched more television (P = .02)" (Schuster. 2014); and that's only the last in a series of studies suggesting that children who engage in more vigorous physical activity are at reduced risk of obesity, while children who are more sedentary are at a significantly greater risk of becoming obese in adolescence, which happens to be the next and last developmental step we're going to discuss in today's waredownloadsoft obesity feature.

Adolescence - Adolescence is a critical phase in the development of our fat stores. While the years before puberty are characterized by both fat cell hypertrophy (the fat cell size increases), hyperplasia (more fat cells are formed) and apoptosis (fat cells die), most experts agree that the number of apoptotic processes in our adipose tissue declines rapidly as we approach puberty.

Figure 6: Difference of total fat mass of girls at age 10, 11, 12, 13; all values relative to girls who had a low and maintained a low activity levels (LL) - HH: high activity at baseline, low later, LH: low activity at baseline, high later, HL: high activity at baseline, low later (Völgyi. 2011).

This decline in the adipose tissue turnover is really bad news and one of the reasons why scientists believe that the "critical window" from the headline of today's waredownloadsoft article closes during puberty:

"It is generally thought that alteration in the size of fat cells in adulthood is achievable but maintenance of reduced fat cell size is likely to be difficult because of the mechanisms that may include, e.g. decreased leptin production. Furthermore, while an increase in adipo-cyte number is possible during adulthood, reversal of fat cell number does not occur. Consequently, adolescence represents an additional critical window when physical activity may affect obesity risk (reducing fat cell accretion) in ways it can-not during adulthood (reducing established fat cell number). " (Street. 2015)

Since adolescence is also associated with an increase in lean mass, including skeletal muscle and bone, it is thus high time to start being, or - better - being even more active. After all, both muscle and bone mass are positively correlated with physical activity levels (Bailey. 1999; Völgyi. 2011).

A 2005 study by D'Andrea et al. shows significant increases in resting energy expenditure after large volume liposuction (all values expressed rel. to baseline). This is the exact opposite of what would happen if the same 4-5% of body fat had been lost by dieting and thus evidence that surgery may help people lose weight without setting them up for the yoyo effect even after the "window of opportunity" closed.

Liposuction to the rescue! I am usually not a fan of cosmetic surgery, but in view of the fact that D’Andrea et al. (2005) were able to show that large-volume liposuction results in "a significantly improved insulin sensitivity, resting metabolic rate, serum adipocytokines, and inflammatory marker levels" in a clinical study conducted with 123 obese women, it is hard to ignore that the surgery knife may help even if the "Window of Opportunity" has closed, already. The reduction in REE in reduced obese individuals is after all one of the main reasons they regain weight (or struggle with weight regain for the rest of their life). If this problem is in fact triggered by the high amount of emptied fat cells that are left behind after losing more than 40lbs, it's only to assume that the surgical removal of fat cells would not lead to the same "pro-weight gain" problems.

If you take a look at the data in Figure 6 it's yet not too late to start being active in puberty. The previously sedentary girls in Völgyi's study (Figure 6 | LH) who started to exercise regularly during puberty, for example, were similarly lean as their "always active" peers (HH). Probably because they expended more energy, but also because their exercise left them less hungry than their sedentary peers ... that sounds like bogus? Well, take a look at the reduced 24h energy intake Thivel et al. measured in youths who were locked in a metabolic chamber in response to high intensity exercise vs. sitting around (Thivel. 2012 | Figure 7) - exercise does not make you hungry.

Figure 7: Much in contrast to what you may expect, obese kids actually eat less, when they are forced to work out. In that, doing high intensity exercise (HIE) is more "satiating" than low intensity (Thivel. 2012).

Now, if exercise curbs your appetite, while being sedentary increases it and its obesogenic consequences, which in turn reduce your willingness and ability to exercise, it is obvious what Street et al refer to when they are talking about "a two way street" (Street. 2015). It's the previously hinted at vicious cycle in which lower physical activity predisposes to obesity, while obesity in turn predisposes to even greater reductions in physical activity.

In view of the previously referenced physiological peculiarities, adolescence appears to be the last stage in our development, where increased activity, alone, can go a long and consequential way. It is thus all the more important to break the cycle of being sedentary <> getting fatter before the transition into adulthood takes place. After all, the currently available research leaves little doubt that physical activity during adolescence will promote an adult body composition and metabolic profile that is associated with a reduced obesity risk, and reduced morbidity: Adult women who were more active adolescents, for example, are 50% less likely to be abdominally obese - even if all covariates are controlled for (da Silva. 2015). Physical activity interventions in adults, on the other hand, yield very ambiguous results. In most cases, however, being more active alone will not make a significant enough difference to trigger fat loss and instigate health improvements.

Shi et al. conducted an interesting experiment that highlight the role of low leptin in weight regain. They fattened rodents up, dieted them down and found that the weight reduced rodents whose weight loss had stagnated after 3 weeks had the same low leptin levels as the normal-weight significantly leaner rodents. The hypothesis is that this is due to having more, but empty fat cells that produce way too little leptin for the total amount of body fat, because the amount of leptin that's produced depends in a non-linear way on the level of fat in the cells. Rodent bogus? Well several human studies showing a reversal of neurological, endocrine and metabolic abnormalities in reduced obese indiv. with leptin (Rosenbaum. 1997, 2005 & 2008) suggest that this may actually be happening in man & woman, too.

So what? With the vicious cycle of being sedentary, getting fat, being even more sedentary and getting even fatter, we are back to our original question which was whether you'd have to stay fat forever if you end up being fat at the end of puberty. I wouldn't go so far as to say that your fate is determined, but it's hard to ignore the evidence that our kids can at least avoid adding additional fat cells and thus increase their chance of life-long leanness by leading an active lifestyle. We, on the other hand are in a very compromised situation. In contrast to studies in adolescents, many studies in adults show that even combined aerobic and resistance training, may effectively shed our love-handles once we are adults (Willis. 2012).

Dieting, on the other hand, may successfully reduce our body weight, but the risk of "refilling" the fat cells we've created as babies, children and adolescents, when the body fat turnover and the natural "apoptotic death" of fat cells stagnates, increases with every pound of extra body fat we've "acquired" as babies, children and teens. Why exactly this is the case has not been fully elucidated, yet. I personally find that Shi's 2009 hypothesis that says (generally speaking) that the high number of small fat cells in people who have gained a lot of fat before adulthood are left with after a diet won't produce enough leptin to signal the body that they've achieved a new steady state. Constant hunger and rapid and easy fat gain even from consuming the "exact" amount of energy they should need are the nasty consequences some of you may have experienced first-hand | Comment!

References:

Bailey, D. A., et al. "A six‐year longitudinal study of the relationship of physical activity to bone mineral accrual in growing children: the University of Saskatchewan Bone Mineral Accrual Study." Journal of Bone and Mineral Research 14.10 (1999): 1672-1679.
Baughcum, Amy E., et al. "Maternal feeding practices and childhood obesity: a focus group study of low-income mothers." Archives of Pediatrics & Adolescent Medicine 152.10 (1998): 1010-1014.
Caruso, V., H. Bahari, and M. J. Morris. "The Beneficial Effects of Early Short‐Term Exercise in the Offspring of Obese Mothers are Accompanied by Alterations in the Hypothalamic Gene Expression of Appetite Regulators and FTO (Fat Mass and Obesity Associated) Gene." Journal of neuroendocrinology 25.8 (2013): 742-752.
Chu, Lisa, et al. "Impact of maternal physical activity and infant feeding practices on infant weight gain and adiposity." International journal of endocrinology 2012 (2012).
Clapp, James F. "Morphometric and neurodevelopmental outcome at age five years of the offspring of women who continued to exercise regularly throughout pregnancy." The Journal of pediatrics 129.6 (1996): 856-863.
da Silva Garcez, Anderson, et al. "Physical Activity in Adolescence and Abdominal Obesity in Adulthood: A Case-Control Study Among Women Shift Workers." Women & health ahead-of-print (2015): 1-13.
Darlington, Anne-Sophie E., and Charlotte M. Wright. "The influence of temperament on weight gain in early infancy." Journal of Developmental & Behavioral Pediatrics 27.4 (2006): 329-335.
Harrod, Curtis S., et al. "Physical activity in pregnancy and neonatal body composition: the healthy start study." Obstetrics & Gynecology 124.2, PART 1 (2014): 257-264.
Li, Ruowei, et al. "Relation of activity levels to body fat in infants 6 to 12 months of age." The Journal of pediatrics 126.3 (1995): 353-357.
Mattran, Kelly, et al. "Leisure-time physical activity during pregnancy and offspring size at 18 to 24 months." Journal of Physical Activity and Health 8.5 (2011): 655.
Nader, Philip R., et al. "Next steps in obesity prevention: altering early life systems to support healthy parents, infants, and toddlers." Childhood Obesity (Formerly Obesity and Weight Management) 8.3 (2012): 195-204.
Reilly, John J. "Low levels of objectively measured physical activity in preschoolers in child care." Medicine and science in sports and exercise 42.3 (2010): 502-507.
Rosenbaum, Michael, et al. "Effects of Weight Change on Plasma Leptin Concentrations and Energy Expenditure 1." The Journal of Clinical Endocrinology & Metabolism 82.11 (1997): 3647-3654.
Rosenbaum, Michael, et al. "Low-dose leptin reverses skeletal muscle, autonomic, and neuroendocrine adaptations to maintenance of reduced weight." Journal of Clinical Investigation 115.12 (2005): 3579.
Rosenbaum, Michael, et al. "Leptin reverses weight loss–induced changes in regional neural activity responses to visual food stimuli." The Journal of clinical investigation 118.7 (2008): 2583.
Schroeder, Mariana, et al. "Post-weaning voluntary exercise exerts long-term moderation of adiposity in males but not in females in an animal model of early-onset obesity." Hormones and behavior 57.4 (2010): 496-505.
Schuster, Mark A., et al. "Changes in obesity between fifth and tenth grades: A longitudinal study in three metropolitan areas." Pediatrics 134.6 (2014): 1051-1058.
Shi, Haifei, et al. "Diet‐induced Obese Mice Are Leptin Insufficient After Weight Reduction." Obesity 17.9 (2009): 1702-1709.
Shindo, Daisuke, Tomokazu Matsuura, and Masato Suzuki. "Effects of prepubertal-onset exercise on body weight changes up to middle age in rats." Journal of Applied Physiology 116.6 (2014): 674-682.
Slining, Meghan, et al. "Infant overweight is associated with delayed motor development." The Journal of pediatrics 157.1 (2010): 20-25.
Street, S. J., J. C. K. Wells, and A. P. Hills. "Windows of opportunity for physical activity in the prevention of obesity." Obesity Reviews (2015).
Taylor, Rachael W., et al. "Rate of fat gain is faster in girls undergoing early adiposity rebound." Obesity research 12.8 (2004): 1228-1230.
Thivel, David, et al. "The 24-h energy intake of obese adolescents is spontaneously reduced after intensive exercise: a randomized controlled trial in calorimetric chambers." PloS one 7.1 (2012): e29840.
Wagener, A., A. O. Schmitt, and G. A. Brockmann. "Early and late onset of voluntary exercise have differential effects on the metabolic syndrome in an obese mouse model." Experimental and Clinical Endocrinology and Diabetes 120.10 (2012): 591.
Whitaker, Robert C., et al. "Early adiposity rebound and the risk of adult obesity." Pediatrics 101.3 (1998): e5-e5.

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Wednesday, November 4, 2015

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Eating More Protein Doesn't Help You Lean Out? Reanalysis of Often-Cited 36-Week Study Corrects Original Conclusion: Threshold Intakes and Changes (!) in Protein Intake Matter!

Is the "Fat Kid" Doomed to Stay Fat Forever? What's the Role of Physical Activity Within a Window of Opportunity?