HIT Your Satellite Cells to Increase Your Gains! Only High Intensity "Cardio" Exercise Will Fuel Your Satellite Cell Pool and Set You Up For Future Muscle Growth.

Image 1: NO-mediated satellite cell
recruitement (Anderson. 2000)

You have read it on the SuppVersity, you have heard about it on Carl Lanore's Super Human Radio and the BodyRX Show and those of you who have seen videos or pictures from the latest New York City Marathon, should actually have been able to infer it from the way the "finishers" looked like. Intensity not duration is what counts, when doing "cardio". Yet, as a very recent (7 days old) study shows (Naito. 2011), High Intensity Training (HIT) will not only burn off your lovehandles, while keeping your muscles intact, it will also prime your musclefibers for future growth by increasing the number of satellite cells, the small dormant mononuclear progenitor cells that are sandwiched between the basement membrane and sarcolemma of the fibers of your muscle and are recruited, whenever your body feels that you could use a little more or have to replace some damaged muscle mass.

While I will go into more detail on how your muscles actually grow in the upcoming parts of the Intermittent Fasting Series, in the course of which I am going to explain how you should train, eat and sleep in order to exploit all three major pathways of skeletal muscle growth, I want to give you a sneak peak at what you are going to learn, by highlighting that protein synthesis, i.e. the accrual of muscle protein in existing myonuclear domains, and the recruitment of satellite cells to replace damaged or add new myonuclei are distinct processes. It should nevertheless be obvious that with all the protein synthesis of the world you will - sooner or later - hit a plateau, when all the existing myonuclei have "blown up" to their maximal size - or as Naito et al. put it: "Increases in the number of satellite cells are necessary for full skeletal muscle growth and hypertrophy" So, whenever the existing myonuclei have reached their "full potential", the only way to keep growing is by adding new myonuclei via satellite cell recruitment. Keep that in mind before you discard the results the following study, because the "HIT rats" did not gain more "active" muscle than the "LIT rats" ;-)

In their experiment Hasashi Naito and his colleagues from the Tokai University and the Juntendo University in Japan put 17-week old (these are old rats!) female Sprague-Dawley rats on one out of four exercise regimen (for a detailed outline of the regimen, cf. table 1):

1. High Intensity, High Duration (90H)
2. High Intensity, Low Duration (30H)
3. Low Intensity, High Duration (90L)
4. Low Intensity, Low Duration (30L)

Table 1: Outline of the exercise
protocol (from Naito. 2011)

In the course of the 10-week study period the rats were exercised five times a week on one of those funky rodent treadmills. What's funny is that despite the fact that, as the scientists say, "[e]lectrical shocks were used sparingly to motivate the animals to run", two of the critters in the high intensity groups refused to do their workouts, which reminds me of what Dr. Layne Norton had to say on one of the past installments of BodyRX Radio: "Most of those who will tell you that they cannot do HIT for whatever reasons are usually just too lazy" - we may thus consider those two lazy rats as evidence for the accuracy of the model... and by the way, it did not save them from being anesthetized and deprived of their plantaris muscle, which was weighed and analyzed for its fiber composition and satellite cell count.

As it was to be expected in view of the high age of the rats, where skeletal muscle mass maintenance, may be considered a success, there were no statistically significant increases in plantaris and/or body mass in any of the treatment groups.

Figure 1: Changes (compared to untrained control) in number of myonuclei and satellite cells per muscle fiber (data calculate base on Naito. 2011)

Despite the absence of measurable skeletal muscle hypertrophy, the pronounced (cf. figure 1) and fiber-type specific (cf. figure 2) increases in satellite cell counts in the high intensity groups may well be considered as the necessary prestage of a hypertophic growth spurt, which could be triggered by appropriate training (which would obviously be strength training) and endocrine (more on that in the conclusion) stimuli.

Figure 1: Satellite cells per muscle fiber in type I (slow twitch) and type II (fast twitch) muscle fibers of rats in the control and the high intensity, high duration (90H) groups (data calculate base on Naito. 2011)

In that, it is also interesting to note that contrary to popular believe, the slow-twitch type I fibers, with their greater number of satellite cells, have an increased propensity for maximal myonuclear numbers, the fable of the "hypertrophy-prone fast-twitch type II" fibers, on the other end, is a consequence of their ability to accumulate more protein per myonucleus. And while I will - as promised in the red box above - dig deeper into that in future installments of Sunday's Intermittent Thoughts, I can already tell you that the fiber composition (not the size!) of professional body builders is almost identical to those of non-strength-trained individuals and thusly fundamentally different from that of strength athletes, like powerlifters (Tesch. 1982) - in order to achieve maximal muscularity you can thusly not neglect your type I fibers!

That being said, both the strength training, which would make use of the increased propensity to grow by recruiting satellite cells to form new myonuclei, as well as the necessary local IGF and MGF responses, which have been shown to decrease with age (Grounds. 2002), were absent in the study at hand. In someone like you, a young, vigorous strength trainee, both stimuli will yet obviously be present in abundance (at least I would hope so ;-). Accordingly, 1-3 high intensity (and in view of the fact that the duration, 30 vs. 90min, did not make a difference probably also high intensity interval) training (HIT or HIIT) sessions per week could not only make your increasingly fat-free muscles shine in their full glory, they will also "precondition" you for future muscle growth by increasing your satellite cell pool. I would thus suggest, you better not join the two lazy rats from the study, and rather find yourself the next best track to do a bunch of sprints ;-)

To Fail or Not to Fail - 5x10 or 10x5? The Energetic Demand of Your Workouts Doesn't Depend on Workloads, Alone

Image 1: PCr, ATP, whatever as long as there was energy left, Arnold kept pumping iron (pun intended ;-)

"To fail or not to fail", this question is probably about as ancient as the hilarious idea to engage in physical activity that is not in one way or another directly related to one of our two most fundamental needs, survival and procreation. Researchers from the Physical Education Department at the Sport Sciences University of the Basque Country and the Department of Health Sciences at the University of Navarra in Spain have recently examined this question from a slightly different angle than most of the articles you have probably seen in and on the various muscle mags and bodybuilding related websites on the Internet. What Esteban M. Gorostiaga and his colleagues wanted to know was:

Are There Significant Differences in Energy Metabolism When you Train to Failure?

Or, put another way: Does it make a difference if you fail from a molecular energetic point of view or is the mere number of reps the most fundamental determinant of the changes in muscle adenine nucleotides, inosine 59-monophosphate (IMP), phosphocreatine (PCr), creatine (Cr), lactate and energy charge during a workout. To answer this question the researchers recruited 6 healthy male volunteers (age 28-40y; BMI 23.3kg/m²; 1-RM_max on unilateral leg press 199+/-43kg) and had them perform a total of 50 repetitions with the same initial load (83% of 1-RM) on two separate occasions, either

• performed to failure, as a quintette of 5 x 10 (sets x reps), or
• stopped before failure, in a 10 x 5 fashion.

On both occasions the subjects rested 2 minutes between the sets. Furthermore, Gorostiaga et al. tried to eliminate "confounding factors", by equating the values of several variables such as initial load and total number of repetitions between both exercise sessions and making sure that whenever a "subjects could not lift the initial load during the following sets due to fatigue" the load was decreased by 15kg until the respective subject was able to complete all 50 repetitions (Gorostiaga. 2012).

Figure 1: Peak power output profiles (average for n=6 subjects) for each exercise during the two experimental conditions: when exercise was 5 sets of 10 repetitions to failure (10REP; open circles), and when exercise was 10 sets of 5 repetitions not to failure (5REP; filled circles; adapted from Gorostiaga. 2012)

It is plain to see from the data in figure 1 that performing all sets to failure (open circles) lead to a significant reduction in total workload (the area under the peak powder curve):

During 5REP all the subjects were able to complete all the repetitions with the initially load assigned (154+/-31 Kg; 83+/-8% of 1RM). During 10REP, however, most of the participants were unable to complete all the repetitions with this starting load, due to failure. The load had to be reduced by 7.2+/-3.8% after 27+/-16 repetitions and was progressively reduced, reaching 85+/-12%(P,0.05) of the initial load at the last repetition. Average load during the 50 repetitions of 10REP was 6.1+/-6.3% lower (P<0.05) than during 5REP. (Gorostiaga. 2012)

If we examine the graph further there are a couple of other interesting things to observe, though:

• the 2nd-3d rep was the one with the maximal power - so much about the value / validity of 1-RM maximum strength tests, then ;-)
• the power progressively declined from the 3rd rep on (35-45%) and that with an astonishing dip after the 5th rep - maybe because subjects are used to do 5 reps, so that this could also be a psychological factor
• while not training to failure with 10 sets of five reps allows to maintain almost identical average peak power on all sets, training to failure with 5 sets of 10 reps resulted in a net reduction of 33% from 812Watts on the first to 569 Watts on the last set
• the average peak power per set was accordingly 28% lower, when the participants trained to failure

What's the "energy charge"? The energy charge was calculated as the quotient of (ATP + 1/2 ADP)/(ATP + ADP + AMP) and does thus quantify the ratio of usable to used energy in the muscle samples.

Yet while the average mean power output changes paralleled those of peak power output in both experimental conditions, the opposite was the case for the aforementioned muscle metabolites - muscle adenine nucleotides, inosine 59-monophosphate (IMP), phosphocreatine (PCr), creatine (Cr), lactate and energy charge - the scientists measured by high-performance liquid chromatography from the muscle biopsies they had taken from the right legs of the subjects on each occasion.

Is light training an option, at all?

Very much in accordance with the subjective experience of many trainees, the data in figure 2 appears to confirm that working out to failure does induce muscular exhaustion, which manifests in the form of physically quantifiable changes in muscle metabolites in the training to failure group

• almost depleted PCr stores in the failure group (85% fall, P<0.05), and 
• reduced ATP (-21%), energy charge (-4%), and  
• reduced adenine nucleotides pool (-20%; ATP + ADP + AMP), in the presence of
• increased IMP (+8600%) and lactate (+1400%) levels

Which stand in stark contrast to the mediocre decrease in of phosphocreatine, the almost unchanged muscle ATP, IMP, energy charge and adenine nucleotide pool and comparatively marginal elevations in blood lactate in the 10 x 5 non-failure group.

Figure 2: Changes in ATP, ADP, AMP, phosphocreatine (PCr) inosine monophosphate (IMP) and lactate from pre to post workout in the 5 x 10 (failure) and the 10 x 5 (no failure) session (data calculated based on Gorostiaga. 2012)

As far as the correlation between these markers and the actual power output during the workout are concerned, the scientist say that they observed a ...

Figure 3: Relationship between muscle lactate concentrations and average peak power (from Gorostiaga. 2012).

• significant linear negative correlation (R²=0.59) was observed between the average changes in peak power output observed during the last two repetitions (expressed in percent of the initial two repetition values) and the decreases in ATP levels (expressed in percent of initial value).
• significant curvilinear negative correlation between the average peak power output changes observed during the last two repetitions of the first and last sets (expressed in percent of the initial two repetition values) and the corresponding levels of muscle lactate. 

From the curvilinear nature of this relationship (see figure 3) Gorostiaga et al. conclude that "when muscle lactate levels do not exceed the upper limit of 10–15 mmol/kg wet muscle, power output changes little from maximum values". The exact opposite is yet the case, when the lactate values exceed this critical upper value and the power output begins to decrease sharply.

Image 2: While training like a sissy will at best produce suboptimal results, maxing out on every set of every workout will work for max. 2-3 weeks until you will not just lose the gains you may have made but end up weaker and with less muscle in the hospital, when an injury or total burn-out forced you to finally see reason. Going to failure on one the last set of a selected exercise for each body group may be a way smarter, safer and more productive way. Combine that with planned 3-RM tests to gauge your strength progress and you should see some nice gains and can keep track of your strength gains without risking burn-out or injury and trust me this has little to do with being a sissy!

Implications: At first sight you may certainly argue that the study does not provide much novel information. If you do however compare the main results to common wisdom about various strength training regimen, the total depletion of the phosphocreatine stores in the "higher" rep group and the increase in IMP levels, of which Gorostiaga et al. rightly argue that they reflect the failure of ATP resynthesis to match ATP hydrolysis rates and eventually feed into the uric acid cycle (as reflected by the 19% increase in the failure group) put an emphasis on the often underestimated energetic and metabolic demand of training to failure. In this context, the pronounced loss of purines from the muscle, as it has also been observed by Hellsten et al. subsequent to profoundly lowered ATP levels in the course of a one-legged HIIT protocol on a cycle ergometer (Hellsten 1999), and the subsequent extraction of urate from the blood by the muscle to restore intramuscular urate levels (remember: urate acts as a free-radical scavenger during intense exercise; cf. Hellsten. 1997) may well be an overlooked factor, when it comes to assessing exercise recovery.

Still, while the former would suggest that you better avoid training to failure altogether and simply hit the gym for a "light" 10 x 5 workout everyday, the minor reduction in PCr (-15% vs. -80%) and the non-existent rise in plasma lactate and urate (no stress = no adaptation?) do indicate that frequent light training session will probably not result in the desired, or at least suboptimal muscular adaptations, which are the physiological bases for the strength and size gains, you are looking for (read all about "The Physiology of Building Muscle"). Moreover, the almost unchanged ATP/ADP ratio (see figure 3), which is the gauge by which AMPK works (cf. "Zoning in on AMPK"), could be the reason why many of the "sissy workout" studies report that strength training would not have the same / any beneficial effect on glucose tolerance, lipid levels and all the other standard parameters of metabolic health scientists usually measure in those trials.

Bottom line: While it is almost certain that you will out-train your own recovery potential by going to failure on every set of every workout, the results of this study put an emphasis on the fundamental difference between physical workloads and their immediate physiological effects (just a reminder, the workload, i.e. weight lifted x reps was identical for both groups). What we are still lacking to derive concrete reliable workout tips from data like this, though, are clear-cut mechanistic or at least probabilistic relationships between the short term effects of and the long-term adaptation to different workout regimen and their respective energetic demands... ah, and by the way, this goes for the incredible popular measurements of post-workout protein synthesis, as well. Until now, no-one can say how much predictive value temporary increases in fractional muscle protein synthesis actually have in terms of long(er) term muscle gains.

References:

• Gorostiaga EM, Navarro-Ame´zqueta I, Calbet JAL, Hellsten Y, Cusso R, et al. (2012) Energy Metabolism during Repeated Sets of Leg Press Exercise Leading to Failure or Not. PLoS ONE 7(7): e40621. 
• Hellsten Y, Tullson PC, Richter EA, Bangsbo J. Oxidation of urate in human skeletal muscle during exercise. Free Radic Biol Med. 1997;22(1-2):169-74.
• Hellsten Y, Sjodin B, Richter EA, Bangsbo J (1998) Urate uptake and lowered ATP levels in human muscle after high-intensity intermittent exercise.Am J Physiol 274: E600–E606.

Work Out 'Till You Drop: After 1h+ of Intense Exercise or an Energy Equivalent of >800kcal Leptin Begins to Plummet!

Image 1: Losing consciousness is very different from losing body fat and while the former may require "burning" more than 800kcal, the latter does not.

Sometimes you read an abstract like that by Mahmoud Hesar Koushki et al. and think "Hmm... that sucks!" Then, you come to think about it and realize "Yeah! That really sucks!" And the thing that sucks in this particular case is the message studies like that are sending out to the public, when they end on statements like "Rising the energy costs of the exercise through increasing the exercise duration, can be one of the factors affecting negative energy balance, leading to positive changes in leptin concentrations." (Hesar Koushki. 2012).

What's good for your obese neighbor...

... must not be good for you! I know, I am repeating myself here, but in view of the fact that my voice obviously has not been heard in Iran, as of yet, I will repeat my novel mantra as often as it takes for people to get it into their stup... ah, I mean stubborn heads and stop sending healthy people into misery.

Figure 1: This is what the study particpants in the Hesa Koushki study had to endure - a "exhaustion exercise session" on the treadmill (Hesar Koushki. 2012)

A good way to achieve that is known as "exhaustive running session" (cf. figure 1), but as you have heard before was still "insufficient" to induce significant decreases in leptin levels in the 23 male students (age 19.58 ± 2.12 yr, BMI 1.63 ± 2.7 kg/m²) who volunteered to participate in this study (cf. figure 2):

Figure 2: Serum leptin, insulin, blood glucose, cortisol and lactate levels of young healthy, but untrained men before and after exhaustive exercise session (Hesar Koushki. 2012)

But what does that tell us? If we were dealing with women, it would probably mean that this type of exercise was insufficient to induce amenorrhea (Chou . 2011), that, when performed once(!), it was not excessive enough to induce a profound enough starvation signal to trick the bodies of athletes or gymrats to believe that they were running the risk of becoming underweight (Köpp. 1997) and that it was not the first step towards muscle and bone loss (Kaufman. 2002). But does this mean that it's safe and effective?

When much is not yet too much, more must not be better either!

Figure 3: If you don't want to burn more energy, more glucose, more fat, and reduce your intramuscular and liver triglyceride stores to ramp up insulin sensitivity and ward off NAFLD, you better stick to 60min+ exercise and 800kcal+ energy expenditure per workout - without eating any carbs, at all, of course! After all, those could negate these "beneficial effects" *sarcasm mode off!*

If we apply standard paradigma of "working out to lose weight" to the finding that short-term intense exercise with an energy expenditure way below 800kcal did not reduce circulating leptin levels and switch off our brains, the (un!)reasonable conclusion would be that

"According to the findings of this study [...] exercise longer than 60 minutes with energy expenditure higher than 800 kcal can be recommended for the reduction of leptin concentration in non-athletes." (Hesar Koushki. 2012)

If we use our brains, though, the take home message would be very different an should rather read like:  "NEVER! Expend more than 800kcal in one workout if you are not leptin resistant and want to make sure that you don't forestall fat loss and mess up your endocrine system." (Dr. Andro ;-)

Fat loss training for non-obese individuals should focus on keeping leptin levels steady!

Once you acknowledge the importance of normal leptin levels for fat loss and overall metabolic health in lean, not leptin resistant individuals, the same review (Bouassida. 2010) the Iranian scientists cite to support their (misleading!) conclusion that it would be basically nonsensical to do intense short bouts of exercise, since those do not reduce circulating leptin levels has to be interpreted in a completely different way.

Just as the complete failure to produce insulin would not just hamper your gains, but have you literally shrivel away, lowering leptin levels in an already lean, if not very lean individual even further will sooner or later whack your metabolism and endocrine system (infertility, low testosterone, amenorrhea, you name it...). Not to mention that you will obviously not be able to derive any of the metabolic benefits of adequate leptin levels and receptor activity (figure 3).

So what can or must be done to keep healthy leptin levels and sensitivity?

Lean, athletic individuals should thus focus on shorter (below 1h), intense and glycolytic workouts (HIIT, lifting weights) and regenerative 'cardio' work in the << 800kcal energy expenditure range and make sure that they...

• get enough sleep - even a moderate sleep debt will increase the production and systemic circulation of TNF-alpha and IL-6 and reduce the expression of adiponectin and leptin in the adipose tissue (Padilha. 2011)
• strategically cycle & refeed on carbohydrates - it stands out of question that a reduction in carbohydrate intake is an effective means to get rid of body fat, but it will work optimally only, if you strategically cycle (higher carb intake on workout, lower carb intake on non-workout days) your carbohydrate intake, integrate regular refeeds (with a 20% caloric deficit every other week) and always eat as much green leafy veggies as it takes to fill you up without ever counting their quasi non-existent carbohydrate content

And while there is some evidence (Teta. 2007, Rodríguez-Carmona. 2012) that would suggest that sodium bicarbonate (baking soda, NaHCO3) to counter the reduction in leptin expression and the use of 12g of ALCAR /day to increase leptin sensitivity (particularly, in older people; cf. Iossa. 2002) could help, as well. Working and eating right for your current metabolic needs will always be the most important factors.

References:

1. Bouassida A, Chamari K, Zaouali M, Feki Y, Zbidi A, Tabka Z. Review on leptin and adiponectin responses and adaptations to acute and chronic exercise. Br J Sports Med. 2010 Jul;44(9):620-30.
2. Chou SH, Chamberland JP, Liu X, Matarese G, Gao C, Stefanakis R, Brinkoetter MT, Gong H, Arampatzi K, Mantzoros CS. Leptin is an effective treatment for hypothalamic amenorrhea. Proc Natl Acad Sci U S A. 2011 Apr 19;108(16):6585-90. Epub 2011 Apr 4. 
3. Coope A, Milanski M, Araújo EP, Tambascia M, Saad MJ, Geloneze B, Velloso LA. AdipoR1 mediates the anorexigenic and insulin/leptin-like actions of adiponectin in the hypothalamus. FEBS Lett. 2008 Apr 30;582(10):1471-6.
4. Digby JE, McNeill E, Dyar OJ, Lam V, Greaves DR, Choudhury RP. Anti-inflammatory effects of nicotinic acid in adipocytes demonstrated by suppression of fractalkine, RANTES, and MCP-1 and upregulation of adiponectin. Atherosclerosis. 2010 Mar;209(1):89-95. .
5. Hesar Koushki M, Hamedinia M, Mollanovruzi A. The response of plasma leptin and some selected hormones to one session of progressive running in non-athlete males. Iranian Journal Of Health And Physical Activity, 2012:3(1).
6. Iossa S, Mollica MP, Lionetti L, Crescenzo R, Botta M, Barletta A, Liverini G. Acetyl-L-carnitine supplementation differently influences nutrient partitioning, serum leptin concentration and skeletal muscle mitochondrial respiration in young and old rats. J Nutr. 2002 Apr;132(4):636-42. 
7. Kaufman BA, Warren MP, Dominguez JE, Wang J, Heymsfield SB, Pierson RN. Bone density and amenorrhea in ballet dancers are related to a decreased resting metabolic rate and lower leptin levels. J Clin Endocrinol Metab. 2002 Jun;87(6):2777-83. 
8. Köpp W, Blum WF, von Prittwitz S, Ziegler A, Lübbert H, Emons G, Herzog W, Herpertz S, Deter HC, Remschmidt H, Hebebrand J. Low leptin levels predict amenorrhea in underweight and eating disordered females. Mol Psychiatry. 1997 Jul;2(4):335-40.
9. Padilha HG, Crispim CA, Zimberg IZ, De-Souza DA, Waterhouse J, Tufik S, de-Mello MT. A link between sleep loss, glucose metabolism and adipokines. Braz J Med Biol Res. 2011 Oct;44(10):992-9. Epub 2011 Sep 2.
10. Punyadeera C, Zorenc AH, Koopman R, McAinch AJ, Smit E, Manders R, Keizer HA, Cameron-Smith D, van Loon LJ. The effects of exercise and adipose tissue lipolysis on plasma adiponectin concentration and adiponectin receptor expression in human skeletal muscle. Eur J Endocrinol. 2005 Mar;152(3):427-36. 
11. Rodríguez-Carmona A, Pérez-Fontán M, Guitián A, Peteiro J, García-Falcón T, López-Muñiz A, García-Buela J, Cordido F. Effect of low-GDP bicarbonate-lactate-buffered peritoneal dialysis solutions on plasma levels of adipokines and gut appetite-regulatory peptides. A randomized crossover study. Nephrol Dial Transplant. 2012 Jan;27(1):369-74.
12. Teta D, Maillard M, Tedjani A, Passlick-Deetjen J, Burnier M. The effect of pH-neutral peritoneal dialysis fluids on adipokine secretion from cultured adipocytes. Nephrol Dial Transplant. 2007 Mar;22(3):862-9.
13. Wolkowicz P, Grenett H, Belousova M, Urthaler F. Activation of leptin expression by an inhibitor of carnitine palmitoyltransferase-1. Int J Obes Relat Metab Disord. 2004 Apr;28(4):649-51.

HIT the Cravings - Eat Less, Improve Your Health & Lose Weight: "Burning 350kcal" at >75% VO2-Max Improves Calorie Balance Doing it at 40% Just Makes You Hungry!

Image 1: Even if the boys in the study at hand still ate "more calories than they expended", HIT would certainly slow their progress from the healthy kid in the left to the obese and more importantly unhealthy one on the right.

Have you ever wondered why the Biggest Losers do survive their almost zero calorie diets? Well, a recent study from the France could well hold the answer (Thivel. 2012): Their intense and often temporarily totally exhausting exercise regimen! "What? That insane cardio + whatever you may call that torture 12h/day ..." - I see you are surprised, because in essence most of the stuff they do appears to (and actually is) totally idiotic. I am however not growing tired of repeating that even taking the stairs easily turns into an high intensity exercise if you have to carry a 200lbs apron of fat from the ground- to say the third floor. If you don't believe it, do 50 lunges with 200lbs and tell me that this ain't "high intensity" ;-)

HIIT holds the key to health and satiety... and that is probably why it facilitates weight loss!

When I think about it, for a morbidly obese person, taking the stairs could in fact be even more intense than the 75% VO2Max high-intensity cycling protocol the 15 obese boys (age 13.5y; BMI: 30.7; waist: 104.3cm; fat mass 38.2%) from the Pediatric Obesity Department of the Children’s Medical Center of Romagnat (France) performed at roughly 3h after ingesting a standardized breakfast, the caloric content of which was matched to the calculated energy expenditure, i.e. rest + exercise-induced (the boys had to cycle until they had performed a workload equivalent to ~350kcal) of the entire morning in order to isolate the effect of exercise intensity from that of energy status on subsequent energy intakes at launch and dinner, as well as macronutrient pereferences, energy expenditure and appetite sensation, which were the other dependent variables, David Thiel and his colleagues recorded after the aforementioned high intensitiy and separate (7-days washout) low intensity (40% VOMax, again 350kcal) exercise and sedentary control conditions.

Figure 1: Energy intake, expenditure and balance of the boys in the three test sessions (calculated based on

If, for the time being, we disregard the beneficial health effect any type of physical activity will have over just sitting around pondering which of those foods in front of you contain "good" and which contain "bad" calories, the (statistically non-significantly) increased "energy balance" in the low intensity exercise condition (cf. figure 1) does in fact confirm Dr. Oz' somewhat skewed summary of Garry Taubes' statement that exercise would "just make you hungry". The statistically significant reduction in energy intake (-6%, p<0.05) and the even more profound decrease (-25%, p<0.01) of the 24h "energy balance" in the high intensity exercise condition, on the other hand, support the (fortunately) evermore popular notion that short and intense exercise sessions, not daily marathons in the "fat burning" zone, are the ideal complement to any dietary intervention that is targeted at loosing weight and improving metabolic and overall health (suggested read: Previous news on HIT / HIIT)

A brief note on the notion of  "dietary interventions": For15 year old boys who habitually consume >3500kcal/day any "dietary intervention" to prevent them from morbid obesity, diabetes and all the other ailments by which large parts of the Western society is plagued, must inevitably include a reduced calorie intake! While the importance of the daily "energy balance" is certainly overblown and any holistic diet + exercise + lifestyle intervention should be designed to induce a natural, satiety-induced reduction in energy intake by combining a reasonable amount of intense exercise with a nutrient-dense diet like, but not necessarily identical to a low-, but - in most cases - better not no-carb "Paleo Diet", complete ignorance towards the amount of food you consume will inevitably compromise your results - no matter how "good" the calories you are consuming may be.

In this context, it is also noteworthy that the reduction in calorie intake in the HIT trial was more pronounced at dinner than at launch and that the non existent differences between the ratings of subjective hunger, fullness or prospective food consumption in the three experimental sessions, cannot be accounted for by changes in the macronutrient composition of the subsequent ad-libitum meals, which were equally "identical" (within statistical margins, obviously) for the high intensity, low intensity and sedentary control session.

Hard and short = full and happy - what more can you ask for?

Image 2: I guess if parents were better role-models and encouraged their children to exercise (with them), childhood obesity would not be such a huge problem, anyways.

If you look for the underlying reason for the voluntarily reduced energy intake in the high intensity exercise condition of the study at hand, the results of another recently published paper by Balaguera-Cortes et al. comes to mind (Balaguera-Cortes. 2012), in which 10 "active" men completed 45min of either aerobic or resistance training in a similar counter-balanced fashion. When the scientists measured the exercise-induced hormonal changes, they found significantly lower levels of the "hunger hormon" ghrelin in the resistance compared to the aerobic exercise condition. Interestingly, though, the energy intake of these normal weight subject at a subsequently provided breakfast buffet was identical in both conditions.

While the very different exercise stimuli of HIT (Thiel study) and HIIT, on the one hand, and resistance training (Belaguera-Cortes study), on the other hand, could account for the differential effects on subsequent energy intake and would thusly support the notion that resistance training alone is not sufficient to induce significant reductions in body weight.  

I feel that further research is needed to establish, the influence of being obese or lean and/or being used to overeat vs. eating at maintenance exerts on the resistance exercise-induced increase in energy intake and the long-term effects of the latter not on body weight, but body composition.